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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

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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

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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

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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

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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

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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