lOMoARcPSD|3537447

CVA & Other diseases

Physical therapy (Our Lady of Fatima University)

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CVA
Differentials: Disconnection syndromes
Epidemiology Split brain
Old > young, M > F, black > white, asian > US Disconnection apraxia/(L) side apraxia
Alexia w/o agraphia/Pure word blindness
Pathophysiology Pure word deafness
Focal infarction and ischemic penumbra Conduction aphasia
Cerebral edema → ↑ ICP → herniation
S/Sx: ↓ level of consciousness, widened pulse pressure, ↑ HR, PCA
Cheyne-Stokes respiration, vomiting, unreacting pupils, Behavioral disorders
papilloedema Akinetic mutism
Abulia
Risk Factors Pseudobulbar affect/emotional dysregulation syndrome
Modifiable (L) (R)
Hypertension cautious impulsive
DM Visual impairment
Heart disease Visual agnosia
Cigarette smoking Pure word blindness
Hypercholesterolemia Anton – denial of blindness
Obesity (L) (R)
TIA simultagnosia depth & distance
Asymptomatic carotid bruit color agnosia
↑ hematocrit/serum fibrinogen prosopagnosia
Non-modifiable Memory deficit
Race Hemisensory deficit
Age *Thalamic pain/Dejerine-Roussy syndrome
Sex
Previous stroke Lacunar
Pure motor
Classification: Temporal Pure sensory
TIA Dysarthria with facial weakness
Reversible ischemic neurologic deficit Dysarthria with clumsy hand
Stroke in evolution Ataxic hemiparesis
Completed stroke
Brainstem
Classification: Pathophysiological
Ischemic Syndrome Area Ipsi Contra
- Thrombotic(40%) Weber medial CN III hemiplegia
- Embolic (20%) basal
- Lacunar(20%) midbrain
- Other (5%) Benedikt tegmetum CN III pain & T°,
Hemorrhagic of midbrain ataxia
- Intracerebral (10%) proprioception,
- Subarachnoid (5%) tremor, chorea,
Locked-In bilateral (+) upward
Classification: Neuroanatomical basal pons gaze only
ICA Millard- lateral pons CN VI, VII hemiplegia
Gubler
MCA Wallenberg lateral CN X & V, pain pain & T°
Contralateral hemiplegia (PICA/Latera medulla & T° (face), (body)
Contralateral hemianesthesia l Medullary ataxia,
Frontal gaze palsy Syndrome) Horner’s
Aphasias nystagmus
(L) (R) AICA cerebellum, CN V, VI, VII, pain & T°
44 Broca Aprosodia brainstem pain & T° (body)
Amelodosia (face), ataxia,
22 Wernicke Affective agnosia Horner’s
Amusia SCA cerebellum, ataxia, pain & T°
Apraxia brainstem Horner’s (body & face)
(L) (R)
39 Gerstmann Examination
40 Ideomotor Anosognosia, Neglect Test & measures – Urinalysis, blood analysis, FBS, thyroid
P Autopagnosia
function test, full cardiac eval, lumbar puncture
Somatoagnosia Figure-ground
Imaging – CT scan, MRI, PET, Doppler, Cerebral angiopgraphy
Ideational Form
Spatial relations Medical Mx
Position in space
Meds: thrombolytics, anticoagulants, antiplatelet,
Topographic
antihypertensive
Vertical Surgery:
Constructional apraxia Endarectomy
Dressing apraxia Aneurysm repair/resection – operative (clipping, trapping,
Contralateral hemianopsia
proximal occlusion), endovascular (coil embolisation, balloon
Dysphagia
remodeling, balloon occlusion, stents)
Evacuation of hematoma
ACA
Contralateral hemiplegia
Others
Contralateral hemianesthesia
Disability Scale – Fugl Meyer, STREAM
Uninhibited neurogenic bladder Greatest recovery – 3-6 months
Primitive reflexes
Palmomental
Predictors
Pout
1 month recovery → 6 month recovery
Grasp/Groping Grip strength at 24 hrs → arm recovery in 3 months
*Gegenhalten/Paratonia Poor Predictors

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coma at onset persistent incontinence • Contralateral hemisensory loss involving mainly the UE
poor cognitive function severe hemiplegia and face (LE is more spared)
prior stroke visual-spatial perceptual deficit • Motor speech impairment: Broca’s or nonfluent aphasia
unilateral hemineglect significant cardiovascular disease with limited vocabulary and slow, hesitant speech
large cerebral lesion multiple neurologic deficits • Receptive speech impairment: Wernicke’s or fluent
lack of return of motor function after 1 month aphasia with impaired auditory comprehension and
fluent speech with normal rate and melody
STROKE • Global aphasia: nonfluent speech with poor
• Stroke is the sudden occurrence of permanent damage to comprehension
an area of the brain caused by a blocked blood vessel • Perceptual deficits: unilateral neglect, depth perception,
or bleeding within the brain. spatial relations, agnosia
• TWO MAJOR CATEGORIES: • Limb-kinetic apraxia
➢ Ischemic Note:
➢ Hemorrhagic PERCEPTUAL – UN – failure to respond to people or objects
Note: presented to the side opposite a brain lesion.
Strokes can be divided into two major categories: Ischemic – Depth perception- ability to determine distances between objects
most common type of stroke and see the world in three dimensions
- affects about 80% of individuals with stroke Apraxia- difficulty in motor planning
- happens when a clot blocks or impairs blood flow, depriving Difficulty making precise movements with
the brain of essential
oxygen and nutrients. • Contralateral homonymous hemianopsia
• etiology • Loss of conjugate gaze to the opposite side
• Atherosclerosis • Ataxia of contralateral limb(s) (sensory ataxia)
• Ischemic Strokes • Pure motor hemiplegia (lacunar stroke)
➢ Cerebral Thrombosis Note:
➢ Cerebral embolus (CE) Strokelike symptoms Other causes of focal brain damage, such
• Hemorrhagic Strokes as traumatic injury to the brain, demyelinating lesions (attacks the
➢ Cerebral Hemorrhage myelin sheath or the cells that produce and maintain it)
➢ Lacunar Stroke Brain tumors AB(N) Cells, brain abscesses (Inflammation and
➢ Subarachnoid Hemorrhage collection of infected material)
➢ epidemiology Homonymous hemianopsia - A homonymous hemianopia is the
• In the Philippines.. loss of part of the field of view on the same side, in both eyes.
Stroke has a prevalence of 0-9% - easily become lost, feel disoriented and unable to navigate
➢ Ischemic stroke 70% safely through the crowd
➢ Hemorrhagic stroke 30% Conjugate - ability to move both eyes in the same direction
• In the US…
➢ 795,000 individuals each year
➢ 610,000 are first attacks Medical treatment
➢ 185,000 are recurrent strokes of stroke
Note: By: Erica D. Cabusas
Women have a lower age-adjusted stroke incidence than men. ❑ Merci Retriever System
However, this is reversed in older ages; women over 85 years of ❑ Penumbra System
age have an elevated risk compared to men. Medical intervention

• Brief background thrombolytics

Modifiable Risk Factors Alteplase (tPA)
❑ Hypertension ❖
0.9 mg/kg (max 90 mg)
❑ Heart disease ❖
to be used <3 hrs. of onset
Ischemic/hypertensive symptoms for maximum
Valvular efficacy
Arrhythmias ❖ converts plasminogen to
❑ Smoking plasmin, degrades fibrin
❑ Diabetes mellitus present in clots, dissolves
❑ Elevated fibrinogen clots and reestablishes blood
❑ Erythrocytosis flow.
❑ Hyperlipidemia Possible adverse effects: The most common complication is
• Types of Strokes bleeding and brain hemorrhage.
1. Transient Ischemic Attacks
• Transient ischemic attacks (TIAs) have historically been anticoagulants
defined as a strokelike event that completely resolves Warfarin (Coumadin), Heparin
within 24 hours. The symptoms of a TIA begin -Used to reduce the risk of blood clots and prevent existing clots
abruptly and may persist for only a few seconds or from getting bigger by thinning the blood.
minutes, followed by apparent full resolution. TIAs
are not trivial events and require a thorough Possible adverse effects: Increased risk of bleeding and
investigation. Those TIAs associated with MRI evidence hemorrhage, hematomas.
of tissue damage carry a particularly high risk of further Antiplatelet therapy
vascular events. Acetylsalicylic acid (Aspirin), Clopidogrel bisulfate (Plavix),
• Signs and symptoms Dabigatran etexilate (Pradaxa), ticlopidine hydrochloride
• Aphasia (Ticlid)
• Ataxia -act by inhibiting platelet aggregation and adhesion.
• Apraxia -Prevent platelets (blood cells) from sticking together; long-term,
• Agnosia low-dose is used to decrease the risk of thrombosis and recurrent
• Anopsia stroke; higher doses may be used in place of anticoagulants
Note: Possible adverse effects: Increased risk of gastric ulcers and
Aphasia, an inability to produce and/or comprehend language bleeding.
ATAXIA the loss of coordination of muscles
Agnosia is the loss of the ability to recognize objects, faces, Antihypertensive agents
voices, or places ACE inhibitors, Alpha-blockers (Minipress), beta-blockers,
Anopsia - defect in the visual field calcium channel blockers, direct vasodilators, diuretics,
postganglionic neuron inhibitors
• Contralateral hemiparesis involving mainly the UE and -Used to control hypertension.
face (LE is more spared) Possible adverse effects: Dizziness, hypotension, among other
symptoms.

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❑ Architectural modifications, assistive devices or orthotics

Angiotensin ii receptor antagonists should be ready before discharge
Telmisartan (Micardis), Losartan Potassium (Cozaar)
-A chemical that triggers muscle contraction around blood
vessels, narrowing them; enlarges blood vessels and reduces
blood pressure.
Possible adverse effects: Dizziness, hypotension, among other • MEDICAL DIAGNOSIS
symptoms. • ECHOCARDIOGRAM
• Uses soundwaves to produce images of the heart
Anticholesterol agents • Commonly used to allow the doctor to see if the heart is
Atorvastatin calcium or Lipitor, rosuvastatin calcium or normally beating and pumping blood
Crestor, Zocor, Mevacor, Lescol • non-invasive
-Lower cholesterol by inhibiting the enzyme in the blood that note:
produces cholesterol in the liver; for management of Use in stroke: can help determine if there is a blood clot na
hypercholesterolemia and mixed dyslipidemias. pwedeng magtravel and magcause ng stroke
Possible adverse effects: Dizziness, headache, insomnia,
weakness. • Computed Tomography (CT)
• Show areas of abnormalities in the brain, and can help to
Antispasmodic/spasmolytics determine if these areas have insufficient blood flow,
Carisoprodol (soma), chlorzoaxazone (Parafon Forte), hemorrhage, or other problems.
Cyclobenzaprine (Flexeril), Diazepam (Valiu), • Less costly than MRI
Methocarbamol (Robaxin), Orphenadrine (Norflex) Note:
-Used to relax skeletal muscle and decrease muscle spasm. A type of x-ray that uses a computer to make cross-sectional
Possible adverse effects: drowsiness, dizziness, dry mouth, images of your body
among other symptoms. Can be sagittal, coronal, etc

antispastics • a. Computed Tomography Angiogram (CTA)

Baclofen (Lioresal), Dantrolene Sodium (Dantrium), • CT scan with an involvement of a contrast media to
Diazepam (Valium), Tizanidine ( Zanaflex) produce pictures of blood vessels and tissues in a part
-Used to relax skeletal muscle and decrease muscle spasm. of your body
Possible adverse effects: May cause drowsiness, dizziness, • The media contrast is injected through an intravenous (IV)
confusion, weakness line started in your arm or hand
Note:
anticonvulsants The media is called a contrast because it “lights up: blood
Carbamazepine (Tegretol), Clonazepam (Klonopin), vessels and tissues that are being tested
Diazepam (Valium), Phenobarbital (Luminal), Phenytoin Gadolinium yung iniinject
(Dilantin) Some patients are allergic to gadolinium
-Used to control seizures; act as a generalized CNS depressant.
Possible adverse effects: May cause drowsiness, ataxia, • b. CT Perfusion of the Head
sedation, among other symptoms. • Uses special x-ray equipment to show which areas of the
Antidepressants brain are adequately supplied with blood
*used to control depression • Provides detailed information about blood flow to the brain
Fluoxetine (Prozac), Monoamine Oxidase Inhibitors, • Cranial Magnetic Resonance Imaging
Sertraline (Zoloft), Tricyclics Amitriptyline • This type of testing is useful to determine the extent of
❖ Possible adverse effects: May cause anxiety, tremor, brain injury and identify potential structural abnormalities
insomnia, nausea. • More effective and sensitive than Computed Tomography
(CT)
Pt intervention Note:
Acute stage The media is called a contrast because it “lights up: blood
❑ Positioning strategies vessels and tissues that are being tested
❑ Improve respiratory and circulatory function Gadolinium yung iniinject
❑ Prevent pressure sores Some patients are allergic to gadolinium
❑ Prevent form deconditioning
POSt acute stage • Magnetic Resonance Angiography (MRA)
❑ 5 days a week for minimum of 3 hours of active • Type of MRI that looks specifically at the body’s blood
rehabilitation per day vessels
❑ Intensive rehabilitation if vitals are stable • Used to evaluate blood vessels and help identify
✓ Improve sensory function abnormalities or identify plaque formation
✓ Flexibility and joint integrity • Non-invasive
✓ Improve strength • Helpful in examining extracranial & intracranial cerebral
✓ Manage spasticity vessels
✓ Improve movement control
✓ Postural control and functional mobility
✓ Improve upper extremity function
✓ Managing shoulder pain
✓ Improve lower limb function
✓ Improve balance
✓ Improve locomotion
✓ Improve aerobic function
✓ Improve feeding and swallowing
✓ Improve motor learning
Patient and family education
❑ Give factual information, counsel family members about
the patients capabilities and limitations
❑ Provide open discussion and communication
❑ Be supportive, sensitive and maintain a positive
supporting nature
❑ Give psychological support
❑ Refer to help groups
Discharge planning
❑ Family member should participate daily in the therapy
session and learn exercises
❑ Home visits should be made prior to discharge

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arthritis (particularly rheumatoid arthritis); and poor nutrition

(including malnutrition due to eating disorders).
• Osteogenesis imperfecta
-Osteogenesis imperfecta is a rare form of osteoporosis that is
present at birth. Osteogenesis imperfecta causes bones to
break for no apparent reason.
OSTEOPOROSIS • Idiopathic juvenile osteoporosis
• INTRODUCTION: -Idiopathic juvenile osteoporosis is rare. It occurs in children
Etiology between the ages of 8 and 14 or during times of rapid
• Results from insufficient bone formation growth. There is no known cause for this type of osteoporosis,
• Excessive bone resorption in which there is too little bone formation or excessive
• Combination of both bone loss. This condition increases the risk of fractures.
• • Bone fractures:
• 15% Postmenopausal Caucasian women (US) • Bruising
• 35%- women older than 65 years • Swelling
• 50%-women older than 50 years have Osteopenia of the • Deformity
femoral neck • Pain
• Risk factors: • Loss of function (compound fx)
• Genetics • Tenderness
• Female gender • Sometimes bone protrusion
• Positive family history • - Pt. may sometimes feel dizziness
• Racial characteristics associate with Caucasian, Asian or • Sick, faint resulting from shock
Hispanic background • Upon injury, a snapping or grinding noise is present
• Low body weight • OSTEOMALACIA
• -Modified Risk Factors: • Worsens bone pain
• Early menopause • Muscle weakness
• Early pregnancy • Dull aching of hips, lower back, pelvis, legs and ribs
• Smoking • Worse at night esp. when pressure is applied
• Sedentary lifestyle • Waddling gait
• Alcoholism • OSTEOPOROSIS
• Low body fat • Back pain (due to collapsed vertebra)
• Low calcium itake • Loss of height over time
• High caffeine intake • Stooped posture
• Prolonged bed rest • Prone to bone fractures much more easily
• Anorexia
• -Medical Risk Factors:
• Corticosteroids
• Diuretics
• Thyroid hormone preparations
• Epidemiology
-Fracture of the vertebrae and fracture of other bones such as
the proximal humerus, distal forearm, wrist proximal femur
(hip), and pelvis.

• Types:
• Type 1 Postmenopausal
-Type 1 or postmenopausal osteoporosis occurs in 5% to 20%
of women, affecting those within 15 to 20 years of
menopause, with a peak incidence in the 60s and early 70s.
The incidence in women is eight times higher than that in men.
The frequency of postmenopausal osteoporosis accounts for
the overall female-male ratio of 2:1 to 3:1.
• Type 2 Involutional
-Type 2 is generally seen in older age population a d has been
referred to as Senile Osteoporosis. Women are more prone to
develop Osteoporosis because of the contribution of the loss
estrogen to accelerated bone loss in the postmenopausal
female population. It occurs in women or men more than 70
years of age and usually is associated with decreased bone
formation along with decreased ability of the kidney to produce
1,25(OH)2D3. The vitamin D deficiency results in decreased
calcium absorption, which increases the PTH level and
therefore bone resorption. In type 2 osteoporosis, cortical and
trabecular bone is lost, primarily leading to increased risk of
hip, long bone, and vertebral fractures.
• Type 3 Secondary Osteoporosis
-Type 3 or secondary osteoporosis occurs equally in men and
women and at any age. In men, most cases are due to disease
or to drug therapy, but in 30% to 45% of affected individuals no
cause can be identified. In various series of osteoporotic De Lisa
patients, secondary osteoporosis accounts for about 40% of • Pharmacologic and nutritional treatment of bone mass
the total number of osteoporotic fractures seen by a physician. deficiency (Skeletal Osteopenia/Osteoporosis)
This type of osteoporosis is associated with a variety of ✓ Treatment of osteoporosis is directed at
conditions, including hormonal imbalances (eg, Cushing's preservation or improvement of bone mass at
syndrome); cancer (notably multiple myeloma); gastrointestinal the specific target sites. Because bone mass is
disorders (especially inflammatory bowel disease causing the principal, although not the only,
malabsorption); drug use (eg, corticosteroids, cancer determinant of fracture, such preservation or
chemotherapy, anticonvulsants, heparin, barbiturates, valporic improvement of bone mass s associated with a
acid, gonadotropin-releasing hormone [GnRH], excessive use reduce risk of fracture.
of aluminum-containing antacids); chronic renal failure; ✓ Mode of action of specific osteoporosis
hyperthyroidism; hypogonadism in men; immobilization; therapies
osteogenesis imperfecta and related disorders; inflammatory
• Nutritional adjuncts

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o Calcium
✓ Mainstay of osteoporosis prevention
and treatment. Generally safe: milk
and dairy products and calcium
supplements are acceptable sources
of calcium.
o Vitamin D
✓ 4 hundred to 800 UI if vitamin D,
administered in a multivitamins form,
is reasonable treatment for
osteoporosis; whether the active
forms of vitamin D such as calcitriol
are beneficial in osteoporosis is
unproven.
o Protein
✓ Protein supplementation has been
shown to favorably affect outcomes in
patients who have sustained hip
fractures.
• Pharmacologic agents
o Bisphosphonates
✓ Have the ability to preserve and
increase bone mass at the spine and
hip, as well as to prevent fractures at
each of these skeletal sites.
o Estrogen
✓ Mainstay of osteoporosis in women.
Data exist to indicate estrogens may
preserve bone mass at multiple
skeletal sites and prevent fracture.
o Calcitonin
✓ Calcitonin studies do indicate its
ability to preserve bone density, and
possibly prevent fractures. One of its
benefits is its potential ability to
decrease pain after acute
compression fracture in the spine,
presumably through a stimulation of
beta-endorphins
o Raloxifene
✓ Raloxifene (Evista) is FDA-approved
in this class, for the treatment of
postmenopausal osteoporosis, and
prevention of bone loss in recently
postmenopausal women; it is not
recommended for relief of
menopausal symptoms (74). The use
of raloxifene
provides modest increases in bone
mass, but reduction in the risk of
vertebral fracture is 40% to 50%, and
there is no reduction in nonvertebral
fractures (45). It also appears to
reduce
the risk of estrogen-dependent breast
cancer, but increases the risk of deep
vein thrombosis to a degree similar to
that of estrogen. Newer research in
this class focuses on increased
benefit to
bones, heart and breast tissue
hormone
o Parathyroid
✓ Parathyroid hormone, or fragments of
the intact peptide molecule may be of
in osteoporosis when administered
parentally. Such as usage is based on
presumed anabolic effect of
parathyroid hormone when
administered as a fragment, and it
may be of value in established
osteoporosis in terms of stimulating
bone formation.
o Experimental therapies
✓ Estrogen agonist or antagonist such
as reloxifene, tamoxifen, idioxifene,
and droloxifene may have value in
preserving bone mass in
osteoporosis.
• Non-FDA-Approved Drugs
o Sodium fluoride
o Calcitriol
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o Other bisphosphonates
o Tibolone
• General Recommendations for Osteoporosis Therapy
✓ The above pharmacology should be
completed by avoidance of life-styles
known to result in bone loss, including
cigarette smoking, excessive alcohol
intake, a lack of exercise, lack of
calcium intake, and so forth
✓ The use of calcium, a multiple vitamin
with vitamin D, and a consideration of
the approved forms of therapy for
osteoporosis may definitely be of
value in preventing progression of
disease.
• PATIENT ASSESSMENT FOR REHABILITION
✓ Depends on accurate diagnosis of the
degree of bone loss, as well as a
determination of the degree of frailty
and propensity of the patient to fall.
• MANAGEMENT OF OSTEPOROSIS-RELATED
DISABILITY
o Psychosocial considerations
o Exercises
1. Principle of specificity
2. Principle of progression
3. Principle of reversibility
4. Principle of initial values
5. Principle of diminishing returns
• Vertebral fracture
o A multidisciplinary team approach is beneficial
to ensuring maintenance of function in this
population. Non-pharmacologic interventions
should be parentally used to manage chronic
back pain. Chronic back pain in the
osteoporotic patient is managed by having the
patient assume adequate recumbent bed rest
for 20-30 minutes twice daily. This program is
supplemented by encouraging adjustments in
life-style, medications, physical agents,
orthoses, and other therapies considered
useful for chronic pain.
• Hip fracture
o These patient require the care of physiatrist,
physical therapist, and occupational therapist,
as well as of nurses and social workers. The
benefits of the multidisciplinary approach have
been documented as resulting in fewer
transfers of acute emergencies, fewer
postoperative complications, improved
ambulation at the time if discharge, and fewer
discharge to nursing homes
• Wrist fracture
o The primary goal of treatment to return of pain-
free normal function of the hand and wrist.
Initial casting usually extends above the elbow
and restricts movement of both elbow and
wrist. During the period of mobilization, usually
6-8 weeks, strength and flexibility should be
maintained in the upper extremities.
• Back supports and bracing in osteoporosis
o Bracing will be of value at certain times and in
certain conditions associated with osteoporotic
fractures. When able, it is best to utilize one’s
own muscles to support the skeleton. However,
bracing is extremely useful to aid the patient
who is in too much pain to function without
support and is also helpful to prevent soft-
tissue deformity and excessive loading of the
vertebral bodies
• Fall and fractures
o Because hip fractures have multifactorial
causes, interventions must aim not only at
increasing muscular strength, balance, and
flexibility and reducing the forces of impact
when a fall occurs. Of utmost importance in the
success of a program aimed at preventing falls
is the educational component in reduction of
risk factors for falling. Home visit from

occupational therapist have been shown to be
helpful in this.
• Mechanism of falls
➢ Risk Factors for Falls
1. Environmental
2. Medical
3. Neuromuscular
4. Demographic
• Fear of falling
❖ Physical medicine and rehabilitation strategies can be of
value in the management of the osteoporotic patient and
are currently underused. These strategies are used to
reduce disability resulting from impairments in bone and
structure, muscle strength, and coordination.
Braddom
Treatment
osteoporosis is a multifactorial condition and its treatment has
several facets, so it requires a team approach. Endocrine
consultation is needed, along with interventions from specialist in
physical medicine and rehabilitation, pharmacology, psychology
and nutrition. The prevention of falls decreases the risk of
fracture. A recent controlled trial demonstrated significant
improvement in risk of fall, balance, and unsteadiness of gait
after 4-week spinal proprioceptive extension exercise dynamic
(SPEED) program.
Exercise
The efficacy of exercise for improving bone mass is supported by
hormonal and nutritional factors. To meet the challenge of
mechanical load, skeletal tissue must have engaged bone mass
and proper architecture to withstand the physical strain that
imposed on it. It is fortunate that normal musculoskeletal
structure is highly adaptable and can meet the challenge of usual
mechanical load.
Posture Training Program and The Osteoporotic Skeletal
Frame
Orthoses and the Osteoporotic Spine
❖ Treatment of Osteoporosis
➢ Medical Therapy of Spinal Osteoporosis
Calcitonin therapy decreases the rate of bone
loss in osteoporotic patients. Calcitonin works
through the inhibition of bone resorption.
➢ Rehabilitation of Patients with Spinal
Osteoporosis
✓ Acute fracture in the spine creates
pain lasts about 1 to 2 weeks and
sometimes requires bed rest. A
transcutaneous electrical nerve
stimulation (TENS) unit might also
help in the treatment of chronic back
pain secondary to spinal osteoporosis
of the type II variety. After 2-week
period, ambulation should be initiated
if possible.
✓ The main reason for the application of
thoracic orthosis is to prevent further
fracture by limiting motion in the
spine.
Therapy depends on the cause and type of osteoporosis. Initially
it is intended to influence the bone metabolism in order to prevent
bone fractures. If bone fractures have already occurred as a
result of osteoporosis, their acute treatment is required: this
means alleviating the pain associated with the fracture as well.
Osteoporosis treatment is also intended to reduce or entirely
eliminate possible permanent complaints.
Left untreated, bone degeneration continues so that the bones •
become increasingly brittle. Beginning with osteoporosis
treatment as early as possible is therefore important.
Orthoses can help stabilise and straighten the spine. They
improve the body posture and activate the torso musculature.
The products shown are fitting examples. Whether a product is
actually suitable for you and whether you are capable of
exploiting the functionality of the product to its fullest depends on
many different factors. Amongst others, your physical condition,
fitness and a detailed medical examination are key. Your doctor
or orthopedic technician will also decide which fitting is most
suited to you. We are happy to support you.
Activation of the musculature
Good treatment options for osteoporosis (bone degeneration) are
available in the meantime. Even at an early stage, promoting
muscle activity is helpful in order to delay the rapid progress of
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lOMoARcPSD|3537447
the disease. The DorsoOsteo Care spinal orthosis was
developed specifically for this purpose.
The mode of operation is simple: The orthosis helps you
straighten your upper body, thereby strengthening your
musculature, increasing bone regeneration and improving your
posture.
The DorsoOsteo Care is easy to put on and made of a soft,
comfortable and breathable material.
Bisphosphonates are a class of drugs that prevent the loss
of bone mass, used to treat osteoporosis and similar diseases.
They are the most commonly prescribed drugs used to treat
osteoporosis.[1] They are called bisphosphonates because they
have two phosphonate(PO(OH)
2) groups.
Evidence shows that they reduce the risk of fracture in post-
menopausal women with osteoporosis.[2][3][4][5][6]
Bone undergoes constant turnover and is kept in balance
(homeostasis) by osteoblasts creating bone
and osteoclasts destroying bone. Bisphosphonates inhibit the
digestion of bone by encouraging osteoclasts to
undergo apoptosis, or cell death, thereby slowing bone loss.[7]
The uses of bisphosphonates include the prevention and
treatment of osteoporosis, Paget's disease of bone, bone
metastasis (with or without hypercalcaemia), multiple
myeloma, primary hyperparathyroidism, osteogenesis
imperfecta, fibrous dysplasia, and other conditions that exhibit
bone fragility.
Bisphosphonates for Osteoporosis
Examples
Generic Name Brand Name
alendronate Fosamax
ibandronate Boniva
risedronate Actonel, Atelvia
zoledronic acid Reclast
You take most bisphosphonates by mouth-every day, once or
twice a week, or even once a month. Zoledronic acid is
given intravenously (IV), usually only once each year. One form
of ibandronate is also given intravenously, usually every 3
months.
How It Works
Bisphosphonates are antiresorptive medicines, which means
they slow or stop the natural process that dissolves bone tissue,
resulting in maintained or increased bone density and strength.
This may prevent the development of osteoporosis.
If osteoporosis already has developed, slowing the rate of bone
thinning reduces the risk of broken bones.
Bisphosphonates may be taken by men or women.
Why It Is Used
Bisphosphonates are commonly used for the prevention and
treatment of osteopenia and osteoporosis.
Bisphosphonates are also used to treat other bone diseases
such asPaget's disease.
How Well It Works
Studies show that bisphosphonates increase bone thickness and
may lower the risk of fractures.1
Side Effects
All medicines have side effects. But many people don't feel the
side effects, or they are able to deal with them. Ask your
pharmacist about the side effects of each medicine you take.
Side effects are also listed in the information that comes with
your medicine.
Here are some important things to think about:
Usually the benefits of the medicine are more important
than any minor side effects.
• Side effects may go away after you take the medicine
for a while.
• If side effects still bother you and you wonder if you
should keep taking the medicine, call your doctor. He or she
may be able to lower your dose or change your medicine. Do not
suddenly quit taking your medicine unless your doctor tells you
to.
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Parkinson’s disease Extrapyramidal- drug induced movements disorders that produce

• Epidemiology acute and tardive symptoms
• Progressive disorder of the central nervous system Wilson’s disease- autosomal recessive genetic disorder in which
• James Parkinson “paralysis agitans” copper accumulates in the body. Manifests n neurological or
• An extrapyramidal disorder by Kinnier Wilson psychiatric and liver symptoms
• Affects 7-10 million people worldwide Note:
• 2% of people older than 65 years of age has PD Alzheimers disease- is a type of dementia that causes
• Second to Alzheimer’s disease problems with memory, thinking and behavior. Symptoms
Note: usually develop slowly and get worse over time, becoming
Progressive disorder of the cns with motor and non motor severe enough to interfere with daily tasks.
symptoms, motor symptoms: rigidity, bradykinesia, tremor. Diffuse lewy body diseas- Lewy body dementia, these abnormal
Extrapyramidal- drug induced movement disorders. proteins are diffuse throughout other areas of the brain, including
the cerebral cortex. The brain chemical acetylcholine is depleted,
• Epidemiology causing disruption of perception, thinking and behavior.
• Increase substantially in the coming years due to the Subsancia nigra-reward and movement
aging of the population
• Common in men than women • Parkinson- plus syndrome
• Average onset: 50-60 years old • Affects the substancia nigra
• Early onset: less than 40 years old • Produces parkinsonian symptoms with other neurological
• Young onset: between 21 and 40 years of age sign
• Juvenile onset: less than 21 years old 1. Alzheimer’s disease- progressive type of dementia
• Etiology 2. Diffuse Lewy body disease (DLBD)
• Can be both genetic and environmental Features:
• Parkinsonism- generic term used to describe a group of • Indistinguishable rigidity and bradykinesia from PD
disorders with primary disturbances in the dopamine • typically do not show measurable improvement from the
systems of the basal ganglia. administration of anti-Parkinson medications such as
1. Idiopathic Parkinsonism levodopa (L-dopa) therapy
2. Secondary Parkinsonism • Cardinal Features:
3. Parkinson-Plus Syndrome • Rigidity
Note: • Bradykinesia
Basal ganglia- a group of structures linked to the thalamus in the • Postural Instability
base of the brain and involved in coordination of movement. • Tremor
• Disruption in daily functions
• Etiology • depression
• PARKINSONISM note:
• Idiopathic Parkinsonism Triad of PD:
• Secondary Parkinsonism • RIGIDITY
1. Postencephalitic Parkinsonism • BRADYKINESIA
2. Toxic Parkinsonism • PSTURAL INSTABILITY
3. Drug-Induced Parkinsonism (DIP)
• Parkinsonism-plus syndrome
1. Alzheimer’s disease
2. Diffuse Lewy body disease (DLBD)
3. Normal pressure hydrocephalus (NPH)
4. Creutzfeldt-Jakob disease (CJD)
5. Wilson’s disease (WD)
6. Juvenile Huntington’s disease
• Parkinson’s disease
• Also known as Idiopathic Parkinsonism
• Idiopathic or genetic mutation
• Most common. 78% are affected
• Two clinical subgroups(symptoms):
1. Postural instability and gait disturbances
2. Tremor predominant
Genes:
1. Casual genes that produces the disease
2. Genes that don’t cause the PD but increase the risk of
developing it
• Secondary parkinsonism
• Postencephalictic Parkinsonism-influenza epidemic of
encephalitis lethargica
• Toxic Parkinsonism- exposed to environmental toxins and
industrial chemicals.
• Drug-induced Parkinsonism- drugs that produce
extrapyramidal dysfunction that mimics signs of PD.
Ex:
1. Neuroleptic drugs
• Rare cases:
• Metabolic conditions
- Hypoparathyroidism
- Hyperparathyroidism
Note:
Postencephalictic- parkinsonian symptoms occurred. may slow
virus na nagiinfect ng brain
- Occurred nung 1917-1926, many indi were affected
Toxic parkinsonism- parkinsonian symptoms occur in harmful
chemicals like AGENT ORANGE- a herbicide in the US. Then
manganese, carbon monoxide etc etc.
MPTP- is a prodrug to the neurotoxin MPP+, which causes
permanent symptoms of Parkinson's disease by destroying
dopaminergic neurons in the substantia nigra of the brain. It has
been used to study disease models in various animal studies.
Drug induced- blocks the dopamine receptors

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IV. Medical Diagnosis • Familial incidence: 5%

❖ The diagnosis of Parkinson disease is primarily clinical made Sullivan:

by a neurologist.
❖ Bedside cognitive evaluation can be normal early in the • Affects 7-10 million people worldwide
disease process. • 2% of people older than 65 years of age has PD
▪ A detailed history of your current and past • Second to Alzheimer’s disease
medications, to make sure you are not taking • Increase substantially in the coming years due to the
medications that can cause symptoms similar to aging of the population
PD. • Common in men than women (1.2 to 1.5 frequently)
▪ A detailed medical history and physical • Average onset: 50-60 years old
examination. • Early onset: less than 40 years old
▪ A detailed neurological examination during which a • Young onset: between 21 and 40 years of age
neurologist will ask you to perform tasks to assess • Juvenile onset: less than 21 years old
the agility of arms and legs, muscle tone, your gait
Etiology:
and your balance.
• Parkinsonism- generic term used to describe a group of
❖ In order to diagnose a patient with Parkinson’s disease, the disorders with primary disturbances in the dopamine
following must be observed/assessed: systems of the basal ganglia
✓ Tremor or paucity of spontaneous movements • Idiopathic parkinsonism or parkinson’s disease- most
✓ Resistance to movement of the limb during ROM common form, affecting 78% of pts.
examination • Secondary parkinsonism is a result from different
✓ Motor examination—which in PD is asymmetric in the identifiable cause
early stages of the disease • Parkinsonism plus syndromes refers to those conditions
✓ Gait observation that mimics PD.
*If a patient uses more than five steps to complete a 180
degree turn, PD should be considered. Parkinson’s disease
✓ It is also helpful to watch for certain cardinal symptoms
such early vertical eye movement abnormalities, early • Idiopathic or genetically identififed
autonomic failure or hyperreflexia, Babinski’s sign, • 2 clinical subgroups:
ataxia and peripheral neuropathy. 1. Postural instability and gait disturbances
2. Tremor predominant
❖ Triad of Parkinsonism
Genetic- represents 10% cases overall. PARK1, PINK1,LRRK2,
➢ Tremor
DJ-1, and glucocerebrosidase, are some examples.
➢ Rigidity 2 categories:
➢ Bradykinesia 1. Casual genes that causes the mutation
2. Associated genes that increases in developing PD.
❖ Parkinson Disease is diagnosed based on the patient’s
medical history and symptoms evaluated during the Secondary Parkinsonism
neurological examination so in order to rule out other
neurological disorders, CT scan, MRI or PET may be used. • Postencpehalictic Parkinsonism
• Toxic Parkinsonism- individuals that are exposed to
❖ The differential diagnosis of Parkinson Disease is wide. The toxins and industrial chemicals
rigidity can be mistaken for the stiffness of arthritis, the • Drug induces parkinsonism- variety of drugs that can
postural changes can be associated to osteoporosis or produce extrapyramidal dysfunction that mimics PD:
degenerative spine disease, the bradykinesia and masklike 1. Neuroleptic drugs
facies can be mistaken for depression. 2. Antidepressant drugs
3. Antihypertensive drugs
• Rare cases: metabolic conditions.
❖ As Parkinson Disease advances: 1. BG calcification
➢ Obstructive and restrictive pulmonary disease 2. Hypothyroidism
➢ Speech can be rapid and monotonous and have low 3. Hyperthyroidism
volume with poor articulation and inappropriate periods 4. Wilson’s disease
of silence
Parkinson-plus Syndrome
➢ Hand writing can become small and cramped
(microphagia)
• A group of neurodegenerative diseases can affect the
➢ Dementia and depression
substancianigra and produce parkinsonian symptoms
Autonomic dysfunction with increased salivation, drooling, along with neurological signs.
orthostasis, increased perspiration, constipation, hyperreflexic • Diseases include:
bladder with incontinence, dysphagia 1. progressive supranuclear palsy (PSPO)
2. Alzheimer’s disease
I. INTRODUCTION 3. diffuse Lewy body disease (DLBD)
4. normal pressure hydrocephalus (NPH)
Parkinson’s disease
5. Creutzfeldt-Jakob disease (CJD)
6. Wilson’s disease (WD)
• A progressive disorder of the central nervous system
7. juvenile Huntington’s disease
• James Parkinson “paralysis agitans”
• An extrapyramidal disorder by Kinnier Wilson

Epidemiology: Lindsay:
Severe and permanent parkinsonism has been inadvertently
produced in individuals who injected a synthetic heroin containing
• Annual incidence: 20 per 10000 the chemical MPTP (1-methyl-4-phenyl-1,2,3,6- tetra/
hydropyridine)
• Prevalence: 90 per 100000

• Sex: Male:Female-3:2

• Age of onset: 50y/old

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