Spinal Cord Disorders UWKS

  

Neurogenic Bladder, Acute Medullar

Compression, and Complete Spinal

Transection

  Christian Kamallan Neurology Department U W K S

  

Anatomy of

the spine Diferent spinal cord levels supply nerves for diferent 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

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

Myotomes

• Segmental nerve root innervating a muscle
• Again important in determining level of injury
• Upper limbs:

  C - Shoulder abduction ₅ C - Wrist extensors ₆ C - Elbow extensors ₇ C - Long fnger fexors ₈

• Lower Limbs :

  L - Hip fexors ₂ L - Knee extensors _3,4 L - S - Knee fexion _{4,5 1} L - Great Toe/Ankle dorsifexion ₅ S - Great Toe/Ankle plantar ₁ fexion

  Anatomy review

• Spinal cord ends at
• Dural sac ends at

  S2

• Terminology
• – Conus medullaris :

  most distal bulbous part

• – Filum termiale :

  tapering part of conus medullaris (mostly fbrous tissue)

• – Cauda equina : distal

  collection of nerve

  Conus vs Cauda

• Spinal cord ends at
• Dural sac ends at

  S2

• Terminology
• – Conus medullaris :

  most distal bulbous part

• – Filum termiale :

  tapering part of conus medullaris (mostly fbrous tissue)

• – Cauda equina : distal

  collection of nerve

  Conus vs Cauda Conus ^Cauda _{Sudden and bilateral onset Gradual and unilateral onset}

  Radicular pain less prominent Radicular pain more prominent _{More low back pain Less low back pain} Symmetric , distal, hyperreflexic _paresis ^{Asymmetric , areflexic paraplegia} Symmetric, bilateral, typically _{perianal area sensory loss, sensory dissociation occurs} ^{Asymmetric, unilateral, typically} _{saddle area, no sensory dissociation} Early spincter signs 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 neurofbromas) _{http://www.emory.edu/ANATOMY/AnatomyManual/back.html}

  

Intramedullary vs

_{Intramedullary Extramedullary} Extramedullary Poorly localized burning pain Prominent radicular pain “sacral sparing” Early sacral sensory loss _{appear later}

Corticospinal tract signs Early spastic weakness in legs

_{(usually malignant lesion) (usually benign lesion)} Usually rapid progression Usually slow progression

  

Cord compression….

One of the only true neurological emergencies…

  where time is of the essence (i.e. drop everything else

you’re doing)

Diferential Diagnosis

• Common causes _{– Fracture – Neoplasm – Spinal infection/abscess – Herniated disk} – Cervical / lumbar stenosis _{– Conus medullaris lipomas} – Spinal hemorrhage
• Mimickers _{– Spinal AVMs – Anterior spinal artery infarction – Plexopathy – Neurosarcoidosis} – Multiple sclerosis / transverse myelitis

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
• – Severe: strangulation of cord with paraplegia

  Mild: minor Asx indentation of thecal sac

• – 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) Refexes 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

Refexes

• Hyperrefexia, upgoing toes (may not be seen in cauda equina lesions)
• Abdominal refexes (helpful if present and asymmetric)

  Above cauda equina, if intramedullary  sparing of sacral dermatomes

• _• At cauda equina  saddle anesthesia

  

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 _•

  Spincters _– Urinary

• Contraction of detrusor muscle innervated by S2-3- _–

  distended bladder  retention ^– Then “decentralized bladder” becomes active and shrinks, bladder wall hypertrophies  _– incontinence, frequency Ask about urination, palpate bladder for fullness, _{content.aspx? http://www.accessmedicine.com/} bladder scan and Foley _{aID=707106&searchStr=neurogenic+} insertion to document urine _bladder

  

Spincters

• Rectal tone
• – External anal sphincter and puborectalis muscle innervated by S3-4
• – Loss of anal tone 

  stool incontinence

• – Similar mechanism for bulbocavernosus

  refex _{http://www.netterimages.com/image/12555.htm} DRE, anal wink,

• – tugging at Foley

  

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
• – Test of choice

  myelography

• – 2nd test of choice

  ADVANTAGES

• – Non-invasive

  ADVANTAGES

• – No procedural complication
• – CSF can be obtained for (e.g. risk of herniation with analysis brain mets, hemorrhage with
• – Safe for claustrophobic coagulopathies, neuro patients deterioration with CSF
• – Safe for ferromagnetic retrieval)

  implant (valves, PM,

• – Visualization of spinal implants, shrapnel) parenchyma, adjacent bone
• – No movement artifact and soft tis
• – Can image entire spine even if subarachnoid block present

  

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 Dose recommended Mild disease , no neurological Sx Forgo steroids _{Moderate disease , minimal} neurological dysfunction, < 80% _{spinal block} ^{Low dose: 10mg x1 IV} _{then 4mg q6h; then taper rapidly when definitive} Rx underway _{Severe disease , significant} neurological dyxfunction _{(paraparetic, paraplegic); > 80% spinal block} ^{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 diference b/w initial dose of 10mg or 100mg for mild disease
• Adverse efects (gastric ulcers, hyperglycemia, psychosis, life threatening infections, etc)

  

Radiotherapy

• RT portal: centered on spine, 2 vertebral bodies above and below myelographic b>No diference in functional outcome or overall survival b/w diferent dosing regi
• Protracted course had better local control of tumour (less recurrence within feld)
• Overall success depends on inherent

  radiosensitivity of tumour, neuro status at

  Surgery ^st

• Needed for tissue Dx if 1 presentation of

  cancer or if spine instability

• Adverse efects (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

• presentation

  Most important Px factors: weakness at

• 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

  

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 defcits (weakness, sensory,

  sphincter) (pattern of weakness, sensory level)
• – localize lesion
>MRI if no contraindication, image whole spine
• Involve all relevant consultants
• No diference between high and low dose Decadron

  • Act fast, prognosis directly related to duration and

  severity of neuro defcits
• Overall poor prognosis, but pain control and

Spinal Cord Injury Classifcation

• Quadriplegia : injury in cervical region all 4 extremities afected
• Paraplegia : injury in thoracic, lumbar or sacral segments 2 extremities afected

  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 refex 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 refexes

  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 arefexic bladder
• Absent of somatic refex activity and faccid muscle paralysis
• – Sphincter = residual tone

Spinal shock

• • return of the bulbocavernosus refex (anal

  sphincter contraction in response to squeezing the glans penis or tugging on the Foley) signifes 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?
• Refex recovery
• – Refex recovery1st = striated muscle of pelvic foor
• – If BCR present: sacral miturition center intact

  Neurogenic shock:

• Triad of i) hypotension ii) bradycardia iii) hypothermia
• More commonly in injuries above T
6<
• Secondary to disruption of sympathetic outfow from T – L
_{1 2}
• Loss of vasomotor tone – pooling of blood
• Loss of cardiac sympathetic tone – bradycardia
• Blood pressure will not be restored by fuid infusion alone
• Massive fuid 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

• Typically in older patients
• Hyperextension injury
• Compression of the cord anteriorly by osteophytes and posteriorly by ligamentum favum
• 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 &amp; some lower extremity movement and sensation
• Due to fexion / 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

  Hyperextension injuries with fractures of the posterior elements of the vertebrae

  Clinically:

• Proprioception afected – 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 afected side

  (corticospinal)

• Loss of proprioception and fne 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 specifc symptoms – back pain
• bowel and bladder dysfunction
• leg numbness and weakness
• saddle parasthesia
Spinal Cord Injuries:

  

In conclusion

• 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

  

refers to dysfunction of the urinary

refers to dysfunction of the urinary

• bladder due to disease of the central

  bladder due to disease of the central

  nervous system or peripheral nerves

  nervous system or peripheral nerves

  involved in the control of micturition involved in the control of micturition (urination). (urination).

  Types of Neurogenic Bladder

  

SPASTIC NEUROGENIC

BLADDER

SPASTIC NEUROGENIC

BLADDER

  LESIONS AT ABOVE T12 LESIONS AT ABOVE T12

  INTERRUPTED AFFERENT SIGNALS

  INTERRUPTED AFFERENT SIGNALS

EXCITATION OF NEURONS BELOW T12

EXCITATION OF NEURONS BELOW T12

SPONTANEOUS CONTRACTION OF DM SPONTANEOUS CONTRACTION OF DM URINARY SPHINCTER SPASMS URINARY SPHINCTER SPASMS

  INTRAVESICAL VOIDING PRESSURE

  INTRAVESICAL VOIDING PRESSURE BLADDER WALL HYPERTROPHY WITH TRABECULATION BLADDER WALL HYPERTROPHY WITH TRABECULATION REDUCED URINE-VOLUME CAPACITY REDUCED URINE-VOLUME CAPACITY UNCONTROLLED URINATION UNCONTROLLED URINATION FREQUENT URINATION FREQUENT URINATION

  LESIONS AT OR BELOW S2/S4 LESIONS AT OR BELOW S2/S4

  INTERRUPTED AFFERENT SIGNALS BELOW S2/S4

  INTERRUPTED AFFERENT SIGNALS BELOW S2/S4 LOW OF SENSATION OF BLADDER FILLING LOW OF SENSATION OF BLADDER FILLING RELAXATION OF DETRUSOR MUSCLE RELAXATION OF DETRUSOR MUSCLE POOR CONTRACTION OF DETRUSOR MUSCLE POOR CONTRACTION OF DETRUSOR MUSCLE

  INTRAVESICULAR PRESSURE

  INTRAVESICULAR PRESSURE BLADDER CAPACITY (2000ML) BLADDER CAPACITY (2000ML) OVERDISTENDED BLADDER OVERDISTENDED BLADDER BLADDER PRESSURE REACHES A BREAK THROUGH POINT BLADDER PRESSURE REACHES A BREAK THROUGH POINT SMALL AMOUNTS OF URINE DRIBBLE SMALL AMOUNTS OF URINE DRIBBLE RESIDUAL URINE RETENTION RESIDUAL URINE RETENTION

• 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.

• • 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 Causes of Neurogenic Bladder

• • Stroke

  • Stroke

  • Parkinson’s disease

• • Parkinson’s disease>

  • Multiple sclerosis

• • Multiple sclerosis>

  • Alzheimer’s disease

• • Alzheimer’s disease>Spina bifida and neural

• Spina bifida and neural disorders resulting from diabetes disorders resulting from diabetes or alcoholism or alcoholism

  

Symptoms of Neurogenic Bladder

Symptoms of Neurogenic Bladder

  Overactive bladder Overactive bladder

  Frequent urination, in the daytime and at night Frequent urination, in the daytime and at night

• (nocturia) (nocturia)

  Stress incontinence Stress incontinence

  Urge incontinence Urge incontinence

  Inability to urinate (urinary retention) Inability to urinate (urinary retention)

  Underactive bladder – bladder is unable to signal Underactive bladder – bladder is unable to signal

• when full when full

Treatment

  Medicines that relax the bladder (oxybutynin, Medicines that relax the bladder (oxybutynin,

• tolterodine, or propantheline) tolterodine, or propantheline)

  Medicines that make certain nerves more active Medicines that make certain nerves more active

• (bethanechol) (bethanechol)

  Botulinum toxin (Botox) Botulinum toxin (Botox)

  GABA supplements GABA supplements

  Antiepileptic drugs

• Antiepileptic drugs

  thank you