Ms Info Health Professionals

Multiple sclerosis information
for health and social care professionals

MS: an overview
Diagnosis
Types of MS
Prognosis
Clinical measures
A multidisciplinary approach to MS care
Self-management
Relapse and drug therapies
Relapse
Steroids
Disease modifying drug therapies
Symptoms, effects and management
Vision
Fatigue
Cognition
Depression
Womens health
Bladder
Bowel
Sexuality
Mobility
Spasticity
Tremor
Pain
Communication and swallowing
Pressure ulcers
Advanced MS
Complementary and alternative medicine
Index
Fourth Edition
Acknowledgements
Acknowledgements
The MS Trust is extremely grateful to all those who

freely gave their expertise, work and time to this
publication.
Steven Bloch, PhD MRCSLT
Lecturer, Division of Psychology and Language
Sciences, University College London.
Sarah Callin, MBBS MRCP(UK)
Consultant in Palliative Medicine, St.Catherines
Hospice, Scarborough.
Maureen Coggrave, PhD MSc RN
Clinical Nurse Specialist, The National Spinal
Injuries Centre, Stoke Mandeville Hospital Senior
Lecturer, Buckinghamshire New University.
Angela Davies Smith, MCSP SRP PGCE
Clinical Specialist Research Physiotherapist, MS
Research Unit, Frenchay Hospital, Bristol.
Verity Dods, MSc BN(Hons) RN
MS Specialist Nurse, Surrey Community Health,
Horley, Surrey.
Nikki Embrey, MSc
Clinical Nurse Specialist (Multiple Sclerosis),
University Hospital of North Staffordshire NHS
Trust, North Midland MS Service.
Gavin Giovannoni, MBBCh PhD FCP(Neurol) FRCP
FRCPath
Professor of Neurology, Blizard Institute, Barts and
The London School of Medicine and Dentistry.
Simon Hickman, MA PhD FRCP
Consultant Neurologist, Royal Hallamshire Hospital,
Sheffield.
Amanda Howarth, PhD RGN BMedSci(Hons)
MSc (Pain Management) Senior Lecturer (Pain),
Faculty of Health and Wellbeing, Sheffield Hallam
University, Sheffield.
Dawn Langdon, MA MPhil PhD AFBPS C Psychol
Professor of Neuropsychology, Royal Holloway,
University of London.
Christine Norton, PhD MA, RN

Professor of Clinical Nursing Innovation, Imperial
College Healthcare and Bucks New University,
London, Nurse Consultant (Bowel Control)
St Marks Hospital.
Jalesh Panicker, MBBS MD DM MRCP(UK)
Consultant Neurologist in Uro-Neurology at the
National Hospital for Neurology and Neurosurgery,
Honorary Senior Lecturer at the UCL Institute of
Neurology, Queen Square, London.
Hugh Rickards, MD FRCPsych
Consultant in Neuropsychiatry, Hon. Reader in
Neuropsychiatry, National Centre for Mental
Health , Birmingham.
Helmut Roniger, MMed(RSA) Dipl Acup FFHom
Consultant Physician, Royal London Hospital for
Integrated Medicine, UCLH, London.
Francoise Schyns, MSc (Pain), MCSP
Senior Physiotherapist, Revive MS Support,
Maryhill, Glasgow.
Vicky Slingsby, BSc(Hons)
MS Specialist Occupational Therapist, Poole
Hospital, Poole, Dorset.
Christina Smith, PhD MRCSLT
Lecturer, Division of Psychology and Language
Sciences, University College London.
Martin Steggall, PhD MSc BSc(Hons) RN PG Cert
Academic Practice Clinical Nurse Specialist (erectile
dysfunction), Barts and The London NHS Trust.
Valerie Stevenson, MBBS MD MRCP
Consultant Neurologist and Lead of the Spasticity
Service, National Hospital for Neurology and
Neurosurgery, Queen Square, London.
Kate Watkiss, RGN RM BSc(Hons)
Multiple Sclerosis Specialist Nurse, Shrewsbury and
Telford Hospitals NHS Trust.
Denise Winterbottom, BSc(Hons)
MS Specialist Nurse, Salford Royal Hospital,
Salford.
Alison Nock, DipCOT

MS Specialist Occupational Therapist, Poole
Hospital, Poole, Dorset.
www.mstrust.org.uk
Multiple sclerosis information for health and social care professionals

Contents
Contents
Section 1
Section 2
Section 3
Section 4
Introduction
MS: an overview
Diagnosis
Types of MS
11
Prognosis
12
Clinical measures
13
17
Self-management
19
22
Relapse
22
Steroids
24
24
Beta interferons and glatiramer acetate
26
Natalizumab
27
Fingolimod
28
Mitoxantrone
29
Disease modifying therapies currently in clinical trials
30
34
Vision
34
Fatigue
36
Cognition
39
Depression
41
Womens health
44
Bladder
47
Bowel
53
Sexuality
59
Mobility
62
Spasticity
66
Tremor
70
Pain
72
75
Pressure ulcers
77
Advanced MS
80
Complementary and alternative medicine 83

Index
telephone 01462 476700
83
90
MS: an overview
Introduction
Introduction
This fourth edition of Multiple sclerosis information for
health and social care professionals has been compiled
by the MS Trust with the help of specialist health and
social care professionals, and people affected
personally by multiple sclerosis (MS). The aim of the
book - and of the MS Trust - is to improve the level of
understanding of MS amongst those who work with,
and care for, people who have the condition. We
recognise the challenge that MS presents for
professionals but hope that professionals will also
acknowledge the challenge for a person receiving a
diagnosis of MS, knowing that they will live for the
rest of their life with the condition, yet having no idea
how it might progress.
The ambition of this book is to:
offer an overview of MS
provide a resource for professionals who work

with people with MS
the provision of equipment and accommodation
the provision of personal care and support
palliative care to enable people to make

choices about end of life care
support for families and carers
the provision of seamless, responsive services.
How successful has implementation of these

principles been? The MS Trust, in partnership with
the Royal College of Physicians, has now carried out
three national audits of NHS MS services in England
and Wales. The findings show real progress with the
development of specialist centres but little progress
with regard to access to rehabilitation, the provision
of equipment, access to palliative care, or joined up
services. Much work clearly remains to be done and
we hope that this publication will support the
professionals who can help to change the situation
and improve the management of MS.
The arrival of disease modifying drugs in the UK

goes back to 1995. NICE assessed the drugs in
2002 and following this the Department of Health
answer some of the questions about the
Risk-sharing Scheme was set up also in 2002. The
management of MS and its symptoms
UK has however been slow to adopt the disease
modifying drugs into routine practice and we still
offer directions for further information through
lag well behind the USA and Europe. The
references and bibliographies.
Department of Health Risk-sharing Scheme allows
There have been two national documents that should all people eligible for the four original disease
have impacted on the management of MS in the UK. modifying drugs to be treated within the NHS and
The first of these was Multiple sclerosis: management of the Scheme has also been the catalyst for the
establishment of specialist centres and a significant
multiple sclerosis in primary and secondary care issued
increase in the number of MS specialist nurses. The
by the National Institute for Health and Clinical
long-term cost efficacy data is being collected and
Excellence (NICE) in 2003. The second was the
analysed on an ongoing basis.
National Service Framework for long-term conditions
launched in 2005. Both documents enshrined
Two further drugs have also been licensed:
principles for good management which included:
natalizumab for people with highly active relapsing
remitting MS and fingolimod for people with rapidly
the provision of person centred services
evolving severe relapsing remitting MS or with high
disease activity despite treatment with a beta
early recognition, prompt diagnosis and
interferon. In both cases these drugs offer a greater
treatment from specialised services
reduction of relapses than the original disease
modifying drugs but have more complex side effects.
emergency and acute management
Further drugs are also in research and development.
early and specialist rehabilitation
MS the disease remains poorly understood by
commissioners and NHS managers. The complexity
community rehabilitation and support
of the condition and the management strategies
means that MS will remain a condition managed in
vocational rehabilitation
partnership between specialist centres and MS
specialist nurses alongside the primary care teams.
www.mstrust.org.uk
Multiple Sclerosis Information for Health and Social Care Professionals

MS: an overview
Section 1
Joined up services to address both health and
social issues are an aspiration for the future.
MS: an overview
Further resources
National Institute for Health and Clinical
Excellence. Multiple sclerosis - management of
multiple sclerosis in primary and secondary care.
NICE Clinical Guideline 8. London: NICE; 2003.
Excellence. Multiple sclerosis - beta interferon and
glatiramer acetate for treatment of multiple
sclerosis. NICE Technology Appraisal Guidance No.
32. London: NICE; 2002.
Department of Health. Cost effective provision of
disease modifying therapies for people with
multiple sclerosis. Health Service Circular
(2002/04) London: Stationery Office; 2002.
Department of Health. The National Service
Framework for long-term conditions. London:
Department of Health; 2005.
Royal College of Physicians, MS Trust. NHS services
for people with multiple sclerosis: a national
survey. London: RCP; 2006, 2008, 2011.
100,000 people in the UK are estimated to have

multiple sclerosis (MS), a chronic neurological
disorder and the most common cause of
neurological disability in young adults1. It is
sometimes benign, frequently remitting, but often
progressive with gradually increasing disability.
Although that disability will vary, the uncertainty
and unpredictability is universal. For most, MS does
not have a significant effect on life expectancy but
for some it may mean facing 50 years of disability
and distress.
Multiple sclerosis was first described in the 1860s by
the French neurologist Jean Martin Charcot yet for
virtually a century little research was carried out into
the condition. Despite much research over recent
years the cause of MS is as yet unproven and the
cure remains elusive. However, much can be done
to manage symptoms and, with the advent of
disease modifying drugs, it is believed that
incremental disability may be slowed.
Good management of MS is a huge challenge to
health and social care professionals because the
disease course is unpredictable, symptoms endlessly
variable and the psychosocial consequences can
impact as profoundly as the physical symptoms. MS
affects all aspects of life, work, social and family life.
People continually have to readapt to changes in
their condition and live with a lifetime of
uncertainty that multiple sclerosis brings. For this
reason, a holistic approach, with the person with
MS and their family at the centre of managing MS,
is essential.
Prevalence
MS is the most common condition of the central
nervous system (CNS) which is made up of the
brain and spinal cord. It is generally diagnosed
between the age of 20 and 40, with women
outnumbering men in a ratio of about 3:12. Though
MS can be diagnosed in very young children and in
people over 65, this is unusual3.
Areas of low, medium and high prevalence of MS
can be identified. It is commonest in temperate
countries (50-120/100,000) decreasing with
proximity to the equator (<5/100,000)4. In the UK,
prevalence is approximately 100-140 per 100,0005
MS: an overview
MS: an overview
in England and Wales. This figure is higher still in

Scotland, especially Shetland and Orkney, where
the highest known prevalence, 200 per 100,000 has
been recorded5.
Putting MS risk in context
1 in 700 people will develop MS
1 in 40 people will develop MS if they have

a first degree relative with the condition
(parent, sibling)
1 in 3 people will develop some form of cancer
1 in 22 people have chronic heart disease
1 in 33 people have diabetes
1 in 500 people have Parkinsons Disease.
Cause
The cause of MS remains unproven, but the
evidence is pointing toward a complex interplay of
epigenetic, environmental and genetic factors that
provoke the immune system to produce an
autoimmune inflammatory response characterised
by transient attacks on those cells that form myelin.
Over time axonal loss and neurodegeneration leads
to accruing disability.
This loss and degeneration starts very early with a
subclinical phase and additional risk factors have
evidence to support their influence. Month and
place of birth, familial risk, gender, diet and levels
of circulating vitamin D3 and UVB exposure
together with smoking associated with HLADRB1
may all play a part. Migration influences risk and
positive Epstein Barr serology, particularly
accompanied by early infectious mononucleosis, is
also likely to increase risk.
The most common, but still speculative, explanation is
that some environmental agent (probably infective)
gains access to the genetically susceptible person
before puberty. Evidence supporting this theory is that
an individual living in the tropics is unlikely to develop
MS but if that person moves to a temperate
environment before the age of puberty they then take
on the risk of the area to which they moved.
Chronic cerebro-spinal venous insufficiency (CCSVI)
is a recent theory proposing that people with
multiple sclerosis have an abnormal narrowing in
veins taking blood from the brain and that this
causes a build up of iron which crosses the blood
brain barrier and damages cells in the central
nervous system. CCSVI needs further research and
if a valid link is found it will need to be established
whether the narrowing is a cause of MS, or
alternatively due to the effect of MS. Treatment, by
percutaneous venoplasty, is as yet based on
incomplete evidence.
Although a genetic component is likely MS is not
hereditary in the conventional sense. Families who
already have a member with MS have a greater risk of
developing the condition than families where no one
has MS. If a parent has MS, the risk for their children is
15-20 times greater than that of the general population
though the risk is still relatively low.
So far there are no conclusive results to explain

what the hereditary process could be, though
there is ongoing work in this area6.
What we do have is evidence that treating early is
critical as it can influence the long-term outcome
for people with MS who may have otherwise faced
a lifetime of disability.
References
1.
Compston A, Coles A. Multiple sclerosis. Lancet

2008;372(9648):1502-17.
2.
Orton SM, Herrera BM, Yee IM, et al. Sex ratio of multiple
sclerosis in Canada: a longitudinal study. Lancet Neurol
2006;5(11):932-6.
3.
Burgess M. Shedding greater light on the natural history

and prevalence of multiple sclerosis. Br J Neurosci Nurs
2010;6(1):7-11.
4.
Richards RG, Sampson FC, Beard SM, et al. A review of the

natural history and epidemiology of multiple sclerosis:
implications for resource allocation and health economic
models. Health Technol Assess 2002;6(10):1-73.
5.
Cook SD, MacDonald J, Tapp W, et al. Multiple sclerosis in

the Shetland Islands: an update. Acta Neurol Scand
1988;77(2):148-51.
6.
Compston A. The genetic epidemiology of multiple sclerosis.

Philos Trans R Soc Lond B Biol Sci 1999;354(1390):1623-34.
MS Trust resources
MS Explained
Kids guide to MS
The young persons guide to MS
Talking with your kids about MS
Further resources
Compston A, Confavreux C, Lassman H, et al.
editors. McAlpines multiple sclerosis. 4th ed.
Philadelphia: Churchill Livingstone; 2006.
Ebers GC. Environmental factors and multiple
sclerosis. Lancet Neurol 2008;7:268-277.
www.mstrust.org.uk

Diagnosis
Diagnosis
Myelin is a fatty substance, which coats the axon
of nerves in the central nervous system (CNS) and
has an insulating effect enabling electrical impulses
to move faster. Damage to myelin results in a
disturbed transfer of information along the axons.
In MS, patches of inflammation may occur in the
myelin, this can result in the myelin itself
becoming damaged. If the inflammation covers a
wide area it can leave a scar (sclerosis); a lesion.
These lesions can appear in many sites throughout
the CNS - hence multiple. Demyelination occurs
when myelin around axons deteriorates and is lost.
There is also an increasing body of evidence to
demonstrate that the axons themselves become
damaged, this axonal loss is a cause of impairment.
Once lost, an axon can never regenerate and this is
thought to account for the progressive disability
which is often part of the condition. Axonal loss is
now believed to occur much earlier in the disease
process than was once thought.
MS can affect any part of the CNS, giving rise to a
variety of physical and sometimes cognitive
symptoms, in addition to the psychosocial
problems that can also result.
Onset
Onset of MS rarely occurs before puberty and is
usually in early adult life. The incidence of onset
rises during the 20s, reaching its peak in the late
20s and early 30s. Initial symptoms are, most
commonly, visual disturbances, including pain in
and around the eyes, blurred or double vision,

sensory problems that take the form of pins and
needles in the hands and feet, weakness,
numbness, balance disorders and fatigue.
Symptoms vary enormously, not only from one
person to another, but also in the same person
from one time of day to another.
Clinically isolated syndrome

85% of people experience an initial onset of
symptoms that is known as clinically isolated
syndrome (CIS). This inaugural event is defined as
an individuals first episode of neurological
symptoms lasting at least 24 hours. Damage may
be monofocal resulting in the experience of a
single symptom (eg optic neuritis) or multifocal
when multiple symptoms might be experienced
(eg incoordination and bladder problems).
Not everyone who experiences CIS will go on to
develop MS and for some there may be no further
symptoms. However, if MRI findings show brain
lesions that are indicative of MS then the chances
of having further relapses and a definite diagnosis
of MS are high1.
Paediatric MS
The onset of MS in childhood and adolescence is
being increasingly recognised2. 3-5% of patients have
onset of MS before the age of 16 with 1% before the
age of 11. Male to female ratio is equal before
puberty, after which it is most common in females
and mirrors the adult ratio of 3:1. 95% of patients
with paediatric MS follow a relapsing remitting
course. Diagnosis in this age group can however be
problematic as symptoms often resemble acute
disseminated encephalomyelitis (ADEM).
healthy nerve cell

axon
nerve cell with damaged myelin
myelin
an axon left without myelin will die
MS: an overview
Diagnosis
Diagnosis
Diagnostic tests
A diagnosis of definite MS is based upon objective

evidence of lesions separated in time and space, ie
relapsing and remitting symptoms affecting at least two
separate areas of the brain or spinal cord. MS can be
difficult to diagnose since there is no single test, or
clinical feature which is exclusive to the condition, and so
other possible causes must be eliminated. Confirmation
of the condition can therefore take some time.
There are three major investigations, all or some of

which may be carried out when MS is suspected
though none are 100% conclusive without supporting
clinical evidence and robust clinical history:
There are established criteria that have to be met to

positively identify MS. These are known as the
McDonald Criteria and are relevant in diagnosis of
both relapsing remitting and primary progressive MS3.
Revision of these criteria in 20104 allows for earlier
diagnosis of MS without any loss of accuracy. This
facilitates earlier use of disease modifying drugs that
may have an impact on later accumulation of disability
for people experiencing relapses.
magnetic resonance imaging (MRI)
neurophysiological tests
examination of cerebrospinal fluid (CSF).
Magnetic resonance imaging (MRI)
MRI is the most sensitive investigation with the

ability to highlight areas of active and non-active
demyelination. MRI creates images by using
magnetic fields and radio waves to monitor the
behavior of hydrogen
atoms in the body,
Figure 1
these are converted
NICE guidance5 states that the individual should be
to create crossinvolved in the diagnostic process and should be
sectional images. The
informed as soon as a diagnosis of MS is considered chemical make up of
reasonably likely. In a study of patient satisfaction
the scars caused by
and timing of diagnosis patients themselves
MS means that they
preferred early diagnosis6. See page 10 - Delivering
show up as white
a diagnosis of MS.
patches on MRI
images, giving a very
The typical diagnostic process
clear picture of the
The GP is usually the first health professional a person
effects of MS on the
will consult when they are experiencing neurological
brain and spinal cord
problems. GPs see on average one new diagnosis of MS
(Figure 1).
every 15 years and are likely to have only three or four
patients with MS in their case load. There is no single
The use of an enhancing agent, such as gadolinium,
clinical feature exclusive to MS and where there are
will show whether a lesion is active or not. In active
unexplained neurological symptoms the GP will refer
inflammatory lesions the blood-brain barrier is
the patient to a neurologist for full neurological
disrupted and the gadolinium leaks into the
examination and paraclinical tests. The neurologist will surrounding brain tissue and can be detected on the
make the diagnosis of MS.
MRI image.
There are specialist MS centres throughout the UK
with access to neurologists who have expertise in
treating MS and a specialist MS team including MS
specialist nurses. Find these on the MS Trust map of
MS services www.mstrust.org.uk/map.
It can be problematic to establish a correlation

between the lesions as revealed by MRI and the
clinical presentation at any given time.
Clinical evidence
to observe abnormalities that are suggestive of

multiple sclerosis
to rule out alternative diagnoses such as tumours

or stroke
to help in the evaluation of patients who have

subjective complaints but few objective signs
of abnormality
as a surrogate marker for disease activity in

clinical trials.
A thorough physical examination of the current

function of the nervous system is made. Specifically,
signs of weakness or stiffness in the limbs and areas of
abnormal/reduced sensitivity on the body surface will
be looked for. Evidence of current or previous damage
in the optic nerve is important (and can be detected
through an ophthalmoscope) as this is a common site
of lesions in MS. However, it is rare to make a certain
diagnosis of MS on clinical evidence alone, since in
many cases such evidence is subjective.
Neurologists use MRI for the following purposes:
www.mstrust.org.uk

Diagnosis
The 2010 revised McDonald criteria for diagnosis of MS4

Clinical presentation
(person presenting to neurologist)
Additional data needed

for MS diagnosis
Two or more attacks; objective clinical

evidence of two or more lesions
None
Two or more attacks; objective clinical

evidence of one lesion
Dissemination in space shown on MRI

or
Up to two MRI detected lesions typical of MS
plus positive cerebrospinal fluid.
or
Await a further relapse suggestive of
dissemination in space (ie affecting another
part of the body)
One attack; objective clinical evidence of two

or more lesions
Dissemination in time demonstrated by MRI

or
Second clinical attack (relapse)
One attack; objective clinical evidence of one

lesion (known as 'clinically isolated syndrome')
Dissemination in space demonstrated by MRI

or
Up to two MRI detected lesions typical of MS
plus positive cerebrospinal fluid AND
dissemination in time demonstrated by MRI
or
Dissemination in time demonstrated by MRI (ie
new lesion seen on MRI at least three months
after the original scan)
or
Second clinical attack (relapse)
Insidious neurological progression suggestive

of multiple sclerosis (typical for primary
progressive MS)
Positive cerebrospinal fluid AND dissemination in

space, shown on MRI or
Abnormal visual evoked potential plus abnormal
MRI AND dissemination in time demonstrated by
MRI or
Continued progression for one year (determined
retrospectively or by ongoing observation)
MS: an overview
Diagnosis
Neurophysiological tests
These relatively simple, non-invasive investigations
are carried out on vision, hearing or sensation to
look specifically for delay in the conduction of
nerve impulses to and from the brain.
The most common test is the visual evoked potential
(VEP). Visual tests involve watching a television screen
that has alternating black and white squares. An
electrode is placed over the visual cortex and a
computer analyses the received visual signal from the
television set. The length of time it takes for the
signal to leave the television set and reach the visual
cortex is known and thus a delay in the signal
transmission can be identified. Such a delay may be
indicative of damage due to an MS lesion.
aspects of their MS healthcare by being given

relevant and accurate information about each choice
and decision.
The Information Standard was devised by the
Department of Health to allow people to recognise
organisations that produce information that is
accurate, evidence-based and unbiased. Certified
organisations can be recognised by the quality mark
below. The MS Trust is a certified organisation.
References
1.
Miller D, Barkhof F, Montalban X, et al. Clinically isolated

syndromes suggestive of multiple sclerosis, part 1: natural
history, pathogenesis, diagnosis and prognosis. Lancet Neurol
2005;4(6):281-8.
2.
Huppke P, Gartner J. A practical guide to paediatric multiple

sclerosis. Neuropediatrics 2010;41(4):157-62.
3.
McDonald WI, Compston A, Edan G, et al. Recommended

diagnostic criteria for multiple sclerosis: guidelines from the
International Panel on the diagnosis of multiple sclerosis. Ann
Neurol 2001;50(1);121-7.
4.
Polman CH, Reingold SC, Banwell B, et al. Diagnostic criteria

for multiple sclerosis: 2010 revisions to the McDonald criteria.
Ann Neurol 2011;69(2):292-302.
The sample of CSF is analysed by electrophoresis

for its protein level and leucocyte count.
Approximately 80% of people with MS have an
elevated immunoglobulin G (IgG) index or
oligoclonal immunoglobulin bands present in the
spinal fluid but not in the serum, indicating
inflammation and immunological disturbance.
5.
National Institute for Health and Clinical Excellence. Multiple

sclerosis - management of multiple sclerosis in primary and
secondary care. NICE Clinical Guideline 8. London: NICE; 2003.
6.
Janssens ACJW, de Boer JB, Kalkers NF, et al. Patients with

multiple sclerosis prefer early diagnosis. Eur J Neurol
2004;11(5):335-7.
7.
Burgess M. The process of adjustment: providing support after

a diagnosis of multiple sclerosis. Br J Neurosci Nurs
2010;6(4):156-60.
Deliviering a diagnosis of MS
8.
Box V, Hepworth M, Harrison J. Identifying the information

needs of people with multiple sclerosis. Nurs Times
2003;99(49):32-6.
Cerebrospinal fluid examination

Examination of the cerebrospinal fluid (CSF) used to
be an important diagnostic aid but the increased use
of MRI has reduced the need for this invasive
procedure. Fluid is drawn off the spinal cord by
means of a lumbar puncture. NICE guidance states
that this should only be used when the situation is
clinically uncertain; however it is still of importance in
the diagnosis of primary progressive MS.
A critical element in the diagnostic process is the

provision and pacing of information. It is recognised
that how a diagnosis is communicated and the
information and support received at this time will
impact on subsequent adjustment to MS7. The
health professional should find out how much and
what information the individual wants to receive8.
Explanations of diagnostic tests should be given.
A diagnosis given badly will be remembered
throughout the life of a patient and can impact
negatively on their adjustment to living with MS.
The importance of patient information in the
management of MS is further highlighted in the
recommendation by NICE that:
People with MS should be enabled to play an
active part in making informed decisions in all
10
MS Trust resources
MS Explained
MS: What does it mean for me?
Clinically isolated syndrome (CIS) factsheet
Map of services www.mstrust.org.uk/map
Further resources
2008;372(9648):1502-17.
Zajicek J, Freeman J, Porter B. Multiple sclerosis
care: a practical manual. Oxford: Oxford University
Press; 2007.
www.mstrust.org.uk

Types of MS
people can have a persistent increase in disability

whilst others may experience plateaux or a more
gradual worsening of symptoms.
Relapsing remitting MS
About 85% of people are diagnosed with the type of
MS that manifests in a series of relapses (sometimes
called an attack or exacerbation) followed by periods of
good or complete recovery - a remission.
A relapse is defined as; the appearance of a new
symptom or the reappearance of old symptoms that
last more than 24 hours. A relapse can last for
considerably longer and may persist for weeks or
months, the average length of a relapse has been
reported as 55 days. The frequency of relapses, the
severity of symptoms experienced and the length of
the gap between attacks are unpredictable. Similarly, it
may sometimes be difficult to determine what is a
fluctuation in symptoms (a day to day worsening or
improvement) and what is a relapse.
On average people with relapsing remitting MS have
one or two attacks a year, but this can vary. It is
possible for symptoms to worsen gradually over time
as recovery from relapses becomes less complete. The
term rapidly evolving severe relapsing remitting MS is
sometimes used for someone who has two or more
disabling relapses in one year and evidence of
increasing lesions on two consecutive MRI scans.
Some people whose MS has been progressive from

onset may also experience occasional relapses, this is
sometimes referred to as relapsing progressive MS.
Benign MS
People with benign MS experience attacks
separated by long periods with no symptoms. The
phrase is sometimes used inaccurately to describe
a period of mild symptoms following diagnosis. As
the defining characteristic of benign MS is the
long-term absence of symptoms, it can only be
diagnosed retrospectively after ten or more years.
Some people with an initial benign course will
eventually start to experience more frequent
relapses and may eventually develop secondary
progressive MS.
relapsing remitting MS
disability
Types of MS
time
Secondary progressive MS
disability
secondary progressive MS
time
primary progressive MS
disability
About 75% of people whose disease pattern begins

with relapsing and remitting symptoms later develop
secondary progressive MS (50% of those with
relapsing remitting MS develop secondary progressive
MS within ten years from diagnosis). The accepted
definition of secondary progressive MS is that a person
must have shown continued deterioration for the past
six months whether or not they have continued to
experience relapses. The transition to secondary
progressive MS is psychologically difficult as people
recognise they have moved into another phase of the
disease and disease modifying medications may no
longer be useful.
time
Some people find that the increase or progression

of disability is very gradual, whilst for others it can
occur more quickly.
About 10% - 15% of people with MS are diagnosed

with a form of MS in which disability increases from
the outset. This is known as primary progressive MS
(or, less commonly, chronic progressive MS). Some
disability
Primary progressive MS
benign MS
time
Adapted from Lublin FD1.
11
MS: an overview
Prognosis
Prognosis
One of the chief characteristics of MS is its
unpredictability from one person to another, from
one day to another, from one time of day to another.
However, some prognostications can be made from
the pattern of the disease over the first five years. For
example, early problems with sensation and eyesight
(as opposed to problems related to the cerebellum
such as unsteadiness and clumsiness) usually indicate
a more favorable form of MS. Younger age at onset is
also a good prognostic sign2.
Factors that influence prognosis3

Favourable
The uncertainty of prognosis can be hard to deal with.

Many people ask if there is any way of identifying
triggers which will cause the condition to worsen but
there is very little proof that any particular event or
circumstance can be identified. There is some evidence
that stressful life events, such as a car accident or severe
emotional stress, can make deterioration more likely. A
meta-analysis7 concluded that there is a consistent
association between stressful life events and subsequent
exacerbation in multiple sclerosis. However even this is
controversial and there is usually little that can be done
to prevent such stresses occurring.
Female
Low rate of relapses per year

(1-5 in five years)
Complete recovery from the first attack
Long interval between first and

second attack
Symptoms predominantly sensory

eg optic neuritis
Younger age of onset - less than 35 years
There is no known reason why someone with MS

should avoid either immunisation8 or a necessary
surgical operation. NICE guidance recommends
people with MS should be offered immunisation
against influenza and have any other immunisations
and surgery that they need.
Low disability at five years from onset.
References
Unfavourable
1.
Lublin FD, Reingold SC. Defining the clinical course of multiple sclerosis:
results of an international survey. Neurology 1996;46(4):907-11.
Male
2.
High rate of relapses per year (3 or more

in first five years)
Vukusic S, Confavreux C. Natural history of multiple sclerosis: risk factors

and prognostic indicators. Curr Opin Neurol 2007;20(3):269-74.
3.
Hutchinson M. Predicting and preventing the future: actively managing

multiple sclerosis. Pract Neurol 2009;9(3):133-43.
Incomplete recovery from the first attack
4.
Short interval between first and

second attack
Cottrell DA, Kremenchutzky M, Rice GP, et al. The natural history of

multiple sclerosis: a geographically based study. 5. The clinical features
and natural history of primary progressive multiple sclerosis. Brain
1999;122(4):625-39.
5.
Symptoms predominantly of motor

involvement eg balance, weakness, ataxia
Sadovnick AD, Ebers GW, Wilson RW, et al. Life expectancy in patients
attending multiple sclerosis clinics. Neurology 1992;42(5):991-4.
6.
Sadovnick AD, Eisen K, Ebers GC, et al. Cause of death in patients

attending multiple sclerosis clinics. Neurology 1991;41(8):1193-6.
7.
Mohr DC, Hart SL, Julian L. Association between stressful life events and
exacerbation in multiple sclerosis: a meta-analysis. BMJ
2004;328(7442):731.
8.
Farez MF, Correale J. Immunisations and risk of multiple sclerosis:

systematic review and meta-analysis. J Neurol 2011;258(7):1197-1206.
Older age of onset - over 35 years
Significant disability at five years

from onset
After 15 years with MS, about half of the

population will still be independent in terms of
walking and the remaining half will need help with
mobility. When people reach the point of requiring
help with walking (EDSS 6.0) they are likely to
progress, irrespective of whether they are having
relapses, or if they have primary or secondary MS4.
12
Long-term studies suggest that MS only has a small

impact on life expectancy of five to ten years
compared to the general population. One study found
that people with more complex disability (EDSS
greater than or equal to 7.5) were more at risk of
potentially life threatening complications - such as
respiratory or cardiovascular problems - that can result
from reduced mobility, and this affected the overall life
expectancy figures5. Frequency of death by suicide has
been found to be 7.5 times higher among patients
with MS compared to the general population6.
MS Trust resources
MS Explained
Primary progressive MS exposed
www.mstrust.org.uk

Clinical measures
Clinical measures
Measurement of a condition as variable as MS is
notoriously difficult but the need for evidencebased decisions has highlighted the importance of
the development of adequate measures1.
Monitoring disease status, evaluating clinical
practice outcomes and interpreting the results of
research interventions require robust
measurements. However choosing the most useful
outcome measure can be problematic2.
For any measure to be acceptable it must be
reliable, reproducible and valid. Reliability concerns
the extent to which scores produced by a scale are
free from measurement error and are able to be
reproduced, validity concerns the extent to which
an instrument measures what was intended. In the
field of health another parameter is also necessary:
whether the measure can detect clinical change in
the attribute being measured even if the change is
small. This property is termed responsiveness.
Clinically useful scales therefore:
reflect the extent of the disease process
are multi-dimensional to reflect the main ways

in which the disease affects an individual
are scientifically sound
are capable of reflecting change over time.
A further consideration is also necessary - are the

aspects of life considered important by the person
with MS the same as those which the clinician
considers important? Assessment of patient reported
outcome measures (PROMs) has become increasingly
common as these provide a means of collecting the
patients views on a treatment efficacy or outcome3.
The ability to detect improvement is also important
but studies in this area have been limited4.
In multiple sclerosis the most commonly used
measure remains the Expanded Disability Status Scale
(EDSS). This is a method of quantifying disability in
multiple sclerosis and monitoring changes in the level
of disability over time. It is widely used in clinical trials
and in the assessment of people with MS.
The EDSS scale ranges from 0 to 10 in 0.5 unit
increments that represent higher levels of
disability. Scoring is based on an examination by a

neurologist. EDSS steps 1.0 to 4.5 refer to people
with MS who are able to walk without any aid and
is based on measures of impairment in eight
functional systems:
pyramidal - weakness or difficulty moving limbs
cerebellar - ataxia, loss of coordination or tremor
brainstem - problems with speech, swallowing

and nystagmus
sensory - numbness or loss of sensations
bowel and bladder function
visual function
cerebral (or mental) functions
other.
Each functional system is scored on a scale of

0 (no disability) to 5 or 6 (more severe disability).
EDSS steps 5.0 to 9.5 are defined by the
impairment to walking. The scale is sometimes
criticised for its reliance on walking as the main
measure of disability.
Although the scale takes account of the disability
associated with advanced MS, most people will
never reach these scores.
EDSS is of limited reliability and is not very
responsive to change. There is a bias towards
physical (especially ambulatory) rather than
cognitive effects of MS. It is not a linear scale and
people with MS spend more time at some levels
on the scale than others. Despite its limitations
EDSS remains the most widely used impairment
assessment scale in MS, particularly in clinical trials.
Scales to monitor impairment:
Expanded Disability Status Scale (EDSS).

This is an observer-rated scale, usually
performed by a neurologist.
Scripps Neurological Rating Scale is based on

the standard neurological examination with an
extra category for bladder, bowel and sexual
dysfunction. Correlation between the Scripps
scale and EDSS is not good and further
psychometric evaluation is necessary.
13
MS: an overview
Clinical measures
Expanded Disability Status Scale (EDSS)
Score
14
Description
1.0
No disability, minimal signs in one functional system (FS)
1.5
No disability, minimal signs in more than one FS
2.0
Minimal disability in one FS
2.5
Mild disability in one FS or minimal disability in two FS
3.0
Moderate disability in one FS, or mild disability in three or four FS. No impairment
to walking
3.5
Moderate disability in one FS and more than minimal disability in several others.
No impairment to walking
4.0
Significant disability but self-sufficient and up and about some 12 hours a day.
Able to walk without aid or rest for 500m
4.5
Significant disability but up and about much of the day, able to work a full day, may
otherwise have some limitation of full activity or require minimal assistance. Able to
walk without aid or rest for 300m
5.0
Disability severe enough to impair full daily activities and ability to work a full day
without special provisions. Able to walk without aid or rest for 200m
5.5
Disability severe enough to preclude full daily activities. Able to walk without aid or rest
for 100m
6.0
Requires a walking aid - cane, crutch, etc - to walk about 100m with or without resting
6.5
Requires two walking aids - pair of canes, crutches, etc - to walk about 20m without resting
7.0
Unable to walk beyond approximately 5m even with aid. Essentially restricted to

wheelchair; though wheels self in standard wheelchair and transfers alone. Up and
about in wheelchair some 12 hours a day
7.5
Unable to take more than a few steps. Restricted to wheelchair and may need aid in
transferring. Can wheel self but cannot carry on in standard wheelchair for a full day
and may require a motorised wheelchair
8.0
Essentially restricted to bed or chair or pushed in wheelchair. May be out of bed itself
much of the day. Retains many self-care functions. Generally has effective use of arms
8.5
Essentially restricted to bed much of day. Has some effective use of arms retains some
self care functions
9.0
Confined to bed. Can still communicate and eat
9.5
Confined to bed and totally dependent. Unable to communicate effectively or

eat/swallow
www.mstrust.org.uk

Clinical measures
Scales to monitor a persons need

for care:
Extended Barthel Index is well-established,

monitoring ten areas of activities of daily living:
bowel, bladder, grooming, toilet use, feeding,
transfer, mobility, dressing, stairs, and bathing
on 0-3 point scales. It does not however
include cognition or communication.
Functional Independence Measure (FIM) is
more detailed than the Barthel scale in that it
includes an assessment of communication and
social cognition and uses 1-7 point rating scales.
Fatigue Severity Scale (FSS) consists of nine

questions focusing on physical symptoms with
an average score ranging from 1-7. Lower
scores indicate less fatigue.
Modified Fatigue Impact Scale (MFIS) a 21

item scale covering physical, cognitive and
psychosocial functioning. Lower scores indicate
less fatigue.
Leeds MS Quality of Life Scale (LMSQoL) is a

recent development and is MS specific.
UK Neurological Disability Scale, formerly

known as the Guys Neurological Disability Scale
(UKNDS/GNDS) is based on 12 areas which are
considered important by neurologists. This
captures many aspects of disabilities that can
be experienced by people with MS and is
commonly used by health professionals in
practice as a basis for assessment.
Health status scales:

All the scales listed in this section are questionnaires
and would be completed by the person with MS
following an introduction from a health professional.
Multiple Sclerosis Impact Scale (MSIS-29)

measures 20 physical and nine psychological
items assessing how much impact they have on
life from the patients perspective. This
combines both quality of life issues and
psychometric testing. High scores indicate
greater disability.
Study Short Form 36 Health Survey (SF36)
measures the health status in eight dimensions
including physical function, pain, general
health, vitality, and social functioning. This
scale is widely used but, because it is not MS
specific, its usefulness can be limited. However
this can allow comparisons of the impact of MS
with other conditions.
MS Quality of Life Instrument (MSQOL 54)

is a variant of the SF36 with an additional
18 items that are specific to MS. Low scores
indicate lower quality of life.
MS Quality of Life Inventory (MSQLI) is

composed of SF36 plus pre-existing established
symptom related scales, this allows
comparisons of specific symptoms across
subject samples and with other illness groups.
Functional Assessment of Multiple Sclerosis

(FAMS) is a quality of life instrument based
on a scale developed within the oncology
environment.
Mobility scales:
The A1 scale is similar to EDSS but gives a

more precise measure within levels 4-6.
Ten metre timed walk. Individual walks

without assistance 10 m and the time is
measured for the intermediate 6m to allow for
acceleration and deceleration.
Rivermead mobility scale covers mobility,

including bed mobility, lying to sitting, transfer
and gait.
Upper limb function:

Nine hole peg test involves the subject placing
nine dowels in nine holes. Subjects are scored on
the amount of time it takes to place and remove
all 9 pegs.
Box and block. A number of small wooden
blocks are placed in one side of a box. The subject
being tested is required to use the dominant
hand to grasp one block at a time and transport
it over a partition and release it into the opposite
side. The test is then repeated with the nondominant hand.
Both are tests of manual dexterity with the former
requiring greater dexterity and can be
administered in less than ten minutes.
15
MS: an overview
Clinical measures
References
Spasticity scales:
Ashworth Scale is most frequently used with a

clinical rating being given after an assessor tests
the passive resistance to passive movement of a
joint. A physiotherapist would normally
administer this scale.
Cognition scales:
Paced Auditory Serial Addition Test (PASAT).

Two variations of this test are used: a two or
three minute version.
Symbol-digit Modalities Test (SDMT).
Both these cognition tests need to be administered

by trained personnel.
Composite assessment scores:

The complexity of the disease and the range of
measures available have now led to research with
the aim of validating composite measures which
encompass the major clinical dimensions that are
of relevance both to the clinician and to the
person with MS.
1.
Thompson AJ, Hobart JC. Multiple sclerosis: assessment of

disability and disability scales. J Neurol 1998;245(4):189-96.
2.
Laidler D. The outcome measure minefield. Way Ahead

2008;12(4):12.
3.
Doward LC, McKenna SP, Meads DM, et al. The

development of patient-reported outcome indices for
multiple sclerosis (PRIMUS) Mult Scler 2009;15(9):1092-102.
4.
van Winsen, Kragt JJ, Hoogervorst ELJ. Outcome

measurement in multiple sclerosis: detection of clinically
relevant improvement. Mult Scler 2010;16(5):604-10.
5.
Rothwell PM, McDowell Z, Wong CK, et al. Doctors and

patients dont agree: cross sectional study of patients and
doctors perceptions and assessments of disability in multiple
sclerosis. BMJ 1997;314(7094):1580-3.
MS Trust resources
Health professional resources
www.mstrust.org.uk/professionals
MS Functional Composite (MSFC) is an example

and includes:
1. Timed walk of 25ft
2. Nine hole peg test
3. PASAT 3 minute version
Each of the test results is standardised using a
reference population and the resulting scores are
averaged to provide a single score. The MSFC is
measured by a unique Z score where an increase
or decrease represents improvement or
deterioration in neurological function.
The MS population is complex and MS requires
sensitive clinical outcome measures that can detect
small changes in disability whilst reliably reflecting
long-term changes in sustained disease
progression. Integration of current and new
outcome measures may be most appropriate and
utilisation of different measures depending on the
MS population and stage of the disease may be
most useful.
16
www.mstrust.org.uk

A multidisciplinary approach to
MS care
Current and emerging disease modifying drug
therapies impact on the course of MS by targeting
immune responses and slowing down the course of
MS. They are an investment for the long-term future
but do not address the impact of symptoms felt.
Expert and effective symptom management
remains key to optimising quality of life for those
living with MS1. Lesions characteristic of MS can
occur anywhere within the central nervous system
resulting in a wide range of diverse symptoms that
may present in many combinations, with variable
intensity and are often difficult to describe. No two
people with MS have exactly the same symptoms.
It is important to consider that most people with
MS may experience only a few of these symptoms
and that the intensity and frequency can vary;
either at any one time or throughout the duration
of the condition. Symptoms can also be influenced
by a number of mediators and moderators such
as core body temperature, stress, concomitant
illness, infection, pressures sores and general health
and wellbeing.
It is essential to discriminate between cause, effect
and association in MS. Understanding the
relationships between primary symptoms,
secondary effects and additional factors will ensure
effective symptom management.
Secondary complications will worsen primary
symptoms. Take pressure sores as an example.
They may be the consequence of untreated
continence problems rather than a symptom of
MS. They will then become a focus for worsening
spasm if spasticity is present as a primary problem.
Less clear perhaps is pain, which may be either a
primary symptom deriving from damage to the
central nervous system or a secondary symptom
such as the effect of bad posture.
Symptoms can be visible and invisible; they may
present an obvious problem or be misattributed, even
missed. The less overt and invisible such as
depression, fatigue, cognitive problems or sexual
dysfunction are often not considered, assessed or
identified and yet impact on quality of life and capacity

to remain in employment as profoundly as some more
apparent symptoms such as impaired mobility.
The diversity and range of symptoms often
necessitates many health and social care
professionals being involved in the care of a person
with MS. A study reported up to 60 workers from
different sources visiting the home of a person with
MS2. NICE guidelines3 state that when several
healthcare professionals are involved with a person
with MS they should work together with the person
and his or her family as a team towards common
agreed goals and using an agreed common
therapeutic approach.
MS can result in very complex multidisciplinary needs,
often with subtle problems remaining unrecognised
and misunderstood. Successful outcomes need true
multidisciplinary working with shared goals. GP,
neurologist, radiologist, rehabilitationist,
physiotherapist, occupational therapist, psychologist,
counsellor, orthotist, dietitian, nurse, continence
adviser, speech and language therapist, pain specialist,
social worker, complementary therapist - all can have
a role to play in helping the person with MS remain
fully engaged with daily life and able to manage
effectively.
Successful management of one symptom may
require the input from several different professionals
and goals that encompass whole lived experience
not just a disparate collection of symptoms.
The MS specialist health professional is pivotal to
collaborative and coordinated care and support for
people with MS. The role involves acting as a
consultant and educational resource for staff striving
towards greater awareness and knowledge of MS in
the health and social arena 4. The MS specialist can
support people with MS to maximise their selfmanagement skills.
Provision of specialist MS services remains
inequitable and for some lack of access to an MS
specialist team may result in not being able to obtain
the right advice at the right time with resultant poor
outcomes. People living with MS may not always
know what is available, useful, and accessible; often
they are young and have a life yet to be lived. The
MS Trust and other voluntary organisations can
provide information to people with MS and signpost
to local services available.
17
MS: an overview
References
1.
Thompson AJ, Toosy AT, Ciccarelli O. Pharmacological

management of symptoms in multiple sclerosis: current
approaches and future directions. Lancet Neurol
2010;9(12):1182-99.
2.
Thompson A, Johnston S, Harrison J, et al. Service delivery in

multiple sclerosis: the need for co-ordinated community care.
MS Management 1997;4(1):11-8.
3.
National Institute for Health and Clinical Excellence.

Multiple sclerosis - management of multiple sclerosis in
primary and secondary care. NICE Clinical Guideline 8.
London: NICE; 2003.
4.
MS Trust, RCN, UKMSSNA, TiMS. A competency framework

for MS specialist services. Letchworth: MS Trust; 2009.
MS Trust resources
Way Ahead newsletter for health
and social care professionals who
support people with MS
Health professional resources
www.mstrust.org.uk/professionals
Map of services
www.mstrust.org.uk/map
18
www.mstrust.org.uk

Self-management
The estimated 100,000 people in the UK who live with

multiple sclerosis require specific skills to live life to the
Self-management
full and successfully manage their condition. Equally,
health professionals have the responsibility through
Self-management is about dealing with the impact
Quality, Innovation, Productivity and Prevention (QIPP)
that a long-term condition has on a persons daily
to promote and support self-management and to
life. The concept of self-management has caused
reduce the need for unscheduled acute admissions.
some confusion within clinical practice over many
The Department of Health7 recognises the need for a
years, and is not always well defined or understood1. systematic transfer of knowledge and power to patients
to empower them to maximise self-management and
There are a number of related terms and definitions choice, engage in decision-making and ensure that
which may be useful.
there is no decision about me without me so that
patients are active participants in all decisions about
Self-management - refers to an individuals ability
their care.
to take control of their health and effectively
manage their chronic illness, with a strong emphasis The concept of self-management began in the 1960s
and it was seen as a method of finding better solutions
on self-efficacy. Understanding a patients attitude
to illness1. Today self-management is seen as an integral
to health and knowledge in this context is
part of the health care system. With the concept of the
important for health professionals.
Expert Patient arising early in the new century, the
Self-care - traditionally indicated the performance
Department of Health began to endorse the initiative
of activities or tasks by the patient or family, which
seeking to empower those with chronic health needs,
were previously carried out by professionals. Selfto take control of their own care and recognised that
care requires knowledge, skills and understanding
professionals can support and provide expertise to
of a condition and its management2. Whilst
maintain independence9.
self-care and self-management are inextricably
linked they are not the same.
Benefits of self-management
Self-help - traditionally has been seen as the act of
helping or improving oneself without relying on
anyone else, it differs from self-management which
is undertaken in partnership.
Self-efficacy - has been described as the belief that
one is capable of performing in a certain manner to
attain certain goals3. The feeling of self worth and
competence to intrinsically motivate an individuals
self-efficacy relates to a persons ability to have
optimistic beliefs, but in contrast to other features of
optimism, perceived self-efficacy explicitly refers to
ones ability to deal with challenging encounters.
Self-management is a concept now evident in
Department of Health initiatives, for example the
Expert patient4 and Supporting people with long term
conditions to self-care5. The aim of promoting selfmanagement is to enable patients to help themselves
to manage their long-term conditions, whilst working
in partnership with the support of services provided by
the National Health Service6. A more recent report
recognises the benefits of self-management7 finding
that investment in targeted self-management
interventions, particularly for people with long-term
conditions, can increase peoples confidence to
manage their health and well-being and improve their
quality of life. The cost effectiveness of this strategy has
also been explored8.
80-90% of all care for people with long-term

conditions is undertaken by the person themself or
their families. This self-management includes eating
well, exercising, taking medicines, keeping in good
mental health, watching for changes, coping if
symptoms get worse and recognising when to seek
help from health professionals.
Supporting self-management in MS involves educating
people about their condition and care, and motivating
people to look after themselves effectively. Selfmanagement support can be seen in two ways: as a
portfolio of techniques and tools that help people to
choose healthy behavior and a fundamental
transforming of the patient caregiver relationship into
a collaborative partnership9. The very nature of chronic
disease management requires a dynamic, positive
approach, encouraging patients to move from a passive
helpless role to a proactive one10. Education is central in
re-establishing a sense of control over the condition11,12.
Key attributes to self management include:
self-efficacy
resource utilisation
collaborative partnerships with health and social

care professionals
education
19
MS: an overview
Self-management
goal setting and monitoring
problem solving and decision-making.
Research has identified that self-management

improves health and quality of life, including:
reduced pain (despite increasing levels of functional
disability); improved mood; reduced visits to the
general practitioner; improved levels of self-efficacy.
Changes were noticed within one month of selfmanagement intervention and resulted in sustained
improvement in the study groups for up to four
years post-intervention13.
Self-management in multiple sclerosis

In 2009, the Consortium of Multiple Sclerosis
Centers14 issued a white paper analysing patient selfmanagement in multiple sclerosis and offering
guidelines for best practices aimed at empowering
patients. These include:
raising awareness among professionals expert in

and providing for patients with MS concerning
the needs for patient self-management
formally evaluating the unmet needs in MS,

considering both patient and provider perspectives
encouraging research on a broad range of MS

self-management strategies and outcomes,
including assessment of the specific components
of self-management programs that are most
effective for patients with MS, as well as their
optimal delivery eg in-person or via telephone,
type of leadership, number of sessions
eliminating any practice barriers to selfmanagement. This should include engaging

patients in all aspects of developing and
administering interventions, such as
implementation, testing and research,
dissemination, and sustainability
developing evidence-based practice.
In MS self-management includes:
20
dealing with symptoms and relapses
making informed choices about medication
making best use of available resources
being a partner with health professionals in

making decisions about treatment
living well and accommodation of MS into

everyday life.
People who are most likely to successfully selfmanage their MS:
have a good understanding of MS
manage the impact of MS on physical,

emotional, social and working life and are able to
make adjustment where necessary
actively participate in making decisions with

health professionals
adopt healthy lifestyles
take action.
Generic self-management programmes

The Expert Patients Programme (EPP) is a free six
week course for people with chronic or long-term
conditions. The course is delivered by trained and
accredited tutors, most of whom are themselves
living with a long-term health condition.
The EPP aims to give people the confidence to take
more responsibility and self-manage their health and
to be active participants in the treatment,
management and care of their condition. Rather
than focusing on health information about specific
conditions, the course looks at general topics
including healthy eating, dealing with pain and
extreme tiredness, relaxation techniques and coping
with feelings of depression.
Work carried out by Professor Julie Barlow of
Coventry University evaluating the expert patient
programme in people with MS found:
reduced severity of symptoms
significant decrease in pain
improved quality of life control and activity
improved resourcefulness and life satisfaction15.
Internal evaluation data8, self-reported from

approximately 1,000 EPP participants, indicates that
the programme provides significant numbers of
people living with long-term conditions with the
confidence and skills to better manage their
condition on a daily basis:
45% felt more confident that they would not let

common symptoms (pain, tiredness, depression and
breathlessness) interfere with their lives
www.mstrust.org.uk

Self-management
38% felt that such symptoms were less severe

four to six months after completing the course
33% felt better prepared for consultations with

health professionals.
MS specific self-management
programmes
Some examples of self-management courses for people
with MS include: Getting to grips with MS, Taking
control and fatigue management programmes.
Getting to grips with MS, Taking control
These MS specific courses are designed for people
newly diagnosed with MS but could be suitable for a
person at any point along the MS trajectory. They
cover disease specific education including research in
MS, health promotion including nutrition, exercise
and physical activity, positive lifestyle adjustments and
managing MS in the workplace. The roles of other
professionals involved in MS management such as
occupational therapists, physiotherapists and
psychologists are explored.
A study of a cohort of people with MS undertaking
self-management programmes found 82% of
participants felt they had been enabled to cope
better as a result of the course, 64% felt they ate a
better diet and 72% felt enabled to alter their
lifestyles as a response to MS11.
Fatigue management
Fatigue is experienced by 70-90% of people with
multiple sclerosis and can have a major negative
impact on peoples lives. As efficacy of pharmaceutical
treatment is modest, fatigue management strategies
play a vital role. These include avoiding the build up of
fatigue and conserving energy. Fatigue management
education delivered in a face to face format in
community settings has been found to significantly
reduce impact of fatigue on daily life, improve quality
of life and increase self-efficacy in randomised trials16.
Other ways of delivering the course such as by
teleconference were also successful17.
5.
Department of Health. Supporting people with long term

conditions to self-care London: DOH; 2007
6.
Kennedy A. Rogers A. Improving self-management skills: a

whole systems approach. Br J Nurs 2010;10(1):734-8.
7.
Expert patients programme. Healthy lives equal healthy

communities - the social impact of self-management.
London: EPP; 2011.
8.
Expert patients programme. Self-care reduces costs and

improves health - the evidence. London: EPP; 2010.
9.
Hughes SA. Promoting self-management and patient

independence. Nurs Stand 2004;19(10):47-52.
10. de Silva D. Helping people help themselves a review of the

evidence considering whether it is worthwhile to support
self- management. London: The Health Foundation ;2011.
11. Embrey N. Information provision for patients with a diagnosis
of multiple sclerosis - do nurses have an impact on selfmanagement? Nurs Times 2005;101(34):34-6.
12. Brechin M, Burgess M, Dunk J, et al. Taking Control - a pack
to facilitate teaching people with newly diagnosed MS. Way
Ahead 2001;5(2):7-8.
13. Lorig K, Ritter PL, Plant K. A disease-specific self-help
program compared with a generalised chronic disease selfhelp program for arthritis patients. Arthritis Rheum
2005;15;53(6):950-7.
14. Fraser R, Johnson E, Ehde D, et al. Patient self-management
in multiple sclerosis. Consortium of Multiple Sclerosis Centers
White Paper. USA: CMSC; 2009.
15. Barlow J, Edwards R, Turner A. The experience of attending a
lay-led, chronic disease self-management programme from
the perspective of participants with multiple sclerosis. Psychol
Health 2009;24(10):1167-80.
16. Mathiowetz V, Finlayson M, Matuska K, et al. A randomised
trial of energy conservation for persons with multiple
sclerosis. Mult Scler 2005;11(5):592-601.
17. Finlayson M, Preissner K, Cho C, et al. Randomised trial of a
teleconferencedelivered fatigue management program for
people with multiple sclerosis. Mult Scler 2011;17(9):1130-40.
MS Trust resources
MS and me a self-management
guide to living with MS
At work with MS managing life and work
Living with fatigue
Diet factsheet
References
1.
Schilling LS, Grey M, Knafl KA. The concept of self-management

of type 1 diabetes in children and adolescents: an evolutionary
concept analysis. J Advan Nurs 2002;37(1):87-99.
2.
Department of Health. Improving care improving lives - self

care - a real choice. London: DOH; 2005.
3.
Bandura A. Self-efficacy: Toward a unifying theory of

behavioral change. Psych Rev 1977; 84(2):191-215.
4.
Department of Health. The expert patient - a new approach to

chronic disease management for the 21st century. London:
DOH; 2001.
Move it for MS DVD

Exercises on the web
www.mstrust.org.uk/exercises
Stay active
www.mstrust.org.uk/stayactive
StayingSmart
www.stayingsmart.org.uk
21

Relapse
Section 2
should explain the procedure to follow if the patient
thinks they may be having a relapse.
Relapse
Approximately 85% of people diagnosed with MS
will have relapsing remitting MS. Relapsing
remitting MS is characterised by a series of relapses
(also referred to as an attack, a flare up, an episode
or exacerbation), interspersed with periods of
remission.
A number of UK MS specialist centres have audited

their relapse management services and developed
protocols to ensure that anyone experiencing a
relapse is assessed and offered appropriate treatment
as soon as possible3,8-11.
Symptoms similar to those of a relapse can occur when

there is an infection, often a urinary or respiratory
infection. It is important to differentiate a relapse from a
A relapse is defined as a sudden episode of symptoms
pseudo-relapse, which is a temporary worsening of preor disability, in the absence of fever or infection, which existing symptoms due to concurrent fever, illness or
lasts at least 24 hours, and is a neurological
infection. Pseudo-relapses never present with new
disturbance typical of MS1. A relapse must occur at
symptoms, often last only a few hours, and management
least 30 days since the start of a previous episode.
should be aimed at treating the underlying infection.
Urinary tract infections may be asymptomatic so routine
Relapses occur spontaneously and are thought to be
screening is recommended3. It is important to rule out
due to an episode of acute inflammation within the
infection before commencing treatment with steroids.
CNS. Frequency of relapses is very variable, some
people will experience several in a year whilst others
Steroids
will be relapse free for many years. In one
If the symptoms of the relapse are not due to infection
retrospective study in a population of 2,477
and are affecting day to day function, treatment with a
relapsing remitting patients, over three quarters
short course of high dose steroids is recommended.
2
experienced a five year relapse-free period . On
Studies have shown that steroids are effective in
average, people will experience approximately 0.6
speeding up recovery from relapses but make no
relapses per year with frequency gradually
difference either to the degree of recovery or to the
3
decreasing during the course of the condition .
long-term progression of the condition4.
People with secondary progressive MS may also
experience superimposed relapses and relapses have
been reported in people with primary progressive MS4.
The symptoms experienced depend on the area of the
brain or spinal cord affected. Typically, a relapse
evolves over a few days, reaches a plateau, and then
remits to a variable degree over a few weeks or
months. Some relapses are relatively mild while others
may cause more serious problems; most relapses do
not require hospitalisation.
Relapses can have a significant impact not only on
physical symptoms but also on social, financial and
psychological well-being of those affected5,6. They
may provoke fresh feelings of bereavement or fear.
People may recover completely in episodes of
remission or may have residual disability.
Incomplete recovery has been found to range from
20 to 60% in different studies7.
Managing relapses
Different centres have different approaches to
managing relapses. For many people, their MS
nurse will be the first point of contact, for others it
could be their neurologist or GP. Following
diagnosis, an MS nurse or other health professional
22
The NICE Clinical Guideline12 recommends that any

individual who experiences an acute episode sufficient
to cause distressing symptoms or an increased
limitation on activities should be offered a short
course of high-dose corticosteroids. The course should
be started as soon as possible after onset of the
relapse and should be either:
intravenous methylprednisolone, 500mg-1g daily,

for between 3-5 days or
high-dose oral methylprednisolone, 500mg-2g

daily, for between 3-5 days.
Frequent (more than three times a year) or prolonged

(longer than three weeks) use of corticosteroids
should be avoided.
A comparison of oral and intravenous corticosteroid
treatments in MS shows that there are no major
differences in clinical outcomes and both treatments
appear to be equally effective and safe13.
In the short-term, the side effects of methylprednisolone
are usually minor and transient, but may include:
indigestion
mood changes/mood swings
www.mstrust.org.uk

Relapse
altered sleep pattern
increased appetite
metallic taste
flushing of the face.
Special care is needed for people who have diabetes,

and for those with previous gastric problems who may
need medication to protect the stomach. Long-term
treatment should normally be avoided due to side
effects including, weight gain, acne, cataracts,
osteoporosis (thinning of the bones, particularly the
head of the thigh bone), and diabetes.
Other treatments
There are many other management considerations
apart from possible treatment with steroids.
Depending on the symptoms, their severity and how
they are affecting daily life, various adjustments and
equipment may be necessary. For example, a mother
with sensory symptoms in her hands might require
help to care for her young baby and to cook.
Someone experiencing problems with walking may
benefit from a walking stick. It may be necessary to
take time off work and/or temporarily reduce activities.
There is evidence that recovery from relapse is
improved if neurorehabilitation is provided at the
same time as steroids are prescribed14. When
someone experiences a sudden increase in disability
or dependence, the NICE Clinical Guideline12
recommends the individual should be:
given support, as required and as soon as practical,

both in terms of equipment and personal care
referred to a specialist neurological
rehabilitation service.
The urgency of the referral should be judged at the

time, and this referral should be in parallel with any
other medical treatment required.
Experiencing a relapse is often a very stressful time for
both people with MS and their families who typically
have a lot of unanswerable questions about when their
symptoms will resolve, whether they will make a full
recovery, the likelihood of further relapses or if the
relapse is the start of a more progressive phase. At this
time the need for reassurance is high. Health
professionals sensitive to these issues can provide the
communication and counselling skills needed.
Reducing the risk of relapses

Disease modifying therapies reduce the number and
severity of relapses. See p24 Disease modifying drug
therapies.
Life style issues may be important in reducing the risk

of relapses. A well-balanced diet and regular exercise
will promote good health and can help reduce the risk
of relapse triggers such as infections. Strong evidence
suggests that relapses can be triggered by infections,
during the three month period after giving birth and
stressful life events15. Vaccinations against influenza,
hepatitis B and tetanus appear to be safe. Surgery,
general and epidural anaesthesia and physical trauma
are not associated with an increased risk of relapses.
References
1.
Polman CH, Reingold SC, Banwell B, et al. Diagnostic criteria for

multiple sclerosis: 2010 revisions to the McDonald criteria. Ann Neurol
2011;69(2):292-302.
2.
Tremlett H, Zhao Y, Joseph J, et al. Relapses in multiple sclerosis are

age- and time-dependent. J Neurol Neurosurg Psychiatry
2008;79(12):1368-74.
3.
Ennis M, Shaw P, Barnes F, et al. Developing and auditing multiple

sclerosis relapse management guidelines. Br J Neurosci Nurs
2008;4(6):266-71.
4.
Sellebjerg F, Barnes D, Filippini G, et al. EFNS guideline on treatment of

multiple sclerosis relapses: report of an EFNS task force on treatment of
multiple sclerosis relapses. Eur J Neurol 2005;12(12):939-46.
5.
Halper J. The psychosocial effect of multiple sclerosis: the impact of

relapses. J Neurol Sci 2007;256 Suppl 1:S34-8.
6.
Kalb R. The emotional and psychological impact of multiple sclerosis

relapses. J Neurol Sci 2007;256 Suppl 1:S29-33.
7.
Leone MA, Bonissoni S, Collimedaglia L, et al. Factors predicting

incomplete recovery from relapses in multiple sclerosis: a prospective
study. Mult Scler 2008;14(4):485-93.
8.
Matheson F, Porter B. The evolution of a relapse clinic for multiple

sclerosis: challenges and recommendations. Br J Neurosci Nurs
2006;2(4):180-6.
9.
Warner R, Thomas D, Martin R. Improving service delivery for relapse

management in multiple sclerosis. Br J Nurs 2005;14(14):746-53.
10. Embrey N, Lowndes C. Benchmarking best practice in relapse

management of multiple sclerosis. Nurs Stand 2003;17(22):38-42.
11. Porter B, Matheson F, Chataway J, et al. Key steps to delivery of a personcentred relapse service [Internet]. Letchworth Garden City: MS Trust; 2010
[cited 2011 Sept 1]. www.mstrust.org.uk/downloads/key_steps.pdf.
12. National Institute for Health and Clinical Excellence. Multiple sclerosis management of multiple sclerosis in primary and secondary care. NICE
Clinical Guideline 8. London: NICE; 2003.
13. Burton JM, OConnor PW, Hohol M, et al. Oral versus intravenous
steroids for treatment of relapses in multiple sclerosis. Cochrane
Database Syst Rev 2009;(3):CD006921.
14. Craig J, Young CA, Boggild M, et al. A randomised controlled trial
comparing rehabilitation against standard therapy in multiple sclerosis
patients receiving intravenous steroid treatment. J Neurol Neurosurg
Psychiatry 2003;74(9):1225-30.
15. Dhooghe MB, Nagels G, Bissay V, et al. Modifiable factors influencing
relapses and disability in multiple sclerosis. Mult Scler 2010;16(7):773-85.
MS Trust resources
Key steps to delivery of a
person-centred relapse service.
www.mstrust.org.uk/downloads/key_steps.pdf.
23

Steroids
Drug therapies
Significant advances have been made in the last fifteen
years in developing drug therapies that offer real
benefit to people who have MS. It is therefore
important that whether a person is newly diagnosed,
or has more advanced MS, they are managed by a
neurologist with special interest in MS.
The aim of effective therapy is to reduce frequency
and severity of relapses, prevent disability directly
attributable to relapses, relieve symptoms, prevent
or delay disability arising from disease progression
and promote tissue repair to treat established
progression. Drugs used in the treatment of MS can
therefore be considered in three categories1:
treatment of relapse - steroids
disease modification
individual symptom relief (described in the sections

on symptoms and symptomatic management).

Disease modifying therapies are used with a view to
changing the long-term course of MS. The disease
modifying drugs currently licensed for MS work by
reducing the number and severity of relapses. As a
result, they have only been found to be effective for
people with relapsing remitting MS and for some people
with secondary progressive MS who continue to relapse.
As yet, there is no disease modifying treatment for
progressive MS, due to the neurodegenerative process
involved; treatment of which is thus based on the
management of symptoms.
Disease modifying therapies licensed to

treat MS
The table right describes the disease modifying
therapies that are licensed in the UK for use in
relapsing remitting MS, secondary progressive MS
and clinically isolated syndrome.
The Association of British Neurologists (ABN) sets out
the prescribing criteria for usage of disease modifying
therapies and these are updated on a regular basis5.
Steroids
Steroids are the standard treatment for a relapse in MS
and have been in use for about 50 years. The NICE
guidelines3 state that any individual who experiences
an acute episode (including optic neuritis) sufficient to
cause distressing symptoms or an increased limitation
on activities should be offered a course of high dose
steroids to be started as soon as possible after the
onset of the relapse. This should be either:
IV methylprednisolone - 500mg-1g daily for

3-5 days or
high-dose oral methylprednisolone - 500mg-2g

daily for 3-5 days.
See page 22 Relapse.
24
www.mstrust.org.uk

Disease modifying treatments

Disease modifying treatments
Generic name
Brand
name
Administration
Dosage
Indication
beta interferon 1a
Avonex
IM, once weekly
30g
RRMS, SPMS, CIS
beta interferon 1a
Rebif
SC, three times

per week
22g or
44g
RRMS, SPMS
beta interferon 1b
Betaferon
SC, alternate days
250g
RRMS, SPMS, CIS
beta interferon 1b
Extavia
SC, alternate days
250g
RRMS, SPMS, CIS
glatiramer acetate
Copaxone
SC, daily
20mg
RRMS, CIS
Gilenya
Oral, daily
0.5mg
only highly
active or rapidly
evolving severe
RRMS
SELF-ADMINISTERED
fingolimod
HOSPITAL-ADMINISTERED
natalizumab
Tysabri
IV infusion,
every 4 weeks
300mg
only highly
active or rapidly
evolving severe
RRMS
mitoxantrone
Novantrone
IV infusion,
every 3 months
for 2 years
12mg/m2
only highly
active MS
Notes:
RRMS: relapse remitting MS; SPMS: secondary
progressive MS; CIS: Clinically isolated syndrome.
IM: Intramuscular; SC: Subcutaneous; IV: intravenous.
Beta interferon 1a and 1b are licensed to treat
secondary progressive MS where relapses are still a
major feature.
Natalizumab is licensed for people with highly active
relapsing remitting MS who have failed to respond to
beta interferon treatment and for people with rapidly
evolving severe relapsing remitting MS (two or more
relapses a year).
Fingolimod has been licensed for the treatment of

rapidly evolving severe relapsing remitting MS (two
or more relapses a year), and as a second line
treatment for people whose MS remains active
despite treatment with one of the beta interferon
drugs or glatiramer acetate.
Mitoxantrone, has not been licensed for use in MS
in the UK although it has in several European
countries and the US. It is therefore used off-license in
some specialist centres.
Infusion of mitoxantrone (20mg) in combination with
methylprednisolone (1g) may also given every four
weeks for six months.
25

Beta interferons and glatiramer acetate
1b, are available for treatment of MS, the

difference resulting from the protein
manufacturing process. Beta interferon modulates
T-cell and B-cell activity and reduces the bloodbrain barrier permeability to inflammatory cells22.
Beta interferons
and glatiramer acetate
Glatiramer acetate and the beta interferons are
different drugs with different modes of action4.
Large randomised trials have demonstrated these
drugs reduce the number and severity of relapses
by approximately 30% and the number of new
lesions on magnetic resonance imaging (MRI)6-12.
Results from clinical trials are reflected in clinical
use13. Beta interferons appear to have beneficial
effects on quality of life and may slow the accruing
of disability for patients with relapsing remitting
MS14 particularly when treatment is started early in
the disease course. However, more evidence is
required to support an influence on the long-term
prognosis of MS15.
The Association of British Neurologists (ABN) has
set out prescribing criteria for the beta interferons
and glatiramer acetate for both relapsing remitting
and, where appropriate, secondary progressive
MS5. The criteria reflect clinical experience that
treatment soon after the onset of MS is more
effective in the long-term than treatment at a later
stage of MS.
A number of studies have indicated that starting
disease modifying treatment after a clinically
isolated syndrome (CIS) - a persons first episode of
neurological symptoms (lasting at least 24 hours) delays the onset of MS and can have long-term
benefits, such as significant suppression of
subsequent relapse and MRI lesion formation16-20. In
spite of this evidence, the use of disease modifying
drug treatment after a CIS remains controversial21.
The current ABN guidelines only recommend that
neurologists consider prescribing disease modifying
drugs after a CIS if there is also MRI evidence
suggesting a high likelihood of developing MS,
and after discussing the risks and the benefits of
treatment with the patient.
Glatiramer acetate is a synthetic combination of

four amino acids, resembling the myelin protein
surrounding nerve fibres. It is thought to lessen the
immune reaction involved in demyelination by
shifting the T helper (Th)1 lymphocytes in patients
with MS towards a predominance of Th2
phenotype and by inducing the expression of antiinflammatory cytokines23,24.
As both the beta interferons and glatiramer acetate
are proteins and would be broken down in the
digestive tract, they are given by either
subcutaneous or intramuscular injection.
Dosage regimes vary and long-term compliance
can be an issue. The disease modifying drugs are
now available in easy-to-use formulations,
including thinner needle size and auto-injector
devices, which improve adherence, convenience,
and help to manage self-injection anxiety in
patients with MS25,26.
There have been a number of comparative studies
between different types of beta interferon, and
between beta interferon and glatiramer acetate.
Most comparisons have shown no major difference
in efficacy although the higher, more frequently
dosed beta interferons (Rebif, Betaferon and
Extavia) may have a greater efficacy than the once
a week regime (Avonex)27-34 in short-term studies of
less than two years. In a minority of people the
immune system reacts to beta interferon and
produces neutralising antibodies that reduce its
efficacy; although neutralising antibodies can
disappear they may persist. Neutralising antibodies
are easily detected by a simple laboratory test.
Interferons are cytokines, small proteins secreted

by cells as a response to a variety of agents, in
particular viruses. The body naturally produces
several types of interferon: the main ones are
alpha, beta and gamma. Alpha interferons are
useful in cancer treatments, whereas gamma
interferons have been found to increase relapses in
MS. Two different forms of beta interferon, 1a and
26
www.mstrust.org.uk

Natalizumab (Tysabri)
Natalizumab (Tysabri)
Natalizumab is administered as a single intravenous
infusion (300mg) via a drip once every four weeks in
a clinical setting under the supervision of a suitably
qualified health professional.
Natalizumab is a recombinant monoclonal
antibody against alpha-4 integrins. This is the first
in a new class of drugs known as selective
adhesion molecule (SAM) inhibitors. They act in
MS by preventing the migration of immune cells
across the blood-brain barrier, which would result
in inflammation and myelin destruction35.
Natalizumab has been licensed for use with people
with highly active relapsing remitting MS (two or
more disabling relapses in one year), and one or
more gadolinium-enhancing lesions on MRI or a
significant increase in T2 lesion load compared
with a previous MRI. Results of large randomised
clinical trials in patients with relapsing remitting
MS showed that over a two year period
natalizumab reduces the occurrence of relapse by
around two thirds, has a 92% reduction in
gadolinium enhancing lesions in MRI, and
produces significant benefits on the risk of
progression of disability and on quality of life36.
Natalizumab has not been studied in CIS
populations.
Health professionals, patients and their carers need
to be aware that natalizumab can be associated
with infections, including the brain infection
progressive multifocal leukoencephalopathy (PML).
PML is a rare, progressive, and potentially fatal
demyelinating disease of the CNS that is caused by
a mutant form of JC virus, which usually remains
latent. The factors leading to activation of the
infection are not fully understood.
treatment duration, especially beyond 2 years
immunosuppressant use prior to receiving

natalizumab
presence of anti-JCV antibodies.
Anti-JCV antibody status identifies different levels of

risk for PML in natalizumab-treated patients. Patients
who are anti-JCV antibody positive are at an
increased risk of developing PML compared to
patients who are anti-JCV antibody negative.
Patients who have all three risk factors for PML carry
the highest risk. The JC virus is present in
approximately 50% of the adult population. As the
JC virus can be acquired at any time, annual testing
is recommended in those who initially test negative.
The Medicines and Healthcare Products Regulatory
Agency (MHRA) has recommended that patients
are made aware of the associated risk of PML with
treatment of natalizumab, especially beyond two
years, and natalizumab should be promptly
discontinued if PML is suspected.
Neutralising antibodies (NAbs)

Treatment with the beta interferon drugs (Avonex,
Betaferon, Extavia and Rebif) and natalizumab
(Tysabri) can lead to the development of
neutralising antibodies (NAbs) in some patients
with MS, which can reduce the effectiveness of
these drugs46,47. Patients can switch to an
alternative treatment to help restore the
effectiveness of disease modifying therapy, and in
some people, the neutralising antibodies will
disappear over time.
The European Medicines Agency (EMA) recently

reviewed natalizumab and the associated risk of
PML37. The report concluded that the risk of PML
increases after two years of treatment, although
this risk remains relatively low (less than three
per 1,000) and the benefits of the drug continue
to outweigh the risks for patients with highly
active relapsing remitting MS37. Three independent
risk factors are associated with an increased risk
of PML38:
27

Fingolimod (Gilenya)
Fingolimod (Gilenya)
Fingolimod works by binding to receptors on the
surface of lymphocytes, called sphingosine-1phosphate receptors (S1P-R). This results in a large
proportion of the lymphocytes becoming retained
in the thymus or secondary lymph organs. By
suppressing the migration of lymphocytes from
circulating in the blood and entering the central
nervous system, fingolimod reduces the
autoimmune attack on nerve cells in the brain and
spinal cord39,40.
In addition, there is evidence that fingolimod may
have a direct effect on nerve cell damage and
stimulate remyelination by modulating the same
sphingosine receptors in the central nervous system41.
Fingolimod is the first disease modifying therapy
for MS which can be taken in an oral formulation,
as a capsule.
The EMA only approved fingolimod (0.5mg, daily)
as a second line disease modifying treatment for
patients with MS who continue to have relapses or
find the relapse rate has increased despite a years
treatment with one of the first line drugs (Avonex,
Betaferon, Copaxone, Extavia, Rebif). It is also
approved for use in patients with rapidly evolving
severe relapsing remitting MS (two or more
relapses a year).
Based on five years of safety data, fingolimod
treatment can cause temporary changes in heart rate,
blood pressure, shortness of breath and macular
oedema (a swelling in the eye affecting vision)42. The
first dose of fingolimod should be taken in hospital so
that these factors can be monitored.
Fingolimod was licensed based on data42-44 from
two major phase III studies in participants with
relapsing remitting MS. Fingolimod showed a 30%
reduction in progression of disability and a
reduction in annualised relapse rate by about 50%.
There is no data on the use of fingolimod in patients
with CIS, progressive MS or as add-on therapy to selfinjectable DMTs. However, in the INFORMS study,
fingolimod is being evaluated for primary progressive
MS based on the evidence that the drug may have a
direct effect on nerve repair40,45.
28
www.mstrust.org.uk

Mitoxantrone
Drugs currently used in MS licensed for other indications

Current thinking surrounding the aetiology of MS is
that it has an autoimmune component.
Immunoregulators have been proven effective in
the treatment of other autoimmune diseases, such
as psoriasis and rheumatoid arthritis, and this
rationale has led to their use in MS.
Immunoregulators commonly work by inhibiting
the division and proliferation of immune cells.
NICE Clinical Guidelines3 recommend that
mitoxantrone (Novantrone) and azathioprine are
reserved for use in specific circumstances, by an expert
in use of the drugs, and with close monitoring of
adverse events. Each specialist MS centre that
prescribes these agents will therefore have local
protocols and clinical guidelines for their use.
There are a number of other agents that have not
been established for use by phase III trials but might
be used to modify the disease course of MS. These
include the immunosuppressants, azathioprine
(Imuran), cyclophosphamide, mycophenolate mofetil
and methotrexate; bone marrow suppression; and
immunomodulatory approaches such as intravenous
immunoglobulin and plasma exchange. The usage of
these agents has decreased since natalizumab and
fingolimod have been licensed.
Mitoxantrone (Novantrone)
Mitoxantrone is licensed in the UK as a chemotherapy
agent and acts by inhibition of DNA repair. Based on
its associated safety profile (especially cardiomyopathy
and treatment-related leukaemia), it is suggested that
mitoxantrone should be used over a short time
(limited to two years) to treat aggressive forms of
relapsing remitting MS or in the early stages of
secondary progressive MS where relapses are still a
significant feature and disease progression is not
controlled by other immunomodulatory drugs48,49.
Recent studies have suggested that the use of shortterm mitoxantrone (for three to six months) as an
induction therapy followed by a maintenance therapy,
such as glatiramer acetate or beta interferon, may be
a beneficial treatment option in patients with active,
aggressive, relapsing remitting MS50,51. There is no
robust evidence to support the use of mitoxantrone in
primary progressive MS, or in the later stages of
secondary progressive MS (EDSS>6.0)52,53.
29

Disease modifying therapies currently in clinical trials for MS
Disease modifying therapies

currently in clinical trials for MS
There is the potential for a more advanced therapeutic
choice in the future if new drugs become available
for MS with more specific targets, such as the
monoclonal antibodies and oral treatments currently
in development. These have the potential of
increasing the therapeutic efficacy and offer some
neuroprotection from MS, albeit they may raise new
safety and tolerability problems. Listed below are
some of the disease modifying therapies that are
most advanced in clinical trials at the current time.
Laquinimod is an oral therapy which shows

immunomodulatory activity by affecting the levels
of certain cytokines and trafficking immune cells
into the CNS. Phase III data on laquinimod showed
a 23% reduction in annual relapse rate, a 36%
decrease in disability progression and a 33%
reduction in brain atrophy after two years of daily
treatment. Laquinimod appeared to have a
favourable safety and tolerability profile. Slightly
lower levels of efficacy were shown in the phase III,
BRAVO, study comparing laquinimod 0.6mg with
interferon beta 1a over a two year period.
Daclizumab is a monoclonal anti-CD25 antibody
which inhibits activation of T-cells. The therapy,
given as an injection under the skin or intravenous
infusions, reduced the number of new or enlarged
lesions in patients by 72% (25% at a lower dose)60.
Daclizumab was generally well tolerated.
Treatment with daclizumab in combination with
beta interferon is significantly more effective than
beta interferon alone for active relapsing MS61. The
current DECIDE trial is a phase III comparator study
with interferon beta 1a.
Teriflunomide is an oral agent which reduces the

numbers of both B cells and T cells. In addition, it
appears to have other immunomodulatory and antiinflammatory actions. Teriflunomide reduced relapse
rate by 31% at high dose (14mg daily) and the risk of
disability progression (sustained for 12 weeks) by
30%54. Various phase III studies are evaluating the
effectiveness of teriflunomide compared to interferon
beta 1a, as add-on therapy with beta interferon, and in
Ocrelizumab (RG 1594), a monoclonal antibody
delaying conversion from a first CIS to clinically
targeting CD20, has demonstrated a significant
definite MS.
reduction in disease activity as measured by brain
lesions (96% for high dose and 89% for low dose)
BG-12 (dimethyl fumarate) is an oral agent, which
and relapse rate (73% for high dose and 80% for
produces both anti-inflammatory and neuroprotective
low dose) over 24 weeks62. This agent is also being
effects by the activation of the NF-E2-related factor 2
studied in patients with primary progressive MS.
(Nrf2) pathway55,56. Phase III results showed that
following two years of treatment BG-12 reduced the
proportion of patients who relapsed by 49%, the
number of lesions measured by MRI scans and the rate
of disability progression by 53% compared with
placebo (38%).
Alemtuzumab (Campath) is a monoclonal antibody
that targets the T-cells involved in destroying myelin.
Alemtuzumab is administered as an annual infusion.
Phase III studies include the CARE-MS I study
comparing alemtuzumab and interferon beta 1a and
CARE-MS II. Initial results from the CARE-MS I showed
that alemtuzumab reduced relapses by 55% compared
to interferon beta 1a over two years58. The effect on
disease progression was comparable, with 8% of the
alemtuzumab group and 11% of interferon beta group
showing a worsening in their disability score. Four year
follow-up data from phase II studies show 91% of
people have no worsening of their disability with
alemtuzumab compared to 68% taking interferon beta
1a, and by five years 65% were free of clinically active
MS compared to 27% on interferon beta 1a57-59.
30
Other research approaches to

modifying the course of MS
It is now recognised that immunomodulatory
drugs are of maximum benefit before axonal
damage has occurred and clinical progression has
been established. The aim of therapies therefore
must be not only to reduce frequency of relapses63
but also to repair neuronal damage and prevent
transition to a secondary progressive course. The
last decade has seen development of therapies that
moderately affect the course of the disease where
inflammation predominates over degeneration.
The challenge to repair and prevent damage
caused by MS remains.
Remyelination using stem cell therapy

Under specific conditions, stem cells have the
ability to divide and potentially differentiate into
cells with special functions such as nerve or muscle
cells. Theoretically, stem cells may have the
potential to restore the damage caused by MS and
www.mstrust.org.uk

may modulate the immune system to prevent

further damage.
Neuronal repair could be achieved by encouraging
stem cells already present in the body to develop
into, for example, oligodendrocytes64. Alternatively,
cells could be transplanted that would go on to
differentiate into a therapeutic cell type.
Research with stem cells is still at a very early stage
and has involved some small clinical trials of
autologous stem cell transplantation (ASCT, also
known as HSTC). ASCT has been shown to induce
remission in people with rapidly evolving relapsing
remitting and secondary progressive MS. Patients
may have either surgical collection from the bone
marrow or drug-induced mobilisation of
haematopoietic stem cells from the bloodstream.
Participants are treated with high dose
immunosuppressants to suppress their immune
system. Bone marrow cells are harvested,
expanded in the clinic, and then returned to the
patients blood stream by infusion.
In 2006, the European Group for Blood and Marrow
Transplantation (EBMT) reported on a retrospective
survey of 178 patients with MS who had received
stem cell transplants for MS65. The analysis showed
that the transplantation of haematopoietic stem cells
produced a slowing down of disease progression in a
sub-set of patients affected by severe, progressive MS.
In 2011, the same group reported mixed results on
the long-term effects of stem cell therapy, after
participants were followed for between two and 15
years66. The stem cell treatment appeared to be most
beneficial for young patients (35 years or less), those
with recent diagnoses, and those with highly
inflammatory MS. Patients with progressive MS
responded less favourably. Overall, 16 of the 35
patients showed a small improvement in EDSS
disability scale, lasting for an average of two years.
Two of these remained improved over seven and
eight years, respectively. Seven worsened during
follow-up, but remained better than their disability
level at the start of treatment, while seven others
worsened. Two deaths were attributed to the
treatment.
Stabilisation of MS was also reported from a pilot

study68 in six people with stem cells derived from
their own bone marrow. In contrast to previous
studies, stem cells were not pre-treated to increase
certain subsets of cells and patients did not receive
immunosuppressive preconditioning before their
bone marrow stem cells were infused intravenously.
This research will continue in a trial with 80 people
with MS.
Research into stem cells is still in a very early stage,
and it is likely to be many years, possibly as much
as twenty years, before stem cell treatments may
become routinely available for the treatment of
MS. More research must be undertaken to ensure
that large numbers of stem cells can be routinely
generated before transplantation into a patient
and that stem cells develop into the specific cell
type that is required. It will also be important to
show that cells can survive, integrate, function and
not cause harm to the recipient.
In the meantime, patients with MS may need to be
cautious of private stem cell treatments that are
not part of clinical trials. The International Society
for Stem Cell Research (ISSCR) has published a
patient handbook69 to help people evaluate stem
cell therapies they may be considering.
Neuroprotection using cannabis derivatives

Clinical trials into cannabis have shown some
symptomatic relief of MS. Sativex (delta-9
tetrahydrocannabinol and cannabidiol) was the
first cannabis-based medicine to be licensed in the
UK for use as a second-line option for MS-related
spasticity. Studies have also shown evidence of
anti-inflammation, promotion of remyelination and
neuroprotection70-72.
CUPID is a long-term research trial looking at
whether tetrahydrocannabinol (THC), one of the
active ingredients in cannabis, can slow the
increase of disability in people with progressive
multiple sclerosis. The trial will also try to assess
the long-term safety of cannabis-based medicines.
References
In another small trial in patients failing on

interferon therapy67, all patients showed no
worsening of disability, and 17 out of 21 improved
EDSS score by at least one point. Also 16 people
experienced no further relapses. This therapy is
being further validated in a larger trial in North and
South America.
1.

2002;359(9313):1221-31.
2.
Polman CH, Reingold SC, Banwell B, et al. Diagnositic criteria for

multiple sclerosis: 2010 revisions to the McDonald criteria. Ann
Neurol 2011;69(2):292-302.
3.

31

4.
Yong VW. Differential mechanisms of action of interferon beta

and glatiramer acetate in MS. Neurology 2002;56(6):802-8.
24. Schrempf W, Ziemssen T. Glatiramer acetate: mechanisms of

action in multiple sclerosis. Autoimmun Rev 2007;6(7):469-75.
5.
Association of British Neurologists. Revised (2009) Association of

British Neurologists (ABN) guidelines for prescribing in multiple
sclerosis. London: ABN; 2009.
6.
Multiple Sclerosis Study Group. Interferon beta 1b in the

treatment of multiple sclerosis: final outcome of randomised
controlled trial. Neurology 1995;45:1277-85.
25. Al-Sabbagh A, Bennet R, Kozma C, et al. Medication gaps in

disease-modifying therapy for multiple sclerosis are associated
with an increased risk of relapse: Findings from a national
managed care database. J Neurol 2008;255(Suppl 2):S79.
7.
8.
9.
Rudick RA, Goodkin DE, Jacobs LD, et al. Impact of interferon

beta 1a on neurologic disability in relapsing remitting multiple
sclerosis. MSCRG group. Neurology 1997;49(2):358-63.
PRISMS (Prevention of Relapses and Disability by Interferon beta1a Subcutaneously in Multiple Sclerosis) Study Group.
Randomised double-blind placebo-controlled study of interferon
beta-1a in relapsing remitting multiple sclerosis. Lancet
1998;352(9139):1498-504.
OWIMS study group. Evidence of interferon beta 1a dose
response in relapsing remitting MS: The OWIMS study.
Neurology 1999;53(4):679-86.
10. PRISMS study group. PRISMS-4: Long-term efficacy of interferonbeta-1a in relapsing MS. Neurology 2001;56(12):1628-36.
11. Johnson KP, Brooks BR, Cohen JA, et al. Copolymer 1 reduces
relapse rate and improves disability in relapsing remitting
multiple sclerosis: results of a phase III multicenter, double-blind,
placebo-controlled trial. The Copolymer 1 Multiple Sclerosis
Study Group. Neurology 1995;45(7):1268-76.
12. Filippi M, Rovaris M, Rocca MA, et al. Glatiramer acetate reduces
the proportion of new MS lesions evolving into black holes.
Neurology 2001;57(4):731-3.
13. Dubois BD, Keenan E, Porter B, et al. Interferon beta in multiple
sclerosis: experience in a British specialist multiple sclerosis
centre. J Neurol Neurosurg Psychiatry 2003;74(9):946-9.
14. Bermel RA, Weinstock-Guttman B, Bourdette D, et al.
Intramuscular interferon beta-1a therapy in patients with
relapsing-remitting multiple sclerosis: a 15-year follow-up study.
Mult Scler 2010;16(5):588-96.
15. Ebers GC, Traboulsee A, Li D, et al. Analysis of clinical outcomes
according to original treatment groups 16 years after the pivotal
IFNB-1b trial. J Neurol Neurosurg Psychiatry 2010;81(8):907-12.
16. Coyle PK. Early treatment of multiple sclerosis to prevent
neurologic damage. Neurology 2008;71(24 Suppl 3):S3-7.
17. Jones JL, Coles AJ. New treatment strategies in multiple sclerosis.
Exp Neurol 2010;225(1):34-9.
18. Comi G, Martinelli V, Rodegher M, et al. Effect of glatiramer
acetate on conversion to clinically definite multiple sclerosis in
patients with clinically isolated syndrome (PreCISe study): a
randomised, double-blind, placebo-controlled trial. Lancet
2009;374(9700):1503-11.
19. Kappos L, Polman CH, Freedman MS, et al. Treatment with
interferon beta 1b delays conversion to clinically definite and
McDonald MS in patients with clinically isolated syndromes.
Neurology 2006;67(7):1242-9.
27. Durelli L, Verdun E, Barbero P, et al. Every-other-day interferon

beta1b versus once weekly interferon beta 1a for multiple
sclerosis: results of a 2 year prospective randomised multicentre
study. Lancet 2002;359(9316):1453-60.
28. Panitch H, Goodkin DS, Francis G, et al. Randomised
comparative study of interferon b1a treatment regimes in MS.
The EVIDENCE trial - (Evidence for interferon dose effect:
European-North American comparative efficacy). Neurology
2002;59:1496-1506.
29. Antonetti F. Fionocchiaro O. A comparison of two recombinant
IFNb preparations used in the treatment of relapsing-remitting
multiple sclerosis. J Interferon Cytokine Res 2002;22:1181-84.
30. Vartanian T. An examination of the results of the EVIDENCE,
INCOMIN and phase III studies of interferon beta products in
the treatment of multiple sclerosis. Clin Ther 2003;25(1):105-18.
31. Smith B, Carson S, Fu R, et al. Drug class review: diseasemodifying drugs for multiple sclerosis: final update 1
report. Portland: Oregon Health & Science University;
2010 ID: 21348046.
32. OConnor P, Filippi M, Arnason B, et al. 250 microg or 500
microg interferon beta-1b versus 20 mg glatiramer acetate in
relapsing-remitting multiple sclerosis: a prospective, randomised,
multicentre study. Lancet Neurol 2009;8(10):889-97.
33. Mikol DD, Barkhof F, Chang P, et al. Comparison of
subcutaneous interferon beta-1a with glatiramer acetate in
patients with relapsing multiple sclerosis (the REbif vs Glatiramer
Acetate in Relapsing MS Disease [REGARD] study): a multicentre,
randomised, parallel, open-label trial. Lancet Neurol
2008;7(10):903-14.
34. Cadavid D, Wolansky LJ, Skurnick J, et al. Efficacy of treatment of
MS with IFNbeta-1b or glatiramer acetate by monthly brain MRI
in the BECOME study. Neurology 2009;72(23):1976-83.
35. Steinman L. Blocking adhesion molecules as therapy for multiple
sclerosis: natalizumab. Nat Rev Drug Discov 2005;4(6):510-18.
36. Polman CH, OConnor PW, Havrdova E, et al. A randomised,
placebo-controlled trial of natalizumab for relapsing multiple
sclerosis. N Engl J Med 2006;354(9):899-910.
37. European Medicines Agency (EMA). Tysabri: European Public
Assessment Report. [cited 2011: July 28]
38. Kappos L, Bates D, Edan G, et al. Natalizumab treatment for
multiple sclerosis: updated recommendations for patient
selection and monitoring. Lancet Neurol 2011;10(8):745-58.
20. Jacobs LD, Beck RW, Simon JH, et al. Intramuscular interferon
beta 1a therapy initiated during the first demyelinating event in
multiple sclerosis. CHAMPS Study Group. N Engl J Med
2000;343(13):898-904.
39. Brinkmann V, Cyster JG, Hla T. FTY720: sphingosine 1phosphate receptor-1 in the control of lymphocyte egress and
endothelial barrier function. Am J Transplant 2004;4(7):1019-25.
21. Aboue Zeid NE, Pittock SJ. Clinically isolated syndromes. In

Lucchinetti CF, Hohlfeld R, editors. Blue books of neurology:
multiple sclerosis 3. Philadelphia: Elsevier; 2010. p 213-14.
40. Miron VE, Hall JA, Kennedy TE, et al. Cyclical and dosedependent responses of adult human mature oligodendrocytes
to fingolimod. Am J Path 2008;173(4):1143-52.
22. Dhib-Jalbut S, Marks S. Interferon-beta mechanisms of action in

multiple sclerosis. Neurology 2010;74(Suppl 1):S17-24.
41. Miron VE, Ludwin SK, Darlington PJ, et al. Fingolimod (FTY720)
enhances remyelination following demyelination of organotypic
cerebellar slices. Am J Path 2010;176(6):2682-94.
23. Duda PW, Schmied MC, Cook SL, et al. Glatiramer acetate
(Copaxone) induces degenerate, Th2-polarized immune
responses in patients with multiple sclerosis. J Clin Invest
2000;105(7):967-76.
32
26. Costello K, Kennedy P, Scanzillo J. Recognising nonadherence in

patients with multiple sclerosis and maintaining treatment
adherence in the long term. Medscape J Med 2008;10(9):225.
42. Cohen J, Barkhof F, Comi G, et al. Oral fingolimod or

intramuscular interferon for relapsing multiple sclerosis. N Engl J
Med 2010;362(5):402-15.
www.mstrust.org.uk

43. Kappos L, Radue EW, OConnor P, et al. A placebo-controlled

trial of oral fingolimod in relapsing multiple sclerosis. N Engl J
Med 2010;362(5):387-401.
44. Khatri B, Barkhof F, Comi G, et al. Comparison of fingolimod
with interferon beta-1a in relapsing remitting multiple sclerosis:
a randomised extension of the TRANSFORMS study. Lancet
Neurol 2011;10(6):520-9.
45. FTY720 in Patients With Primary Progressive Multiple Sclerosis
(INFORMS). ClinicalTrials.gov website:
clinicaltrials.gov/show/NCT00731692.
61. Wynn D, Kaufman M, Montalban X, et al. Daclizumab in active

relapsing multiple sclerosis (CHOICE study): a phase 2,
randomised, double-blind, placebo-controlled, add-on trial with
interferon beta. Lancet Neurol 2010;9(4):381-90.
62. Kappos L, Calabresi P, OConnor P, et al. Efficacy and safety of
ocrelizumab in patients with relapsing-remitting multiple
sclerosis: results of a phase II randomised placebo-controlled
multicenter trial. Mult Scler 2010;16(Suppl 10):S33
63. Lublin FD. Effects of relapses on residual deficit in MS.
Neurology 2003;61(11):1528-1532.
46. Vartanian T, Slberg Srensen P, Rice G. Impact of neutralizing

antibodies on the clinical efficacy of interferon beta in multiple
sclerosis. J Neurol 2004;251(Suppl 2):25-30.
64. Huang JK, Jarjour AA, Nait Oumesmar B, et al. Retinoid X

receptor gamma signaling accelerates CNS remyelination. Nat
Neurosci 2011;14(1):45-53.
47. Srensen PS, Hyldgaard Jensen PE, Haghikia A, et al.

Occurrence of antibodies against natalizumab in relapsing
multiple sclerosis patients treated with natalizumab. Mult Scler
2011;17(9):1074-8.
65. Saccardi R, Kozak T, Bocelli-Tyndall C, et al. Autologous stem

cell transplantation for progressive multiple sclerosis: update of
the European Group for Blood and Marrow Transplantation
autoimmune diseases working party database. Mult Scler
2006;12(6):814-23.
48. Hartung HP, Gonsette R, Konig N. Mitoxantrone in progressive

multiple sclerosis: a placebo controlled, double blind,
randomised, multicentre trial. Lancet 2002;360(9350):2018-25.
49. Marriott JJ, Miyasaki JM, Gronseth G, et al. Evidence Report: The
efficacy and safety of mitoxantrone (Novantrone) in the
treatment of multiple sclerosis: Report of the Therapeutics and
Technology Assessment Subcommittee of the American
Academy of Neurology. Neurology 2010;74(18):1463-70.
50. Boggild M. Rationale and experience with combination
therapies. J Neurol 2006;253(Suppl 6):vi45-vi51.
51. Le Page E, Leray E, Taurin G, et al. Mitoxantrone as induction
treatment in aggressive relapsing remitting multiple sclerosis:
treatment response factors in a 5 year follow-up observational
study of 100 consecutive patients. J Neurol Neurosurg Psychiatry
2008;79(1):52-6.
52. Edan G, Morrissey S, Le Page E. Rationale for the use of
mitoxantrone in multiple sclerosis. J Neurol Sc. 2004;223(1):
35-9.
53. Martinelli Boneschi F, Rovaris M, Capra R, eta. Mitoxantrone
for multiple sclerosis. Cochrane Database Syst Rev 2005:(4);
CD002127.
54. OConnor PW, Wolinsky JS, Confavreux C, et al. A placebocontrolled phase III trial (TEMSO) of oral teriflunomide in
relapsing multiple sclerosis: clinical efficacy and safety outcomes.
Mult Scler 2010:16(Suppl 10);S23.
66. Fassas A, Kimiskidis VK, Sakellari I, et al. Long-term results of

stem cell transplantation for MS: a single-center experience.
Neurology 2011;76(12):1066-70.
67. Burt RK, Loh Y, Cohen B, et al. Autologous non-myeloablative
haemopoietic stem cell transplantation in relapsing-remitting
multiple sclerosis: a phase I/II study. Lancet Neurol
2009;8(3):244-53.
68. Rice CM, Mallam EA, Whone AL, et al. Safety and feasibility of
autologous bone marrow cellular therapy in relapsingprogressive multiple sclerosis. Clin Pharmacol Ther
2010;87(6):679-85.
69. International Society for Stem Cell Research. Patient handbook
on stem cell therapies. Illinois: ISSCR; 2008.
70. Zajicek J, Sanders H, Wright DE, et al. Cannabinoids in multiple
sclerosis (CAMS) study: safety and efficacy data for 12 months
follow up. J Neurol Neurosurg Psychiatry 2005;76(12):1664-9.
71. Baker D, Jackson SJ, Pryce G. Cannabinoid control of
neuroinflammation related to multiple sclerosis. Br J Pharmacol
2007;152(5):649-54.
72. Zajicek JP, Apostu VI. Role of cannabinoids in multiple sclerosis.
CNS Drugs 2011;25(3):187-201.
55. Moharregh-Khiabani D, Linker RA, Gold R, et al. Fumaric acid

and its esters: an emerging treatment for multiple sclerosis. Curr
Neuropharmacol 2009;7(1):60-4.
56. Lukashev M, Zeng W, Ryan S, et al. Activation of Nrf2 and
modulation of disease progression in EAE models by BG00012
(dimethyl fumarate) suggests a novel mechanism of action
combining anti-inflammatory and neuroprotective modalities.
Mult Scler 2007;13(Suppl 2):S149.
57. Coles AJ, Compston DA, Selmaj KW, et al. Alemtuzumab vs
interferon beta-1a in early multiple sclerosis. N Engl J Med
2008;359(17):1786-1801.
58. Jones JL, Anderson JM, Phuah CL, et al. Improvement in disability
after alemtuzumab treatment of multiple sclerosis is associated
with neuroprotective autoimmunity. Brain 2010;133(8):2232-47.
59. Twyman C. [PD-003] More alemtuzumab relapsing-remitting
multiple sclerosis patients are free of clinical disease activity at
five years. AAN 63rd Annual Meeting; 2011 April 9-16; Hawaii,
USA.
60. Rose JW, Burns JB, Bjorklund J, et al. Daclizumab phase II trial in
relapsing and remitting multiple sclerosis: MRI and clinical
results. Neurology 2007;69(8):785-9.
MS Trust resources
Disease modifying drug therapy
Fingolimod (Gilenya) factsheet
Mitoxantrone (Novantrone) factsheet
Natalizumab (Tysabri) factsheet
Stem cells factsheet
Drug research
www.mstrust.org.uk/research
33

Vision
Section 3
Vision
Multiple sclerosis can affect vision by various
mechanisms, although frank blindness is very rare
in MS. The NICE clinical guideline states that each
professional in contact with a person with MS
should consider whether the individuals vision is
disturbed, by considering, for example, the
individuals ability to read the text of a newspaper,
book or other written material and to see
the television.
If there are some problems with vision it is
worthwhile initiating an optometrist assessment to
ascertain whether the visual problem can be
helped by glasses. Any individual who experiences
reduced visual acuity, despite using suitable
glasses, should be referred for a specialist opinion.
The optometrist can assess whether the visual
problem may be caused by an eye problem that is
not due to MS, such as cataracts or macular
degeneration. A decision can therefore be made as
to whether the visual problem is best dealt with in
an ophthalmology or neurology clinic.
Some visual problems that are specific to MS are:
Optic neuritis
Optic neuritis is the most common eye problem in
MS. It is the first manifestation of MS in up to 30%
of cases and most people with MS will have optic
neuritis at some point during their disease course.
It is characterised by an inflammation and
demyelination of the optic nerve. The optic nerve
is the second cranial nerve that joins the eye to the
brain, transmitting the retinal image to the brain.
Optic neuritis usually presents with unilateral
impairment of vision, although bilateral cases can
occur. There is usually some degree of pain behind
the eye and pain on eye movement, although 10%
of cases are painless. The visual impairment comes
on acutely and vision can get progressively worse
for up to two weeks. The degree of visual loss can
vary from mild blurring through to loss of light
perception in the affected eye. There is loss of
colour vision, decreased ability to see contrast and
a visual field defect in the affected eye. The visual
field defect is usually over the central part of vision
and is termed a central scotoma.
On examination there will usually be a defect in the
34
pupils reaction to light in the affected eye called a

relative afferent pupillary defect. The optic nerve head
may appear swollen when viewed through an
ophthalmoscope, although in over half the cases the
nerve head is not swollen because the part of the
optic nerve that is affected is away from the eye. In
these cases the condition is often termed retrobulbar
optic neuritis.
Optic neuritis can usually be diagnosed on clinical
grounds, although sometimes further tests are
needed. These can include blood tests, magnetic
resonance imaging (MRI) of the orbits and brain
(Figure 1), an electrical test called visual evoked
potentials and a lumbar puncture.
Spontaneous recovery of vision usually starts to occur
by the third week. Most recovery takes place over the
next three months, although there are signs of
recovery for up to two years following an episode of
optic neuritis. Most people with optic neuritis make a
good recovery, although 10% are left with significant
visual impairment. Despite a good recovery of visual
acuity there are often subtle defects in colour vision
or contrast sensitivity. Vision can often get transiently
worse in the affected eye due to heat or exercise. This
is called Uhthoffs phenomenon.
Treatment in the acute phase with a short course of
high dose oral or intravenous corticosteroids will
speed up recovery, although their use has not been
shown to affect the final level of visual recovery.
Optic neuritis may occur as a one-off. In a third of
cases it can recur, in either eye. Only about 2% of
people, though, will develop permanent blindness
due to repeated attacks of optic neuritis. About 60%
of people who present with optic neuritis will go on
to develop MS. The risk of conversion to MS can be
ascertained by looking for asymptomatic brain MS
lesions on MRI. If there are no brain lesions then the
long-term risk of MS is 20%; the risk rises to 80% if
any brain lesions are seen.
Double vision (diplopia)

Double vision (diplopia) may be another early
symptom of MS. This occurs when the nerve
pathways that control eye movements are
damaged. It is due to a misalignment of the two
eyes so that they look in slightly different directions
and they may not move together in a coordinated
fashion. The nerve pathways commence in the
brainstem, which is a common site of relapses in
MS (Figure 2). Diplopia may be accompanied by
vertigo, nausea and unsteadiness (ataxia). If
www.mstrust.org.uk

Vision
diplopia occurs as part of a relapse then it will

usually recover. This recovery may be speeded up
by treatment with corticosteroids, as described
above. If the diplopia is persisting, particularly in
someone with progressive MS, then putting a prism
in one lens of glasses or patching one eye can
abolish the double vision.
Nystagmus
Nystagmus is the repetitive to-and-fro motion of the
eyes. The movement can be horizontal, vertical or
have a rotational component. It may just occur with
eye movements, when it is termed gaze-evoked
nystagmus. This is often asymptomatic, but is clearly
seen by an observer. In progressive MS nystagmus can
occur in the primary position of gaze. This can then
cause the symptom of oscillopsia, where there is a
failure to maintain fixation and therefore objects
appear to move and vision is blurred. This can be very
disabling and it can cause a significant reduction in
visual acuity. This is a very difficult symptom to treat.
Initial studies have indicated that gabapentin and
memantine may be effective.
On-going visual problems
gabapentin. J Neurol 2010;257(3):322-7.

Thurtell MJ, Joshi AC, Leone AC, et al. Crossover
trial of gabapentin and memantine as treatment
for acquired nystagmus. Ann Neurol
2010;67(5):676-80.
Vedula SS, Brodney-Folse S, Gal RL, et al.
Corticosteroids for treating optic neuritis. Cochrane
Figure 1
Coronal MRI of the orbits in an individual
with acute optic neuritis showing an
inflamed optic nerve (arrowed).
If there are persisting difficulties with vision, despite all

available treatment, then the person with MS may
benefit from being registered as having a sight
impairment. In addition, a referral to a low vision
service should be made, to see if there are specific
areas where help can be given, such as the provision of
appropriate magnifying devices to permit reading.
Further resources
Armstrong RA. Multiple sclerosis and the eye.
Ophthalmic Physiol Opt 1999;19(Suppl 2):S32-S42.
Davis EA, Rizzo JF. Ocular manifestations of multiple
sclerosis. Int Ophthalmol Clin 1998;38(1):129-39.
Frohman EM, Froham TC, Zee DS, et al. The neuroophthalmology of multiple sclerosis. Lancet Neurol
2005;4(2):111-21.
Figure 2
Axial (left) and coronal (right) MRI of the
brain in an individual with MS showing a
lesion in the brainstem (arrowed) that was
responsible for acute double vision.
Hickman SJ, Dalton CM, Miller DH, et al. Management

of optic neuritis. Lancet 2002;360:1953-62.
Multiple sclerosis - management of multiple sclerosis
in primary and secondary care. NICE Clinical
Guideline 8. London: NICE; 2003.
Starck M, Albrecht H, Pllmann W, et al. Acquired
pendular nystagmus in multiple sclerosis: an examinerblind cross-over treatment study of memantine and
35

Fatigue
Fatigue
Fatigue can be described as an overwhelming
sense of tiredness, lack of energy and feeling of
exhaustion. More formally, it has been defined as
a subjective lack of physical and/or mental energy
that is perceived by the individual or caregiver to
interfere with the usual and desired activity1. MS
fatigue is different from normal tiredness and does
not correlate with age, severity of MS or mood.
Fatigue is reported to be the most common
symptom experienced by people living with MS. In
a survey of 2,265 people with MS2, 94%
experienced fatigue, with 87% reporting an impact
on their activities of daily living, which was between
moderate to high. Fatigue is often described as an
invisible symptom and is variable in nature. Fatigue
can be the predominant reason for disability, even
early on in the disease course and is reported to be
one of the key factors most likely to influence people
to give up their jobs. Mental fatigue can affect
learning, memory, attention and concentration.
Fatigue has a huge impact on participation in
everyday tasks, work, leisure and social activities and
can therefore impact on psychological well-being.
A good explanation of fatigue is important early on
in treatment as MS fatigue exacerbates symptoms
and people can fear that they are having a MS
relapse. The symptoms will subside after rest which
distinguishes them from a relapse.
Brain scans of people who have fatigue show that
they use larger areas of the brain to carry out
activities than people without fatigue. This would
mean that more brain power is required to carry
out an activity, which may cause fatigue3.
Fatigue can be classified as primary or secondary
fatigue depending on its cause1.
Types of fatigue
Primary fatigue
Primary fatigue describes aspects of fatigue that
are thought to be directly related to the disease
process but much of the understanding of these
features remains theoretical.
Short-circuiting fatigue is sometimes known as
nerve fibre fatigue or conduction block where
36
performance deteriorates during continued/sustained

activity but responds to a short rest break allowing
activity to be resumed. For example, a person with
MS may notice he or she is starting to limp when
walking for a while but after a short rest walking has
improved. Research suggests that a build up of
sodium ions during continued activity, sometimes
referred to as flooding, causes a conduction block,
while stopping the activity allows time for the cell
membrane to return to its resting state4.
Lassitude refers to an overwhelming tiredness not
directly related to participation in activity or
exercise. The pathogenesis of lassitude is even
more poorly understood, although various
immunological theories have been suggested.
Heat sensitive fatigue is well recognised in MS and
has long been considered a unique dimension of MS
fatigue differentiating it from fatigue in other
conditions. A rise in body temperature of as little as
half a degree can interfere with nerve conduction
and cause fatigue. This is often described as
Uhthoffs syndrome where symptoms can become
worse with an increase in body temperature5.
Secondary fatigue
Secondary fatigue is not unique to MS; it relates to
factors that can be generalised across a variety of
chronic and disabling conditions. The relationship
between these factors is complex and their influence
on the overall experience of fatigue is often difficult
to discern. However, the ability to isolate these
contributory factors can be invaluable in the medical
management of fatigue since many secondary
factors can be avoided or treated directly6.
Medications may cause tiredness or drowsiness as
a side effect, for example baclofen, commonly
used in the treatment of spasticity. Side effects of
the beta interferon disease modifying therapies
have also been documented as having a negative
impact on fatigue7. It should be noted if there is a
correlation between a change in fatigue levels and
a change in medication.
Exertion or increased effort required by the body if
mobility or coordination is affected, can cause
fatigue. Reduced activity can also lead to
deconditioning of the muscles and cardiovascular
system, resulting in a less efficient use of energy
and therefore the experience of more fatigue.
Infection, for example having a cold, flu or
urinary tract infection, can all be associated with
www.mstrust.org.uk

Fatigue
increased tiredness and the need to rest, therefore

worsening fatigue.
Disturbed sleep can exacerbate fatigue and may
be due to symptoms that can be alleviated or
lessened, for example spasms, pain, urinary
urgency at night, depression or anxiety.
Depression or low mood can affect motivation
and activity and increase lethargy therefore
exacerbating fatigue.
Environment including lighting and temperature
are crucial, as poor lighting increases visual effort
and heat can exacerbate fatigue. The general
layout of home and work environments should be
ergonomic to allow energy to be used efficiently.
Also, walking distance and number of stairs need
to be considered.
Fatigue management
Explanation and information may be the only tools
necessary for people with MS to accept that some
fatigue is inevitable, to help them minimise
precipitating factors and manage their lifestyle to
accommodate the problem.
For other people further help may be necessary
and various fatigue management programmes
have been developed and are well documented1.
This approach to managing fatigue relies on a
person reflecting on their own fatigue and the way
that it affects their daily life. A fatigue diary can
help in this process. The approach does not take
fatigue away but aims to make living with fatigue
easier. Fatigue management requires a coordinated
approach involving family and colleagues as well as
health professionals8,9.
The principles are as follows:
Take frequent rests
Balance activities with rests and learn to allow time
to rest when planning a days activities. Rest means
doing nothing at all and it is better to take short
frequent rests rather than one long one. It is
crucial to rest before fatigue sets in. Some people
also find relaxation techniques helpful.
Prioritise activities
Prioritising activities can mean that you save energy
for the things you really want or need to do. Decide if
jobs could be done by other people, consider outside
help, and consider jobs that could be cut out of your
daily routine or done less often, such as ironing.

Plan ahead
A daily or weekly timetable can be useful to schedule
activities and rest in a balanced way. Spread heavy
and light tasks throughout the day. Set realistic
targets and breakdown large complicated tasks into
smaller stages that can be spread throughout the
day. Time, not task is a good rule to work to.
Organise living and work spaces
This involves looking at energy effectiveness/
efficiency when carrying out daily activities at home,
work and in leisure. This may involve re-organising
desks or cupboards, or adjusting the temperature or
lighting.
Adopt a good posture
Activities should be carried out in a relaxed and
efficient way minimising stress on the body, which
will in turn save energy. Maintain an upright and
symmetrical posture during all tasks and rest on a
perching stool while carrying out tasks if necessary.
Avoid excessive twisting and bending.
Lead a healthy lifestyle
Keep generally fit. Exercise is essential but should be
balanced with rests. Physiotherapists can advise on
specific exercises that may be relevant. Eat a well
balanced diet and remember that excess weight,
alcohol and smoking can all have a negative impact
on fatigue.
An occupational therapist can offer education
regarding both fatigue management principles and a
practical problem-solving approach. As well as clinical
guidelines which support fatigue management
programmes, research demonstrates that a fatigue
management programme for people with MS that
combines cognitive behavioural and energy saving
approaches, is effective in reducing fatigue severity
and increasing self-efficacy10.
Generally, medicines targeted at fatigue should not
be used routinely. However, a small clinical benefit
might be gained from taking amantadine
(Symmetrel, Lysovir) which has been shown to
reduce fatigue in 20-40% of people with mild to
moderate MS. Amantadine is generally well tolerated
with mild side effects including constipation, nausea,
anxiety and hyperactivity. It is suggested that the dose
is taken in the middle of the day to avoid problems of
insomnia or vivid dreams from the drug being taken too
close to the individuals normal bedtime11,12.
37

Fatigue
Modafinil is a drug that promotes wakefulness and is

licensed for treating people experiencing excessive
sleepiness due to narcolepsy. Research has
suggested that it may be an effective treatment for
the management of multiple sclerosis fatigue in
some people where sleepiness is a factor in their
fatigue14. However following the findings of a safety
review, the European Medicines Agency
recommended that the use of modafinil should now
only be associated with narcolepsy.
References
1.
Multiple Sclerosis Council for Clinical Practice Guidelines.

Fatigue and multiple sclerosis. Washington DC: Paralysed
Veterans of America; 1998.
2.
Hemmett L, Holmes J, Barnes M, et al. What drives quality of

life in multiple sclerosis? QJM 2004;97(10):671-6.
3.
Tartaglia M, Narayanan S, Francis SJ, et al. The relationship

between diffuse axonal damage and fatigue in multiple
sclerosis. Arch Neurol 2004;61(2):201-7.
4.
Herndon, RM. Fatigue in multiple sclerosis. Int J MS Care

1999;1(1):7-11.
5.
Guthrie TC, Nelson DA. Influence of temperature changes on

multiple sclerosis: critical review of mechanisms and research
potential. J Neurol Sci 1995;129(1):1-8.
6.
Kesselring J, Thompson A. Spasticity, ataxia and fatigue in

multiple sclerosis. Ballieres Clin Neurol 1997;6(3):429-45.
7.
Simone IL, Ceccarelli A, Tortorella C, et al. Influence of

interferon beta treatment on quality of life in multiple
sclerosis patients. Health Qual Life Outcomes 2006;4:96.
8.
Sauter C, Zebenholzer K, Hisakawa J, et al. A longitudinal

study on effects of a six-week course for energy conservation
for multiple sclerosis patients. Mult Scler 2008;14(4):500-5.
9.
Mathiowetz VG, Matuska KM, Finlayson ML, et al. One-year

follow-up to a randomized controlled trial of an energy
conservation course for persons with multiple sclerosis. Int J
Rehabil Res 2007;30(4):305-13.
MS Trust resources
Living with fatigue
MS and me: a self-management
guide to living with MS
Diet factsheet
Further resources
Harrison S. Fatigue management for people with
multiple sclerosis. 2nd edition. London: College of
Occupational Therapists; 2007.
Hubsky EP, Sears JH. Fatigue in multiple sclerosis:
guidelines for nursing care. Rehabil Nurs
1992;17(4):176-80.
Krupp LB. Fatigue in multiple sclerosis. Int MS J
1996;3(1):9-17.
Krupp LB, Pollina A. Mechanisms and management
of fatigue in progressive neurological disorders.
Curr Opin Neurol 1996;9(6)456-60.
Excellence. Multiple sclerosis - management of
multiple sclerosis in primary and secondary care.
10. Thomas P, Thomas S, Kersten P, et al. Multi-centre

randomized controlled trial to assess the effectiveness of a
group-based cognitive behavioural approach to managing
fatigue. Paper presented at MS Frontiers Conference (UK
Multiple Sclerosis Society); 2011 23-24 June; London, UK.
11. Krupp LB, Coyle PK, Doscher C, et al. Fatigue therapy in
multiple sclerosis: results of a double-blind, randomized,
parallel trial of amantadine, pemoline, and placebo.
Neurology 1995;45(11):1956-61.
12. Pucci E, Branas P, DAmico R, et al. Amantadine for fatigue in
multiple sclerosis. Cochrane Database Syst Rev
2007;(1):CD002818.
13. Rammohan KW, Rosenberg JH, Lynn DJ, et al. Efficacy and
safety of modafinil (Provigil) for the treatment of fatigue in
multiple sclerosis: a two centre phase 2 study. Neurol
Neurosurg Psychiatry 2002;72(2):179-83.
14. Littleton ET, Hobart JC, Palace J. Modafinil for multiple
sclerosis fatigue: does it work? Clin Neurol Neurosurg
2010;112(1):29-31.
38
www.mstrust.org.uk

Cognition
Cognition
Reasoning and judgment, including new learning,

problem solving and behavioural regulation may be
impaired but, because of the subtle nature of
reasoning, this problem is often much less obvious.
Because MS is often thought of as primarily a

physical disease, problems with attention and
memory are often overlooked. On formal laboratory
tests, about half of all people with MS experience
some inefficiency in concentration, or other mental
tasks (known as cognitive difficulties)1-3.
Speed of information processing is the most

vulnerable cognitive domain. This is particularly
noticeable when people have to deal with
information coming from different directions
(multi-tasking).
Cognitive difficulties in MS can affect4:
relationships and families
competence in legal and financial matters
adjustment to disability
ability to benefit from rehabilitation
employment
driving
quality of life.
Attention and concentration lapses can also cause

problems, especially when there are distractions in
the environment, such as a busy office.
Visuo-spatial perception is also sometimes
impaired, although less often.
Cognitive functions which are less likely to be affected
by MS include: language, remote knowledge, old
knowing, previously learned motor skills (eg riding a
bicycle), long-term automatic social skills.
Therapy
Cognitive problems can arise early in the course of

the disease although the greater the disease
duration and severity the more likely significant
problems are to occur. As with physical symptoms,
MS may affect some cognitive functions whereas
others may be left intact. This is important because
it gives the person assets with which to
compensate for (and sometimes mask) deficiencies.
Cognitive symptoms can worsen during relapse
and improve during remission but more commonly
symptoms develop slowly and gradually over time.
Although cognitive dysfunction is a sensitive area to
broach with people with MS and their families, it is
now generally accepted that openly recognising the
problem is considerably more helpful than pretending
it does not exist, or misunderstanding why problems
are occurring. Recognition opens the door to
support, acceptance, constructive discussion and
possible compensatory strategies5,6.
Two studies have suggested that disease modifying

drugs may offer some protection from cognitive
decline in MS7,8.
Neuropsychologists, speech therapists and
occupational therapists are able to assist people in
understanding, assessing and managing cognitive
problems in MS. The objectives of cognitive
rehabilitation are to support the person with MS in
maintaining:
independence
reliability as a family and community member
capacity to contribute to society.
Coping strategies
Generally, two complementary approaches may
be employed:
a retraining approach whereby progressively

more challenging exercises are given by
health professionals and used to strengthen
impaired function
a compensatory approach, which might involve,

for example, memory prompts or the recording
of information.
Forms of cognitive dysfunction

Memory loss is probably the commonest problem.
Apart from the obvious difficulties presented by
everyday forgetfulness, memory loss also has
implications in terms of learning new skills.
39

Cognition
There are many practical compensatory strategies

which can be employed and a number of
publications which people with MS and their
families may find useful 9,10.
use of large page-to-a-day diary and establish

systematic habits of consulting it11
use technology eg dictaphones, bleepers,
mobile phones11
establish a fixed routine, eg always keeping

things in the same place
do only one thing at a time and remove

distractions (background noise, TV, etc)
use white boards, post-it notes or notebooks,

especially by the phone
avoid doing jobs which need concentration

when fatigued or anxious.
11. Johnson KL, Bamer AM, Yorkston KM, et al. Use of cognitive
aids and other assistive technology by individuals with multiple
sclerosis. Disabil Rehabil Assist Technol 2009;4(1):1-8.
MS Trust resources
Cognition factsheet
StayingSmart
www.stayingsmart.org.uk
It is worth remembering that some medications

including those used to counteract pain, fatigue and
depression may have a negative impact on cognition.
References
1.
Gingold J. Facing the cognitive challenges of multiple

sclerosis. 2nd ed. New York: Demos; 2011.
2.
Chiaravalloti ND, DeLuca J. Cognitive impairment in multiple

sclerosis. Lancet Neurol 2008;7(12):1139-51.
3.
Benedict RH, Zivadinov R. Risk factors for and management

of cognitive dysfunction in multiple sclerosis. Nat Rev Neurol
2011;7(6):332-42.
4.
Langdon DW. Cognition in multiple sclerosis. Curr Opin

Neurol 2011;24(3):244-9.
5.
Gingold J. Mental sharpening stones: manage the cognitive

challenges of multiple sclerosis. New York: Demos; 2008.
6.
OBrien AR, Chiaravalloti N, Goverover Y, et al. Evidencebased cognitive rehabilitation for persons with multiple
sclerosis: a review of the literature. Arch Phys Med Rehabil
2008;89(4);761-9.
7.
Fischer JS, Priore RL, Jacobs LD, et al. Neuropsychological

effects of interferon beta1a in relapsing multiple sclerosis.
Multiple Sclerosis Collaborative Research Group. Ann Neurol
2000;48(6):885-92.
Kappos L, Freedman MS, Polman CH, et al. Long-term effect

of early treatment with interferon beta-1b after a first clinical
event suggestive of multiple sclerosis: 5-year active treatment
extension of the phase 3 BENEFIT trial. Lancet Neurol
2009;8(11):987-97.
9.
Kapur N. Managing your memory: a manual for improving

everyday memory skills. Southampton: Wessex Neurological
Centre; 2001.
10. Clare L, Wilson BA. Coping with memory problems: a

practical guide for people with memory impairments, their
relatives, friends and carers. Bury St Edmunds: Thames Valley
Test Company; 1997.
40
www.mstrust.org.uk

Depression
triggers, relevant anniversaries as well as the cause

of a persons episode, experience of treatment and
final outcome.
Depression
Experience of living with MS - as with many other
chronic conditions - can undoubtedly result in a low
mood. This however should be clearly distinguished
from clinical depression, which is common in
people with MS1.
Health professionals should be mindful of an
individuals mental health as well as their physical
health at all stages of clinical intervention. Health
professionals will then be better placed to
encourage their patients to work towards
maintaining stable mood and preventing the
likelihood of developing the disabling symptoms of
low mood and anxiety alongside the already
challenging symptoms associated with MS.
Health professionals need to be explicit in their

discussions with patients about any history of
depression and risk of recurrence. Plans for
monitoring and identifying any early warning signs
should also be put in place. Health professionals
who see a patient on a regular basis are well
placed to notice changes in mood or personality
between appointments.
Risk factors for clinical depression in the
general population include a history of significant
loss, a family history of mental illness, major
trauma or significant health problems. Depression
is thought to be more common in women. It is
also more prevalent in the 20-50 age range and
following retirement.
Depression and MS
It is estimated that about half of all people with MS
will experience an episode of depression at some
stage, regardless of their clinical presentation. This
may be recurrent in some and persistent in others. In
one study, 28% of people with MS could be
described as depressed at any one time2.
These factors are also relevant to people with MS,

but there are other specific risk factors3. There
seems to be an increased risk for people who have:
People who experience depression may not
recognise it as such or may find it difficult to talk

about how they feel. The stigma that is associated
with mental health problems also acts as a barrier to

discussion about the symptom.
In some cases, depression may not be experienced as

a reaction to the complexities of living with MS but
as a symptom due to lesions in certain parts of the
brain that directly affect mood and cause depression.
Risk factors and prevention

As part of an initial assessment, most health
professionals will obtain a good history of an
individuals physical health. The same is not always
true for mental health.
Health professionals can play an important role in
preventing depression by being aware of risk factors
and can help people think about protective
strategies and introducing changes, where possible
and acceptable, to minimise risk.
It is important to know if there is a relevant family
or individual history, to understand any previous
shorter disease duration

greater disease severity
lower education
lower age
less social support.
Some people also experience alteration in their

mood just before or after a relapse.
There appears to be no correlation between risk of
depression and extent of disability.
Many of the drugs prescribed for other symptoms
of MS can have low mood as a side effect. Drugs
that can lower mood include steroids, beta
interferons and muscle relaxants.
These factors need to be considered in the early
part of a persons care and any relevant risk factors
recorded in the notes and shared with the
individual and their GP. Advice should be given on
prevention. This is particularly important as
depression can exacerbate and amplify many of
the primary symptoms associated with MS.
41

Depression
Anxiety disorders are also common in people with

MS4, with an estimated 25% of people experiencing
them, but these are often overlooked and
undertreated.
The mnemonic DEPRESSION - below can be

useful in determining the psychological needs of
people with MS.
Diagnosis
D - Diagnosis
Diagnosis of depression is often missed by health

professionals. It is an essential diagnosis to make
and responds to treatment5,6.
How are you dealing emotionally

with the diagnosis of MS?
E - Expression
Observe mood and facial

expression
P - Pleasure
What things do you

enjoy most?
R - Remorse
Do you feel guilty about

things you have or have
not done?
Do you feel a burden to your
family/friends?
E - Explore
Past personal or family history

or psychiatric illness?
S - Sadness
How would you best

describe your mood?
S - Stress
Do you experience stress

and/or anxiety?
How do you deal with this?
What activities do you avoid
due to stress/anxiety?
Has your concentration
decreased?
I - Insomnia
How well do you sleep?

Do you experience early
morning wakening?
Do you experience initial
insomnia/inability to sleep?
O - Others
How is illness perceived in

your family?
How do others perceive
your mood?
N - Nutrition
How is your appetite?

Do you taste and enjoy food?
Have you gained/lost weight?
Individuals and their families play a key role in

identification and diagnosis of depression. Health
professionals rely on their descriptions of the
symptoms experienced to identify the best way of
managing or treating the condition.
Symptoms such as sleep or appetite disturbance, poor
concentration, fatigue or weight loss are not particularly
useful in the diagnosis of depression in people with MS.
This is because they are common symptoms in people
with MS who do not have depression.
Symptoms which can aid the diagnosis of
depression in people with MS include pervasive low
mood (low mood all the time and in every situation)
for at least two weeks; mood particularly bad at a
certain time of day (diurnal variation in mood);
negative thoughts about self, the world and the
future which are out of context with the level of
disability; suicidal ideas and the lack of ability to
take pleasure in routine things such as eating,
talking, watching TV or walking; especially things
that would have given pleasure in the past.
NICE recommends7 asking two key questions to
identify those who might be depressed:
during the last month, have you often been

bothered by feeling down, depressed or hopeless?
during the last month, have you often been

bothered by having little interest or pleasure in
doing things?
Reproduced by kind permission of Bernie Porter,

MS Nurse Consultant, The National Hospital for
Neurology and Neurosurgery.
42
www.mstrust.org.uk

Depression
Treatment
Various approaches have proven effective in
treating depression and the individual should play
a key role in deciding which treatment plan works
best for them.
In addition to the NICE guideline for managing
depression in long-term conditions7, a significant
amount of research supports the use of low level
interventions in the first instance. These include
advice on sleep hygiene and exercise, ensuring
better peer and social support and treating any
pain and other physical symptoms.
If further treatment is required, the options are
antidepressant medication and psychotherapy,
which are often used in combination.
MS Trust resources
Depression factsheet
Further resources
Excellence. Depression: the treatment and
management of depression in adults. NICE Clinical
Linde K, Berner MM, Kriston L. St Johns wort for
major depression. Cochrane Database Syst Rev
2008;(4):CD000448.
Selective serotonin reuptake inhibitors (for

example, Prozac) can be useful and tricyclic
antidepressants, such as imipramine and
amitriptyline, are also sometimes prescribed.
The psychotherapeutic approach may involve
identifying the cause of depression, and trying to
alter negative patterns of thinking and behaviour
into a more positive approach and may include
cognitive behavioural therapy (CBT).
References
1.
Remick RA, Sadovnick AD. Depression and suicide in multiple

sclerosis. In: Thompson AJ, Polman C, Hohlfeld R, editors.
Multiple sclerosis: clinical challenges and controversies.
London: Martin Dunitz Ltd; 1997. p243-9.
2.
McGuigan C, Hutchinson M. Unrecognised symptoms of

depression in a community-based population with multiple
sclerosis. J Neurol 2006;253(2):219-23.
3.
Bamer AM, Cetin K, Johnson KL, et al. Validation study of

prevalence and correlates of depressive symptomatology in
multiple sclerosis. Gen Hosp Psychiatry 2008;30(4):311-7.
4.
Korostil M, Feinstein A. Anxiety disorders and their clinical

correlates in multiple sclerosis patients. Mult Scler
2007;13(1):67-72.
5.
Sadovnick AD, Eisen K, Ebers GC, et al. Cause of death in

patients attending multiple sclerosis clinics. Neurology
1991;41(8):1193-6.
6.
Remick RA, Sadovnick AD. Depression and suicide in multiple

sclerosis. In: Thompson AJ, Polman C, Hohlfeld R, editors.
Multiple sclerosis: clinical challenges and controversies.
London: Martin Dunitz Ltd; 1997. p248.
7.

Depression in adults with a chronic physical health problem:
treatment and management. NICE Clinical Guideline 91.
London: NICE; 2009.
43

Womens health
Contraception
Womens health
Women with MS outnumber men by 3:11 and disease
activity appears related to hormonal fluctuations by as
yet, poorly understood mechanisms. Hence there are
special considerations that need to be taken into
account for women with MS, and the health
professional requires an understanding of the impact
of menstruation, pregnancy and menopause on MS.
Menstruation
Many women report cyclical changes in MS
symptoms and feel that their symptoms deteriorate
two to three days prior to the onset of their
menstrual period and improve once bleeding has
started. A few small studies have confirmed this
anecdotal evidence though more work undoubtedly
needs to be done in this area2-4.
In one small study5 it was found that 78% of women
had premenstrual worsening of their MS symptoms in
one or more of the menstrual cycles analysed.
Symptoms most likely to increase pre-menstrually were
limb weakness, pain and nocturia. Additionally,
another small scale study found that those on
combined oral contraception reported that their
MS symptoms worsened during the pill-free week6.
A greater understanding of this menstrual cycle effect
by women with MS and health professionals would
help to reduce anxiety associated with an unexpected
increase in symptoms.
Current data suggests that premenstrual symptoms
alone cannot account for the change in MS symptoms
and other hormonally related factors may be
important. It is tempting to assume that the decline in
the level of oestrogens accounts for premenstrual
deterioration in MS symptoms. Research into MS and
pregnancy7,8 points to oestrogen having a protective
effect as it may suppress autoimmunity. Unfortunately
solutions are rarely simple and an obvious question
that comes to mind is if oestrogen is so beneficial,
why do more women than men have MS? Sadly this
paradox is still to be solved.
Women who are disabled by MS and who are no
longer contemplating having children may want to
consider ceasing menstruation by hormonal means.
They should be encouraged to explore available
options with their GP or practice nurse. Adopting this
strategy may benefit carers particularly where a male is
looking after a female partner and the couple find this
aspect of care particularly difficult to deal with.
44
All forms of birth control are available for people

with MS, although various factors should be taken
into account when decisions about contraception
are being made. These include patient choice,
ease, comfort, effectiveness, interaction with
medications, and physical limitations such as loss
of dexterity or spasticity.
There are no contraindications specific to women
with MS for oral contraceptives, although it is
recommended9 that there should be discussion with a
physician since certain drugs, including antibiotics,
phenytoin and carbamazepine, may reduce oral
contraceptive effectiveness. It should be borne in
mind that there is an increased risk of thrombosis
associated with immobility, and the usual checks on
weight, smoking and so on should be made as for
any other woman contemplating oral contraceptives.
If cognitive impairment affects the womans ability to
take daily oral contraceptives reliably, then a
transdermal weekly patch may be a good alternative.
Good manual dexterity is needed for the use of
barrier contraceptives, such as diaphragm,
condoms and spermicides; hand tremor, weakness
or sensory loss could therefore be problematic. It
may be prudent to inform women with MS that
using a diaphragm may increase the likelihood of
bladder infections.
Intrauterine devices (IUD) have been shown to be
generally safe, effective and easy to use. Hormonereleasing IUDs (eg Mirena coil) have the advantage
of reducing menstrual flow and duration10.
Another option is a progesterone implant, again
requiring no maintenance and effective for up to
five years. Progesterone can also be injected on a
three monthly basis.
Pregnancy
Because MS is most commonly diagnosed in
women aged between mid 20s and early 30s, the
question of pregnancy is an important one. The
main issues are: the effect of the pregnancy on the
mother with MS, the overall outcome of the
pregnancy in terms of the babys health, and the
risk that the baby will inherit MS. A study
investigating the concerns of pregnant women
with MS11 identified labour, delivery issues, breast
feeding and short and long-term parenting issues.
The unpredictability of MS resulting in uncertainty
permeated many of these concerns.
www.mstrust.org.uk

Womens health
Effect of pregnancy on the mother

with MS
Until 1950 and the publication of Tillmans paper12
on the effect of pregnancy on MS and its
management, women with MS were advised to
avoid pregnancy. Since 1950, many researchers in
both retrospective and prospective studies have
borne out Tillmans findings that pregnancy has no
long-term effect on disability. However, there are
still many myths and misconceptions about MS
and pregnancy and some people (including health
professionals) express disapproval when a woman
with MS becomes pregnant.
In common with many other autoimmune diseases
(rheumatoid arthritis, myasthenia gravis, for
example), fewer disease events may be
experienced during pregnancy for women with
relapsing remitting MS, especially during the third
trimester. This suggests that there is some
protection from pregnancy-related hormones.
However, that protection does not seem to apply
to women with progressive disease. During the
three months postpartum the risk of a relapse
increases. Overall, however, pregnancy does not
affect disease outcome or level of disability, and a
two year follow up study determined that birth
relapse risk is similar to that in the pre-pregnancy
year13. While one small scale study suggested that
breast feeding may offer a degree of protection
against postpartum relapse14, a second, larger
study found that breast feeding did not reduce the
relapse rate post delivery15.
NICE guidance states that women with MS should
be offered the most appropriate analgesia for them
during delivery. Concerns are sometimes expressed
regarding the use of epidural anaesthesia, but
there is no evidence that epidural administration of
drugs has any effect on relapse rate or disability16.
The incidence of instrumental or caesarean section
deliveries has been shown to be no higher for
women with MS. Although a small study
concluded that women with MS were more likely
to have assisted vaginal deliveries than those
without17, a larger scale Canadian study refuted
these findings18.
Overall outcome of the pregnancy in

terms of the babys health
There is no increased risk of miscarriage, foetal
malformations, stillbirths, birth defects or infant
mortality when the mother has MS.
Risk that the baby will inherit MS

MS is not hereditary and the majority of people who
develop MS have no previous family history of the
condition. However, family studies have revealed that
there is a higher, but still small, risk of developing MS
for someone with a relative with the condition19. In
the general population in the UK, the risk of
developing MS is about 1 in 700. The risk is higher
for people who already have someone with MS in
their family. On average, the risk for first degree
relatives (parents, children, siblings) of someone with
MS is about 1 in 40. For second degree relatives
(cousins, uncles/aunts, nephews/nieces) it is around 1
in 100. While there is a genetic predisposition to MS,
the actual risk is considered low and should not deter
a couple from starting a family.
Other factors
When considering pregnancy other factors may
need to be taken into account. Many of the drugs
used in the treatment of MS are inadvisable during
pregnancy and breastfeeding. Steroids may be used
with relative safety in pregnancy20. However, many
pregnant women choose not to have steroids,
particularly as they have no bearing on the degree
of recovery from the relapse.
There is limited data on the use of disease
modifying therapies in pregnancy. Women are
usually advised to cease treatment three months
before attempting to become pregnant, and
recommence once breast feeding has ended.
Immunosuppressive and some symptom
management drugs may cause physical defects in
the developing embryo.
As more evidence emerges regarding the link
between MS and vitamin D, it is prudent for women
with MS to supplement with vitamin D during
pregnancy, if they are not already doing so. Vitamin
D supplementation during pregnancy may lower
the MS risk for the foetus, as well as provide other
health benefits, and is now recommended (at a low
dose) for all women21. However, as yet there is no
clear guidance on appropriate dosage for pregnant
women with MS.
Another consideration is the level of disability of the
mother and the availability of help with the care of
the baby, should this be necessary. Women with MS
should be encouraged to plan for the postnatal
period, in the event of relapse, utilising practical
help from family and friends, or statutory assistance
eg from social services, or via the health visitor. Local
45

Womens health
MS mother and baby groups can be invaluable in

providing peer support and preventing feelings of
isolation. Levels of fatigue should also be taken into
account, bearing in mind that this common symptom
can be exacerbated by the pregnancy itself and by
subsequent disturbed nights.
MS is unpredictable and therefore decisions about
having children can be difficult to make. The
health professional can achieve a great deal by
encouraging exploration of all the issues, many of
which will be uncomfortable, and providing up to
date information and support.
Menopause
Menopause does not appear to have any effect on
MS either positive or negative, although there has
been little research in this area22. However, there is
anecdotal evidence, as well as a few small studies,
indicating that symptoms which worsen during
menopause may be responsive to hormone
replacement therapy (HRT). The majority of women
with MS who have used HRT report improvement
rather than deterioration in their condition, but any
potential benefit must be evaluated against possible
risks. Since loss of bone density and osteoporosis may
be a problem for people with MS23, the beneficial
effect of HRT on reducing the risk of osteoporosis
should be taken into account.
Health screening
It is important that women with MS should be
offered all relevant health screening, for example
for cervical and breast cancer24. Unfortunately
access to screening tests can be restricted for
women with chronic disabling conditions, due to
substantial physical barriers (eg mobile breast
screening units with steps) thus limiting health
promoting activities critical to a healthy life25.
References
1.
2.
46
Orton SM, Herrera BM, Yee IM, et al. Sex ratio of multiple
sclerosis in Canada: a longitudinal study. Lancet Neurol
2006;5(11):932-6.
Smith R, Studd JW. A pilot study of the effect upon multiple
sclerosis of the menopause, hormone replacement therapy
and the menstrual cycle. J R Soc Med 1992;85(10):612-3.
3.
Zorgdrager A, De Keyser J. Menstrually related worsening

symptoms in multiple sclerosis. J Neurol Sci 1997;149(1):95-7.
4.
Houtchens MK, Gregori N, Rose JW. Understanding

fluctuations of multiple sclerosis across the menstrual cycle.
Int J MS Care 2000;2(4):7-14.
5.
Wilson S. Premenstrual worsening of MS symptoms. Way

Ahead 2001;5(3):14.
6.
Holmqvist P, Hammar M, Landtblom AM, et al. Symptoms of

multiple sclerosis in women in relation to cyclical hormone
changes. Eur J Contracept Reprod Health Care
2009;14(5):365-70.
7.
Confavreux C, Hutchinson M, Hours MM, et al. Rate of

pregnancy-related relapse in multiple sclerosis. N Engl J Med
1998;339(5):285-91.
8.
Devonshire V, Duquette P, Sadovnick AD. The immune

system and hormones: review and relevance to pregnancy
and contraception in women with MS. Int MS J
2003;10(2):44-50.
9.
Birk K, Giesser B, Werner MA. Fertility, pregnancy, childbirth

and gynecologic care. In: Kalb RC, editor. Multiple sclerosis:
the questions you have - the answers you need. 3rd ed. New
York: Demos Medical Publishing; 2004. p329-46.
10. Andersson K, Odlind V, Rybo G. Levonorgestrel-releasing and

copper-releasing (Nova T) IUDs during five years use: a
randomized comparative trial. Contraception 1994:49(1):56-72.
11. Smeltzer SC. The concerns of pregnant women with multiple
sclerosis. Qual Health Res 1994;4(4):480-502.
12. Tillman AJ. The effect of pregnancy on multiple sclerosis and
its management. Res Publ Assoc Res Nerv Ment Dis
1950;28:548-82.
13. Confavreux C, Vukusic S, Adaleine P, et al. Pregnancy and
multiple sclerosis (the PRIMS study): two-year results.
Neurology 2001;56(Suppl 3):A197.
14. Langer-Gould A, Huang SM, Gupta R, et al. Exclusive
breastfeeding and the risk of postpartum relapses in women
with multiple sclerosis. Arch Neurol 2009;66(8):958-63.
15. Portaccio E, Ghezzi A, Hakiki B, et al. Breastfeeding is not
related to postpartum relapses in multiple sclerosis.
Neurology 2011;77(2):145-50.
16. Vukusic S, Hutchinson M, Hours M, et al. Pregnancy and
multiple sclerosis (the PRIMS study): clinical predictors of
postpartum relapse. Brain 2004;127(6):1353-60.
17. Jalkanen A, Alanen A, Airas L. Pregnancy outcome in women
with multiple sclerosis: results from a prospective nationwide
study in Finland. Mult Scler 2010;16(8):950-5.
18. van der Kop ML, Pearce MS, Dahlgren L, et al. Neonatal and
delivery outcomes in women with multiple sclerosis. Ann
Neurol 2011;70(1):41-50.
19. Compston A. The genetic epidemiology of multiple sclerosis.
Philos Trans R Soc Lond B Biol Sci 1999;354(1390):1623-34.
20. Ferrero S, Pretta S, Ragni N. Multiple sclerosis: management
issues during pregnancy. Eur J Obstet Gynecol Reprod Biol
2004;115(1):3-9.
21. National Institute for Health and Clinical Excellence.
Antenatal care: routine care for the healthy pregnant
woman. NICE Clinical Guideline 62. London: NICE; 2008.
22. Coyle PK, Halper J. Meeting the challenge of progressive
multiple sclerosis. New York; Demos Medical Publishing:
2001. p93.
23. Hearn AP, Silber E. Osteoporosis in multiple sclerosis. Mult
Scler 2010;16(9):1031-43.
24. Stuifbergen A, Becker H. Health promotion practices in women
with multiple sclerosis: increasing quality and years of healthy
life. Phys Med Rehabil Clin N Am 2001;12(1):9-22.
25. Smeltzer SC. Preventive health screening for breast and cervical
cancer and osteoporosis in women with physical disabilities.
Fam Community Health 2006;29(1 Suppl):35S-43S.
MS Trust resources
Pregnancy and
parenthood factsheet
www.mstrust.org.uk

Bladder
incontinence will occur if the contraction pressures

are too high for the muscles at the bladder outlet to
hold on.
Bladder
Bladder problems are one of the most common
symptoms reported by people with MS with studies
frequently citing around 75% of people
experiencing this symptom1. They tend to occur as
MS advances, appearing on average six years into
the illness, although one in ten people may report
symptoms at the time of initial onset2. This
highlights the importance of raising bladder issues
in routine assessments.
Poor bladder control is disabling and many regard
this as one of the most constraining aspects of their
MS3. Unpredictable urinary urgency with a danger
of incontinence can cause a person to become
housebound, unwilling to venture out where access
to toilets is uncertain. Although urinary urgency
and frequency are the most common problems,
many people with MS can experience difficulty in
completely emptying their bladder. In some
situations, such as prior to going out, they can find
it difficult to initiate passing urine even in the
absence of urgency. They may have a reduced flow
rate, an interrupted stream and the sensation of
incomplete bladder emptying. It is important to
emphasise that much can be done to improve this.
Figure 1
medial
frontal
lobes
pontine
micturition
centres
L3,4,5,S1
Lower limbs
S2,3,4
uro-genital
function
Bladder disorders that occur in MS are of two distinct

types: overactivity and incomplete emptying4.
Overactivity
Bladder overactivity is usually the problem a person
with MS is most aware of. It results in a tendency for
the bladder to contract unpredictably and sometimes
uncontrollably, this results in urgency, frequency and
urgency incontinence. At its worst, the bladder may
seem to have a life of its own.
In health, the bladder behaves a bit like a balloon
although there is a significant difference - unlike a
balloon it has a special property that enables it to
expand without raising internal pressure. This
remarkable property is the result of its nerve supply
from the spinal cord, from controlling centres within
the brain; particularly the micturition centre situated
at the base of the brain (Figure 1). With spinal cord
disease this connection is disrupted and the special
property lost resulting in an overactive bladder. The
bladder, after only partial filling, develops
spontaneous, insuppressible contractions that
provoke a sense of urinary urgency. Urinary
This diagram shows how nerves supplying the legs

branch off the spinal cord, above those to the bladder.
The micturition centre at the base of the brain is
shown by a large black dot. If there is disease affecting
the spinal cord (in the cervical cord area, a common
site for demyelination in MS), neural impulses between
the micturition centre and the nerves to the bladder
will be interrupted, as will impulses between the brain
and nerves to the legs. For this reason difficulty with
walking is usually associated with poor bladder control
in multiple sclerosis: both problems can be the result
of spinal cord disease5,6. The effect of this is
unfortunate because bladder control deteriorates at
the same time as mobility worsens; making it
increasingly difficult to respond to bladder urgency by
hurrying to the toilet.
Another feature of the impaired nerve supply to the
bladder muscle is that the normal capacity is
47

Bladder
diminished, causing urinary frequency. In health,

the bladder has a capacity of between 300 and
500ml (about a pint of fluid), whereas the capacity
in people with bladder problems due to MS may
be reduced to 100ml or less. This increases the
frequency of emptying from every three to five
hours (depending on how much is drunk) to
hourly or worse in the day and at night.
Incomplete emptying
Although some people with MS are aware that
their bladders do not empty properly, others with
the same problem are not. For many, needing to
void again soon after doing so is usually an
indicator that bladder emptying is poor. Research
has shown that if people with MS thought they
were not emptying their bladder properly, they
were usually correct. However, of those who
thought they were emptying completely, about
half were wrong and were surprised to find how
much urine they had been leaving behind6. This
results in hesitancy and retention.
Incomplete bladder emptying is the result of two

things going wrong, both of which are due to spinal
cord malfunction:
the muscle which surrounds the bladder outlet

tube (urethral sphincter) does not relax when the
bladder muscle contracts, thus resulting in an
interrupted flow
the neural impulses that normally keep the

bladder muscle contracting until it is completely
empty do not get down the spinal cord. When the
bladder does contract, the contractions, although
frequent, are poorly sustained.
Management
In 2009 stakeholders involved in continence care,
including neurologists, urologists, primary care
professionals, MS nurses and nursing groups,
formulated a set of guidelines for managing bladder
problems in MS. Expert consensus was reached after
discussion, and recommendations agreed on review of
literature and expert opinion (Figure 2).7
Figure 2
Abbreviations
DDAVP
Desmopressin
CISC
Clean intermittent self-catheterization
Buzzer
Suprapubic vibration device
BoNT/A
Botulinum toxin A
Walking
unaided
IDC
Indwelling catheter
Walking mostly
without aids
Walking mostly
with aids
Antimuscarinics
+/- DDAVP
Chairbound
Antimuscarinics
+ CISC
Buzzer
+/- DDAVP
BoNT/A
Bedbound
Antimuscarinics
+ CISC/IDC
BoNT/A
IDC
time
48
www.mstrust.org.uk

Bladder
The consensus states that a person with MS who

complains of lower urinary tract symptoms must
be assessed by a suitably trained health
professional who is knowledgeable about MS and
its effects on lower urinary tract function.
Dipstick tests of the urine must be

undertaken in patients with new symptoms of
bladder dysfunction. The first step is to test for
a urinary tract infection (UTI). UTIs can
themselves worsen bladder symptoms.
Importantly, they can also worsen other
neurological symptoms, and potentially
precipitate an MS relapse.
If there is reason to suspect incomplete bladder
emptying measurement of post micturition
residual volume; the volume left behind after
passing urine, should be carried out prior to
any treatment intervention.
Urodynamic investigation with filling cystometry

and pressure/flow studies of voiding should be
carried out in those who are refractory to
conservative treatment or whose symptoms have
significant impact on daily life and there is a need
to undergo further investigations.
It is recommended that for most people with MS,

bladder problems can be successfully managed
based upon a simple algorithm (Figure 3)7. Any
person with residual volume in excess of 100ml
should be offered the opportunity to learn clean
intermittent self-catheterisation.
Reviewing someones daily fluid intake, both quantity

and type of fluid, by completing a voiding diary is
valuable. Fluid intake needs to be individualised,
however intake of between one and two litres a day is
recommended7. Pelvic floor exercises may be helpful
especially when symptoms are mild.
Figure 3
Abbreviations
UTI
Urinary tract infection
PVR
Post void residual volume
49

Bladder
Management of overactive bladder

Antimuscarinics
Antimuscarinic medications block the messages
that initiate bladder contractions and reduce
frequency of bladder emptying. The names of the
commonly prescribed drugs are given in Table 1.
These can be very effective in managing an
overactive bladder8 but risk causing a dry mouth as
common side effect. A dry mouth is evidence that
an effective dose is being taken. It is important to
adjust and titrate medication slowly, adding
additional doses over intervals of weeks, so that
the bladder remains under control but the mouth
is not too dry. Artificial saliva may be prescribed, in
either tablet or spray form if a dry mouth becomes
too uncomfortable. Oxybutinin patches have been
found to reduce this side effect.
Antimuscarinic medication can exacerbate problems

when the bladder does not empty properly. In this
situation, the medication, whilst lessening the tendency
for the bladder to contract, also impairs its already poor
emptying ability (Figure 4). The management strategy is
to resolve incomplete bladder emptying as the first step.
Figure 4
Antimuscarinic
Medication
Residual
Urgency &
Frequency
Table 1
50
Generic name
Brand Name
Dose
Frequency
Propantheline
Pro-Banthine
15mg
Three times a day
Tolterodine tartrate
Detrusitol
2mg
Twice a day
Tolterodine tartrate
Detrusitol XL
4mg
Once a day
Trospium chloride
Regurin
20mg
Twice a day
Oxybutynin chloride
Ditropan
2.55mg
Two to four times a day
Oxybutynin chloride XL
Lyrinel XL
530mg
Once a day
Propiverine hydrochloride
Detrunorm
15mg
One to four times a day
Darifenacin
Emselex
7.515mg
Once a day
Solifenacin
Vesicare
510mg
Once a day
Fesoterodine
Toviaz
48mg
Once a day
www.mstrust.org.uk

Bladder
Botulinum toxin
For some people, the measures outlined above
will not provide adequate bladder control.
Injecting botulinum toxin into the bladder wall
was first reported in Switzerland over ten years
ago and is highly effective in reducing urgency
and incontinence. In people with MS, the
injections have been shown to be effective in
managing detrusor over-activity and to improve
symptoms of urgency, frequency and
incontinence. It also improves quality of life9.
A consistent response is seen in patients who
receive repeat injections10. However bladder
emptying is almost always affected by this
procedure so acceptance to carry out clean
intermittent self-catheterisation is crucial. The
procedure can be done under local anaesthetic
as an outpatient and the benefit seems to last for
around a year. This treatment is recommended
for those who have not responded to
antimuscarinic medications, and are willing to
perform clean intermittent self-cathetirasation7.
Other approaches
Posterior tibial nerve stimulation (a procedure for
stimulating the nerve behind the ankle) has
recently has been found to help with overactive
bladder symptoms in people with MS11.
Management of incomplete
bladder emptying
Clean intermittent self-catheterisation (CISC)
A persistent post void residual volume in excess
of 100ml indicates that clean intermittent selfcatheterisation should be offered7. This technique
has been in use for nearly 40 years12 resulting in
the single greatest improvement in managing the
bladder problems of MS13. This must be initiated
and taught by a urology specialist nurse or
continence advisor.
People have varied responses to the suggestion
that they should self-catheterise, some react with
horror and fear. Fortunately, most people decide
to try the technique once the fundamentals of
pelvic anatomy have been explained (particularly
important for women), reassurance given that it
will not hurt, is not invasive, the discretion of the
catheter shown, the personalised nature of the
procedure emphasised and the technique
expertly demonstrated. Talking to someone who
has previously mastered the method can be
helpful for some who are novice.
CISC will help reduce bladder symptoms of

accumulating urine that cannot be eliminated
naturally. The procedure will benefit those with
symptoms of difficulty in voiding as well as those
who have urinary frequency and urgency because
of bladders that are persistently nearly full.
The recommended regime to self-catheterise is
two or three times a day and, if nocturnal frequency
is problematic, last thing before bedtime. The
patient will become the expert on how often he/she
should carry out their CISC. Some find it necessary
to catheterise four or six times in 24 hours. More
frequent CISC may indicate that bladder storage
capacity is poor and antimuscarinic medications
need to be increased.
Lack of motivation is a common cause of failure,
and there are also some medical conditions that
make it impossible. Poor hand function due to
weakness or tremor is a major difficulty. A general
benchmark is that people who can write and
feed themselves are likely to have the necessary
manual dexterity to self-catheterise. Lower limb
spasticity or spasm may make thigh abduction
difficult but with appropriate management CISC
may still be possible.
Other approaches
There is some evidence that supra pubic vibration
(a buzzer) can improve bladder emptying for
those with both incomplete bladder emptying and
detrusor overactivity14.
Night-time urinary frequency and

nocturnal incontinence
Nocturnal incontinence and night-time urinary
frequency are two of the worst problems
associated with urinary impairment. For most
people with MS, symptoms are helped significantly
by taking an oral antimuscarinic and carrying out
CISC, before going to bed. Sometimes, despite
these measures, difficulties persist and
desmopressin at night may be effective as it
reduces the volume of urine produced overnight
by the kidneys (when they are at their most
productive). Its action lasts for 3-6 hours and,
despite its mode of action, is safe when taken
precisely as instructed. Desmopressin is usually
taken as a spray. It can be used during the daytime
but it is essential that the user realises the possible
dangers of retaining too much water if it is used
more than once in 24 hours15. It should not be
prescribed to people over 65.
51

Bladder
Bladder management in advanced MS

With advancing disease, drugs, CISC and
botulinum toxin may prove inadequate or
unsuitable. An indwelling catheter inserted suprapubically, can transform the life of a person with
MS. It is important that regular review, advice and
support is sustained and is appropriate to the
current level of disability or impairment7.
MS Trust resources
Bladder factsheet
A UK consensus on the management
of the bladder in multiple sclerosis
With the advent of botulinum toxin, the need for

surgical intervention has diminished significantly.
However there may be individuals whose symptoms
are intractable and who may benefit from surgery
and they should be under specialist care.
References
1.
Marrie RA, Cutter G, Tyry T, et al. Disparities in the

management of multiple sclerosis related bladder symptoms.
Neurology 2007;68(23):1971-8.
2.
de Seze M, Ruffion A, Denys P, et al. The neurogenic bladder

in multiple sclerosis: review of the literature and proposal of
management guidelines. Mult Scler 2007;13(7):915-8.
3.
Nortvedt MW, Riise T, Myhr KM, et al. Reduced quality of life

among multiple sclerosis patients with sexual disturbance and
bladder dysfunction. Mult Scler 2001;7(4);231-5.
4.
Chancellor MB, Blaivas GJ. Urological and sexual problems in

multiple sclerosis. Clin Neurosci 1994;2(3-4):189-95.
5.
Miller H, Simpson CA, Yeates WK. Bladder dysfunction in

multiple sclerosis. Br Med J 1965;1(5445):1265-9.
6.
Betts CD, DMellow MT, Fowler CJ. Urinary symptoms and the
neurological features of bladder dysfunction in multiple
sclerosis. J Neurol Neurosurg Psychiatry 1993;56(3):245-50.
7.
Fowler CJ, Panicker JN, Drake M, et al. A UK consensus on the

management of the bladder in multiple sclerosis. J Neurol
8.
Andersson KE. Antimuscarinics for treatment of overactive

bladder. Lancet Neurol 2004;3(1):46-53.
9.
Kalsi V, Gonzales G, Popat R, et al. Botulinum injections for the

treatment of bladder symptoms of multiple sclerosis. Ann
Neurol 2007;62(5):452-7.
10. Khan S, Game X, Kalsi V, et al. Long-term effect on quality

of life of repeat detrusor injections of botulinum neurotoxin-A
for detrusor overactivity in patients with multiple sclerosis.
J Urol 2011;185(4):1344-9.
11. de Seze M, Raibaut P, Gallien P, et al. Transcutaneous
posterior tibial nerve stimulation for treatment of the
overactive bladder syndrome in multiple sclerosis: results of a
multicenter prospective study. Neurourol Urodyn
2011;30(3):306-11.
12. Lapides J, Diokno AC, Silber SJ, et al. Clean, intermittent selfcatheterization in the treatment of urinary tract disease. J Urol
1972;107(3):458-61.
13. Winder A. Intermittent self-catheterisation. Nurs Times
2002;98(48):50.
14. Prasad RS, Smith SJ, Wright H. Lower abdominal pressure
versus external bladder stimulation to aid bladder emptying in
multiple sclerosis: a randomised controlled study. Clin Rehabil
2003;17(1):42-7.
15. Tubridy N, Addison R, Schon F. Long term use of
desmopressin for urinary symptoms in multiple sclerosis. Mult
Scler 1999;5(6):416-7.
52
www.mstrust.org.uk

Bowel
Bowel
Although bowel problems are common in patients
with MS they are generally under reported and
neglected1. Wiesel2 reported that the prevalence
of bowel dysfunction in patients with multiple
sclerosis is higher than in the general population.
Up to 70% of patients complain of constipation
or faecal incontinence, which may coexist2,3.
Sullivan and Ebers4 also reported that 53% of
people with MS complained of constipation and
another study of a large number of people with
MS found that 43% had constipation and 53%
faecal incontinence.
Bowel dysfunction is a source of considerable
ongoing distress in many patients with MS.
Symptoms related to the bladder and bowel are
reported by patients as an important symptom
limiting their ability to work2. Management of
bowel problems is influenced by many factors,
including peoples expectations of what is
normal, tradition, and culture5. Bowel control is
extremely complex, involving a delicate
coordination of many different nerves and muscles.
Overall bladder and bowel dysfunction has been
linked to lower limb dysfunction, meaning that
paralysis of legs and walking difficulties are often
accompanied by bladder and bowel problems,
thus compounding management difficulties.
Managing dysfunction begins with assessment by
an experienced health professional followed by
ongoing collaboration with the individual to
develop an approach which meets their particular
needs. Assessment should be repeated as an
individuals needs change. In the absence of
research evidence from studies with MS patients,
findings in other similar patient groups, such as
spinal cord injury, should be used to inform care.
Neurological control
In order to have voluntary control of defaecation
(continence), it is necessary to have sensation of
the presence of stool in the rectum, sometimes
referred to as the call to stool. This sensation
occurs when the faeces move into the rectum,
stretching the rectal walls and triggering messages
of the need to evacuate to be sent via the sensory
pathways to the sacral spinal cord and brain.
Sensory information will differentiate between solid
or liquid stool or flatus in the rectum. In response

to sensory messages motor impulses reach the
anorectum from the brain and sacral spinal cord to
coordinate reflex activity and to allow voluntary
relaxation of the anal canal for evacuation; if
defaecation is not convenient, the urge to
defaecate can be voluntarily suppressed, stool
moves back up into the rectum and away from the
anal canal.
Damage to any part of this pathway, may reduce
or completely interrupt transmission of motor and
sensory nerve impulses resulting in reduced or lost
sensation and control over voluntary muscle
function leading to faecal incontinence.
Damage to autonomic nerve pathways in the
spinal cord alters colonic motility due to impaired
parasympathetic and sympathetic input. This may
result in rapid transit and loose stool but more
often results in slower transit and constipation.
Reduced motility and impaired reflex coordination
of the pelvic floor, left or descending colon,
rectum and anal canal can result in evacuation
difficulties. These pathophysiological problems are
compounded by reduced mobility, polypharmacy,
spasticity and fatigue6.
Management
Bowel dysfunction, particularly faecal incontinence,
has a significant negative impact on the quality of
life of individuals. It may be an important
contributor to the decision to stop working, and
may result in social isolation and admission to
residential care. Minimising the impact on the
individual and their family is important.
The NICE guidance on management of MS6
specifically identifies bowel problems as significant
and commonly encountered by patients. The
guidelines suggest that all health professionals in
contact with individuals with MS should have in
mind the possibility of bowel dysfunction. Where
an individual reports problems with bowel function
an assessment should be undertaken to clearly
identify the problem and to support the
development of an individualised bowel
management programme.
There are few published studies to support bowel
management for people living with MS, so much of
the following is based on evidence and experience
from the spinal cord injured population.
53

Bowel
aluminium antacids, antibiotics, antimuscarinics,

antiepileptics, antidepressants, calcium
supplements, diuretics, iron tablets, opiates
Aims
The aim of managing bowel dysfunction depends
on the main symptom.
Faecal incontinence - providing predictable,

effective and reliable evacuation at a chosen time.
Constipation - promoting an appropriate stool

form with easy, effective evacuation on a
regular basis.
diet - appetite, frequency of meals/snacks, intake

of fruit, vegetables and wholegrain foods
fluid intake - volume and type
bowel function - sensation of need for evacuation,

voluntary control - ability to defer defaecation
for how many minutes after first urge
frequency of evacuation
stool form - use the Bristol Scale7 to describe stool

form. Abnormal stool such as black-tarry, pale or
bloody stool should prompt further investigation
which may include onward referral
frequency of faecal incontinence - volume and

stool type
other symptoms - abdominal bloating, passage

of flatus, pain, rectal bleeding, haemorrhoids,
fissures etc
current/previously tried methods of managing - if

any - oral laxatives, rectal stimulants, use of pads
duration of bowel care
A simple bowel diary completed for one week

before assessment is a very useful adjunct. This
should record timing, frequency and stool form at
evacuation. Methods used to assist evacuation
(laxatives, rectal stimulants, digital interventions),
episodes of faecal incontinence and other problems
should all be noted. A record of dietary and fluid
intake can also be useful.
level of dependence in bowel care - who provides

care if required
accessibility/suitability of toilet facilities - refer to

local community occupational therapist if
appropriate
impact on social and work life.
The assessment should consider:
In either case where an individual has faecal urgency,

impaired mobility and therefore difficulty accessing a
toilet in a timely way, or where help is required with
toileting, promoting a regular routine, which allows
evacuation to occur at an appropriate time, is essential.
This is sometimes referred to as a pre-emptive
approach; bowel evacuation and care is prompted at
a suitable time when it is most manageable so preempting faecal incontinence or urgency at other
times. Regular effective emptying of the bowel also
helps to avoid the build up of constipated stool and
development of faecal impaction.
Assessment
A bowel assessment should be holistic in nature,
focusing on the objectives identified by the
individual and placing the bowel issue in the
context of the wider impact of MS for that
individual. Co-morbidities should also be
considered, an individual with MS may also
experience gastrointestinal morbidity and referral
for gastroenterological or colorectal opinion may
be warranted.
54
Individuals with MS will often be taking multiple

medications. Where new medications are
commenced or changes made to dosage, the
patient should be educated to be alert for changes
in bowel function and if necessary to seek advice.
type of MS and level of disability
brief medical history - including gut-related

disease/surgery, obstetric history
Ideally, the assessment will include a digital rectal

examination. This allows visual assessment of the
perianal area, assessment of anal tone, sensation and
voluntary anal squeeze, presence and type of stool in
the rectum, local problems such as anal stricture,
prolapse, haemorrhoids, fissure etc.
medication - including over-the-counter and

complementary or alternative medicines. The
following groups of drugs are associated with
altered stool consistency, most often constipation:
Radiographic colonic transit studies and anorectal

physiology tests may be undertaken in some centres.
However, the usefulness of such tests in managing
neurogenic bowel dysfunction has yet to be established.
www.mstrust.org.uk

Bowel
Interventions
Diet
The impact of dietary fibre on bowel function in
individuals with MS is not clear. However, the general
health benefits of an adequate intake of soluble and
insoluble fibre through fruit, vegetables and whole
grain foods are well recognised. The individual should
be encouraged to aim for five portions of fruit and
vegetables daily with one or two portions of
wholegrain foods. Their intake should be increased
gradually to avoid abdominal bloating or flatulence,
and will be dependent on ability to eat and appetite.
Fruit and vegetables may be fresh, frozen or dried; a
standard portion is 80g. Impact on bowel function
can be assessed as the diet is gradually changed and
amended as necessary.
Fluid intake
The normal function of the large bowel is to
absorb water. In conditions where transit time is
extended, greater water absorption occurs
resulting in increased risk of constipation.
Inadequate fluid intake is also a factor. A good
guide in assessing fluid intake is to observe the
colour of the patients urine8, pale straw coloured
urine indicates an adequate intake, darker urine
suggests that intake should be increased. While
water, which is free of any additives, is the ideal
any fluid that the patient will drink should be
encouraged to maintain pale straw coloured urine.
Defaecation dynamics
In patients presenting with constipation who are
able to use the toilet, correct positioning when
toileting can promote improved evacuation of
stool. Feet should be supported and the knees
should be higher than the hips in a quasi-squatting
position. Bracing the abdominal muscles and
bulging the abdominal wall outwards to increase
abdominal pressure may assist the passage of stool
without raising intrarectal pressures unduly.
Opening the bowels over a toilet is the norm for
adults and all reasonable efforts should be made to
facilitate this. This may require adaptation of the
toilet or bathroom. An occupational therapist
assessment of the patients own environment and
appropriate risk assessment for carers giving bowel
care in the home is required.
Establishing a routine
Having a regular routine is fundamental to gaining
control over bowel function and avoiding
constipation. The routine should be developed
individually and be designed to fit into the individuals

life. Frequency of bowel care may range from once or
twice daily to alternate days and some flexibility
should always be maintained9.
Establishing appropriate stool consistency
Stool consistency is described here using the Bristol Stool
Form Chart7, a copy of which can be found below.
The Bristol Stool Form Scale

Type 1
Seperate hard lumps, like nuts (hard to pass)
Type 2
Sausage-shaped but lumpy
Type 3
Like a sausage but with cracks on its surface
Type 4
Like a sausage or snake, smooth and soft
Type 5
Soft blobs with clear-cut edges (passed easily)
Type 6
Fluffy pieces with ragged edges, a mushy stool
Type 7
Watery, no solid pieces ENTIRELY LIQUID
55

Bowel
useful where dietary fibre cannot be increased

and are suitable for long term use. They should
not be used in existing bowel obstruction or
faecal impaction. They take a few days to become
effective and may cause flatulence and abdominal
distension especially when first used. They should
be used daily in a regular pattern.
If the stool is too soft or loose it is difficult to control

and can contribute to incontinence. A bulking agent
such as Fybogel may help, along with increasing
wholegrains such as wholemeal bread which help to
absorb liquid. However, there is a risk of soft
impaction or overloading of the bowel with soft bulky
stool in immobile individuals with slow colonic transit
when using bulking agents.
Where the stool is constipated and diet alone has
not been effective a number of laxatives which
soften stool and/or stimulate colonic activity are
available. It is important to match the introduction
or increase in stool softeners or stimulant laxatives
with planned management of evacuation. People
usually begin with small doses of laxatives and
increase gradually until the appropriate stool
consistency is achieved; if the stool becomes too
soft the laxative should be reduced gradually.
Osmotic laxatives such as lactulose and

macrogols (Movicol, Idrolax) act by retaining
fluid in the bowel due to osmotic action. They
produce a softer bulkier stool. They take up to
three days to become effective and may cause
bloating and flatulence. Small regular doses to
achieve optimal stool consistency may be best
as doses large enough to cause evacution may
result in incontinence.
Stimulant laxatives, such as senna and

bisacodyl, stimulate intestinal motility. They
take 8-12 hours to be effective. They are used
to promote evacuation of stool and so are only
taken 8-12 hours prior to planned evacuation
of the bowel. While they are usually
recommended for short-term use in the general
population, in individuals with neurogenic
bowel dysfunction, long-term use is more usual
and they form part of the individuals ongoing
bowel mangement programme.
Assisting evacuation of stool

Being able to initiate bowel evacuation at a
chosen time is an important part of achieving
managed continence. This can be done by
using pharmacological or digital rectal
stimulation for those with reflex activity.
Bristol Stool Form Scale 4 is identified as the optimal

stool form for the general population and for those
with intact evacuatory reflexes. Some individuals prefer
to have a more formed stool (Bristol Stool Form 3) as
this gives them more control over evacuation; for
instance individuals without evacuatory reflexes who
use manual evacuation of stool as their main method
of evacuation. Care should be taken to avoid
development of constipation in the longer term.
Abdominal massage
Abdominal massage is used by up to 30% of individuals
with neurogencic bowel dysfunction9,10. It is regarded as
a non-invasive technique to encourage stool transit, and
while it may not eradicate the need for laxatives it may
reduce it11 and improve quality of life in constipated
individuals. Massage may be used before and after
digital rectal stimulation, insertion of stimulants or
digital removal of faeces to aid evacuation12. McClurg
and Lowe-Strong13 also describe a technique for
massage, and suggest regular use not directly associated
with bowel evacuation can be beneficial.
Laxatives
Where stool form is not optimal due to slow transit
or evacuation difficulty, oral laxatives may be used
to improve stool form and evacuation.
Rectal stimulants
Suppositories or micro enemas are used to trigger
reflex rectal contractions to expel stool in
individuals who have reflex activity in the
anorectum. Glycerin, Lecicarbon E and bisacodyl
suppositories (ranging from milder to stronger)
may be used; Micralax, Microlette and Norgalax
mini enemas may also be tried, usually when
suppositories have not been effective.
Types of laxatives:
56
Bulk forming laxatives include ispaghula

(Fybogel, Regulan, Isogel), methylcellulose
(Celevac), sterculia (Normacol). They must be
taken with ample fluids to avoid obstruction; a
good general fluid intake is essential. They may be
Digital rectal stimulation

Where an individual has reflex activity in the
anorectum and is unable to voluntarily expel
stool from the rectum, digital rectal stimulation
(DRS) may be used to initiate defaecation at a
chosen time. The technique stimulates
increased reflex muscular activity in the rectum,
raising rectal pressure to expel stool, and relaxes
www.mstrust.org.uk

Bowel
the external anal sphincter, thus reducing outlet

resistance2,12,14,15. It also stimulates movement of
stool into the rectum. It is often required in
addition to the use of pharmacological rectal
stimulants but for some patients digital rectal
stimulation alone is effective. It can be conducted
by the individual themselves if able or by a
suitably trained nurse or carer.
Manual evacuation of stool
The need for and importance of manual
evacuation of stool has been recognised in recent
publications16,17. Manual or digital removal of stool
involves the insertion of a single gloved, lubricated
finger into the rectum to break up and/or remove
stool18. It is a very common intervention amongst
individuals with neurogenic bowel dysfunction9
and is used by individuals with no anorectal
reflexes19 as their main method of evacuation. It
can be conducted by the individual themselves if
able or by a suitably trained nurse or carer.
Caution has been expressed in one text because
the risk of stimulation of the vagus nerve in the
rectal wall can slow the clients heart20 but this is an
uncommon side effect, rarely seen in practice.
Transanal irrigation
Warm water (body temperature 36-38C) is instilled
into the rectum and colon using a hand or electric
pump or by gravity. This both stimulates colonic
reflex activity and mechanically washes stool out.
A small number of different systems are available
and irrigation using either system can be given by a
carer. Two recent reviews have suggested that
transanal irrigation is superior to bowel management
using suppositories21,22 but laxatives may still be
required to maintain an effective programme.
Irrigation can provide improved outcomes in terms of
duration and completeness of evacuation, but it does
not suit every patient and reliable selection criteria
have yet to be identified. Assessment by an
experienced health professional, and careful teaching
and supervision of the irrigation technique increase
the likelihood of success.
Biofeedback
Biofeedback is a behavioural therapy which aims to
educate a patient about bowel function, diet and
fluids, and re-educate them in terms of their
muscle function and bowel control23. Psychological
and emotional support is also offered. Biofeedback
may be useful for individuals with mild to
moderate MS symptoms24, and is offered at many
specialist colorectal centres.
Sacral nerve stimulation (SNS)

SNS is delivered via an implanted device which provides
continuous low amplitude stimulation of the sacral
nerve plexus25 which is interrupted to allow defaecation.
Intact sacral nerves are required; SNS is not effective in
individuals with complete spinal cord injury26. The
benefits of this technique for individuals with
neurogenic constipation and faecal incontinence are still
undergoing exploration26,27.
Stoma formation for bowel management
For some individuals neurogenic bowel dysfunction
and its management have such a severe impact on
quality of life that they opt for a stoma to alleviate
the problem. Approximately 3.5% of individuals with
spinal cord injury in the UK have a stoma to manage
their bowel dysfunction28 and the outcomes appear
very good in this highly selected group29,30. The
numbers of individuals with MS who make the
same choice is unknown but for some individuals a
stoma can significantly reduce the impact of bowel
dysfunction on their lives when all other options
have been explored.
Containment products
The goal of effective bowel management is to enable
the individual to achieve managed continence; the use
of containment products as the main method of
management is only a choice where all other options
have been explored and found ineffective. There is a
wide range of equipment and disposable items, both
body-worn and to protect bedding etc available to
choose from31.
References
1.
DasGupta R, Fowler CJ. Bladder, bowel and sexual dysfunction

in multiple sclerosis: management strategies. Drugs
2003;63(2):153-6.
2.
Wiesel PH, Norton C, Glickman S, et al. Pathophysiology of

bowel dysfunction in multiple sclerosis. Eur J Gastroenterol
Hepatol 2001;13(4):441-8.
3.
Bakke A, Myhr KM, Gronning M, et al. Bladder, bowel and

sexual dysfunction in patients with multiple sclerosis - a cohort
study. Scand J Urol Nephrol Suppl 1996;179:61-6.
4.
Sullivan SN, Ebers GC. Gastrointestinal dysfunction in multiple

sclerosis. Gastroenterology 1983;84(6):1640.
5.
Powell M, Rigby D. Management of bowel dysfunction:

evacuation difficulties. Nurs Stand 2000;14(47):47-51.
6.

7.
Heaton KW, Radvan J, Cripps H, et al. Defaecation frequency

and timing, and stool form in the general population: a
prospective study. Gut 1992:33(6):818-24.
8.
British Dietetic Association 2007. Fluid why you need it and

how to get enough. www.bda.uk.com/foodfacts/fluid.pdf
[accessed August 2011]
57

Bowel
9.
Coggrave M. Neurogenic continence part 3: bowel

management strategies. Br J Nurs 2008;17(11):706-10.
10. Han RR, Kim JH, Kwon BS. Chronic gastrointestinal problems
and bowel dysfunction in patients with spinal cord injury.
Spinal Cord 1998;36(7):485-90.
11. Lms K. Abdominal massage to manage constipation. Nurs
Times 2010;107(4):26-7.
12. Coggrave M. Management of the neurogenic bowel. Br J
Neurosci Nurs 2005;1(1);6-13.
13. McClurg D, Hagen S, Hawkins S, et al. Abdominal massage
for the alleviation of constipation symptoms in people with
multiple sclerosis: a randomized controlled feasibility study.
Mult Scler 2011;17(2);223-33.
14. Wiesel P, Bell S. Bowel dysfunction: assessment and
management in the neurological patient. In: Norton C,
Chelvanayagam S, editors. Bowel continence nursing.
Beaconsfield: Beaconsfield Publishers; 2004. p.181-203.
15. Consortium for Spinal Cord Medicine. Clinical practice
guidelines: Neurogenic bowel management in adults with
spinal cord injury. J Spinal Cord Med 1998;21(3):248-93.
16. Royal College of Nursing. Digital rectal and manual removal
of faeces. Guidance for Nurses. London: RCN; 2004.
17. National Patient Safety Agency. Ensuring the appropriate
provision of manual bowel evacuation for patients with an
established spinal cord lesion. National Patient Safety
Information 01. London: NPSA; 2004.
18. Kyle G, Prynn P, Oliver O. A procedure for the digital
removal of faeces. Nurs Stand 2005;19(20):339.
19. Stiens S, Bergman S, Goetz LL. Neurogenic bowel
dysfunction after spinal cord injury: clinical evaluation and
rehabilitative management. Arch Phys Med Rehabil
1997;78(3 Suppl):S86-102.
20. Sonnenberg A, Tsou VT, Muller AD. The institutional colon:
a frequent colonic dysmotility in psychiatric and neurologic
disease. Am J Gastroenterol 1994;89(1):62-6.
21. Christensen P, Krogh K. Transanal irrigation for disordered
defeacation: a systematic review. Scand J Gastroenterol
2010;45(5):517-7.
22. Emmanuel A. Review of the efficacy and safety of transanal
irrigation for neurogenic bowel dysfunction. Spinal Cord
2010;48(9):664-73.
23. Burch J, Collins B. Using biofeedback to treat constipation,
faecal incontinence and other bowel disorders. Nurs Times
2010;106(37):18,20-1.
29. Branagan G, Tromans A, Finnis D. Effect of stoma formation

on bowel care and quality of life in patients with spinal cord
injury. Spinal Cord 2003;41(12):680-3.
30. Munck J, Simoens Ch, Thill V, et al. Intestinal stoma in
patients with spinal cord injury: a retrospective study of 23
patients. Hepatogastroenterology 2008;55(8):2125-9.
31. Cottenden A. Management with Continence Products. In:
Abrams P, Cardozo L, Khoudry S, et al, editors. Incontinence:
basics and evaluation. Bristol: International Continence
Society; 2005. p 149-255.
MS Trust resources
Bowel factsheet
Diet factsheet
Bibliography
Fowler CJ, Panicker JN, Emmanuel A, editors.
Pelvic organ dysfunction in neurological disease.
Cambridge: Cambridge University Press; 2010
Bywater A, While AE. Management of bowel
dysfunction in people with multiple sclerosis.
Br J Comm Nurs 2006;11(8):333-41.
Coggrave M. Management of neurogenic bowel.
Br J Neurosci Nurs 2005;1(1):6-13.
Coggrave M, Wiesel PH, Norton C. Management
of faecal incontinence and constipation in adults
with central neurological diseases. Cochrane
Excellence. Faecal incontinence: the management
of faecal incontinence in adults. NICE Clinical
24. Wiesel PH, Norton C, Roy AJ, et al. Gut focused behavioural
treatment (biofeedback) for constipation and faecal
incontinence in multiple sclerosis. J Neurol Neurosurg
Psychiatry 2000;69(2):240-3.
25. Kenefick NJ, Christiansen J. A review of sacral nerve
stimulation for the treatment of faecal incontinence.
Colorectal Dis 2004;6(2):75-80.
26. Jarrett ME, Mowatt G, Glazener CH, et al. Systematic review
of sacral nerve stimulation for faecal incontinence and
constipation. Br J Surg 2004; 91(12):1559-69.
27. Brill SA, Margolin DA. Sacral nerve stimulation for the
treatment of faecal incontinence. Clin Colon Rectal Surg
2005;18(1):3841.
28. Coggrave M, Norton C, Wilson-Barnett J. Management of
neurogenic bowel dysfunction in the community after spinal
cord injury: a postal survey in the United Kingdom. Spinal
Cord 2009;47(4):323-30.
58
www.mstrust.org.uk

Sexuality
Sexuality
The NICE clinical guideline1 states that MS may
disturb the normal sexual physiology and may result
in other impairments that make normal sexual
behaviour difficult. This may make it difficult for the
person to establish or maintain relationships and as
both aspects are important they should be
recognised together.
Epidemiology
Sexual problems are common in multiple sclerosis.
Estimates of the frequency of sexual dysfunctions vary
from 50 to 90% in men and 40 to 80% in women,
depending on the severity of disability of the group
and duration of illness2-5. Such reports tend to focus on
physical problems and the total impact of a change in
an individuals sexuality is often overlooked.
Sexual dysfunction correlates positively with the
presence of other disabilities in particular bladder and
bowel symptoms, sensory disturbance of the genitalia,
weakness of the pelvic floor and spasticity6-8. The
associated factors may be recognised as risk factors
and alert health professionals to the possibility of sexual
dysfunction. In common with other symptoms of MS
those of sexual dysfunction can also relapse and remit.
Studies have estimated that over 50% of people with
neurological disorders may experience sexual
dysfunction, but only approximately 25% express
concern about problems they may have9,10. People do
not always voice their concerns and health
professionals are sometimes reluctant to enquire but
people with MS should be offered the opportunity to
discuss any issues or problems. The NICE clinical
guideline1 recognises the importance of enjoying sexual
health regardless of illness or disability and states,
Every person (or couple) with MS should be asked
sensitively about or given opportunity to remark upon,
any difficulties they may be having in establishing
sexual or personal relationships.
Types of dysfunction
MS symptoms such as spasticity, and tertiary

dysfunction can be seen as a result of the psychosocial
impact such as depression or changes within the
relationship. It is important to establish in which of
these areas the sexual problem is presenting.
Medication commonly contributes to sexual
dysfunction; for example, tricyclic antidepressants
are associated with erectile dysfunction and the
selective serotonin reuptake inhibitors are associated
with delayed or absent orgasm or ejaculation.
Loss of desire may result from depression or changes
within the dynamics of the relationship. People
should be offered information about locally available
counselling and supportive services such as
Relate. Psychosexual counselling may be appropriate
for some.
The very nature of sexual problems can make
discussion difficult for both people with MS and
healthcare professionals. Individuals may not be
aware that MS can affect sexual functioning and
assessment of these needs is important.
Men with MS
The commonest dysfunction in the excitement
phase is erectile dysfunction which brings a
significant impact on quality of life3,12. This is often a
primary symptom, a direct result of demyelination.
However, assessment must include psychosexual
and relationship factors as well as the physical
aetiology since the cause of sexual dysfunction is
often multifactorial. Erectile dysfunction may also be
the first sign of cardiovascular disease13.
The PDE5 inhibitors, sildenafil (Viagra), vardenafil
(Levitra) and tadalafil (Cialis) are the most popular first
line treatments and are probably effective in 70-80% of
men. A double-blind, randomised trial involving 217
men with MS found that sildenafil significantly
improved erections (90% of patients) compared with
placebo (24% of patients)14. NICE guidance1
recommends that men with persisting erectile
dysfunction who do not have contraindications should
be offered 25-100mg sildenafil.
Kaplan11 divided the sexual response cycle into three

Tadalafil has the advantage of being effective for up
phases - desire, excitement and orgasm.
to 36 hours which may mean less planning and
pressure to have sexual intercourse to a schedule. In
Sexual problems can be described as primary,
secondary or tertiary2. People with MS may experience an Italian study, 72 of 92 (78%) men with MS
responded to 10-20mg doses of tadalafil, with
dysfunctions as a consequence of one or all of the
statistically significant improvements in erectile
above. Primary dysfunction is caused directly by
function and in sexual satisfaction scores15.
demyelination, for example numbness in the genital
area. Secondary sexual dysfunction occurs as a result of
59

Sexuality
Side effects most commonly experienced with PDE5

inhibitors include headache, flushing, rhinitis (nasal
congestion) and dyspepsia. The only absolute
contraindication to PDE5 inhibitors is concurrent
nitrate therapy and nicorandil.
Where someone does not respond to PDE5 inhibitors
they should be assessed for general and specific
factors that might worsen erectile dysfunction; these
might include depression, anxiety, vascular disease,
diabetes and other medications. Alternative
treatments such as alprostadil or intra cavernosal
papverine could then be considered, or intraurethral
applications (eg MUSE), or a constriction ring.
Vacuum devices are excellent at preventing penile
atrophy and should be considered as an adjunct to
pharmacological management.
Medications may not on their own solve
psychological or relationship issues, but can be
helpful in conjunction with counselling.
Women with MS
Most of our knowledge regarding sexual
functioning has been derived from studies in men.
Understanding of female sexual dysfunction is
gradually increasing in what has previously been a
neglected area.
Problems may include loss of libido, lack of vaginal
lubrication, difficulty in achieving orgasm, pain
during intercourse and numbness. As with men,
both psychological and neurological factors are
components of sexual dysfunction.
Partners and relationships

Masters and Johnson17 observed that there is no such
thing as an uninvolved partner. The turmoil of
emotions, which may occur in response to the onset of
disability, impacts upon the partner and may alter their
need for autonomy and intimacy. A change in roles
within a relationship from an equal partnership to one
of carer and cared for substantially alters the
dynamics of the relationship. In addition the effects of
cognitive changes on the relationship may need to be
addressed. Some couples may adjust and adapt to a
new type of relationship but others may experience
great distress. Identified risk factors within relationships
are the presence of a progressive condition,
relationships begun before the onset of disability and
the presence of a sexual dysfunction10,18-20. The
importance of intimacy and communication within
couples is vital as people often have difficulty talking
about problems with each other.
People who are not in a relationship

Sexual expression is no less of an issue for those not
currently in a relationship. Often there is a greater
degree of reticence about asking for help. Concerns
about sexual functioning with a new partner, or
about finding a partner in the face of mobility
problems, continence and other difficulties, need the
opportunity to be voiced.
Helping individuals and couples with

sexual and/or relationship difficulties
A commonly used model in facilitating discussion of

sexual dysfunction is known as the P-LI-SSIT model.
This is a hierarchical model that can be applied by any
health professional to the point at which they feel able
Women may experience alteration in the excitement to operate21,22. The components of the acronym are
phase and work is being carried out in this area,
pyramidal; many people will benefit from the first
however trials have found that sildenafil is not
intervention but few from the fourth.
effective in women16. There have not been many
advances in the therapeutic options, with reliance
P - giving people permission to discuss sex and
on topical lubricants and creams. Poor vaginal
relationship worries. Professionals should be able to
lubrication can easily be solved by liberal application pick up cues or ask specifically about sex and
of water-based lubricants such as Sylk or Senselle.
relationship issues. MS can have quite an effect on
the more intimate side of life. Has that caused you
Changed sensation in the genital area may respond to any concern?
treatment such as carbamazepine or amitriptyline.
Some women find that the use of vibrators and other
LI - providing limited information about any areas of
sexual aids increases the intensity of stimulation.
concern. This can be done by whoever the person
Education can also be important in helping women to with MS has confided in. If they feel unable to provide
explore other means of achieving orgasm and
information, then having listened to the problem they
additional erogenous zones. Partners could be
can make a referral to another agency such as a
encouraged to experiment to find new ways to
sexual dysfunction clinic, counselling or Relate.
approach altered sexual functioning and not lose sight Acknowledgement of the problem and empowerment
of the fact that this can be fun.
to look further for help is very important.
60
www.mstrust.org.uk

Sexuality
SS - providing specific suggestions, for example

about how to manage continence problems to
allow sexual intimacy, managing fatigue,
positioning to avoid spasm or pain. Many of these
suggestions are made most appropriately by a
professional with knowledge of neurological
problems rather than just skill in treating sexual
dysfunction.
IT - intensive therapy. Specialised psychosexual
therapy. The majority of problems can be dealt
with earlier in this model.
All health care professionals can undertake the first
step in the P-LI-SS-IT model providing they are
prepared to listen. This alone can be of immense
therapeutic benefit.
15. Lombardi G, Macchiarella A, Del Popolo G. Efficacy and

safety of tadalafil for erectile dysfunction in patients with
multiple sclerosis. J Sex Med. 2010;7(6):2192-200.
16. DasGupta R, Wiseman OJ, Kanabar G, et al. Efficacy of
sildenafil in the treatment of female sexual dysfunction due
to multiple sclerosis. J Urol 2004;171(3):1189-93.
17. Masters WH, Johnson VE. Human sexual response. London: J
& A Churchill Ltd; 1966.
18. Halvorsen JG, Metz ME. Sexual dysfunction, part 1:
Classification, etiology and pathogenesis. J Am Board Fam
Pract 1992;5(1):51-61.
19. Abrams KS. The impact on marriages of adult-onset
paraplegia. Paraplegia 1981;19(4):253-9.
20. Woollett SL, Edelmann RJ. Marital satisfaction in individuals
with multiple sclerosis and their partners; the interactive
effect of life satisfaction, social networks and disability. Sex
Marital Therapy 1988;3(2):191-6.
21. Annon JS. The behavioural treatment of sexual problems:
brief therapy. New York: Harper and Row; 1976.
22. Taylor B, Davis S. Using the extended PLISSIT model to
address sexual healthcare needs. Nurs Stand 2006 21(11):
35-40.
References
1.

2.
Foley FW, Sanders A. Sexuality, multiple sclerosis and

women. Mult Scler Management 1997;4(1):3-9.
3.
Tepavcevic D, Kostic J, Basuroski I, et al. The impact of sexual

dysfunction on the quality of life measured by MSQoL-54 in
patients with multiple sclerosis. Mult Scler 2008;14(8):1131-6.
4.
Zorzon M, Zivadinov R, Monti Bragadin L, et al. Sexual

dysfunction in multiple sclerosis: a 2-year follow-up study.
J Neurol Sci 2001;187(1-2):1-5.
5.
Demirkiran M, Sarica Y, Uguz S, et al. Multiple sclerosis

patients with and without sexual dysfunction: are there any
differences? Mult Scler 2006;12(2):209-14.
6.
Hulter BM, Lundberg PO. Sexual function in women with

advanced multiple sclerosis. J Neurol Neurosurg Psychiatry
1995;59(1):83-6.
7.
Vas CJ. Sexual impotence and some autonomic disturbances

in men with multiple sclerosis. Acta Neurol Scand
1969;45(2):166-82.
8.
Fraser C, Mahoney J, McGurl J. Correlates of sexual

dysfunction in men and women with multiple sclerosis. J
Neurosci Nurs 2008;40(5):312-7.
9.
Szasz G, Paty D. Maurice WL. Sexual dysfunctions in multiple

sclerosis. Ann NY Acad Sci 1984;436:443-52.
MS Trust resources
MS and sex: a guide for men
MS and sexuality: a guide for women
Further resources
Kessler TM, Fowler CJ, Panicker JN. Sexual
dysfunction in multiple sclerosis. Expert Rev
Neurother 2009;9(3):341-50.
Fletcher SG, Castro-Borrero W, Remington G, et al.
Sexual dysfunction in patients with multiple
sclerosis: a multidisciplinary approach to evaluation
and management. Nat Clin Pract Urol
2009;6(2):96-107.
10. Chandler BJ, Brown S. Sex and relationship dysfunction in

neurological disability. J Neurol Neurosurg Psychiatry
1998;65(6):877-80.
11. Kaplan HS. The new sex therapy: active treatment of sexual
dysfunction. New York: Brunner/Mazel; 1974.
12. Zorzon M, Zivadinov R, Bosco A, et al. Sexual dysfunction in
multiple sclerosis: a case-control study. I. Frequency and
comparison of groups. Mult Scler 1999;5(6):418-27.
13. Kirby M, Jackson G, Betteridge J, et al. Is erectile dysfunction
a marker for cardiovascular disease? Int J Clin Pract
2001;55(9):614-8.
14. Fowler CJ, Miller JR, Sharief MK, et al. A double blind,
randomised study of sildenafil citrate for erectile dysfunction
in men with multiple sclerosis. J Neurol Neurosurg Psychiatry
2005;76(5):700-5.
61

Mobility
Physical problems can be divided into

primary problems which arise as a direct result
of neurological damage
Mobility
Mobility can be defined as the ability to
independently and safely move oneself from one
place to another. In MS, altered movement is one
of the more common symptoms and may be due
to focal weakness or tightness in a muscle group.
Although this section considers a physiotherapeutic
approach to these problems, it must be
remembered that mobility can be adversely
affected by altered sensation, fatigue, visual
disturbance, ataxia, pain or depression. These
symptoms and effects are dealt with elsewhere in
this book, as is spasticity, which can be a major
contributory factor to mobility problems.
It is important to distinguish between habilitation and

rehabilitation. The former enables the individual to
continue with their present lifestyle, whilst the latter
enables them to return to the best level possible
following a relapse or period of inactivity.
wheelchair and seating
walking aids: sticks, elbow crutches, delta

walkers, rollators (4 wheeled walkers)
The therapy regime should be realistic and relevant in

order to lead to improvement. Wherever possible,
people with MS should be encouraged to start exercise
early in their disease course. Maintaining ability is easer
than regaining ability. One challenge in MS is the
individuals ability to comply with a routine. It is
difficult for fit people to persevere with exercises
without becoming bored and disheartened; if you add
the problem of pain, fatigue and disability then
motivation can become an even greater challenge.
Group sessions in a proactive atmosphere can be
useful at all stages, however some people may prefer
to exercise at home.
splinting and orthotics
Group physiotherapy
appropriate home adaptations: hoists, stair lifts,

transfer aids, bath aids, railings.
Other factors with a major impact on mobility and

which may need to be considered include:
This section describes the physiotherapeutic

approach, considers group exercise, the
importance of good positioning and individual
exercises to encourage this, and describes the use
of functional electrical stimulation (FES) and
fampridine.
Groups need to meet in a venue which is local, easily

accessible, with ramps, good transport and parking
and with disabled toilets nearby. Group therapy should
be pitched at the appropriate level of ability and
should suit different interests. It should be viewed as a
supplement to individual therapy.
Groups have many advantages including:
the opportunity to educate and teach preventative

strategies to more than one person. Groups are
more economical than one to one so can often
continue to provide support by running for longer
periods. Ongoing individual physiotherapy for
people with MS is not a reality in most areas
improved attendance and motivation to increase

activity levels
a positive way of monitoring progress, and

picking up any problems before complications
arise and therefore making appropriate referrals
to other professionals when required
social interaction leading to friendships, mutual

support and empowerment through sharing
new ideas and coping strategies
A physiotherapy approach
Physiotherapy aims to prevent unnecessary
complications such as contractures, poor gait
patterns, pressures sores and muscle imbalance. It
addresses poor co-ordination, balance issues and
reduces the risk of falls. It promotes exercise which
is valuable in the reduction of fatigue, weakness
and social isolation through becoming housebound. Physiotherapy may also help with
depression, which affects a high proportion of
people living with MS. One of the goals of
physiotherapy is to educate and to motivate
people to reach their full potential at any stage of
their condition. Thus, physiotherapy promotes
well-being and quality of life of the individual
throughout the whole spectrum of their condition.
62
secondary problems which arise as complications

of altered movement and which are preventable.
www.mstrust.org.uk

Mobility
promotion of a positive mental attitude by

encouraging individuals to go out of the house
reduction of stress level by incorporating

elements of relaxation and teaching better
breathing techniques.
Each person should be assessed individually before

entering a class, and be given a home exercise
regime when appropriate. At each class, a realistic
goal could be set for every attendee to work on
before the following class.
realistic, regular and long-term input from a

physiotherapist. A multidisciplinary approach is
vital for both the person with MS and the carer.
Exercises can be made more attractive by variety:
hydrotherapy - individually and in groups
equipment - treadmills, Swiss balls, poles,

weights, cycles, vibrating plates, standing
frame, parallel bars, pulleys, parachutes
games - involving coordination, hand-eye

control, cognitive skills and functional
movements, from simple throwing and
catching to competitive work
Tai Chi, yoga, Chi Qung, Pilates, circuit

training, dance (movement with music) and
other similar classes
attendance at a gym and local exercise

referral schemes
hippotherapy - a physiotherapeutic treatment

using the movement of the horse to challenge
balance, core stability, increase body awareness
and stretch tight soft tissue structures.
The goals of a group exercise routine include:
maintaining good posture - looking at

positioning in chairs, wheelchairs, cars
or at work
maintaining correct dynamic and static

balance mechanisms
maintaining standing to encourage

weightbearing
avoiding muscle imbalance - maintaining

muscle strength and length, so a good daily
stretching regime needs to be established
pacing to reduce fatigue
reducing complications
developing a healthy self-image
developing body awareness which allows better

strategies for standing and walking
increasing stamina and blood circulation
maintaining supple joints and reducing pain
improving motivation and compliance

with exercises
improving mood.
Education plays a vital role at all stages of MS. The

person with MS needs to be involved in the
treatment plan as an active participant, as well as
learning about the condition and how to minimise
complications and to maximise potentials. He/she
needs to take responsibility for the quality of routine
which, to be effective, should be carried out
regularly, if possible daily. Management is a 24 hours
a day, seven days a week challenge. In order to
achieve maximum benefit, long-term care and
support are needed, involvement of family, carers and
friends, and forward planning of activities to ensure
pacing and maximum enjoyment of life.
Posture and positioning

Group activities can be beneficial for those who are
newly diagnosed and/or have minimal disability. If
groups are kept small then those who are
moderately disabled can also benefit but they may
need some individual input from carers or
physiotherapists. If appropriate, partners or carers
may be involved and shown how to help with a
basic stretching routine, positioning and manual
handling. Those with severe disability need ongoing support, long-term care facilities and
Posture describes the position one holds ones

body in, whether sitting, standing or even lying
down. If one has good posture, it will prepare
and allow one to move in the way one wants.
It is common for people with MS to adopt a
compensatory posture, which, in the long term
can exacerbate symptoms (eg spasms, pain)
and worsen mobility problems.
63

Mobility
Posture should be assessed:
Figure 1
In a chair:
Does the person slump?
Are they seated one-sided?
Have they got diminished breath
control/quiet voice/ability to swallow?
Do they have to hold on with their hands to
keep their trunk stable?
Does their head stay upright through the
course of the day?
In a wheelchair:
All the above questions apply in addition to:
Is the chair giving the required support to the
individuals back, head, seat, thighs and feet?
Is the chair contributing to poor posture?
Is the chair light enough to be self-propelled?
Is the person comfortable?
In bed:
Do they lie in the windswept position (body
flat and legs turned to one side)?
Do they hold their head to one side?
Do they go into spasms?
Are the heels rubbing too much?
Do they seem comfortable?
Changes in positioning can become habitual,
leading to further problems of poor circulation,
increased risk of infections, pressures sores,
shortening of muscles, stiffening of joints, increased
spasms and general discomfort and pain.
Many people are unaware of postures that they adopt
because of the brains ability to adapt when its
equilibrium is compromised. For example, if one leg
does not work or feel right, the body will adopt a
one-sided stance in order to stand up while shifting
the weight away from the problematic side. If that
compensation is not corrected, then the changes in
posture could become permanent. A physiotherapist
can advise on measures to prevent and/or correct
postural problems and improve comfort when seated
and when in bed.
Individual exercises
A variety of simple exercises can be done at home.
All of these exercises can be done in a chair; some
can also be done in bed.
Breathing exercises (e.g. deep breathing, whistling,
singing, blowing in a balloon) will encourage
diaphragmatic control and increased air flow and
64
circulation. Subsequently, people will usually sit up

straighter and improve their posture automatically.
Stretching exercises that elongate the trunk muscles
eg stretching forward across a table while sitting;
holding a stick or a cardboard tube and raising it
above the head or reaching out to the side; yogatype exercises.
Balance exercises are very valuable to improve postural
awareness (eg standing in front of the kitchen counter
and with a chair behind, trying to stand unsupported;
balance from one leg to the other, from heel to toe and
then find the middle so that the body weight is
distributed equally on both feet; Tai Chi).
Core stability exercises aimed at improving the
control of the trunk in response to disturbances
generated by movements of the limbs eg bridging,
pelvic tilt, quadruped arm and/or leg stretch,
Pilates-type exercises (Figure 1).
Using a regular trigger for daily activity can make
exercise easy to remember. This could be exercising
whilst waiting for the kettle to boil or checking posture
when looking in the mirror to comb hair.
Functional electrical stimulation

People with MS often experience foot drop where
the foot drags along the ground or hangs down
when walking. Functional electrical stimulation (FES)
applies electrical stimulation to unresponsive or weak
muscles and forces functional movement.
To be suitable for the treatment, the individual needs to
be able to walk, even if only a few metres with a stick or
crutch. By wearing a foot switch triggered stimulator,
the person with MS - with corrected dropped foot - can
maintain use of walking muscles for longer.
In January 2009, NICE issued guidance that FES
can be offered routinely as a treatment option for
people with foot drop caused by damage to the
brain or spinal cord.
www.mstrust.org.uk

Mobility
The use of FES is growing, with an increasing number

of centres offering the treatment. An assessment by a
physiotherapist trained in the use of FES is required to
ensure that the treatment will be suitable for the
individual. The physiotherapist will also make sure
that the pads are placed properly and that the
equipment is being used most effectively.
Fampridine (Fampyra)
Fampridine, a potassium channel blocker, may be
effective for those whose walking impairment has
been caused by reduced nerve transmission.
Fampridine works by blocking some of the
chemical processes in nerves to allow electrical
signals to continue travelling along damaged
nerves to stimulate muscles.
Fampridine, taken as one 10mg tablet twice daily,
is licensed for the improvement of walking in adult
patients with MS who have walking disability
(EDSS 4-7).
In clinical trials, approximately one third to one
half of people taking fampridine found walking
speed improved, with an average improvement of
about 25%. Initial treatment should be limited to a
two week trial to identify responders. A timed
walking test eg timed 25 foot walk, should be used
to evaluate improvement. Side effects can include
dizziness, nausea, some agitation or wakefulness,
back pain and balance disorders. At higher doses
the risk of more serious side effects, including
seizures, increases. For this reason it is important
not to exceed the recommended daily dose.
Further resources
Ashburn A, Lennon S, Mokone S. Developing a
physiotherapy service for patients with multiple
sclerosis. Int J Ther Rehabil 1997;4(12):654-70.
DeSouza L, Bates D, Moran G. Multiple sclerosis.
In: Stokes M, editor. Neurological physiotherapy.
London: Mosby International Ltd; 1998. p133-48.
Edwards S. Neurological rehabilitation. Edinburgh:
Churchill Livingstone; 2001.
Freeman JA, Gear M, Pauli A, et al. The effect of core
stability training on balance and mobility in ambulant
individuals with multiple sclerosis: a multicentre series
of single case studies. Mult Scler 2010;16(11):1377-84.
Gear M, Freeman J, Hunter H. Core stability
training in MS. Way Ahead 2011;15(3):8-9
Goodman AD, Brown TR, Edwards KR, et al. A phase
3 trial of extended release oral dalfampridine in
multiple sclerosis. Ann Neurol 2010;68(4):494-502.
Kasser S. Exercising with multiple sclerosis: insights

into meaning and motivation. Adapt Phys Activ Q
2009;26(3):274-89.
Lord SE, Wade DT, Halligan PW. A comparison of two
physiotherapy treatment approaches to improve walking
in multiple sclerosis: a pilot randomized controlled study.
Clin Rehabil 1998;12(6):477-86.
Functional electrical stimulation for drop foot
of central neurological origin. NICE Interventional
procedure guidance 278. London: NICE; 2009.
Multiple sclerosis: management of multiple sclerosis in
primary and secondary care. NICE Clinical Guideline
Pope P. Night-time postural support for people with
multiple sclerosis. Way Ahead 2007;11(4):6-8.
Solari A, Filippini G, Gasco P, et al. Physical rehabilitation
has a positive effect on disability in multiple sclerosis
patients. Neurology 1999;52(1):57-62.
Schyns F, Paul L, Finlay K, et al. Vibration therapy in
multiple sclerosis: a pilot study exploring its effects on
tone, muscle force, sensation and functional
performance. Clin Rehabil 2009;23(9):771-81.
Silkwood-Sherer D, Warmbier H. Effects of
hippotherapy on postural stability in persons with
multiple sclerosis: a pilot study. J Neurol Phys Ther
2007;31(2):77-84.
Snook EM, Motl RW. Effect of exercise training on
walking mobility in multiple sclerosis: a meta-analysis.
Neurorehabil Neural Repair 2009;23(2):108-16.
Wiles CM, Newcombe RG, Fuller KJ, et al. Controlled
randomised crossover trial of the effects of physiotherapy
on mobility in chronic multiple sclerosis. J Neurol
MS Trust resources
Are you sitting comfortably?
a self-help guide to good posture
and positioning
Falls: managing the ups and downs of MS
Functional electrical stimulation (FES) factsheet
Fampridine (Fampyra) factsheet
Exercises for people with MS
65

Spasticity
Spasticity
Spasticity can be a complex and challenging
symptom to manage in neurological conditions and is
a common symptom experienced by people with
multiple sclerosis. The ongoing management of
spasticity requires teamwork between the person with
spasticity, their regular carers, and members of the
multidisciplinary team1,2. In a survey 84% of people
with MS reported symptoms of spasticity with one
third rating it as moderate or severe3.
Table 1. Features of the upper motor neurone

syndrome9
What is spasticity?
The true nature of spasticity is still not clearly
understood. The most common definition used is:
a motor disorder characterised by a velocity
dependent increase in tonic stretch reflexes with
exaggerated tendon jerks, resulting from hyperexcitability of the stretch reflex, as one component
of the upper motor neurone syndrome4. More
succinctly spasticity has been defined as the
velocity dependent increase in resistance of a
passively stretched muscle5.
More recently these definitions have been
challenged by a European working group as
narrow and limiting. Specifically this group
identified that the term spasticity is used differently
by clinical and research communities and
concluded that spasticity is not a pure motor
disorder, or just a result of the hyper-excitable
stretch reflex or dependent on the velocity of the
stretch. They suggested a new definition as,
Disordered sensorimotor control, resulting from
an upper motor neurone lesion, presenting as
intermittent or sustained involuntary activation
of muscles6.
The resistance to passive movement caused by
spasticity is generated by abnormalities in the control
of movement by the central nervous system (CNS).
As well as this neural involvement of spasticity there
are also biomechanical changes, which occur both in
muscles and connective tissue, which through disuse
and immobility can lead to reduced range of
movement or contractures7. Increased resistance to
passive movement felt by the clinician, often referred
to as hypertonia, may be caused by a combination
of spasticity, which is neurally generated, and
biomechanical changes in the muscle and connective
tissue. Together these changes can significantly
affect function8.
66
Spasticity is one component of the upper motor

neurone syndrome9 that occurs as a result of
acquired damage to any part of the CNS,
including the spinal cord. It has a range of effects,
which can be categorised into positive and
negative features (Table 1). Most people will
present with a combination of features. One or
several of the positive features will influence the
resistance to passive movement. Often people are
described as having spasticity, but it is likely they
will also have other features of the upper motor
neurone syndrome.
Positive
features
Negative
features
Spasticity
Weakness
Spasms (flexor,
extensor, adductor)
Increase in
tendon reflexes
Loss of dexterity
Fatiguability
Clonus
Positive support
reaction
Extensor plantar
responses
Why does spasticity occur?

The control and regulation of normal skeletal muscle
activity involves a complex combination of
descending motor commands, reflexes and sensory
feedback from the brain, spinal cord and peripheral
sensation. During normal movement, influences from
the cerebral cortex, basal ganglia, thalamus and
cerebellum, travelling via upper motor neurones
adjust, reinforce and regulate the lower motor
neurone which connects directly via peripheral nerves
to the muscle to form smooth, coordinated muscle
activity and maintenance of posture.
In simple terms spasticity occurs when there is
damage to these descending upper motor neurone
tracts (eg a plaque in MS) which interrupts the
regulation of spinal cord and lower motor neurone
www.mstrust.org.uk

Spasticity
activity. This can result in enhanced lower motor

neurone activity and an increase in muscle activity,
in response to peripheral stimuli (eg muscle stretch,
a urinary tract infection or pressure ulcer)10,11.
Consequences of spasticity
Spasticity can affect physical activities such as
walking, transferring, picking up objects, washing,
dressing and sexual activity. It can also have an
emotional impact, on for example, mood, self-image
and motivation12-14. Safety in sitting and lying can also
be compromised due to spasms or persistent poor
positioning15,16 which can lead to the development of
contractures. This can potentially lead to restricted
mobility and social isolation.
Symptoms of the upper motor neurone syndrome are
not always detrimental and they may even be
positive in improving vascular flow and assisting in
transfers and even walking17. Therefore the treatment
of spasticity needs to be carefully selected and
reviewed over time in order to meet the individuals
aims and to maintain and promote function.
Management and treatment

of spasticity
Two core principles of spasticity management
are2,15,16:
Optimising an individuals posture and
movement through use of appropriate seating,
stretching and exercise programmes2.
Preventing or managing factors that may
increase spasticity and spasms. Primarily
exacerbations can occur from cutaneous stimuli
such as skin irritation, pressure sores, ingrown
toenails, tight fitting orthoses. Visceral stimuli
including incomplete bladder emptying,
constipation, bowel impaction and infections, for
example urinary tract infections, can be triggers2, 10.
Patterns of movement in function and sustained
postures throughout the day and night can also
aggravate spasticity and spasms.
These principles need to be regularly considered
and reviewed over time and used in conjunction
with medical treatments. Pivotal to their success is
ongoing multidisciplinary teamwork across hospital
and community settings working collaboratively
with the person with spasticity to effectively
manage their symptoms1,2.
A multidisciplinary approach
Effective communication between disciplines is vital
to enhance the management of an individuals
spasticity. Each discipline can be seen to have
specific expertise within the team. However this is
not exclusive and teamwork is essential1,2.
Nurses have a significant role in educating a
person on managing trigger factors and about the
available treatments to manage spasticity. They
can provide ongoing support and advice to a
person and their family as they live with and adjust
to managing spasticity and spasms over time.
Physiotherapists can carry out specific treatments
to assist an individual to manage muscle tone
particularly the biomechanical changes. Treatment
may include appropriate exercise programmes that
may encompass stretches, active exercises or
standing. Advice can also be given regarding
posture and positioning throughout the day.
Occupational therapists can play a key role in
assessing and recommending appropriate
adaptations to an individuals environment and
advising on how to maximise activities of daily
living within the context of spasticity. Appropriate
seating is of particular importance in spasticity
management.
Occasionally the expertise of speech and language
therapists can be sought when spasticity affects
neck and facial muscles18.
Medical management is important in terms of
assessing, prescribing and evaluating the use of
antispasticity drugs. In conjunction with other
members of the team, doctors can decide the
appropriate timing and selection of more
invasive treatments.
Inpatient rehabilitation may be appropriate to
provide a more thorough assessment of an
individuals spasticity throughout a 24 hour period
and to allow a more detailed management
programme to be developed.
Sometimes despite optimal physical management
programmes and optimisation of trigger factors
pharmacological measures are necessary.
Depending on the pattern of spasticity these can
be generalised or focal.
67

Spasticity
Generalised treatments19
Baclofen acts on the CNS and is the most
commonly used antispasticity drug. To avoid side
effects it needs to be started at low doses, slowly
increased and stopped at a dose that does not
cause unwanted side effects. The effect of an oral
baclofen dose can last between 4-6 hours so doses
need to be taken regularly to ensure adequate
control of symptoms. Side effects can include
weakness, drowsiness and dizziness.
Gabapentin is useful for treating spasticity
and spasms. It is particularly helpful in managing
spasticity when pain is associated with it.
Side effects can include drowsiness, dizziness
and fatigue.
The NICE clinical guideline states that the
following should only be given if treatment with
baclofen or gabapentin is unsuccessful or side
effects are unmanageable.
Tizanidine also works on the CNS and needs to be
introduced slowly to avoid side effects. Regular
blood tests should be performed to ensure there is
no adverse effect on liver function. Side effects can
include weakness, drowsiness and dry mouth.
Diazepam or clonazepam can be used alone or in
combination with other drugs. Their daytime use is
limited by sedative side effects, but if taken prior to
sleep they can be very useful in managing
nocturnal spasms. Side effects can include
drowsiness and dizziness.
Dantrolene is the only antispasmodic drug that
works directly on the muscles rather than on the
CNS. It can be used in combination with other
drugs. Often it is not well tolerated and can cause
nausea, vomiting, diarrhoea and weakness. Regular
blood tests need to be completed to ensure no
adverse effect on liver function.
Sativex is a cannabis extract which works on the
cannabinoid receptors in the brain and spinal cord.
It is licensed in MS as an add-on therapy for those
people whose spasticity and spasm has not
responded to the other available drugs20, 21. It is
available as an oral spray. Side effects can include
dizziness, sleepiness and feelings of light
headedness. Occasionally the spray can cause
soreness in the mouth so it is important to change
the spray site regularly. About half of people with
68
MS will respond to Sativex; whether someone is a

responder can be identified after a four week trial of
the drug. The dose of Sativex is then controlled by
varying the number of sprays taken each day.
Focal treatments
Botulinum toxin can be injected into muscles and
acts as a neuromuscular block which causes the
targeted muscle to become temporarily weak. It can
take 10-14 days for the full effect to be felt. It must
be used in conjunction with physiotherapy/
occupational therapy and an exercise programme to
maximise effect and to promote an ongoing change
in the spasticity once the toxin has worn off (approx.
three months)2, 22,23.
Phenol or alcohol motor point injections. The injection
permanently destroys nerve fibres in the injected muscle.
Some nerves may partially regrow, causing the effect to
wear off after several weeks or months. Injections can
however be repeated if necessary.
Intrathecal therapies
Intrathecal baclofen acts by binding to gamma
aminobutyric acid (GABA) receptors and results in
inhibition of mono and polysynaptic spinal reflexes24
with associated reduction in spasm, clonus and pain.
A concentration of GABA receptors is situated in the
intrathecal space of the spinal cord. Delivering
baclofen intrathecally accentuates its antispasticity
effect whilst minimising the troublesome systemic
side effects associated with oral intake.
An implanted pump can deliver baclofen directly to this
area and can be used to treat generalised lower limb
spasticity25-27. It requires commitment from the person
with MS, not only during the trial and implant phase,
but also for its ongoing maintenance of regular reservoir
refills and pump replacements2. It is however an
extremely effective treatment and is being used earlier in
people with MS to improve their walking28.
Intrathecal phenol is a permanent destructive
procedure29. It can be helpful for some people,
to treat very severe spasms that do not respond
to other drug treatments. The effects of an injection can
sometimes wear off but can be repeated if necessary.
Negative effects on lower limb sensation, sexual
function, bladder and bowel management can occur so
appropriate patient selection is critical to ensure effective
strategies are in place to manage these30.
www.mstrust.org.uk

Spasticity
Intrathecal treatments require a detailed clinical

governance framework to ensure safety of
administration, an example of guidelines and nursing
care plans from one service have been published2.
Surgery
Occasionally orthopaedic or neurosurgical procedures
may be recommended. These can include myelotomy
(severing of tracts in the spinal cord) and rhizotomy
(resection of posterior roots)31,32.
Complementary therapies
Some individuals with spasticity report that
complementary therapies such as acupuncture can
help relieve symptoms.
References
1.
Thompson AJ, Jarrett L, Lockley L, et al. Clinical management of

spasticity. J Neurol Neurosurg Psychiatry 2005;76(4):459-63.
2.
Stevenson VL, Jarrett L. Spasticity management: a practical

multidisciplinary guide. Oxford: Informa Health Care; 2006.
3.
Rizzo, MA, Hadjimichael OC, Preiningerova J, et al. Prevalence

and treatment of spasticity reported by multiple sclerosis
patients. Mult Scler 2004;10(5):589-95.
4.
Lance JW. Symposium synopsis. In: Feldman RG, Young RR,

Koella WP, editors. Spasticity, disordered motor control.
Chicago: Year Book Medical Publishers; 1980. p485-94.
Letchworth Garden City: MS Trust; 2010.

16. Jarrett L. The role of the nurse in the management of
spasticity. Nurs Residential Care 2004;6(3):116-9.
17. Losseff N, Thompson AJ. The medical management of
increased tone. Physiotherapy 1995;81(8):480-4.
18. Leary S, Jarrett L, Lockley L, et al. Intrathecal baclofen therapy
improves functional intelligibility of speech in cerebral palsy.
Clin Rehabil 2006;20(3):228-31.
19. Beard S, Hunn A, Wright J. Treatments for spasticity and pain
in multiple sclerosis: a systematic review. Health Technol Assess
2003;7(40);1-111.
20. Novotna A, Mares J, Ratcliffe S, et al. A randomized, double
blind, placebo-controlled, parallel-group, enriched-design
study of nabiximols (Sativex) as add-on therapy, in subjects
with refractory spasticity caused by multiple sclerosis. Eur J
Neurol 2011;18(9):1122-31.
21. Collin C, Ehler E, Waberzinek G, et al. A double-blind
randomized placebo-controlled parallel-group study of Sativex
in subjects with symptoms of spasticity due to multiple
sclerosis. Neurol Res 2010;32(5):451-9.
22. Turner-Stokes L, Ashford S. Serial injections of botulinum toxin
for muscle imbalance due to regional spasticity in the upper
limb. Disabil Rehabil 2007;29(23):1806-12.
23. Royal College of Physicians. Spasticity in adults: management
using botulinum toxin. National guidelines. London: RCP; 2009.
24. Davidoff RA, Sears ES. The effects of Lioresal on synaptic
activity in the isolated spinal cord. Neurology
1974;24(10):957-63.
25. Penn RD, Savoy SM, Corcos D, et al. Intrathecal baclofen for
severe spinal spasticity. N Engl J Med 1989;320(23):1517-21.
5.
Brown P. Pathophysiology of spasticity. J Neurol Neurosurg

Psychiatry 1994;57(7):773-7.
26. Porter B. A review of intrathecal baclofen in the management

of spasticity. Br J Nurs 1997;6(5):253-62.
6.
Pandyan AD, Gregoric M, Barnes MP, et al. Spasticity: clinical

perceptions, neurological realities and meaningful
measurement. Disabil Rehabil 2005;27(1/2):2-6.
27. Jarrett L, Leary S, Porter B, et al. Managing spasticity in people

with multiple sclerosis - a goal-oriented approach to intrathecal
baclofen therapy. Int J MS Care 2001;3(4):10-21.
7.
Carr J, Shepherd R. The upper motor neurone syndrome. In:

Neurological rehabilitation: optimizing motor performance.
Oxford: Butterworth-Heinemann; 1998. p85-203.
28. Erwin A, Gudesblatt M, Bethoux F, et al. Intrathecal baclofen in

multiple sclerosis: too little, too late? Mult Scler 2011:17(5):623-9.
8.
Dietz V. Spastic movement disorder: what is the impact of

research on clinical practice? J Neurol Neurosurg Psychiatry
2003;74(6):820-6.
9.
Greenwood R. Introduction: spasticity and upper motor

neurone syndrome. In: Sheean G, editor. Spasticity
rehabilitation. London: Churchill Communications; 1998.
10. Sheean G. Neurophysiology of upper motor neurone

syndrome and spasticity. In: Barnes MP, Johnson GR, editors.
Upper motor neurone syndrome and spasticity: clinical
management and neurophysiology. Cambridge: Cambridge
University Press; 2001.
29. Bonica JJ. Neurolytic blockade and hypophysectomy. In: Bonica

JJ. The management of pain. 2nd edition. Philadelphia: Lea &
Febiger; 1990. p1980-3.
30. Jarrett L, Nandi P, Thompson AJ. Managing severe lower limb
spasticity in multiple sclerosis: does intrathecal phenol have a
role? J Neurol Neurosurg Psychiatry 2002;73(6):705-9.
31. Lazorthes Y, Sol JC, Sallerin B, et al. The surgical management
of spasticity. Eur J Neurol 2002;9(Suppl 1):35-41.
32. Mittal S, Farmer JP, Al-Atassi B, et al. Long-term functional
outcome after selective posterior rhizotomy. J Neurosurg
2002;97(2):315-25.
11. Stevenson VL, Marsden JF. What is spasticity? In: Stevenson V,

Jarrett L, editors. Spasticity management: a practical
multidisciplinary guide. Oxford: Informa Health Care; 2006. p314.
12. Ward N. Spasticity in multiple sclerosis. J Community Nursing
1999;13(7):4-10.
13. Porter B. Nursing management of spasticity. Primary Health
Care 2001;11(1):25-9.
14. Currie R. Spasticity: a common symptom of multiple sclerosis.
Nurs Stand 2001;15(33):47-52.
MS Trust resources
Spasticity and spasms factsheet
Care pathway: the role of the
health care professional in the
management of spasticity.
15. Keenan L, Stevenson V, Jarrett L. Care Pathway: The role of the

health care professional in the management of spasticity.
69

Tremor
Measurement of tremor
Tremor
Tremor is a complex movement disorder
characterised by involuntary uncontrolled
movements. It consists of oscillating movements of
the upper limb at a frequency of 3-8Hz and may
be present when a person is voluntarily
maintaining a posture against gravity (postural
tremor), or during voluntary movement (kinetic
tremor) especially during target directed
movement (intention tremor). The tremor
amplitude increases during visually guided
movements towards a target and occurs at the
termination of the movement1. This can be
observed during the finger to nose test2 when as
the finger approaches the nose the tremor
amplitude increases. It is uncommon in MS to
experience tremor when the body is fully
supported (rest tremor) although head and neck
tremor can still be present when lying down. In
some cases there is visual involvement, nystagmus,
and severe tremor has been found to correlate
with the presence of dysarthria.
Ataxia often exists alongside tremor and is a term
used to describe abnormal movements occurring
during voluntary activity including lack of
coordination, dysmetria (inaccuracy in achieving a
target), dysdiadochokinesia (inability to perform
movements of constant force and rhythm) and
delay in movement.
At least one third of the MS population experience
tremor1 but estimates vary. In 5-10% of those
experiencing tremor it will be severe, causing a
high level of disability and a loss of independence
in activities of daily living. Tremor can occur
gradually or can appear rapidly. It may occur in
one arm only but frequently occurs in both, with
one arm usually more affected than the other.
Stress, anxiety, emotional upset and fatigue can
make tremor worse.
Cause of MS related tremor

The exact mechanism of tremor is unknown but is
thought to be due to lesions in the cerebellum and
its connections. The cerebellum is responsible for
coordinating movement and smooth muscle activity.
Damage to the basal ganglia is also thought to
cause tremor although the mechanism is unclear3.
70
The Fahn Tremor Rating Scale4 and the 0-10

Tremor Severity Scale5 have both been validated
for use in MS. The International Cooperative Ataxia
Rating Scale (ICARS) has been shown to be a
reliable and repeatable measure for ataxia6.
Impact of tremor on people with MS?

Tremor is one of the most disabling symptoms of
MS causing the person to become dependent as
many daily activities such as writing, eating,
dressing and personal hygiene become difficult
to perform.
Tremor can be socially isolating. The person with
tremor will often avoid situations that make their
difficulties obvious. As tremor most commonly
occurs during purposeful movement, people may
avoid eating and drinking in public, attending
social events, shopping etc.
Treatment for tremor

Tremor remains one of the most difficult MS
symptoms to manage7,8. A multidisciplinary team
(MDT) approach is required. Physiotherapist,
occupational therapist, MS specialist nurse, speech
and language therapist, psychologist, neurologist
and neurosurgeon may all be involved at some
point in the management of MS related tremor.
Treatment can include advice on compensation
strategies, physiotherapy, adaptations, drug
treatments and surgery.
Compensation strategies
Movements that involve reaching away from the
body, especially target-directed movements
(intention tremor) make tremor amplitude
increase. Strategies such as pressing the elbow
firmly to the side of the trunk may reduce distal
tremor although this also reduces reach.
Frequently people with tremor also have postural
instability or insufficient trunk support which can
make controlling movements more difficult. There
are ways to compensate for the tremor to reduce
its impact such as reducing forward reach, leaning
against an arm rest, or using a head rest and back
support to give more postural stability but this in
turn can also limit function.
People with head tremor (titubation) may attempt
to stabilise the head against the shoulder in an
attempt to reduce the tremor. The use of a head
www.mstrust.org.uk

Tremor
rest may reduce head tremor and make activities

such as watching television easier.
Holding the wrist of the active hand with the other
hand may help with tasks such as grooming.
The use of wrist weights has been of limited
benefit in dampening tremor. They can be helpful
if worn during eating in cases of mild/moderate
tremor. Prolonged use should be avoided as it has
been shown to increase the amplitude of tremor
after the weights have been removed.
clinical trials. Botulinum toxin has been used with

some success to treat intrusive head tremor in
people with MS1. Cannabinoids appear ineffective3.
Surgery
Stereotactic lesional surgery to the thalamus may be
used in severe cases of tremor12. Deep brain
stimulation or thalamic stimulation, which has been
used successfully in treatment of Parkinsons, may
also offer a new approach. The outcomes of these
approaches are continuing to be evaluated13,14.
References
Some people find that mentally practicing or

visualising a movement before attempting it can
reduce tremor.
Physiotherapy
Physiotherapy treatment and advice can help
manage tremor. The approach often used is aimed
at stabilising the proximal limb and trunk.
Maintaining joint range of movement and muscle
length will allow better posture and movement.
Adaptations
Adaptation is a key element to coping with tremor.
Fatigue makes tremor worse and so planning the
days activities appropriately is important. New
methods for daily activities may be found and aids
adopted where useful. Aids for eating and drinking
may be of benefit to people with moderate to
severe tremor. Writing is often one of the first
activities that may be stopped as handwriting
becomes illegible. Developments in assistive
technology can offer some help9. Voice activation,
keyboard modifications and dedicated software
programmes can enable independent use of a
computer and charities such as AbilityNet10 can be
a useful resource.
Experimental studies have shown that cooling of
the arms markedly reduced intention tremor
severity in patients with MS, the benefit is transient
lasting for 30 minutes and therefore may be
beneficial prior to performing specific tasks11.
1.
Alusi SH, Worthington J, Glickman S, et al. A study of tremor

in multiple sclerosis. Brain 2001;124(4):720-30.
2.
Feys P, Davies Smith A, Jones R, et al. Intention tremor rated

according to different finger-to-nose test protocols: a survey.
Arch Phys Med Rehabil 2003;84:79-82.
3.
Koch M, Mostert J, Heersema D, et al. Tremor in multiple

sclerosis. J Neurol 2007;254:133-45.
4.
Hooper J, Taylor R, Pentland B, et al. Rater reliability of Fahns

tremor rating scale in patients with multiple sclerosis. Arch
Phys Med Rehabil 1998;79(9):1076-9.
5.
Alusi SH, Worthington J, Bain PG, et al. Evaluation of three

different ways of assessing tremor in multiple sclerosis. J
Neurol Neurosurg Psychiatry 2000;68:756-60.
6.
Storey E, Tuck K, Hester R, et al. Inter-rater reliability of the

International Cooperative Ataxia Rating Scale (ICARS). Mov
Disord 2004;19(2):190-2.
7.

8.
Mills RJ, Yap L, Young CA. Treatment for ataxia in multiple

sclerosis. Cochrane Database Syst Rev 2007;24(1):
CD005029.
9.
Feys P, Romberg A, Ruutiainen J, et al. Assistive technology to

improve PC interaction for people with intention tremor. J
Rehabil Res Dev 2001;38(2):235-43.
10. AbilityNet - www.abilitynet.org.uk [Accessed Sept 2011]

11. Feys P, Helsen W, Liu X, et al. Effects of peripheral cooling on
intention tremor in multiple sclerosis. J Neurol Neurosurg
Psychiatry 2005;76:373-9.
12. Alusi SH, Aziz TZ, Glickman S, et al. Stereotactic lesional surgery
for the treatment of tremor in multiple sclerosis: a prospective
case-controlled study. Brain 2001;124(8):1576-89.
13. Yap L, Kouyialis A, Varma RK. Stereotactic neurosurgery for
disabling tremor in multiple sclerosis: thalmotomy or deep
brain stimulation? Br J Neurosurg 2007;21(4):349-54.
14. Thevathasan W, Schweder P, Joint C, et al. Permanent tremor
reduction during thalamic stimulation in multiple sclerosis. J
Neurol Neurosurg Psychiatry 2011;82(4):419-22.
Drug treatments
There are no drugs specific for tremor and therapy
using drugs licensed for other conditions has
limited benefits. Beta-blockers may show some
functional improvement whilst clonazepam and
isoniazid are of little or no benefit. These drugs
have not been evaluated for tremor in MS in
71

Pain
and self-administered therapies such as TENS

and massage.
Pain
Pain is common in people with MS. Studies have
reported prevalence ranging from 30%1 to 90%2-5
and it is often one of the presenting symptoms6.
Pain in MS includes altered sensations such as pins
and needles, numbness, crawling or burning
feelings through to more classical symptoms of
musculoskeletal pain.
The pain experienced by people with MS can be
persistent or paroxysmal. Pain negatively impacts
upon quality of life for people with MS7 and this
includes impairment of physical and emotional
functioning. Management of pain in MS is complex
and success can be elusive.
The pain experienced by people with MS can be:
primary, or neuropathic, a direct result of nerve

damage, or
secondary, or nociceptive, a consequence of

musculoskeletal complications of posture,
seating etc.
The NICE Clinical Guideline for the management of

MS in primary and secondary care8 recommends that
each professional in contact with a person with

MS should ask whether pain is a significant
problem for the person, or whether it is a
contributing factor to their current clinical state
all pain, including hypersensitivity and
spontaneous sharp pain, suffered by a person
with MS should be subject to full clinical
diagnosis, including a referral to an appropriate
specialist service if needed.
Assessment and treatment of pain

Pain is a complex, multidimensional phenomenon. It is
an unpleasant experience, particularly when combined
with the other symptoms of MS. It impacts upon many
aspects of an individuals psychosocial and spiritual
well-being, is often difficult for the person with MS to
articulate or describe, and can be difficult to cope with.
A number of factors can amplify existing pain; heat,
cold, fatigue, loss of sleep, mobility problems,
financial insecurity, feelings of low self-esteem,
loneliness and depression. The importance of
developing coping strategies is paramount and
can include relaxation, distraction, exercise regimes
72
People with MS can experience pain due to problems

other than their MS. 7% of the general population have
experienced pain for three months or more9 and other
factors such as arthritis, rheumatism, previous injuries
and surgery need to be taken into consideration.
Simply acknowledging the validity of pain felt brings
some reassurance, particularly if the individual has
experienced a negative response from some health
professionals.
When people with MS present with pain they must be
assessed to identify causative factors and the impact of
pain on their life, prior to drawing up a treatment plan.
If pain remains unresolved, a referral should be made
to a specialist multidisciplinary pain team8 or pain
clinic.
Broadly speaking, there are two types of pain:
neuropathic (neurogenic) pain and nociceptive pain.
People with MS may experience either type or both
types and the pain may be continuous or intermittant
and constant or variable in intensity. Treatment aims to
minimise the level of pain and to develop coping
strategies for day to day living.
Neuropathic pain
People with MS can experience neuropathic pain
due to demyelination of the nerves in the brain
and spinal cord.
Neuropathic pain or nerve pain can be experienced in
different ways by individuals. It can manifest as
dysaethesia or paraesthesia. These abnormal sensations
may be variously described as burning, shooting,
stabbing, crawling, prickling, itching, tingling, pins and
needles, tightness and/or hypersensitivity.
Trigeminal neuralgia is a severe facial pain, which
occurs 300 times more frequently in people with MS
than in the general population10. In extreme cases
surgery may be performed to alleviate the pain but this
may leave the face numb.
Lhermittes sign is an unpleasant sensation similar to an
electric shock that shoots down the spine into the legs,
often triggered by head movement and attributed to
demyelination in the cervical area.
Banding, also known as the MS hug is a feeling of
constriction, tightness or being squeezed around the chest.
Optic neuritis is a common early symptom of MS
although it can occur at any time. A sharp knife-like
www.mstrust.org.uk

Pain
pain behind the eyes is caused by inflammation of

the optic nerve, often accompanied by disruption to
vision. It usually responds successfully to treatment
with steroids.
Ligament damage can also occur in MS because of

hyperextension of the knee when walking; the
subsequent swelling of the knee can cause
significant pain.
Treatment of neuropathic pain
Treatment of nociceptive pain
The main focus of the treatment of neuropathic pain

is drug therapy5,11. The NICE guideline for MS8
recommends anticonvulsants such as carbamazepine
or gabapentin, or using antidepressants such as
amitriptyline. The NICE guideline for neuropathic
pain12 indicates amitriptyline or pregabalin as first
line treatments.
Nociceptive pain is generally managed more

successfully than neuropathic pain.
These drugs affect the chemical transmission of pain

signals with a resultant reduction of symptoms, but
they can cause unpleasant side effects such as
drowsiness, dizziness, nausea and blurred vision. Some
people find the side effects of the drugs intolerable and
therefore choose not to take them. Controlled titration
of the dose and support from health professionals
minimises side effect risk and builds tolerance until side
effects wear off.
Other treatments for neuropathic pain include TENS
(see below) and complementary therapies such as
acupuncture and aromatherapy13.
If the neuropathic pain remains uncontrolled after
initial treatments have been tried, the individual
must be referred to a specialist pain service8.
Nociceptive pain
Nociceptive pain, commonly referred to as
musculoskeletal pain, is the type of pain experienced
when someone hurts themself, has an accident or
surgery. Damage to muscles, tendons, ligaments and
soft tissue results in nociceptive pain. Muscle spasm
and spasticity, common symptoms of MS, can also be
a source of nociceptive pain.
Many people with MS experience lower back pain,
especially if immobility or fatigue means that they are
sitting down for much of the time. Sitting places the
lower back under more strain than standing and nerves
can easily become compressed or pinched. Equally, an
alteration of gait may place unusual stresses on the
discs between the vertebrae. Such stress can cause
damage to the discs and trapped nerves which results
in pain in the part of the body served by these nerves.
The NICE guideline for MS8 recommends that every

person with MS who has musculoskeletal pain
secondary to reduced or abnormal movement,
should be assessed by specialist therapists to see
whether exercise, passive movement, better seating
or other procedures might be of benefit.
If these approaches are unsuccessful, the individual
should be offered appropriate analgesic medicines.
These range from paracetamol and codeine-based
preparations, through to anti-inflammatory drugs and
opiates, in combination with drugs such as baclofen,
tizanidine and Sativex for spasm if indicated.
Any person with MS who has continuing unresolved
secondary musculoskeletal pain should be
considered for transcutaneous nerve stimulation
(TENS see below) or antidepressant medication14.
Cognitive behavioural and imagery treatment methods
should be considered in a person with MS who has
musculoskeletal pain only if the person has sufficiently
well-preserved cognition to participate actively.
Other treatments indicated include trigger point
injections, nerve blocks and complementary
therapies such as acupuncture and aromatherapy13.
Relaxation techniques can also be helpful.
Treatments that should not be used routinely for
musculoskeletal pain include ultrasound, low-grade
laser treatment and anticonvulsant medicines.
Use of TENS for the management of pain
Transcutaneous electrical nerve stimulation (TENS) is

the application of electricity to relieve pain. It is not a
new treatment; carvings from Egypt dating back to
2500BC illustrate the use of electric fish for the
treatment of pain15. TENS units deliver a small electrical
current to the sensory cutaneous nerve endings
through electrically conductive pads. A buzzing,
prickling, tingling sensation is experienced when the
Heavy lifting and awkward turning and bending can
machine is switched on. TENS is recommended in the
also contribute to back and leg pain. These movements NICE guideline8 for people with musculoskeletal pain
may irritate the spinal nerves causing the muscles at
who have not responded to medication, but it can be
the side of the spine to go into spasm; these muscle
used in conjunction with medication and also for
flexor spasms can be very painful and disabling.
neuropathic pain16-17.
73

Pain
TENS machines are battery powered, usually by a

regular 9 volt battery. Machines should have the
facility for a constant mode (also known as
continuous or conventional), a burst mode (also
known as acupuncture TENS), and a modulation
mode. On the constant mode (high frequency/low
intensity) a constant tingling sensation is felt, on
burst mode (low frequency/high intensity) a pulsing
sensation, and on modulation mode (variation of
pulse duration and frequency in a cyclical pattern) an
increase and decrease in the tingling sensation is felt.
To accommodate these three modes the machine
should have the facility to alter the pulse rate
(frequency) and pulse width. TENS units either have
one or two channels allowing the use of either two or
four pads. The dual channel machines are preferable
to allow coverage of a larger area or treatment of two
separate areas. The self-adhesive pads are
recommended if the machine is to be used over a
long period of time, as they are much easier to use.
It is thought that TENS relieves pain by several
mechanisms. The main principle behind the effect
of TENS is the gate control theory of pain18.
Electrical impulses are conducted more quickly
than pain impulses and subsequently provide a
competitive barrage of sensory input in the dorsal
horns. This enhanced sensation inhibits the activity
of the spinal cord pain neurons. Researchers
hypothesise that TENS may stimulate the
production of endorphins and encephalins, the
bodys own natural analgesics at spinal cord level
especially if used at low frequency when sharper
and more intense pulses are experienced19.
TENS has been found to be as effective as the
antidepressant drug nortryptiline for pain in multiple
sclerosis and has fewer potential side effects20.
McAlpines multiple sclerosis. 4th ed. London: Churchill Livingstone;

2005. p389-436.
7.
Motl RW, McAuley E. Symptom cluster and quality of life:

preliminary evidence in multiple sclerosis. J Neurosci Nurs
2010:42(4):212-6.
8.

sclerosis: management of multiple sclerosis in primary and
9.
Bowsher D. In: Carroll D, Bowsher D, editors. Pain: management

and nursing care. Oxford: Butterworth-Heinemann; 1994.
10. Thompson AJ. Multiple sclerosis: symptomatic treatment. J Neurol

1996;243(8):559-65.
11. Thompson AJ, Toosy AT, Ciccarelli O. Pharmacological management
of symptoms in multiple sclerosis: current approaches and future
directions. Lancet Neurol 2010;9(12):1182-99.
12. National Institute for Health and Clinical Excellence. Neuropathic
pain - pharmacological management of neuropathic pain in
adults in non-specialist settings. NICE Clinical Guideline 96.
London: NICE; 2011.
13. Howarth AL, Freshwater D. Examining the benefits of aromatherapy
massage as a pain management strategy for patients with multiple
sclerosis. J Res Nurs 2004;9(2):120-8.
14. Saarto T, Wiffen PJ. Antidepressants for neuropathic pain. Cochrane
Database Syst Rev 2007;17(4):CD005454.
15. Walsh DM. TENS: Clinical applications and related theory. New
York: Churchill Livingstone; 1997.
16. Mattison PG. Transcutaneous electrical nerve stimulation in the
management of painful muscle spasm in patients with multiple
sclerosis. Clin Rehabil 1993;7(1):45-8.
17. Cruccu G, Aziz TZ, Garcia-Larrea L, et al. EFNS guidelines on
neurostimulation therapy for neuropathic pain. Eur J Neurol
2007;14(9):952-70.
18. McMahon S, Koltzenburg M, editors. Wall and Melzacks textbook
of pain. 5th edition. Edinburgh: Churchill Livingstone; 2005.
19. Sjolund BH, Eriksson M, Loeser JD. Transcutaneous nerve stimulation
of peripheral nerves. In: Bonica JJ, editor. The management of pain.
2nd edition. Philadelphia: Lea & Febiger; 1990. p1852-61.
20. Chitsaz A, Janghorbani M, Shaygannejad V, et al. Sensory
complaints of the upper extremities in multiple sclerosis: relative
efficacy of nortryptiline and transcutaneous electrical nerve
stimulation. Clin J Pain 2009;25(4):281-5.
References
1.
74
Clifford DB, Trotter JL. Pain in multiple sclerosis. Arch Neurol

1984;41(12):1270-2.
2.
Hirsh AT, Turner AP, Ehde DM, et al. The prevalence and impact
of pain in multiple sclerosis: physical and psychologic
contributors. Arch Phys Med Rehabil 2009;90(4):646-51.
3.
OConnor AB, Schwid SR, Herrmann DN, et al. Pain associated

with multiple sclerosis: systematic review and proposed
classification. Pain 2008;137(1):96-111.
4.
Archibald CJ, McGrath PJ, Ritvo PG, et al. Pain prevalence,

severity and impact in a clinic sample of multiple sclerosis
patients. Pain 1994;58(1):89-93.
5.
Solaro C, Messmer Uccelli M. Pharmacological management

of pain in patients with multiple sclerosis. Drugs 2010;70(10):
1245-54.
6.
Miller D, Compston A. The differential diagnosis of multiple

sclerosis. In: Compston A, Confavreux C, Lassmann H, editors.
MS Trust resources
Pain factsheet
Further resources
Kerns RD, Kassirer M, Otis J. Pain in multiple
sclerosis: a biopsychosocial perspective. J Rehabil
Res Dev 2002;39(2):225-33.
The British Pain Society. Recommended guidelines for
pain management programmes for adults: a
consensus statement prepared on behalf of the British
Pain Society. London: British Pain Society; 2007.
www.mstrust.org.uk


Many people with multiple sclerosis experience
communication or swallowing difficulties. Early
referral to a speech and language therapist is
important to ensure that problems are fully
investigated and appropriate intervention and
support provided. The therapist will provide advice
that aims to improve or maintain communication
and swallowing abilities, or will suggest strategies
to adapt to the effects of changes in normal
function. This will involve working with the person
with MS as well as family members where
appropriate. Speech and language therapy is
ongoing throughout the course of the disease.
Communication
Communication is central to quality of life and
integral to maintaining relationships. Changes in
the ability to communicate can impact on social
participation and emotional wellbeing.
At a physical level, MS can affect the production of
speech, usually by delays in messages passing
through affected nerve pathways to the muscles
involved in speech production. The term used to
describe this problem is dysarthria. Very precise
control and coordination of a range of muscles is
required for speech and anything affecting the
muscles of breathing, larynx, tongue, lips or jaw
can result in alterations in speech intelligibility.
Darley1 studied 168 people with MS and found
41% displayed dysarthric speech. Hartelius2 found
that 62% of their MS sample reported speech and
voice impairments. Symptoms are variable with
some people experiencing a mild reduction in
volume when tired or a slight slurring of speech at
the end of the day. In more severe cases speech
can be totally unintelligible.
There has been very little research into the effects of
speech therapy on people with MS. Work reported so
far does indicate that therapy can be beneficial3.
General advice may include reducing background
noise before speaking, saying half words on each
breath, speaking slowly and facing listeners when
speaking. Speech exercises may be beneficial if the
problem is mild (eg to assist breath control for
volume). Developments in technology mean that
there are a range communication aids which can
assist some people with very dysarthric speech.
A small number of people with MS develop

dysphasia, or impairment of language function, but
this is unusual. Associated problems include
difficulty understanding and producing written and
/or spoken words. Together with physical speech
difficulties, cognitive problems can also impact on
daily life4. A strong association between dysarthria
and cognitive-linguistic deficit, in people with
chronic progressive type multiple sclerosis has
recently been reported5. The main deficits relate to
attention, memory and speed of processing
information, so that difficulties in retrieving the
name of something or being unable to concentrate
in a noisy environment are often experienced.
The most effective help is based on explanation,
understanding and sharing of ideas. If the speech and
language therapist can build up a trusting relationship
with the person with MS and their family, then
problems relating to speech and communication can
be discussed and solutions explored.
Swallowing
Dysphagia (difficulty in swallowing) is present in
around 30% of people who have MS6,7 and can
increase to over 60% in people who have advanced
MS8. It is particularly prevalent in individuals whose
MS includes involvement of the brainstem.
Swallowing difficulties can affect all four stages of
swallowing (oral preparatory, oral, pharyngeal and
oesophageal), and can include difficulty chewing,
pocketing food in the cheek, fluids escaping from
between the lips, residue in the pharynx after the
pharyngeal swallowing, and episodes of
coughing/choking when eating or drinking. These
difficulties can be caused by weakness, impaired
coordination and spasticitiy, or some combination
of each. Severity of dysphagia is variable.
A speech and language therapist will assess safety and
efficiency of swallowing through clinical (eg history
from the individual, oro-motor examination,
observation of eating and drinking, questionnaires) and
possibly instrumental assessment (videofluoroscopy or
fibro-optic endoscopic evaluation). Following
assessment, rehabilitation can be undertaken, where
the therapist will engage with the individual and, if
appropriate, the family, and advise on posture, possible
exercises, manoeuvres, consistencies of food and
drink, and the eating environment.
If swallowing is considered unsafe (eg the person is
experiencing recurrent chest infections), inefficient
75

(eg the person takes a long time to eat or drink, or

is unable to maintain their weight through their
oral intake), or is having an effect on quality of life,
alternative ways of obtaining nutritional intake may
be recommended. This is most likely to be
percutaneous endoscopic gastrostomy (PEG)
feeding. A PEG can be used alongside oral intake
so that the person can eat and drink for pleasure
while the PEG provides the required nutrients and
calories. It is important that the decision to fit a
PEG is fully discussed and is carefully considered by
the person with MS and their family.
Ultimately, the most effective management of
communication and swallowing in MS results from
close collaboration between the person with MS,
the speech and language therapist and other
professionals and carers.
References
1.
Darley FL. Motor speech disorders. Philadelphia: WB

Saunders; 1975.
2.
Hartelius L, Runmarker B, Andersen O. Prevalence and

characteristics of dysarthria in a multiple sclerosis incidence
cohort: relation to neurological data. Folia Phoniatr Logop
2000;52(4):160-77.
3.
Hartelius L, Wising C, Nord L. Speech modification in

dysarthria associated with multiple sclerosis: an intervention
based on vocal efficiency, contrastive stress, and verbal repair
strategies. J Med Speech Lang Pathol 1997;5(2):113-39.
4.
Langdon DW. Cognition in multiple sclerosis. Curr Opin

Neurol 2011;24(3):244-9.
5.
Mackenzie C, Green J. Cognitive-linguistic deficit and speech

intelligibility in chronic progressive multiple sclerosis. Int J
Lang Commun Disord 2009; 44(4):401-20.
6.
Hartelius L, Svensson P. Speech and swallowing symptoms

associated with Parkinsons disease and multiple sclerosis: a
survey. Folia Phoniatr Logop 1994;46(1):9-17.
6.
Poorjavad M, Derakhshandeh F, Etemadifar M, et al.

Oropharyngeal dysphagia in multiple sclerosis. Mult Scler
2010;16(3):362-5.
7.
De Pauw A, Dejaeger E, Dhooghe B, et al. Dysphagia in

multiple sclerosis. Clin Neurol Neurosurg
2002;104(4):34551.
dysphagia. Nurs Times 1996; 92(50):26-9.

Marchese-Ragona R, Restivo DA, Marioni G, et al.
Evaluation of swallowing disorders in multiple
sclerosis. Neurol Sci 2006;27(Supp 4):S335-37.
Murdoch B, Theodoros D, editors. Speech and
language disorders in multiple sclerosis. London:
Whurr Publishers; 2000.
Restivo DA, Marchese-Ragona R, Patti F.
Management of swallowing disorders in multiple
sclerosis. Neurol Sci 2006;27(Supp 4):S338-40.
Thompson AJ. Multiple sclerosis: symptomatic
treatment. J Neurol 1996;243(50):559-65.
Yorkston KM, Klasner ER, Bowen J, et al.
Characteristics of multiple sclerosis as a function of
the severity of speech disorders. J Med Speech
Lang Pathol 2003;11(2):73-84.
Yorkston KM, Klasner ER, Swanson KM.
Communication in context: a qualitative study of
the experiences of individuals with multiple
sclerosis. Am J Speech Lang Pathol
2001;10(2):126-37.
Yorkston K, Miller R., Strand E. Management of
speech and swallowing in degenerative diseases.
Austin,Texas: Pro-Ed Inc; 1995.
Further resources
Baylor C, Yorkston K, Bamer A, et al. Variables
associated with communicative participation in
people with multiple sclerosis: a regression analysis.
Am J Speech Lang Pathol 2010;19(2):143-53.
Calcagno P, Ruoppolo G, Grasso MG, et al.
Dysphagia in multiple sclerosis - prevalence and
prognostic factors. Acta Neurol Scand
2002;105(1):40-3.
Herbert S. A team approach to the treatment of
76
www.mstrust.org.uk

Pressure ulcers
Causes
Pressure ulcers
Skin, as the largest organ of the body, is crucial for
our health and well-being yet is often taken for
granted1. Whilst MS itself does not directly affect the
skin there are a number of symptoms which can put
people with MS at higher risk of skin breakdown.
These include trauma wounds due to sensation
changes and balance impairments, leg oedema and
increased risk of pressure ulcers due to spasticity,
reduced mobility and cognitive function2.
Pressure ulcers, also referred to as pressure sores,
bed sores, or decubitus ulcers, are areas of localised
damage to the skin, which in adults usually occur
over bony prominences in any area of the body3.
Pressure ulcers may range from minor breaks to
very large deep areas of dead tissues extending
over many square centimetres and down to bone.
Once present they can be difficult to heal, and can
cause general malaise and worsening of most
impairments, and they carry a risk of generalised or
localised infections. The European Pressure Ulcer
Advisory Panel (EPUAP) classification system4 for
pressure ulcers highlights that damage can be
occurring even when the skin is not broken.
Pressure sores are caused by a combination of

factors both outside and inside the body. The
three external factors which can cause pressure
ulcers either on their own or in any combination
are pressure, shear and friction5.
Pressure is the most important factor in pressure
ulcer development5. Pressure in the seated position
for example is caused by the downward forces of
the body weight that compress the soft tissues of
the buttocks against the sitting surface (Figure 1).
This in turn occludes the delicate blood capillary
network which supplies the soft tissues. Pressure is
at its greatest in the area near bone, particularly
the ischial tuberosities where pressure is known to
be three to five times as great as that on
surrounding tissues6.
Figure 1
The NICE clinical guideline for management of MS

states that prevention and management of pressure
ulcers is a key priority. Each pressure ulcer should be Shearing forces can also deform and disrupt tissue
reported, the cause investigated and action taken to and so damage the blood vessels. Shearing occurs
when the body weight is sliding against a surface,
reduce the risks of recurrance2.
for example when poorly seated or sliding down a
bed away from a back rest. Whilst the skeleton and
Patients and carers should be taught to check for
nearby tissues move, the skin on the buttocks
signs of pressure ulcers on a daily basis.
European Pressure Ulcer Advisory Panel (EPUAP) guide4 to pressure ulcer classification
Grade Evidence
1
Non-blanchable erythema of intact skin. Discolouration of the skin, warmth, oedema, induration
or hardness may also be used as indicators, particularly on individuals with darker skin.
Partial thickness skin loss involving epidermis, dermis, or both. The ulcer is superficial and
presents clinically as an abrasion or blister.
Full thickness skin loss involving damage to or necrosis of subcutaneous tissue that may
extend down to, but not through, underlying fascia.
Extensive destruction, tissue necrosis, or damage to muscle, bone, or supporting structures

with or without full thickness skin loss.
77

Pressure ulcers
remains still. During this process the blood

capillaries become distorted, damaged or occluded
leading to skin ischemia (deprivation of blood) and
pressure ulcers can develop.
Damage due to friction differs in that it causes visual
damage to the surface of the skin and may be more
superficial. It is caused when two surfaces rub together,
often skin against a bed or a chair surface. Any moisture
present on the skin as a result of excessive sweating or
incontinence will exacerbate the problem5.
Patients and carers should be advised of warning

signs that can increase the risk of developing a
pressure ulcer. Questions to consider:
are you eating or drinking less than usual?
is moving becoming more difficult?
is your skin regularly exposed to moisture?
is your skin prone to being very dry, sore

or red?
There are a number of additional factors that are

known to place people at higher risk of acquiring
pressure ulcers. People with MS, particularly those with
more advanced disease, may fit into every category:
neurologically compromised
impaired mobility or who are immobile3
impaired nutrition7
obese or underweight8
poor posture
have you been ill recently?

have you lost or gained a lot of weight recently?
has there been any change in your level
of spasms?
The latter point can be an indicator of skin

breakdown as this can be a trigger for spasms. These
can then cause friction and shearing forces on the
skin and a vicious cycle can be entered whereby the
spasms cause the wound to worsen and the wound
exacerbates the spasms.
using equipment, such as seating or beds, which Every person with MS who uses a wheelchair should be
does not provide appropriate pressure relief9.
assessed for their risk of developing a pressure ulcer2.
The individual should be informed of the risk, and
The development of a pressure ulcer is known to
offered appropriate advice. Whenever they are admitted
result in high costs both in human and financial
to hospital (for whatever reason), their need for
terms9. The possible pain, systemic illness, reduced
pressure-relieving devices and procedures should be
self-esteem and independence can result in a major assessed. The assessment should be clinical, specifically
burden of sickness and impact on quality of life for
taking into account the risk features associated with
both patients, their families and carers10-12.
MS, and not simply the recording of a pressure ulcer
risk score; it should lead to the development and
Prevention
documentation of an action plan to minimise risk.
Prevention is far better than cure and most pressure
ulcers can be avoided by good anticipatory
Treatment and the
management.
multidisciplinary approach
There are a range of interconnecting factors
A number of risk assessment tools have been
which need to be tackled to in order to treat
developed to assist in the identification of those
existing pressure sores and prevent them developing
individuals at risk of developing pressure ulcers
again in the future. The involvement of a
including the Norton Scale, Waterlow scoring system
multidisciplinary team will often be required to
and the Braden score13. However, in evaluations of the achieve a positive outcome. Health professionals
effectiveness of these scales there is clearly variation in from different disciplines will need to work together
their sensitivity of predicting those at elevated risk13
and might include:
particularly when, as is frequently the case with an MS
patient, they fall into a younger age category as many
MS specialist nurse
district nurse
tools heavily weight older age. A factor frequently
GP
continence adviser
excluded from such tools is the presence or impact of
spasms which can result in shearing and friction on the
neurophysiotherapist dieticians
skin. This therefore highlights the importance of using
risk assessment tools and scales as an adjunct to, but
wheelchair services
speech and
not a replacement for, clinical judgement14.
language therapist.
78
www.mstrust.org.uk

Pressure ulcers
Simple tips for the prevention of pressure ulcers:

Reduce pressure
When possible alter position, even slightly, every 20 minutes

during the day. If seated this could take the form of rolling slightly
from cheek to cheek in the chair.
Appropriate equipment cushions & mattresses
This includes: bed15, armchair, wheelchair, car seat, office chairs, all
equipment when on holiday, hospital or away from home for any
reason. Seek advice from a district nurse or occupational therapist.
Avoid any form of ring cushion as this can occlude blood vessels
and cause pressure damage itself.
Nutrition
Eat a well balanced diet. Advice and diet sheets can be obtained from
a dietician. Even a short period of not eating well increases the risk of
skin damage, particularly if you are unwell with flu for example
Hygiene and skin care
Skin should routinely be kept clean and fresh. Avoid allowing skin
to be wet. Check for red areas on the skin once or twice a day.
Reddened areas should fade within minutes when pressure is
relieved. If they do not, seek advice from a district nurse.
Transferring
Obtain good instruction and support in transfer techniques and

correct use of equipment. Avoid sliding and pushing when this may
result in friction.
Positioning
Learn correct positioning for comfort and pressure relief,

particularly when seated.
11. Franks PJ, Moffatt CJ. Quality of life issues in chronic wound
management. Brit J Comm Nurs 1999;4(6):283-9.
References
1.
2.
3.
4.
5.
Docherty C, Rose C. Skin disorders. In Alexander MF, Runciman

12. Elliott TR, Shewchuk RM, Richards JS. Caregiver social
P, editors. Nursing Practice: Hospital and home - the adult.
problem-solving abilities and family member adjustment to
Edinburgh: Churchill Livingstone; 1994.
recent-onset physical disability. Rehab Psychol
1999;44(1):104-23.
sclerosis: management of multiple sclerosis in primary and
secondary care. NICE Clinical Guideline 8. London: NICE; 2003. 13. Deeks JJ. Pressure sore prevention: using and evaluating risk
assessment tools. Brit J Nurs 1996;5(5):316-20.
Allman RM. Pressure ulcer prevalence, incidence, risk factors
14.
Rycroft-Malone J, McInnes E. Pressure ulcer risk assessment
and impact. Clin Geriatr Med 1997;13(3):421-36.
and prevention. Technical Report. London; RCN: 2000.
European Pressure Ulcer Advisory Panel and National Pressure
Ulcer Advisory Panel. Pressure ulcer prevention: quick reference 15. National Institute for Health and Clinical Excellence. The use
of pressure relieving devices for the prevention of pressure
guide. Washington DC: National Pressure Ulcer Advisory
ulcers in primary and secondary care. NICE Clinical Guideline
Panel; 2009.
Dealey C. The care of wounds: a guide for nurses. 2nd ed.
Oxford: Blackwell Science Ltd; 1999.
6.
McClement E. Pressure sores. Nurs Times 1984;2(21):S1-3:6.
7.
Casey G. The importance of nutrition in wound healing. Nurs

Stand 1998;13(3):51-2.
8.
Gallagher SM. Morbid obesity: a chronic disease with an

impact on wounds and related problems. Ostomy Wound
Manage 1997;43(5):18-24,26-7.
9.
National Institute for Health and Clinical Excellence. The

management of pressure ulcers in primary and secondary care.
10. Clay M. Pressure sore prevention in nursing homes. Nurs Stand

2000;14(44):45-50,52,54.
Resources from the MS Trust

Are you sitting comfortably?:
a self-help guide to good posture
and positioning
79

Advanced MS
Advanced MS
Advanced stages of MS may require the expertise
and input of palliative care services to achieve the
best quality of life when the illness is limiting time
left and needs are complex. It can integrate skilled
multidisciplinary assessment and management of
MS with appropriate support for the social,
psychological and spiritual needs of someone with
MS reaching the end of their life. It will support
families or carers, many of whom have lived for
many years with the consequence of MS. It can
ensure those decisions and wishes about dignity in
dying with MS, perhaps made whilst living with
MS, are appropriately acted upon and any changes
to those early choices are promptly recognised and
care choices reviewed.
It is now accepted that palliative care provision
should be available for all patients with life-limiting
illnesses, regardless of diagnosis and should not be
restricted to the last few days, weeks or months of
life. Input for MS may be variable over a lengthy
time span.
Those involved in the day to day care of someone
with advanced MS will be involved in providing
general palliative care. Specialist palliative care
input should be considered where there is an
expected lifespan of 6-12 months, intractable
symptoms, complex psychosocial needs and
when discussion or support is needed in advance
care planning.
Holistic assessment and support

MS is a variable condition with a wide spectrum of
clinical presentations yet each individuals experience
of MS is uniquely felt and influenced by many factors;
individual coping mechanisms, past experiences and
available support. The key to getting it right for
each individual is to listen to their narrative and know
what matters to them in the moment and the time
they perceive left to them. Holistic assessment
identifies physical, emotional, social and spiritual
needs, preferences or challenges. These are unlikely
to be static or fixed.
The living end of MS has often been filled with
uncertainty and unpredictability; the dying end
may be no different.
As MS advances previous decisions may change
and pro-active reassessment and review will be
80
required. This will avoid crisis led decision making

and likely accompanying distress. Patients with
advanced MS are housebound and assessment and
review should be carried out in the patients home
or usual place of residence.
Spiritual needs are often overlooked, avoided or
superficially addressed. Nearing the end of life and
imminent death often triggers spiritual questions or
fears and if unexplored can lead to significant distress.
Symptom control
A survey of patients with advanced MS cited that on
average patients experienced around nine different
symptoms1. Pain, spasms and fatigue were the most
common symptoms. Swallowing and
communication problems, shortness of breath and
nausea together with depression and cognitive
impairment will also affect quality of life.
MS symptoms can become refractory to treatment,
fluctuate in intensity or worsen with progression of
MS. Symptoms may be:
primary - a direct result of MS itself
secondary - resulting from primary symptoms
tertiary, arising from the social and

psychochological problems of primary and
secondary symptoms.
Carer needs
Families and carers provide invaluable support for
patients with advanced MS, but the role is
demanding and can place carers under significant
emotional and physical strain. Carer needs often go
unrecognised. The families of people with MS may
have experienced many years of living with the
consequences of MS and they will have a range of
responses, questions, anxieties and needs that must
be addressed. It is important to provide both
practical and emotional support for carers as well as
to consider respite options for families.
Estimating prognosis
Confident prognosis at any stage of MS is difficult
and in advanced MS there is a risk of sudden
deterioration and death from an infection2. Intimate
knowledge of someone with MS will help to gauge
the rate of clinical deterioration and possible time
frames. A framework for end of life care in long term
neurological disease, published by the National End
of Life Care Programme, describes triggers that can
help to identify when a patient may be approaching
the end of life3:
www.mstrust.org.uk

Advanced MS
swallowing problems
recurring infection
Figure 1
marked decline in physical status
England and Wales
first episode of aspiration pneumonia
Mental Capacity Act 20054
significantly worsening cognitive function
Scotland
weight loss
significant complex symptoms.
Adults with Incapacity (Scotland) Act 20005
Northern Ireland
Deterioration may extend over many years and
death usually occurs from respiratory or other
overwhelming infection.
Planning for the future

People with MS should be afforded the right of self
determination regarding their future care
preferences or life-prolonging treatments. The
initiation, pacing and any revisiting of any
discussion about these choices must be led by the
person with MS at a time they choose and it is
critical to identify the cues they give. Some may
fear that cognitive decline or communication
impairment will prevent them articulating clearly
their wishes at some point in the future. Some will
not wish to enter into such a dialogue and prefer
avoidance techniques.
Untreated depression and unidentified cognitive
impairment in MS will negatively influence wishes
and must be appropriately managed as part of the
process of determining future directives.
The family and loved ones may also wish to be
involved in discussion, but it may be that the
person with MS wishes to have a private,
confidential talk with a trusted other.
Each of the four UK nations has statutory guidance
on safeguarding the wishes of people with mental
capacity and those who do not have mental
capacity and it is a duty of care for health care
professionals to understand and follow the
appropriate guidance (Figure 1).
The dying phase

MS is not in itself a terminal condition; the vast
majority of people with MS live their normal life span
and die of conditions completely unrelated to MS. In
one study, death occurred as a consequence of the
Currently no primary legislation

Mental Capacity Bill in preparation (Oct 2011)
secondary complications of chronic disease, such as
pneumonia and septicaemia, in 50% of people with
advanced MS2. The proportion of deaths due to
stroke, myocardial infarctions and malignancies was
similar to the general population.
Recognising and acknowledging that someone
with MS has finally reached the dying phase of life
can be a challenge. Many features of progressing
MS such as increasing weakness, deteriorating
functional ability, difficulty in swallowing and
cognitive impairments can also be features of
imminent death in terminal disease.
As a life is ending for someone with MS
information must be shared with the patient and
the family and checked for understanding. They
may have become accustomed to symptoms
fluctuating in intensity and may not have insight
into the significance or finality of change. They
may have lived with change or progression for
many years. They may need reassurance that
ceasing to eat and drink is a normal part of the
dying process and not the cause of deterioration.
Intrusive or uncomfortable MS symptoms together
with other common end stage symptoms must
continue to be pro-actively managed. Key drug
interventions are likely to include the following
medications or their equivalents:
Midazolam
agitation/
muscle relaxation
Hysocine butylbromide
respiratory secretions
Diamorphine
pain
81

Advanced MS
Recognised tools are available to facilitate the

assessment and management of patients at the end
of life. With appropriate training, tools such as the
Liverpool Care Pathway for the Dying Patient have
been shown to improve the quality of care provided
to dying patients6. The pathway helps ensure key
needs are regularly assessed including areas which
are often overlooked such as spiritual and
psychosocial needs as well as guiding professionals
with appropriate anticipatory prescribing.
References
82
1.
Higginson IJ, Hart S, Silber E, et al. Symptom prevalence

and severity in people severely affected by multiple sclerosis.
J Palliat Care 2006;22(3):158-65.
2.
Sadovnick AD, Eisen J, Ebers GC, et al. Cause of death in

patients attending multiple sclerosis clinics. Neurology
1991;41(8):1193-6.
3.
National Council for Palliative Care, Neurological Alliance,

National End of Life Care Programme. Improving end of life
care in long term neurological conditions: a framework for
implementation. London; National End of Life Care
Programme; 2010.
4.
Department for Constitutional Affairs. Mental Capacity Act

2005 code of practice. London: The Stationery Office; 2007.
5.
Scottish Government. Adults with Incapacity (Scotland) Act

2000: A short guide to the Act. Scottish Government:
Edinburgh; 2008.
6.
Marie Curie Palliative Care Institute Liverpool. The Liverpool

Care Pathway for the Dying Patient. Liverpool: Marie Curie
Palliative Care Institute Liverpool; 2010.
Further resources
Department of Health. End of Life Care Strategy:
promoting high quality care for all adults at the
end of life. London: Department of Health; 2008.
NHS End of Life Care Programme. Capacity, care
planning and advance care planning in life limiting
illness. A guide for health and social care staff.
London: Department of Health; 2011.
MS Society. MS and palliative care: a guide for
health and social care professionals. London: MS
Society; 2006.
Dying Matters - www.dyingmatters.org. [Accessed
Sept 2011]
Brown JB, Sutton L. A neurological care pathway
for meeting the palliative care needs of people
with life-limiting neurological conditions. Int J
Palliat Nurs 2009:15(3):120-7.
www.mstrust.org.uk

Section 4
Complementary and
alternative medicine
Complementary and alternative medicine (CAM)
refers to those forms of treatment which are not
widely in use by orthodox healthcare professionals.
Complementary refers to those treatments that are
used in conjunction with orthodox medicine.
Alternative refers to those treatments that are used
instead of more conventional approaches.
(41%), omega-3 fatty acids (37%), vitamins E

(28%), B (36%), and C (28%), homeopathy
(26%), and selenium (24%) were cited most
frequently. Most respondents (69%) were satisfied
with the effects of CAM. Compared with
conventional therapies, CAM rarely reported
unwanted side effects (9% vs 59%).
Bowling5 lists other common reasons for using
CAM which include decreasing the severity of MS
related symptoms, increasing control, improving
health, and using methods that allow for the
interrelation of mind, body and spirit.
Risks and benefits

Which therapies?
Robust evidence that CAMs are effective in MS is
lacking. The benefits of most therapies, including
acupuncture, aromatherapy, yoga and
homeopathy, are based on anecdotal reports.
However, a systematic review by Huntley and
Ernst1 found that there were some therapies that
were evidence-based. These include nutritional
therapy, body work, psychotherapy and imagery,
neural therapy, massage and reflexology. The NICE
guidelines for management of multiple sclerosis in
primary and secondary care2 suggest that fish oils,
magnetic field therapy, tai chi and multimodal
therapy may also be of benefit.
There is also evidence that supports the benefits
of mindfulness based intervention, progressive
muscle relaxation technique, positivity to promote
benefit-finding in MS and cognitive behavioural
therapy (CBT).
Whilst some CAMs carry a low risk and can be

beneficial in treating MS symptoms, others can be
potentially harmful and can interact with
conventional treatments for MS3.
A person with MS should be encouraged to discuss
any alternative treatments they are considering and
to inform their doctors and other health professionals
if they decide to use any2. People with MS should be
encouraged to evaluate any alternative therapy
themselves, including the risks, the costs (financial
and inconvenience) and the perceived benefits.
They should be encouraged to visit only
practitioners who are registered with the relevant
professional bodies and to source supplements, for
example, from reliable sources.
Therapies with limited published

evidence of efficacy in MS
Bodywork
Why CAM is chosen in MS

Complementary therapies are very popular with MS
patients. It has been reported that between one half
and three quarters of individuals with MS use CAMs
in various parts of the Western world, with the
majority using CAMs in a complementary way3.
A survey of 1,573 patients in Germany, found that
the main reasons for the use of CAM in individuals
with MS was the low level of satisfaction and the
high rate of side-effects with conventional
treatments, as well as brief consultation time with
physicians4. In comparison with conventional
medicine, more patients displayed a positive
attitude toward CAM (44% vs 38%), with 70%
reporting lifetime use of at least one method.
Among a wide variety of CAM, diet modification
In bodywork, a therapist has a hands-on guiding

role to the individuals limbs and muscles.
The use of some manipulative techniques such as
chiropractic and osteopathy appears to be fairly
widespread amongst people with MS6. There is no
literature specifically focusing on these forms of
manipulation in MS, but there is a single blind
randomised controlled trial of Feldenkrais
bodywork7. The intent behind this approach is to
reorganise the muscular and nervous system
manually, which allows for improved functioning
and promotes strength, flexibility and ease of
movement. Sessions last about 45 minutes and focus
on a particular movement pattern which may be
problematic. The therapist tries to help identify what
the patient feels and then expands the range of
83

feeling to improve function. This approach is not

unlike that of the Alexander Technique.
Craniosacral therapy has been shown to help with
urinary tract symptoms. In a small prospective
cohort study 28 patients showed a significant
improvement in post void residual volume, lower
urinary tract symptoms and quality of life8.
duration of the study.

After four weeks, both groups showed improvement
in constipation symptoms but the massage group
improved significantly more. Participants reported
that the massage was relaxing and also gave some
empowerment because of self-management.
Reflexology
Neural therapy
This is a technique using small quantities of local
anaesthetic injected into specific areas of the body,
principally old scars and areas that correspond to
acupuncture points. It has been widely used in
Germany and Austria since 1928, mainly for
problems arising from scars, but one double-blind
placebo controlled trial9 investigated 21 patients with
MS randomised into active (n=11) and placebo
(n=10) groups. The active treatment was 1%
lignocaine hydrochloride and placebo was 0.9%
saline. Each patient received two treatments per
week, consisting of injections at points into the ankles
and also around the greatest circumference of the
skull. There were no significant side-effects.
Functional ratings at follow-up, between two and
three and a half years later, showed an overall long
term improvement in 59% compared with placebo.
Improvement rates were similar for all forms of MS.
Massage
Massage is very popular and appears to be very
helpful for some of the musculoskeletal symptoms of
MS. It also seems to help general well-being. One
study involved 24 patients with MS randomly
assigned to either a 45 minute massage twice weekly
for five weeks or to no treatment10. The massage
group had significantly lower anxiety and a less
depressed mood by the end of the study and had
significantly improved in self-esteem, body image
and image of disease progression. No conclusions
however, were drawn about physical characteristics.
Abdominal massage has been shown to help
constipation in a small study11. 30 people with both
MS and constipation were recruited then randomly
allocated to a massage or a control group. The
massage group participants were provided with
advice on bowel management and they or their
carers were taught how to deliver abdominal
massage. They were recommended to perform it
daily for four weeks, each session lasting 10-15
minutes. The control group received bowel
management advice only. A physiotherapist visited
all the participants in their own homes for the
84
Reflexology involves stimulating points on the soles of

the feet which are said to influence the physiology
throughout the body. In one study12, 71 patients were
randomised to either reflexology treatment with
manual pressure on specific points on the feet and
massage of the calf area, or to nonspecific massage of
the calf area only. 53 patients completed the study
and there were significant improvements in the mean
scores of paraesthesia, urinary symptoms, muscle
strength and spasticity.
Another study involving 73 patients found a very
significant (50%) reduction of pain VAS (Visual
Analogue Scale) score and improved quality of life
maintained over 12 weeks. However, there was no
difference between the sham and real reflex-point
treated group13. This result shows a powerful and very
significant but unspecific effect which questions some
of the traditional beliefs about reflexology. It is very
similar to emerging evidence in acupuncture where a
powerful unspecific needling effect is observed
independent of precise needle point location.
Psychotherapy and imagery

One study14 followed 33 patients with MS and trained
half of them in relaxation sessions involving the use of
imagery, focusing on imagining the repair of damaged
myelin and positive immune system responses. The
control group followed their normal medical
treatment. After a six week course of treatment, the
imagery group had a significant decrease in anxiety
but there were no changes in other psychological
variables or in MS symptoms. The authors comment
that this is a simple cost effective approach which can
significantly reduce anxiety in people with MS.
A randomised controlled trial of group
psychotherapy in MS15 showed it to be beneficial for
those with mild to moderate depression, again with
no change in disability scores.
Mindfulness based intervention

Mindfulness is a form of meditation whereby
individuals become nonjudgementally aware of the
present moment. A randomised, single-blind
www.mstrust.org.uk

controlled trial involving 150 people demonstrated

that mindfulness based intervention, as opposed to
usual care, improved health related quality of life,
fatigue and depression for up to six months post
intervention. Mindfulness training can help those
with MS better cope with the unpredictable
changes they may experience with the disease, as
well as have a greater appreciation of the positive
things that they still have in their lives16.
Progressive muscle relaxation technique

One study involving 66 patients with MS using a
quasi-experimental method, provided modest
support for the effectiveness of progressive muscle
relaxation technique on quality of life of patients
with MS compared with no intervention17.
Another study of 50 people with MS used a
crossover design with a four week break between
treatment phases18. It compared the effects of
reflexology and progressive muscle relaxation
training on psychological and physical outcomes.
The Short Form 36 (SF-36) and General Health
Questionnaire 28 were used pre and post each of
the six week treatment phases. State Anxiety
Inventory, salivary cortisol levels, systolic and
diastolic blood pressure and heart rate data were
collected pre and post the weekly sessions.
Positive effects were reported for both treatments.
All the chosen measures, except for three SF-36
scales, recorded significant changes.
Encouragingly, despite the four week break, most
outcome measures did not return to their pretreatment baseline levels.
Positivity to promote benefit finding in MS

After experiencing a stressful or traumatic event,
many individuals report positive changes in their
lives. This is known as benefit finding. One study of
127 people with MS, used two distinct conceptual
frameworks of positive affect and optimism,
examining their effects as mediators on the
relationship between improved depression and
enhanced benefit-finding. It found that depression
improved over time with increased benefit
finding, the relationship being significantly
mediated by both increased optimism and
increased positive affect19.
Cognitive behavioural therapy

The premise of cognitive behavioural therapy is that
what people think affects how they feel emotionally
and how they behave. During times of emotional
distress, the way a person sees and judges themselves

may become more negative. CBT therapists aim to
work jointly with the person to help them begin to see
the link between unhelpful thinking styles and
mood. This may empower a person to have more
control over negative emotion and to bring about
changes in unhelpful behaviour. CBT can be used to
help people with a range of conditions including MS.
A randomised control trial where 72 patients with
MS fatigue were randomly assigned to eight weekly
sessions of CBT or relaxation training (RT),
demonstrated that both CBT and RT appeared to be
clinically effective treatments for fatigue in MS
patients. The effect for CBT was greater than RT20.
A systematic review of psychological interventions
for MS, which searched 19 databases, found that
there was reasonable evidence that cognitive
behavioural approaches were beneficial as
treatment and in helping people adjust to and cope
with having MS21.
Another study which was quasi-experimental in
design, evaluated the effectiveness of a cognitivebehavioural program for women with MS in which 37
women participated in a five week intervention period.
It found significant improvements in the participants
perceived health competence, indices for adaptive and
maladaptive coping and most measures of
psychological well-being. The positive changes were
maintained during the six month follow up period22.
Dietary supplementation
The advice most commonly given by dieticians is to
try to follow a healthy diet with low saturated fat
intake, increased intake of fish and lean meats, fresh
vegetables and fruit and whole grain cereals.
It might be helpful to remember that a diagnosis of
MS represents to many people a total loss of control.
Through diet, control of the body can appear to be
regained and, in some cases therefore, dietary
manipulation is undertaken as much for psychological
and emotional reasons as for any other.
Nutritional therapy
There have been many attempts to link dietary
pattern and the geographic distribution of MS. It
appears that diets high in gluten and milk are much
more common in areas with a higher prevalence of
MS, but most interest has centred around the role of
dietary fat. The most well known approach is the
Swank Diet, recommended by Dr R Swank since
85

194823. He recommends a saturated fat intake of no

more that 10g per day, a daily intake of 40-50g of
polyunsaturated oils, at least a teaspoon of cod liver
oil daily and a consumption of fish three or more
times a week. An impressive cohort of patients was
amassed and followed up for many years and very
significant decrease in expected relapses and onset
of disability was demonstrated. His studies have
been widely criticised for lacking a control group
and for inclusion criteria which are not particularly
well defined and may reflect the milder end of the
MS spectrum.
The emphasis on dietary fat was quite extensively
investigated in at least three double-blind studies
using supplementation with linoleic acid24-26. The
results of these studies were quite mixed, with two
showing an effect and one not, but a combination
analysis suggested that patients supplementing
with linoleic acid had a smaller increase in
disability and reduced severity and duration of
relapses compared with controls27. There have
been many discussions about these trials and the
results are by no means unequivocally accepted.
Some feel that the dose of linoleic acid used in
these trials was too low.
In 2003, the NICE guidelines2 recommended that
17-23g per day of linoleic acid might reduce
disease progression. This amount may be
consumed in many forms including full fat
sunflower margarine or sunflower, safflower or
sesame seed cooking oils. However, subsequent
meta-analysis28 has concluded that there was no
major effect on disease progression.
Many people with MS supplement their diet with
evening primrose oil or flax seed oil. Again there is
debate about a reasonable dose, but it does seem
that there is some evidence that a diet high in
essential fatty acids is helpful in slowing the onset
of disability in MS.
Dietary manipulation and supplementation is the
kind of approach taken by naturopaths. The
literature is well reviewed by Murray and Pizzorno29
and most particularly, by Bowling and Stewart30.
Claims that food allergies may be present in MS have
not been upheld by research. Private allergy testing is
often expensive and real food allergies are rare in
adults. However, if allergies are suspected, testing at
an expert NHS centre is recommended.
86
St Johns wort
Clinical trials and meta-analyses31,32 provide support
that St John`s wort is efficacious in the treatment
of mild to moderate depression. Whilst St John`s
wort appears safe and tolerable, it can potentially
interact with other medications including
anticonvulsants, warfarin, antidepressants and oral
contraceptives3.
Echinacea and other immunestimulating supplements

Claims that individuals with MS should sometimes
take echinacea and other immune stimulating
supplements is incorrect and potentially
dangerous. The effects of medications, such as
methotrexate and interferons, on liver function can
be increased by echinacea3.
Vitamin D
There is a high level of interest in vitamin D and its
potential benefits in MS.
As well as the advantages of treating osteopenia and
osteoporosis to which MS patients are prone, it could
potentially have a preventative and disease modifying
effect. Additionally, low vitamin D levels have been
linked to the potential development of MS, increased
relapse rate and more severe disability3.
Vitamin D is generally thought to be safe but there
are also some concerns that high doses could
cause hypercalcaemia in the long-term. Daily
recommended doses are based on the effective
treatment of rickets. There is no consensus on the
appropriate amount to take in MS.
Low dose naltrexone (LDN)

It has been claimed that low doses of naltrexone,
an opiate receptor antagonist which is used in
opiate addiction, can be beneficial in MS. There
are anecdotal reports of symptomatic benefits and
improvements in quality of life. LDN is thought to
increase endorphin levels by stimulating the
immune system.
An Italian pilot study involved 40 people with
primary progressive MS. Participants received 4mg
of LDN for six months, with researchers looking
primarily at safety but also at the effect on
spasticity, pain, fatigue, depression and quality of
life. The results showed LDN was safe and welltolerated. There was a significant reduction of
spasticity during the trial, but half the participants
reported an increase in pain. There were no
www.mstrust.org.uk

significant changes to measures of fatigue,

depression or quality of life33.
noted35. A recent case report found acupuncture

helpful for MS related fatigue and weakness36.
The University of California in San Francisco (UCSF)

has studied the effects of LDN on quality of life in 80
people with MS. Results showed LDN significantly
improved quality of life (specifically mental health,
pain, and self-reported cognitive function) as
measured by the MS Quality of Life Inventory.
However, no impact was observed on symptoms
such as fatigue, bowel and bladder control, sexual
satisfaction, and visual function. Vivid dreaming was
reported during the first week of treatment, but no
other adverse effects were reported34.
One very small study37 did suggest that

acupuncture has a role in helping spasticity.
Another small uncontrolled study demonstrated a
significant reduction (60%) in urinary urge
frequency after electro-acupuncture which was
similar to treatment with tolterodine38.
LDN appears to be well tolerated and generally

safe, but the trial results have been variable and
inconsistent. Additional studies are required to
establish safety and efficacy3.
As LDN stimulates the immune system, it should not
be taken by people also taking immunosuppressant
drugs, or other drugs that reduce the activity of the
immune system such as steroids.
CAM therapies with only anecdotal

evidence of benefit for people with MS
Acupuncture
In its oldest form, acupuncture is a form of
traditional Chinese medicine. Traditional Chinese
physiology describes the running of energy (Chi) in
meridians which are believed to course just below
the surface of the skin over the whole body. The
insertion of very fine needles into these meridians at
pre-defined points is held to rebalance blocked or
excessive energy flow and so cure symptoms. It is
complicated to learn this sort of approach.
There is a simpler and more readily available
Western form of acupuncture, which relies on the
phenomenon that inserting a needle into a painful
muscular trigger-point seems to deactivate the
point and the pain which radiates from it.
There are very few controlled trials of acupuncture
in MS. Clinical experience suggests that
acupuncture is very helpful for some people,
particularly in relieving cramps, spasms and
bladder symptoms. A small study compared minimal
acupuncture with Chinese acupuncture and found
minimal acupuncture significantly more effective. No
other statistically significant difference between the
groups was found. No major adverse events were
Aromatherapy
Six percent of 848 patients with MS, who
responded to a mail survey in British Columbia39,
used aromatherapy to help manage their
condition. However, there are no scientific studies
supporting the use of aromatherapy.
There is no doubt though, that many people feel it
is a worthwhile therapy, perhaps because of its
effect on mood and its possible promotion of
sleep. One author however40 feels that
aromatherapy cannot be recommended in the
treatment of any form of neurological disease until
more studies are available.
Yoga
Yoga uses a combination of physical postures,
breathing exercises, relaxation and meditation to
try and reach optimal physical and mental health.
There are few studies in MS, but many anecdotes
reinforce the view that deep relaxation and the
strengthening of muscle control which can be
achieved using yoga can be extremely beneficial
for people with MS. Oken carried out a
randomised controlled trial of weekly Iyengar yoga
and exercise in 69 people with MS. Significant
improvements were seen in measures of fatigue
and quality of life in the yoga and exercise groups
compared to the control but no effects on mood
or cognitive dysfunction were reported41.
Homoeopathy
Homoeopathy is a complementary medical system
which uses preparations of substances whose
effects, when administered to healthy subjects,
correspond to the manifestations of the disorder in
the individual. It was developed by Samuel
Hahnemann (1755-1843) and is now practised
throughout the world. Recent large-scale metaanalyses of randomised controlled clinical trials of
homoeopathy42,43 have confirmed activity over
placebo in a wide range of conditions. In the UK,
there are only a small number of homoeopathic
hospitals in the NHS yet homoeopathy is widely
87

used by people with MS. There are no clinical trials

of homoeopathy in MS in the literature although
there are case reports of improvements in
symptoms44 and wide clinical experience.
Case study, anecdotal and clinical experience suggest
that homoeopathy is extremely effective for some
symptoms such as spasms, bladder problems and
diplopia experienced by those with MS. Long term
homoeopathic treatment does seem to help some
symptoms, both physically and psychologically45.
activity may increase as opposed to being reduced.

Health professionals should at least be aware when
individuals are using CAMS, encouraging them to
discuss the risks versus benefits with their
neurologist or MS nurse.
References
1.
Huntley A, Ernst E. Complementary and alternative therapies

for treating multiple sclerosis symptoms: a systematic review.
Complement Ther Med 2000;8(2):97-105.
2.

Multiple sclerosis - management of multiple sclerosis in
primary and secondary care. NICE Clinical Guideline 8.
London: NICE; 2003.
3.
Bowling AC. Complementary and alternative medicine and

multiple sclerosis. Neurol Clin 2011;29(2):465-80.
4.
Schwarz S, Knorr C, Geiger H, et al. Complementary and

alternative medicine for multiple sclerosis. Mult Scler
2008;14(8):1113-9.
5.
Bowling AC. Complementary and alternative medicine and

multiple sclerosis. 2nd ed. New York: Demos; 2007.
6.
Fawcett J, Sidney JS, Riley-Lawless K, et al. An exploratory

study of the relationship between alternative therapies,
functional status, and symptom severity among people with
multiple sclerosis. J Holistic Nurs 1996;14(2):115-29.
7.
Johnson SK, Frederick J, Kaufman M, et al. A controlled

investigation of bodywork in multiple sclerosis. J Altern Comp
Med 1999;5(3):237-43.
8.
Raviv G, Shefi S, Nizani D, et al. Effect of craniosacral therapy

on lower urinary tract signs and symptoms in multiple
sclerosis. Complement Ther Clin Pract 2009;15(2):72-5.
9.
Gibson RG, Gibson SL. Neural therapy in the treatment of

multiple sclerosis. J Altern Complement Med 1999;5(6):543-52.
Hyperbaric oxygen therapy

Hyperbaric oxygen therapy (HBO) involves breathing
oxygen through a mask in a pressurised chamber.
Treatment regimens vary slightly but usually consist of
an initial course of around 20 treatments, each lasting
an hour, spread over one month. Follow up treatment
is then needed at less frequent intervals. Those who
practise this therapy report improvement both in
bladder symptoms and fatigue.
Case reports of benefit following HBO therapy in
people with MS, and positive effects of HBO in
experimental allergic encephalitis (the animal model
of MS) led to clinical investigations in people with MS.
A systematic review assessed the evidence from
14 controlled trials of HBO therapy in people with
chronic MS46. Six of the trials identified were excluded
from the review as they were of poor methodological
quality according to pre-defined criteria. Of the eight
remaining trials, one reported a positive result and
seven reported negative results for HBO therapy. The
authors of the review concluded that: We cannot
recommend the use of hyperbaric oxygen in the
treatment of MS. However, it should be noted that
there are approximately 50 MS therapy centres
around the UK where this therapy has long been
available and it continues to prove popular with many
people with MS.
The role of health professionals in CAMs

Some health professionals may not feel comfortable
with discussing CAMs with patients due to lack of
knowledge or because they feel cynical about CAMs.
Nevertheless individuals with MS do use and will
continue to use CAMS. It is important that
potentially beneficial therapies are not dismissed,
particularly when there is evidence to support their
use. However, it is equally important to balance this
against those therapies that can be harmful, can
interact with or may be used instead of conventional
treatments, particularly if this means that disease
88
10. Hernandez-Reif M, Field T, Theakston H. Multiple sclerosis

patients benefit from massage therapy. J Bodywork
Movement Ther 1998;2(3):168-74.
11. McClurg D, Hagen S, Hawkins S, et al. Abdominal massage
for the alleviation of constipation symptoms in people with
multiple sclerosis: a randomised controlled feasibility study.
Mult Scler 2011;17(2):223-33.
12. Siev-Ner I, Gamus D, Lerner-Gevea L, et al. Reflexology
treatment relieves symptoms of multiple sclerosis: a
randomised controlled study. Mult Scler 2003;9(4):356-61.
13. Hughes CM, Smyth S, Lowe-Strong AS. Reflexology for the
treatment of pain in people with multiple sclerosis: a doubleblind randomised sham-controlled clinical trial. Mult Scler
2009;15(11):1329-38.
14. Maguire BL. The effects of imagery on attitudes and moods
in multiple sclerosis patients. Altern Ther Health Med
1996;2(5):75-9.
15. Crawford JD, McIvor GP. Group psychotherapy: benefits in
multiple sclerosis. Arch Phys Med Rehabil 1985;66(12):810-3.
16. Grossman P, Kappos L, Gensicke H, et al. MS quality of life,
depression, and fatigue improve after mindfulness training: a
randomised trial. Neurology 2010;75(13):1141-9.
17. Ghafari S, Ahmadi F, Nabavi M, et al. Effectiveness of applying
progressive muscle relaxation technique on quality of life of
patients with multiple sclerosis. J Clin Nurs 2009;18(15):2171-9.
18. Mackereth PA, Booth K, Hillier VF, et al. Reflexology and
progressive muscle relaxation training for people with
www.mstrust.org.uk

multiple sclerosis: a crossover trial. Complement Ther Clin

Pract 2009;15(1):14-21.
19. Hart SL, Vella L, Mohr DC. Relationships among depressive
symptoms, benefit-finding, optimism, and positive affect in
multiple sclerosis patients after psychotherapy for depression.
Health Psychol 2008;27(2):230-8.
20. van Kessel K, Moss-Morris R, Willoughby E, et al. A randomised
controlled trial of cognitive behavior therapy for multiple
sclerosis fatigue. Psychosom Med 2008;70(2):205-13.
21. Thomas PW, Thomas S, Hillier C, et al. Psychological
interventions for multiple sclerosis. Cochrane Database Syst
Rev 2006;(1):CD004431.
22. Sinclair VG, Scroggie J. Effects of a cognitive-behavioral
program for women with multiple sclerosis. J Neurosci Nurs
2005;37(5):249-57, 276.
23. Swank RL. Multiple sclerosis: twenty years on low fat diet.
Arch Neurol 1970;23(5):460-74.
24. Millar JH, Zilkha KJ, Langman MJ, et al. Double-blind trial of
linoleate supplementation of the diet in multiple sclerosis. Br
Med J 1973;1(5856):765-8.
25. Bates D, Fawcett PR, Shaw DA, et al. Polyunsaturated fatty
acids in treatment of acute remitting multiple sclerosis. Br
Med J 1978;2(6149):1390-1.
39. Wang Y, Hashimoto S, Ramsun D, et al. A pilot study for the

use of alternative medicine in multiple sclerosis patients with
special focus on acupuncture. Neurology 1999;52(2):A550.
40. Hirsch AR. Aromatherapy: art, science, or myth? In:
Weintraub MI, editor. Alternative and complementary
treatment in neurologic illness. Philadelphia: Churchill
Livingstone; 2001. p128-51.
41. Oken BS, Kishiyama MA, Zajdel D, et al. Randomised
controlled trial of yoga and exercise in multiple sclerosis.
Neurology 2004;62(11):2058-64.
42. Linde K, Clausius N, Ramirez G, et al. Are the clinical effects
of homoeopathy placebo effects? A meta-analysis of placebo
controlled trials. Lancet 1997;350(9081):834-43.
43. Cucherat M, Haugh MC, Gooch M, et al. Evidence of clinical
efficacy of homoeopathy. A meta-analysis of clinical trials. Eur
J Clin Pharmacol 2000;56(1):27-33.
44. Johnston L. Conium in a case of multiple sclerosis. J Am Inst
Homeopathy 1990;83(1):12-15.
45. Whitmarsh TE. Homoeopathy in multiple sclerosis.
Complement Ther Nurs Midwifery 2003;9:5-9.
46. Kleijnen J, Knipschild P. Hyperbaric oxygen for multiple
sclerosis. Review of controlled trials. Acta Neurol Scand
1995;91(5):330-4.
26. Paty DW. Double-blind trial of linoleic acid in multiple

sclerosis. Arch Neurol 1983;40(11):693-4.
27. Dworkin RH, Bates D, Millar JH, et al. Linoleic acid and
multiple sclerosis: a reanalysis of three double-blind trials.
Neurology 1984;34(11):1441-5.
28. Farinotti M, Simi S, Di Pietrantonj C, et al. Dietary
interventions for multiple sclerosis. Cochrane Database
Syst Rev 2007;(1):CD004192.
29. Murray MT, Pizzorno JE. Multiple sclerosis. In: Pizzorno JE,
Murray MT, editors. Textbook of natural medicine. 2nd ed.
Edinburgh: Churchill Livingstone; 1999. p1415-23.
30. Bowling A C, Stewart TM. Current complementary and
alternative therapies for multiple sclerosis. Curr Treat Options
Neurol 2003;5(1):55-68.
31. Linde K, Ramirez G, Mulrow CD, et al. St Johns wort for
depression - an overview and meta-analysis of randomised
clinical trials. BMJ 1996;313:253-8.
32. Ernst E. St. Johns wort as antidepressive therapy. Fortschr
Med 1995;113(25):354-5. [Article in German]
33. Gironi M, Martinelli-Boneschi F, Sacerdote P, et al. A pilot
trial of low-dose naltrexone in primary progressive multiple
sclerosis. Mult Scler 2008;14(8):1076-83.
MS Trust resources
Diet factsheet
Low dose naltrexone (LDN) factsheet
Vitamin D factsheet
Exercises for people with MS
Further reading
Bowling AC. Complementary and alternative
medicine and multiple sclerosis. 2nd ed.
New York: Demos; 2006.
British Medical Association. Complementary
Medicine: new approaches to good practice.
Oxford: Oxford University Press; 1993.
34. Cree BA, Kornyeyeva E, Goodin DS. Pilot trial of low dose
naltrexone and quality of life in MS. Ann Neurol
2010;68(2):145-50.
35. Donnellan CP, Shanley J. Comparison of the effect of two types
of acupuncture on quality of life in secondary progressive
multiple sclerosis: a preliminary single-blind randomised
controlled trial. Clin Rehabil 2008;22(3):195-205.
36. Foell J. Does acupuncture help in helping the ones you
cannot help? The role of acupuncture in facilitating adaptive
processes. Acupunct Med 2011;29(1):61-4.
37. Miller RE. An investigation into the management of the
spasticity experienced by some patients with multiple
sclerosis using acupuncture based on traditional Chinese
medicine. Compl Ther Med 1996;4:58-62.
38. Tjon Eng Soe SH, Kopsky DJ. Multiple sclerosis patients with
bladder dysfunction have decreased symptoms after electroacupuncture. Mult Scler 2009;15(11):1376-7.
89
hpbook.10.11.5K
Multiple Sclerosis Trust

Spirella Building, Bridge Road
Letchworth Garden City
Hertfordshire SG6 4ET
T 01462 476700
E info@mstrust.org.uk
www.mstrust.org.uk
Registered charity no. 1088353
Index
Index
Advanced MS
80
Alemtuzumab
30
Expanded Disability
Status Scale see EDSS
83
Expert Patient
20
70
Fampridine
65
Fatigue
36
Alternative medicine
Ataxia
Baclofen
68
Bed sore
77
Benign MS
11
Beta interferon
24-26
BG-12
30
Bladder
47
Bowel
53
Breastfeeding
45
Cannabis (See also Sativex) 31

Cerebrospinal fluid
10
Childbirth
45
Chronic cerebro-spinal
6
venous insufficiency (CCSVI)
Clean intermittent selfcatherisation (CISC)
51
Clinical measures
13
Clinically isolated syndrome
Cognition
39
Cognitive dysfunction
39
Communication
75
Complementary therapies
83
Concentration
39
Constipation
54
Continence see
Incontinence
Core stability
64
Fatigue management
course
FES
65
Fingolimod
33
Functional electrical
stimulation see FES
Gabapentin
68
Glatiramer acetate
26
Hyperbaric oxygen
88
Immunisation
12
Incontinence - bladder
47
Incontinence - faecal
53
LDN
86
Low dose naltrexone

see LDN
Lumbar puncture
77
Depression
41
Diagnosis
Diet
Diplopia
Disease modifying
drug therapies
Double vision
EDSS
90
8
55, 85
34
10
13-14
Erectile dysfunction
59
Exercise
62
34
Outcome measures
13
Paediatric MS
Pain
72
Palliative care
80
Physiotherapy
62
Pilates
64
Posture
63
Pregnancy
44
Pressure ulcer
77
Prevalence
Primary progressive MS
11
Prognosis
12
Relapse
22-23
Relapsing remitting MS
11
Risk of MS
Sativex
68
Secondary progressive MS
11
Self-management
19
Severe MS
80
59
Spasms
66
Magnetic resonance
imaging see MRI
Spasticity
66
Speech
75
Memory
39
Stem cells
30
Menopause
46
Steroids
Menstruation
44
Swallowing
75
McDonald criteria
22, 24
22, 24
Mitoxantrone
29
TENS
73
Mobility
62
Teriflunomide
30
MRI
MS, types
8
11
Musculoskeletal pain see

Nociceptive pain
24-29
34
35
Optic neuritis
Sexual dysfunction
Methylprednisolone
Decubitus ulcer
21, 37
Nystagmus
Natalizumab
27
Nerve pain see

Neuropathic pain
Transcutaneous electrical nerve

stimulation see TENS
Tremor
70
Vaccination
12
VEP
10
Vision
34
Visual evoked potentials see VEP
Neuropathic pain
72
Vitamin D
Neutralising antibodies
27
Women's health
Nociceptive pain
73
www.mstrust.org.uk
6, 45, 86
44

Index
We hope you find the information in this book helpful. If you would like to speak with someone about any
aspect of MS, contact the MS Trust information team and they will help find answers to your questions.
This book has been provided free by the Multiple Sclerosis Trust, a small UK charity which works to
improve the lives of people affected by MS. We rely on donations, fundraising and gifts in wills to be able
to fund our services and are extremely grateful for every donation received, no matter what size.
MS Trust information service

Helping you find the information you need
The MS Trust offers a wide range of publications, including a newsletter for
health and social care professionals Way Ahead and the MS Information
Update, which provides an ongoing update on research and developments in
MS management.
For a full list of MS Trust publications, to sign up for Way Ahead

and much more visit our website at
www.mstrust.org.uk
Freephone
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email
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write
MS Trust
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Letchworth Garden City
SG6 4ET
This publication will be reviewed in three years

MS Trust
Multiple sclerosis information for health and social care professionals. Fourth edition.
ISBN 1-904 156-24-X
2011 Multiple Sclerosis Trust
Registered charity no. 1088353
All rights reserved. No part of this book may be produced, stored in a retrieval system or transmitted in any form by any means,
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Multiple sclerosis information

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The MS Trust is extremely grateful to all those who

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Alison Nock, DipCOT

Multiple sclerosis information for health and social care professionals

A multidisciplinary approach to MS care

Relapse and drug therapies

Disease modifying drug therapies

Beta interferons and glatiramer acetate

Disease modifying therapies currently in clinical trials

Symptoms, effects and management

Communication and swallowing

Complementary and alternative medicine 83

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provide a resource for professionals who work

the provision of equipment and accommodation

the provision of personal care and support

palliative care to enable people to make

support for families and carers

the provision of seamless, responsive services.

How successful has implementation of these

The arrival of disease modifying drugs in the UK

Multiple Sclerosis Information for Health and Social Care Professionals

100,000 people in the UK are estimated to have

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in England and Wales. This figure is higher still in

Putting MS risk in context

1 in 700 people will develop MS

1 in 40 people will develop MS if they have

1 in 3 people will develop some form of cancer

1 in 22 people have chronic heart disease

1 in 33 people have diabetes

1 in 500 people have Parkinsons Disease.

So far there are no conclusive results to explain

Compston A, Coles A. Multiple sclerosis. Lancet

Burgess M. Shedding greater light on the natural history

Richards RG, Sampson FC, Beard SM, et al. A review of the

Cook SD, MacDonald J, Tapp W, et al. Multiple sclerosis in

Compston A. The genetic epidemiology of multiple sclerosis.

Multiple Sclerosis Information for Health and Social Care Professionals

and around the eyes, blurred or double vision,

Clinically isolated syndrome

healthy nerve cell

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A diagnosis of definite MS is based upon objective

There are three major investigations, all or some of

There are established criteria that have to be met to

magnetic resonance imaging (MRI)

examination of cerebrospinal fluid (CSF).

Magnetic resonance imaging (MRI)

MRI is the most sensitive investigation with the

It can be problematic to establish a correlation

to observe abnormalities that are suggestive of

to rule out alternative diagnoses such as tumours

to help in the evaluation of patients who have

as a surrogate marker for disease activity in

A thorough physical examination of the current

Neurologists use MRI for the following purposes:

Multiple Sclerosis Information for Health and Social Care Professionals

The 2010 revised McDonald criteria for diagnosis of MS4

Additional data needed

Two or more attacks; objective clinical

Two or more attacks; objective clinical