Cns case-extramedullary compressive myelopathy, Q&A
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Transcript of Cns case-extramedullary compressive myelopathy, Q&A
1
What are the compressive causes for acute paraplegia?
ACUTE PARAPLEGIA
COMPRESSIVE CAUSES vertebral fracture or dislocation secondory to
trauma,secondaries,tuberculosis Disc prolapse Subdural haematoma / Epidural haematoma Haematomyelia Spinal epidural abscess bleeding from AV malformations
What are non-compressive causes of acute paraplegia?
NON COMPRESSIVE CAUSES
Demyelinating disease(TRANSVERSE MYELITIS) MS, Devic’s disease
Infective- Herpes zoster, HSV1,HSV2 Vascular –anterior spinal artery thrombosis Autoimmune-SLE,SARCOID
Mention a few causes of acute painful paraplegias
1. Anterior spinal artery thrombosis2. Vasculitis3. Sickle cell anaemia4. Subarachnoid hemorrhage5. Decompression sickness
What are the compressive causes for chronic paraplegia?
CHRONIC PARAPLEGIA
COMPRESSIVE CAUSES
1 DISEASES OF VERTEBRAL COLUMN osteitis (TB, syphilis) cervical spondylosis secondaries spine primary spinal tumour
2 DISEASES OF MENINGES Arachnoiditis(TB syphilis ) meningeal infiltration
3 INTRAMEDULLARY EXTRAMEDULLARY TUMOURS Meningioma /neurofibroma Lipoma Ependymoma Intramedullary metastasis
What are the non compressive causes for chronic paraplegia?
CHRONIC PARAPLEGIA
NON COMPRESSIVE CAUSES
• Multiple sclerosis• Subacute combined degeneration • HTLV 1• Lathyrism• Motor neuron disease• Radiation myelopathy• Hereditary spastic paraplegia
What are the types of bladder dysfunction that can occur in these patients
• Spastic or hyperreflexic bladder• Autonomous or atonic bladder• Motor paralytic bladder• Sensory paralytic bladder
Spastic bladder
• Occurs in lesions above the level of sacral centers and below the pontine center
• Loss of normal inhibition of detrusor during filling• Symptoms of frequency, urgency and urge
incontinence are seen• Bladder capacity is reduced but residual urine is
increased• Detrusor sphincter dyssynergia occurs• Bulbocavernous and superficial anal reflexes are
preserved
Atonic bladder
• Seen in complete lesions below T12 involving cauda equina and conus medullaris
• Bladder is paralysed and there is no sensation of bladder fullness
• Detrusor tone is abolished• Inability to initiate micturition, overflow
incontinence and increased residual volume are present
• Absent bulbocavernous and superficial anal reflexes
WHAT COMPLICATIONS OCCURRED IN THIS PATIENT AFTER SURGERY
post surgical worsening of motor weakness
Possibilities
1 AV malformation bleed2post surgical subdural /epidural haematoma3haematomyelia4Infections spinal epidural abscess5 damage to the cord during surgery
Haematomyelia
• Rare presentation• Hyperacute onset of symptoms that involve
spinal tracts (motor ;sensory or both)• Causes: truma;av malformation;bleeding
diathesis• Pathology involves bleeding into epidural or
subdural space causing compressive myelopathy
Spinal epidural abcess
• Staph aureus • Trauma to the back• Furunculosis /spinal surgery/ epidural
infusion(anesthesia)/cauda equina epidural abscess• Bactremia seeding of spinal epidural space or vertebrae osteomyelitis with extension into epidural space
Clinical presentation of spinal epidural abscess
• Low grade fever• Intense low back ache• Radicular pain• Headache with nuchal rigidity• Rapidly progressive paraparesis wih sensory loss
with sphincter paralysis• Spine tenderness• Examination: signs of complete or partial
transverse cord lesion
What are the differences between compressive and non compressive lesions
FINDING COMPRESSIVE LESION NON COMPRESSIVE LESION
BONY CHANGES Present Absent
ROOT PAIN Present Absent
SENSORY LEVEL Definite upper level No definite level(EXCEPT ATM)
ZONE OF HYPERAESTHESIA Maybe present Absent
ONSET Usually gradual Usually acute
SYMMETRY Usually asymmetrical Usually symmetrical
What are the differences between a INTRAMEDULLARY lesion and
EXTRAMEDULLARY lesion
FINDING INTRAMEDULLARY LESION EXTRAMEDULLARY LESION
RADICULAR PAIN Uncommon Common
VERTEBRAL PAIN Uncommon Common
FUNICULAR PAIN Common Less common
UMN SIGNS Late Early
LMN SIGNS Prominent and diffuse Unusual, if present are segmental
SENSORY INVOLVEMENT Disassociated sensory lossContralateral loss of pain and temperature with ipsilateral loss of proprioception
FINDING INTRAMEDULLARY LESION EXTRAMEDULLARY LESION
PARASTHESIA PROGRESSION Descending Ascending
SACRAL SPARING Absent Present
TROPHIC CHANGES Common Uncommon
BLADDER INVOLVEMENT Early Late
VERTEBRAL TENDERNESS Absent Present
CSF ANALYSIS Froin’s syndrome rare Froin’s syndrome common
Name the various types of clinical presentation of spinal cord syndromes
1. Complete cord transection2. Brown – sequard syndrome3. Central lesions like syringomyelia4. Posterolateral column syndrome like sub acute
combined degeneration5. Posterior column syndrome like tabes dorsalis6. Anterior horn cell syndrome7. Combined anterior horn cell – pyramidal tract
syndrome like Amyotrophic lateral sclerosis8. Anterior spinal artery syndrome
COMPLETE CORD transection
• All ascending tracts from below and descending tracts from above are interrupted
• Affects motor sensory and autonomic functions• Causes– Trauma– Metastatic carcinoma– Multiple sclerosis– Spinal epidural haematoma– Autoimmune disorders– Post vaccinial syndromes
• SENSORY– All sensations are affected– Sensory level is usually 2 segments below the level of lesion.– Segmental paresthesia occur at the level of lesion.
• MOTOR– Paraplegia due to corticospinal tract involvement– First spinal shock followed by hypertonic hyperreflexic paraplegia– Loss of abdominal and cremastric reflexes– At the level of lesion LMN signs occur
• AUTONOMIC– Urinary retention and constipation.– Anhidrosis ,trophic skin changes, vasomotor instability below the level of
lesion– Sexual dysfunction can occur
BROWN SEQUARDS SYNDROME
• Due to damage to one lateral half of spinal cord• SENSORY
– Ipsilateral loss of proprioception due to posterior column involvement
– Contralateral loss of pain and temperature due to involvement of lateral spinothalamic tract
• MOTOR– Ipsilateral spastic weakness due to descending corticospinal tract
involvement– LMN signs at the level of lesion
• Caused by extramedullary lesions• Usually caused by penetrating trauma or tumour
CENTRAL CORD SYNDROME
• Most common cause is syringomyelia• Other causes are hyperextension injuries of neck,
intramedullary tumours and trauma• Associated with Arnold chiari type 1 and 2 and
dandy walker malformation• SENSORY– Pain and temperature are affected– Touch and proprioception are preserved– Dissociative anaesthesia– Shawl like distribution of sensory loss
CENTRAL CORD SYNDROME
• MOTOR– Upper limb weakness > Lower limb weakness
• Other features include– Horners syndrome– Kyphoscoliosis– Sacral sparing– Neuropathic arthropathy of shoulder and elbow
joint• Prognosis is fair
POSTERIOR COLUMN SYNDROME
• Occurs due to neurosyphilis, diabetes mellitus• Usually occurs 10 to 20 years after infection• SENSORY– Impaired position and vibration sense in LL– Tactile and postural hallucinations can occur– Numbness or paresthesia are frequent complaints– Sensory ataxia– Positive Rhomberg’s sign, sink sign and Lhermittes
sign
• Abadie’s sign positive• Urinary incontinence• Absent knee and ankle jerk (areflexia,
hypotonia)• Abdominal and laryngeal crisis can occur• Charcots joint• Miotic and irregular pupil not reacting to light• Argyl Robertson pupil
POSTEROLATERAL COLUMN DISEASE
• Some of the causes– Vitamin B12 deficiency– AIDS– HTLV associated myelopathy– Cervical spondylosis
• SENSORY– Paresthesia in feet– Loss of proprioception and vibration in legs– Sensory ataxia– Positive Rhomberg’s sign
• Bladder atonia• MOTOR– Corticospinal tract involvement – spasticity,
hyperreflexia, bilateral Babinski sign• AIDS – associated dementia and spastic
bladder is present• HTLV associated myelopathy – slowly
progressive paraparesis and an increase in CSF IgG antibodies to HTLV1
ANTERIOR HORN CELL SYNDROMES
• MOTOR– Weakness, atrophy and fasciculations– Hypotonia with depressed reflexes– Muscles of trunk and extremities are affected
• Sensory system is not affected
• Anterior horn cell with pyramidal tract syndrome occurs in amyotrophic lateral sclerosis
• Affects both the anterior horn cells and corticospinal tract• Both LMN and UMN signs occur• Ant horn cell - Paresis, atrophy, fasciculations• Corticospinal tract – Paresis, spasticity and extensor plantar
response• Usually unilateral with muscle weakness• DTR often exaggerated• Superficial reflex - abdominal reflex is preserved• Bulbar and pseudo bulbar involvement occurs• Sensory system is not affected
ANTERIOR SPINAL ARTERY SYNDROME
• Conus medullaris is frequently involved.lies opposite to vertebral bodies T12 and L1.
• MOTOR– Flaccid and areflexic paraplegia
• SENSORY– Loss of pain and temperature– Preservation of position and vibration
• AUTONOMIC– Urinary incontinence– Spinal cord infarction usually occurs in T1 to T4 and L1 segment
• Occurs due to syphilitic arteritis, aortic dissection, atherosclerosis of aorta, SLE, AIDS, AV malformation
POST SPINAL ARTERY SYNDROME
• UNCOMMON• Loss of proprioception and vibratory sense• Pain and temperature is preserved• Absence of motor deficit
2
What are the cognitive dysfunction associated with paraplegia
Cognitive dysfunction in paraplegia
• Multiple sclerosis• HIV myelopathy with encephalopathy• Tabes dorsalis with general paresis of Insane• Subacute combined degeneration• Cerebral diplegia• Chronic hydrocephalus
What are the cerebral causes of paraplegia
Cerebral paraplegia
• The lower limbs and bladder (micturition centre) are represented in the paracentral lobule
• Lesions in this area produce paraplegia with bladder disturbances (retention) and cortical type of sensory loss
• Trauma: in parasaggital area• Tumour :parasaggital meningioma• Thrombosis: arterial : unpaired anterior cerebral artery• venous :sagittal sinus thrombosis• Internal hydrocephalus• cerbral diplegia
Cranial nerves and paraplegia
CRANIAL NERVES IN PARAPLEGIA
• Multiple sclerosis• Tabes dorsalis• Friedrich’s ataxia• Devic’s disease• Vitamin B12 deficiency• Hereditary spastic paraplegia• GBS
3
Paraplegia in flexion and
paraplegia in extension
• Muscle tone is maintained by spinal reflex arc, extrapyramidal system, corticospinal system and cerebellar inputs
• Partial transection of cord leading to selective corticospinal tract loss increase the role of the extrapyramidal tract resulting in increased tone of antigravity muscles resulting in PARAPLEGIA IN EXTENSION
• In complete transection of the cord, the spinal reflex arc takes over and there is a relative increase in the tone of flexors resulting in PARPALEGIA IN FLEXION
Paraplegia in extension
• pyramidal tract involved• Spinal cord lesion incomplete• Increased tone in extensors (antigravity muscles)• Hyperactivity of knee ankle jerks with clonus• Extensor spasm of lower limbs legs in adduction
and external rotation• Mass reflex absent• Prognosis better
Paraplegia in flexion
• Pyramidal tract extrapyramidal system involved
• Flexor spasticity• Legs thighs flexed• Knee ankle reflex absent Absent clonus• Mass reflex present • Worst prognosis
Mass reflex
• Any stimulation below the level of lesion produces an introceptive stimulus producing:
• Flexor spasm• Emptying of bladder and bowel• Seminal emission• Profuse sweating and piloerection
What are the causes of paraplegia with absent deep tendon reflexes
1. Neural shock(spinal)2. Radiculitis – the jerk whose root is involved
will be absent3. Peripheral neuropathy – bilateral ankle jerks
will be absent4. Reflex activity may be absent in presence of
severe infection due to suppression
4
WHAT ARE THE CAUSES OF PARAPLEGIA WITHOUT SENSORY LOSS
1. Hereditory spastic paraplegia2. Lathyrism 3. GB syndrome4. Amyotropic lateral sclerosis5. Fluorosis6. Erb’s spastic paralegia
PARAPLEGIA AND ATAXIA
• TABES DORSALIS• SUB ACUTE COMBINED DEGENERATION• PERIPHERAL NEUROPATHY
5
What are the important clinical features of tuberculosis spine
• Hematogenous spread• Most commonly involves lower thoracic and
upper lumbar vertebrae• Usually two contiguous vertebrae are involved
What are the causes of paraplegia in TB
• Subluxation and dislocation of vertebra• Granulation tissue• Arachnoiditis• Endarteritis• Cold abscess• Tuberculous myelitis• pachymeningitis
6
What is the ANATOMY OF THE LESION AND LEVELS OF LOCALISATION IN SPINAL CORD
DISEASE?
1. Motor level2. Sensory level3. Reflex level4. Autonomic level5. Vertebral level
What are the diagnostic clinical signs of lesions of spinal cord at various levels
FORAMEN MAGNUM
• Atrophy of sternomastoid muscle• Downbeat nystagmus• C2 sensory loss and cerebellar signs• Horner’s syndrome• Lower cranial nerve palsies
C5 – C6 lesion• LMN weakness of elbow flexors and extensors and spastic weakness of
lower limbs
• C5 lesion– Absent biceps and supinator reflexes– Inverted supinator jerk– Exaggerated triceps and finger flexor reflex– Sensory loss below the neck and anterior shoulder
• C6 lesion– Absent biceps, triceps and supinator reflexes– Exaggerated finger flexor reflex– Same as above but sparing of lateral arm
C7 lesion
• Weakness of wrist and finger flexors and extensors and spastic paraparesis
• Preserved biceps and supinator reflexes• Exaggerated finger flexor reflex• Inverted triceps reflex• Sensory loss at and below 3rd and 4th digits,
medial forearm and arm
C8 – t1 lesion
• Weakness of small muscles of the hand with spastic paraparesis
• C8 lesions leads to absent triceps and finger flexor reflex
• T1 lesions spare triceps reflex• Unilateral or bilateral Horner’s syndrome• Sensory involvement from the 5th digit, medial
forearm and arm
Thoracic lesions
• T4 – sensory impairment below the nipples• T6 or higher – absent abdominal reflexes• T10 – positive Beevor’s sign• T12 – preservation of abdominal reflex
L1 lesion
• All muscles of the lower limb are weak• Sensory loss below the groin• Absent cremasteric reflex• Brisk knee and ankle reflexes
L2 lesion
• Spastic paraparesis• Absent cremasteric reflex• Knee jerk may be depressed• Ankle jerk is brisk• Normal sensation on upper anterior aspect of
thigh
L3 lesion
• Preservation of hip flexion and leg adduction• Absent knee jerk• Exaggerated ankle jerk
L4 LESION
• Preservation of hip flexion, knee flexion, leg extension and adduction
• Absent knee jerk• Exaggerated ankle jerk• Normal sensation on upper anterior aspect of
thigh and superomedial aspect of knees
L5 LESION
• Normal hip flexion and adduction and leg extension
• Knee jerk is preserved• Ankle jerk is exaggerated• Sensory function is preserved in the anterior
aspect of thighs, medial aspect of legs, ankles and soles
What are the differences between a conus medullaris lesion and cauda equina
lesion
FINDING CONUS MEDULLARIS LESION CAUDA EQUINA LESION
SYMMETRY Symmetrical involvement of both lower limbs
Asymmetrical involvement of both lower limbs
ROOT PAIN Absent Present, usually severe
SENSORY INVOLVEMENT Bilateral saddle anesthesia Asymmetrical sensory loss
BULBOCAVERNOUS AND ANAL REFLEXES Absent Depends on involved roots
BLADDER AND BOWEL INVOLVEMENT Common Less common
PLANTAR REFLEX Extensor Flexor or not elicitable
What is the management of neoplasm induced paraplegia?
• Glucocorticoids to reduce cord edema (up to 40 mg of dexamethasone daily)
• Local radiotherapy to the symptomatic lesion (3000 cGy in 15 daily fractions)
• Specific therapy for the underlying tumour type• Surgical decompression by laminectomy or
vertebral body resection in severe cases• Fixed motor deficits once established have very
poor prognosis