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.
COMPRESSIVE NONCOMPRESSIVE Bony changes No bony changes Root pains No root pains Upper level of No definite level sensory loss present Zone of Absent hyperesthesia may be present
Compressive Non compressive Usually gradual Usually acute onset onset Asymmetrical involvement of Symmetrical limbs involvement of Bladder bowel limbs disturbance occurs Occurs but late
Symptoms Intra medullary Extra medullaryRadicular pain nil commonFunicular pain common Less commonVertebral pain unusual commonUMN signs late earlyLMN signs Prominent and diffuse Unusual /segmentalSensory involvement Descending AscendingprogressionSphincter involvement Early LateTrophic changes Common UnusualDissociated sensory loss Yes NoSacral sensation Spared Lost
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 2Â° to heroin abuse, spinal A-V malformation
Investigation MRI shows swelling of spinal cordManagement Methylprednisolone injection followed by oral prednisoloneGood recovery occur in 30% of cases
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.
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.
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.
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)..
Skin care issues (Pressure sores) DVT Loss of bladder control & UTI Loss of bowel control Loss of sensory function Loss of motor function Depression
Based on etiology Compressive – decompressive surgery ATM – steroids Supportive care Physiotherapy
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