Paraplegia

SPINAL CORD

VERTEBRAL LEVEL

From cervical segments- subtract 1 From upper thoracic segments- subtract 2 From lower thoracic segments- subtract 3 Lumbar 1-2 segments- T10 vertebra Lumbar 3-4 segments- T11 vertebra Lumbar 5 segments- T12 vertebra

SPINAL SHOCK is the phenomena surrounding transection of the spinal

cord that leads to temporary loss or depression of all or most spinal reflex activity below the level of a spinal lesion.

the period of spinal shock can last from hours to 6 weeks.

In the acute stage, there will be hypotonic paralysis, areflexia, loss of sensory function and dysautonomia. Patient shows retention of the bladder due to the impaired reflex of emptying the bladder.

In post acute stage, first autonomic reflexes come to normal.

In the chronic stage, there will be hypertonic paralysis, hyper-reflexia, spastic-reflex bladder. Patient at this stage shows incontinence.

Causes of flaccid paralysis

Anterior horn cells-poliomyelitis

Nerve root- radiculitis cauda equina

Peripheral nerves- GB syndrome,peripheral neuropathy

Myoneural junction- myasthenia gravis

Muscles – myopathy

hysterical

Causes of spastic paraplegia

CompressiveExtraduralPott`s diseaseMetastatic carcinoma

from breast, lung prostate

Multiple myelomaHerniated disc , fractureCervical spondylosis

IntraduralMeningioma ,

lymphoma ,metsEpidural abscessIntramedullarySpinal cord tumor

VascularArteriovenous malformationAntiphospholipid syndrome and other

hypercoagulable states InflammatoryMultiple sclerosis Transverse myelitisSarcoidosisVasculitis

Infectious Viral: HZV, HSV-1 and -2, CMV, HIVBacterial and mycobacterial: Listeria, syphilis, Mycoplasma pneumoniaeParasitic: schistosomiasis, toxoplasmosis MetabolicVitamin B12 deficiency (subacute combined

degeneration)

Syringomyelia

Trauma Tumour Tuberculosis Thrombosis Transverse myelitis

Differences between compressive and non compressive paraplegia

COMPRESSIVE NONCOMPRESSIVE

Bony changes Root pains Upper level of

sensory loss present

Zone of hyperesthesia may be present

No bony changes No root pains No definite level

Absent

Usually gradual onset

Asymmetrical involvement of limbs

Bladder bowel disturbance occurs

Usually acute onset

Symmetrical involvement of limbs

Occurs but late

Compressive Non compressive

Symptoms Intra medullary Extra medullary

Radicular pain nil common

Funicular pain common Less common

Vertebral pain unusual common

UMN signs late early

LMN signs Prominent and diffuse Unusual /segmental

Sensory involvement progression

Descending Ascending

Sphincter involvement Early Late

Trophic changes Common Unusual

Dissociated sensory loss Yes No

Sacral sensation Spared Lost

Transverse myelitis

Inflammation of the spinal cord at a single level. Symptoms develop rapidly and include limb weakness, sensory disturbance, bowel and bladder disturbance, back pain, and radicular pain. Recovery generally begins within 3mo. but is not always complete.

Causes: Idiopathic (thought to be autoimmune mechanism) Infection Vaccination Autoimmune disease e.g. SLE, sarcoidosis MS Malignancy Vascular e.g. thrombosis of spinal arteries, vasculitis 2° to

heroin abuse, spinal A-V malformation

Investigation MRI shows swelling of spinal cord Management Methylprednisolone injection followed by

oral prednisoloneGood recovery occur in 30% of cases

Spinal cord infarction

Anterior spinal artery infarction produces paraplegia or quadriplegia, sensory loss affecting pain/temperature but sparing vibration/position sensations (supplied by posterior spinal arteries), and loss of sphincter control.

Onset sudden or evolving over minutes or a few hours.

Associated conditions: aortic atherosclerosis, dissecting aortic aneurysm, hypotension.

Therapy is directed at the predisposing condition.

Subacute combined degeneration (vitamin B12 deficiency)

Paresthesia in hands and feet, early loss of vibration/position sense, progressive spastic/ataxic weakness, and areflexia due to associated peripheral neuropathy; mental changes and optic atrophy may be present. Diagnosis is confirmed by a low serum B12 level and a positive Schilling test. Treatment is vitamin replacement.

Hereditary spastic paraparesis

Isolated progressive paraparesis runs in some families. Inheritance is variable. Additional features including cerebellar signs, wasted hands and optic atrophy are sometimes seen. The paraparesis is usually mild and progresses slowly over many years. Some cases have dystonic features and respond to levodopa.

Syringomyelia

Tubular cavities (syrinxes) form close to the central canal of the spinal cord. As the syrinx expands, it compresses nerves within the spinal cord. Typically presents with wasting and weakness of hands and arms, and loss of temperature and pain sensation over trunk and arms (cape distribution)..

COMPLICATION

Skin care issues (Pressure sores) DVT Loss of bladder control & UTI Loss of bowel control Loss of sensory function Loss of motor function Depression

TREATMENT

Based on etiology Compressive – decompressive surgery ATM – steroids Supportive care Physiotherapy