Neurogenic Bladder, Acute Medullar

Compression, and Complete Spinal

Transection

Christian Kamallan
Neurology Department
UWKS
Anatomy of the
spine
Different spinal
cord levels supply
nerves for different
regions of the
body
 Physiology and function
• Grey matter – sensory and motor nerve cells

• White matter – ascending and descending

tracts
• Divided into - dorsal
- lateral
- ventral
http://www.accessmedicine.com/content.aspx?aID=2904376
• Posterior column and lateral corticospinal
tract crosses over at medulla oblongata

• Spinothalamic tract crosses in the spinal cord

and ascends on the opposite side

NB to understand this as it helps to understand

the clinical features of injury patterns and the
neurological deficit
 Dermatomes
• Area of skin innervated by sensory axons
within a particular segmental nerve root
• Knowledge is essential in determining level of
injury
• Useful in assessing improvement or
deterioration
Downloaded from: Rosen's Emergency Medicine (on 29 April 2009 06:34 PM)
© 2007 Elsevier
 Myotomes
• Segmental nerve root innervating a muscle
• Again important in determining level of injury

• Upper limbs:
C5 - Shoulder abduction
C6 - Wrist extensors
C7 - Elbow extensors
C8 - Long finger flexors
T1 - Small hand muscles
• Lower Limbs :
L2 - Hip flexors
L3,4 - Knee extensors
L4,5 - S1 - Knee flexion
L5 - Great Toe/Ankle dorsiflexion
S1 - Great Toe/Ankle plantar flexion
 Anatomy review
• Spinal cord ends at L1-L2

• Dural sac ends at S2

• Terminology
– Conus medullaris: most
distal bulbous part
– Filum termiale: tapering
part of conus medullaris
(mostly fibrous tissue)
– Cauda equina: distal
collection of nerve roots

http://en.wikipedia.org/wiki/Filum_terminale
 Conus vs Cauda
• Spinal cord ends at L1-L2

• Dural sac ends at S2

• Terminology
– Conus medullaris: most
distal bulbous part
– Filum termiale: tapering
part of conus medullaris
(mostly fibrous tissue)
– Cauda equina: distal
collection of nerve roots

http://en.wikipedia.org/wiki/Filum_terminale
 Conus vs Cauda
Conus
Sudden and bilateral onset
Radicular pain less prominent
More low back pain
Symmetric, distal, hyperreflexic
paresis
Symmetric, bilateral, typically
perianal area sensory loss,
sensory dissociation occurs
Early spincter signs
Cauda
Gradual and unilateral onset
Radicular pain more prominent
Less low back pain
Asymmetric, areflexic paraplegia
Asymmetric, unilateral, typically
saddle area, no sensory
dissociation
Late spincter signs
 The real estate of cord
compression…location is key!
• Intradural intramedullary:
– astrocytomas, ependymomas,
hemangioblastomas (primary
spinal tumours)

• Intradural extramedullary:
– Meningiomas
– nerve sheath tumours
(schwannomas and
neurofibromas)

• Epidural: metastases
http://www.emory.edu/ANATOMY/AnatomyManual/back.html
 Intramedullary vs Extramedullary
Intramedullary Extramedullary

Poorly localized burning pain Prominent radicular pain

“sacral sparing” Early sacral sensory loss

Corticospinal tract signs Early spastic weakness in legs

appear later

Usually rapid progression Usually slow progression

(usually malignant lesion) (usually benign lesion)
 Cord compression….
One of the only true neurological
emergencies…
where time is of the essence (i.e.
drop everything else you’re doing)
 Differential Diagnosis
• Common causes
– Neoplasm
– Fracture
– Cervical / lumbar stenosis
– Herniated disk
– Spinal infection/abscess
– Spinal hemorrhage
– Conus medullaris lipomas

• Mimickers
– Anterior spinal artery infarction
– Spinal AVMs
– Multiple sclerosis / transverse myelitis
– Neurosarcoidosis
– Plexopathy
 Location (Neoplasm)

Thoracic spine 60%

Lumbosacral spine 30%
Cervical spine 10%
 Pathophysiology - Epidural Mets
1) Hematogenous spread to bone marrow
– Most common mechanism
– Most at vertebral mass

2) Direct invasion through intervertebral foramina from paravertebral

source
– Second most common mechanism
– Typical of lymphoma

3) Retrograde venous spread

– With increased abdominal pressure, abdo/pelvis venous system
drains via Batson paravertebral plexus to epidural venous plexus
– Common for pelvic tumours (prostate)
 Pathophysiology - Cord Damage
• Severity
– Mild: minor Asx indentation of thecal sac
– Severe: strangulation of cord with paraplegia

• Progression
– Epidural venous plexus obstructed  BBB breakdown 
vasogenic edema  PGD (hence utility of steroids)
– First WM involved  demyelination
– Then GM involved  cord ischemia / infarction
– Irreversible damage if prolonged compression with cord
infarction (> 1 week)
 What is malignant spinal cord
compression?
• Occurs when cancer cells grow
in/near to spine and press on the
spinal cord & nerves

• Results in swelling & reduction in

the blood supply to the spinal
cord & nerve roots

• The symptoms are caused by the

increasing pressure
(compression) on the spinal cord
& nerves
 Epidemiology
• Most common
– Adults: lung, breast, prostate, lymphoma, sarcoma,
kidney
– Children: Ewing’s sarcoma, neuroblastoma, germ cell
neoplasms, Hodgkin’s lymphoma

• In cancer patients
– likelihood of epidural spinal cord compression 5-yrs
before death = 2.5%
– Vertebral metastases >>> ESCC
 That being said…

all patients with new back pain and

known malignancy have spinal cord
compression until proven otherwise
Now that you’ve thought of the Dx,
focus Hx and exam on:
1) Back pain
2) Weakness
3) Reflexes
4) Sensory loss
5) Spincter control
 Back Pain
• Initial complaint in 96%
• May precede neuro Sx by days or years (duration
related to tumour growth rate); average 7 weeks
• Constant, worse with coughing, sneezing, straining,
exercise
• Worse when supine (as opposed to disc disease)
• May be radicular (L’hermitte sign in cervical lesion,
“tight rope / band around chest” in thoracic lesions)
• Percuss / palpate chest to better localize pain
 Weakness
• Present in 80% initially (50% ambulatory; 35%
paraparetic; 15% paraplegic)
• Rate of progression depends on tumour growth
rate (30% become paraplegic in 1 week)
• Usu. paraplegia = cord infarction (likely
irreversible)
• Pattern of weakness depends on site of
compression
– e.g. above conus = pyramidal pattern
– T6-T10: Beevor sign
 Reflexes
• Hyperreflexia, upgoing toes (may not be seen
in cauda equina lesions)
• Abdominal reflexes (helpful if present and
asymmetric)
 Sensory loss
• Present in 78% of patients at diagnosis
• “Pins and needles,” “numb”
• Look for sensory level
– Begin distally, then ascend (use pin, go all the way up to
neck)
– Look for Brown-Sequard syndrome
– Usu 1-5 levels below actual compression
• Pattern as per site of compression
• Above cauda equina, if intramedullary  sparing of sacral
dermatomes
• At cauda equina  saddle anesthesia
 Spincters
• Urinary
– Contraction of detrusor muscle
innervated by S2-3-4
– Initially flaccid and distended
bladder  retention
– Then “decentralized bladder”
becomes active and shrinks,
bladder wall hypertrophies 
incontinence, frequency
– Ask about urination, palpate
bladder for fullness, bladder scan
and Foley insertion to document
urine volume
http://www.accessmedicine.com/content.aspx?
aID=707106&searchStr=neurogenic+bladder
 Spincters

• Rectal tone
– External anal sphincter
and puborectalis muscle
innervated by S3-4
– Loss of anal tone  stool
incontinence
– Similar mechanism for
bulbocavernosus reflex
– DRE, anal wink, tugging at
Foley http://www.netterimages.com/image/12555.htm
 What to image
• Always image entire spine:
– Spinal cord is shorter than vertebral spinal
column; imaging LS spine means you’re not
imaging the cord at all
– Exam is not always reliable for level of
compression
– Multiple sites of deposits are frequent in epidural
spinal cord metastases (1/3 of patients)
 Diagnosis
• MRI • CT myelography
– Test of choice – 2nd test of choice

ADVANTAGES ADVANTAGES
– Non-invasive – CSF can be obtained for
– No procedural complication (e.g. risk of analysis
herniation with brain mets, – Safe for claustrophobic
hemorrhage with coagulopathies, patients
neuro deterioration with CSF retrieval) – Safe for ferromagnetic implant
– Visualization of spinal parenchyma, (valves, PM, implants,
adjacent bone and soft tissues shrapnel)
– Can image entire spine even if – No movement artifact
subarachnoid block present
– Needed to plan radiation and Sx
 Treatment
• The obvious…
– Abscess: ABX, Sx
– Hematoma: correct coagulopathy, Sx
– Fracture / stenosis: Sx
• Goals of treatment for epidural metastases
– Pain control
– Preserve or improve neurological function
 Steroids (Decadron)
Initial presentation
Mild disease, no neurological Sx
Moderate disease, minimal
neurological dysfunction, < 80%
spinal block
Severe disease, significant
neurological dyxfunction
(paraparetic, paraplegic); > 80%
spinal block
Dose recommended
Forgo steroids
Low dose: 10mg x1 IV
then 4mg q6h;
then taper rapidly when definitive
Rx underway
High dose: 100mg x1 IV
then 24mg q6h x at least 72 hours
then taper gradually when
definitive Rx underway
 Steroids
• Clearly improve neurological outcome
• It seems no difference b/w initial dose of 10mg
or 100mg for mild disease
• Adverse effects (gastric ulcers, hyperglycemia,
psychosis, life threatening infections, etc)
 Radiotherapy
• RT portal: centered on spine, 2 vertebral bodies
above and below myelographic block
• No difference in functional outcome or overall
survival b/w different dosing regimens
• Protracted course had better local control of tumour
(less recurrence within field)
• Overall success depends on inherent radiosensitivity
of tumour, neuro status at onset of RTX, timing of
RTX (earlier better)
 Surgery
• Needed for tissue Dx if 1st presentation of cancer or
if spine instability
• Adverse effects (wound closure, infection, spinal
instability, nonfusion)
• May worsen pain
• Older trials (posterior approach):
– Sx + RTX = RTX alone
• Recent trials (anterior approach):
– Sx + RTX > RTX alone
• Future direction more geared toward Sx?
• Careful case-by-case selection
 Supportive

• Pain management (steroids usually relieve

pain, opioids help)
• Bedrest not helpful (except if has spine
instability)
• VTE prophylaxis: heparin sc, TED stockings,
compression
• Catheterization, laxatives
• Pressure sores
 Prognosis
• Most important Px factors: weakness at presentation
• Duration of Sx prior to presentation correlate with Px
• Sparing of sphincter and sacral sensory = good Px
• Px depends on radiosensitivity of tumour
• Children overall prognosis better than adults
• Median survival 6 months
• Recurrence rate 20%
 Early detection
– Inform patients with cancer who are at risk of MSCC
• information about the symptoms of MSCC
• what to do & who to contact if symptoms develop

– Discuss with the MSCC coordinator immediately patients

with cancer who have symptoms of spinal metastases &
neurological symptoms or signs suggestive of MSCC
• view as an emergency.

– Discuss with the MSCC coordinator within 24 hours patients

with cancer who have symptoms suggestive of spinal
metastases
 Take Home Messages
• Suspect spinal cord compression in all patients with cancer
and back pain, +/- weakness, sphincter signs
• Goal of history and exam:
– assess severity of neuro deficits (weakness, sensory, sphincter)
– localize lesion (pattern of weakness, sensory level)
• MRI if no contraindication, image whole spine
• Involve all relevant consultants
• No difference between high and low dose Decadron
• Act fast, prognosis directly related to duration and severity of
neuro deficits
• Overall poor prognosis, but pain control and optimize neuro
status crucial for palliation
 Spinal Cord Injury Classification
• Quadriplegia :
injury in cervical region
all 4 extremities affected

• Paraplegia :
injury in thoracic, lumbar or sacral segments
2 extremities affected
Injury either:

1) Complete

2) Incomplete
Complete:
i) Loss of voluntary movement of parts
innervated by segment, this is irreversible
ii) Loss of sensation
iii) Spinal shock
Incomplete:

i) Some function is present below site of

injury
ii) More favourable prognosis overall
iii) Are recognisable patterns of injury, although
they are rarely pure and variations occur
 Spinal Shock vs Neurogenic Shock

Spinal Shock :

• Transient reflex depression of cord function below level of

injury
• Initially hypertension due to release of catecholamines
• Followed by hypotension
• Flaccid paralysis
• Bowel and bladder involved
• Sometimes priaprism develops
• Symptoms last several hours to days
 Spinal shock
• Spinal shock : A period of decreased excitability of spinal cord at
and below level of lesion (all reflexes disappeared)
• Suppression of autonomic activity as well somatic activity
– a brief period of tachycardia and hypertension
– Followed by Neurogenic shock: prolonged bradycardia,
hypotension, reduction in cardiac output
– Acontractile and areflexic bladder
• Absent of somatic reflex activity and flaccid muscle paralysis
– Sphincter = residual tone
– retention (catheter / SPC / CISC)
• Last 6-12 weeks
 Spinal shock
• return of the bulbocavernosus reflex (anal
sphincter contraction in response to squeezing
the glans penis or tugging on the Foley)
signifies the end of spinal shock,
• Bladder contraction: Last to recover
• Majority of recovery in 1st 6 months
• More subtle changes up to 2 -5 years?
• Reflex recovery
– Reflex recovery1st = striated muscle of pelvic floor
– If BCR present: sacral miturition center intact
Neurogenic shock:
• Triad of i) hypotension
ii) bradycardia
iii) hypothermia
• More commonly in injuries above T6
• Secondary to disruption of sympathetic
outflow from T1 – L2
• Loss of vasomotor tone – pooling of blood
• Loss of cardiac sympathetic tone – bradycardia
• Blood pressure will not be restored by fluid infusion
alone
• Massive fluid administration may lead to overload
and pulmonary edema
• Vasopressors may be indicated
• Atropine used to treat bradycardia
 Types of incomplete injuries
i) Central Cord Syndrome

ii) Anterior Cord Syndrome

iii) Posterior Cord Syndrome

iv) Brown – Sequard Syndrome

v) Cauda Equina Syndrome

i) Central Cord Syndrome :

• Typically in older patients

• Hyperextension injury
• Compression of the cord anteriorly by
osteophytes and posteriorly by ligamentum
flavum
• Also associated with fracture dislocation and
compression fractures
• More centrally situated cervical tracts tend to
be more involved hence
flaccid weakness of arms > legs
• Perianal sensation & some lower extremity
movement and sensation may be preserved
ii) Anterior cord Syndrome:
• Due to flexion / rotation
• Anterior dislocation / compression fracture of
a vertebral body encroaching the ventral canal
• Corticospinal and spinothalamic tracts are
damaged either by direct trauma or ischemia
of blood supply (anterior spinal arteries)
Clinically:
• Loss of power
• Decrease in pain and sensation below lesion
• Dorsal columns remain intact
ii) Posterior Cord Syndrome:
Hyperextension injuries
with fractures of the posterior elements of
the vertebrae

Clinically:
• Proprioception affected – ataxia and
faltering gait
• Usually good power and sensation
iv) Brown – Sequard Syndrome:
• Hemi-section of the cord
• Either due to penetrating injuries:
i) stab wounds
ii) gunshot wounds
• Fractures of lateral mass of vertebrae
Clinically:
• Paralysis on affected side (corticospinal)
• Loss of proprioception and fine discrimination
(dorsal columns)
• Pain and temperature loss on the opposite
side below the lesion (spinothalamic)
v) Cauda Equina Syndrome:
• Due to bony compression or disc protrusions
in lumbar or sacral region

Clinically
• Non specific symptoms – back pain
- bowel and bladder dysfunction
- leg numbness and weakness
- saddle parasthesia
 In conclusion
Spinal Cord Injuries:
• Devastating event to both patient and
family.
• Huge impact on society
• After receiving First – World care in
tertiary institutions, many of our patients
return to impoverished communities
• Here they face huge challenges in terms of
survival
NEUROGENIC BLADDER
 DEFINITION

•refers to dysfunction of the urinary bladder

due to disease of the central nervous
system or peripheral nerves involved in the
control of micturition (urination).
SPASTIC NEUROGENIC
BLADDER
 LESIONS AT ABOVE T12

INTERRUPTED AFFERENT SIGNALS

EXCITATION OF NEURONS BELOW T12

SPONTANEOUS CONTRACTION
URINARY SPHINCTER SPASMS
OF DM
INTRAVESICAL VOIDING
UNCONTROLLED URINATION
PRESSURE
BLADDER WALL HYPERTROPHY
WITH TRABECULATION

REDUCED URINE-VOLUME
CAPACITY FREQUENT URINATION
FLACCID NEUROGENIC
BLADDER
 LESIONS AT OR BELOW S2/S4
INTERRUPTED AFFERENT SIGNALS BELOW S2/S4

LOW OF SENSATION OF BLADDER FILLING

RELAXATION OF POOR CONTRACTION OF
DETRUSOR MUSCLE DETRUSOR MUSCLE

INTRAVESICULAR PRESSURE

BLADDER CAPACITY (2000ML)

OVERDISTENDED BLADDER
BLADDER PRESSURE REACHES A RESIDUAL
BREAK THROUGH POINT
URINE
SMALL AMOUNTS OF URINE DRIBBLE RETENTION
 FLACCID BLADDER

•A flaccid, or hypotonic, bladder ceases to contract

fully, causing urine to dribble out of the body. Besides
the complications that stem from urine dripping,
rashes can occur in the area where urine pools. This
type of bladder disorder occurs when the volume of
urine is large but the pressure is low.
SPASTIC BLADDER

•A spastic, or reflex, bladder occurs when

the volume of urine is normal or small, but
there are involuntary contractions, causing
a person to feel the need to urinate even
when he doesn't need to release urine
Causes of Neurogenic Bladder

•Stroke
•Parkinson’s disease
•Multiple sclerosis
•Alzheimer’s disease
•Spina bifida and neural
disorders resulting from diabetes
or alcoholism
 Symptoms of Neurogenic Bladder

•Overactive bladder
•Frequent urination, in the daytime and at night
(nocturia)
•Stress incontinence
•Urge incontinence
•Inability to urinate (urinary retention)
•Underactive bladder – bladder is unable to signal
when full
 Treatment

•Medicines that relax the bladder (oxybutynin,

tolterodine, or propantheline)
•Medicines that make certain nerves more active
(bethanechol)
•Botulinum toxin (Botox)
•GABA supplements
•Antiepileptic drugs
thank you