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What is the role of anticoagulants in the immediate treatment of acute ischaemic stroke ?

What is the role of anticoagulants in the immediate treatment of acute ischaemic stroke ?  Anticoagulants (including unfractionated heparin, low molecular weight heparin or specific thrombin inhibitors) offer no short- or long-term benefits in the immediate treatment of acute ischaemic stroke. Although the risks of deep venous thrombosis or pulmonary embolus are significantly reduced, these benefits are offset by a dose-dependent increased risk of intracranial or extracranial bleeding.

What is the role of thrombolysis in acute stroke ?

What is the role of thrombolysis in acute stroke ?  Treatment with intravenous tissue plasminogen activator (tPA) when administered within 3 hours after onset of the ischaemic event (and in the absence of any sign of brain injury on CT) improves clinical outcome at 3 months (N Engl J Med 1995; 333: 1581-7). The CT scan in these patients must be examined very carefully for evidence of hemispheric brain ischaemia, which may increase the risk of deterio-ration, with or without cerebral haemorrhage, after thrombolytic treatment. An over-view of previous trials found significant excesses of early and total deaths, and of symptomatic and fatal intracranial haemorrhages, after acute thrombolysis, but a significant reduction in death or dependency in patients randomized to treatment within 3 hours of stroke onset (Lancet 1997; 350: 607-14). It remains unclear which patients are most likely to benefit or be harmed.

What are the measures used to determine the outcome after an acute stroke ?

What are the measures used to determine the outcome after an acute stroke ? Some of the standard measures include: * Barthel index is a reliable and valid measure of the ability to perform activities of daily living such as eating, bathing, walking and using the toilet. • Modified Rankin Scale is a simplified overall assessment of function in which a score of 0 indicates the absence of symptoms and a score of 5 shows severe disability. • Glasgow Outcome Scale is a global assessment of function in which a score of 1 indicates good recovery, a score of 2 moderate disability, a score of 3 severe disability, a score of 4 survival but in a vegetative state, and a score of 5 death. • NIH Stroke Scale, a serial measure of neurological deficit, is a 42-point scale that quantifies neurological deficits in 11 categories. For example, a mild facial paralysis is given a score of 1 and complete right hemiplegia with aphasia, gaze deviation, visual field deficit, dysarthria and sensory loss is

What are the causes of hemiplegia ?

What are the causes of hemiplegia ?   About 80% of all strokes are due to cerebral infarction resulting from thrombotic or embolic occlusion of a cerebral artery (J Neural   Neurosurg Psych 1990; 53: 16-22). The remaining 20% are caused by either intracerebral or subarachnoid haemorrhage.   Elderly: • Vascular event (thrombosis, embolism or haemorrhage). • Tumour. • Subdural haematoma. • Syphilis.   Youth:   • Multiple sclerosis.  • Tumour.  • Trauma.   • Embolism (look for underlying valvular heart disease, atrial fibrillation).  • Connective tissue disorder. • Neurosyphilis.   • lntracranial infection: look for underlying acquired immune deficiency syndrome (AIDS), otitis media, cyanotic heart disease.

What are the clinical features of spinal cord compression from epidural metastasis ?

What are the clinical features of spinal cord compression from epidural metastasis ?  The initial symptom is progressive axial pain, referred or radicular, which may last for days to months. Recumbency frequently aggravates the pain, unlike the pain of degenerative joint disease where it is relieved. Weakness, sensory loss and incon-tinence typically develop after the pain. Once a neurological deficit appears, it can evolve rapidly to paraplegia over a period of hours to days. In suspected cases MR! of the spine must be done by the next day. About 50% of cases in adults arise from breast, lung or prostate cancer. Compression usually occurs in the setting of dis-seminated disease. It is at the thoracic level in 70% of cases, lumbar in 20% and cervical in 10%, and occurs at multiple, non-contiguous levels in less than half of the cases. The tumour usually occupies the anterior or anterolateral spinal canal. CSF findings are non-specific in metastatic epidural compression. The cell coun

What is the characteristic type of diplegia in cerebral palsy ?

What is the characteristic type of diplegia in cerebral palsy ?  Diplegia associated with prematurity is a striking clinical entity striking for the symmetry of neurological signs, for their distribution, for the relatively good intelli-gence of the patients, and for the comparative absence of seizures, the disability often being purely motor without sensory deficits.

How do you localize the lesion to the 1st sacral root level ?

How do you localize the lesion to the 1st sacral root level ?   • Muscular weakness: plantar flexors, extensor digitorum brevis, peroneus longus, hamstrings.   • Deep tendon reflexes affected: ankle jerk.   • Radicular pain/paraesthesia: buttock, back of thigh, calf and lateral border of the loot.   • Superficial sensory deficit: lateral border of the foot.

How do you localize the lesion to the 5th lumbar root level ?

How do you localize the lesion to the 5th lumbar root level ?   • Muscular weakness: hamstrings, peroneus longus, extensors of all the toes.   • Deep tendon reflexes affected: none.   • Radicular pain/paraesthesia: buttock, posterolateral thigh, anterolateral leg, dorsum of [bot.   • Superficial sensory deficit: dorsum of the foot and anterolateral aspect of the leg.

What do you know about tropical spastic paraplegia ?

What do you know about tropical spastic paraplegia ?  This is seen in Japan, the Caribbean and parts of western Africaand South America where women, more often than men, in their third and fourth decades have spastic paraparesis with neurogenic bladder. Viral infection with human T-lympbotrophic virus I has been implicated as a cause of this disorder.

What do you know about hereditary spastic paraplegia ?

What do you know about hereditary spastic paraplegia ? This is an autosomal dominant condition, first described by Seeligmuller and Strumpell, in which spasticity is more striking than muscular weakness. The age of onset is variable and the condition has a relatively benign course. When the onset is in childhood, there may be shortening of the Achilles tendon, often requiring surgical lengthening. There is usually no sensory disturbance.

Where is the lesion in patients with spastic weakness of one leg ?

Where is the lesion in patients with spastic weakness of one leg ?  The lesion may be localized to the spinal cord or the brain.  Progression to involve the arm does not help to differentiate between the spinal cord or the brain.  Similarly, spread to the opposite leg does not necessarily indicate that the lesion is the spinal cord.  Full investigation would include radiography of the spine and CT, but if the latter is normal then myelography may be required.

What do you know about transverse myelitic syndrome ?

What do you know about transverse myelitic syndrome ? • Causes include: trauma, compression by bony changes or tumour, vascular disease. • All the tracts of the spinal cord are involved. • The chief clinical manifestation is spastic or flaccid paralysis. • The lesion can be incomplete cord compression or total cord transection:

What are the causes of spastic paraparesis ?

What are the causes of spastic paraparesis ?   Youth: • Trauma. • Multiple sclerosis. • Friedreich's ataxia. • HIV.   Adults': • Multiple sclerosis. • HIV (Neurology 1989; 39: 892). • Trauma (motor vehicle or diving accident). • Spinal cord tumour (meningioma, neuroma). • Motor neuron disease. • Syringomyelia. • Subacute combined degeneration of the cord (associated peripheral neuropathy). • Tabes dorsalis. • Transverse myelitis. • Familial spastic paraplegia.   Elderly: • Osteoarthritis of the cervical spine. • Vitamin deficiency. • Metastatic carcinoma. • Anterior spinal artery thrombosis. • Atherosclerosis of spinal cord vasculature.

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