Handbook of clinical neurology
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The cerebrospinal fluid (CSF) is a bodily fluid, which is both easily accessible and the most proximate to the pathological alterations of multiple sclerosis (MS). Consequently, the analysis of this fluid provides an important window into the pathological underpinnings of this disease. For example, for years, it has been known that the CSF of MS patients contains oligoclonal gamma immunoglobulins (IgG), which are synthesized within the central nervous system and presumably relate to the immune dysfunction, which is characteristically found in MS. ⋯ Thus, patients without a definite diagnosis who have CSF IgG bands are significantly more likely to develop definite MS compared to those patients without such a banding pattern. Other biological molecules can also be found in the CSF including neurofiliment, myelin basic protein (MBP), glial fibrillary acidic protein (GFAP), tau, neuronal cell adhesion molecule (NCAM), and the growth associated protein (GAP-43). However, the value of measuring these (and other) CSF constituents for both diagnostic and prognostic purposes and for following response to therapy is still to be determined.
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Increased survival of critically ill patients has focused the attention on secondary complications of intensive care unit (ICU) stay, mainly ICU-acquired weakness (ICUAW). ICUAW is relatively common with significant impact on recovery. Prolonging mechanical ventilation and overall hospitalization time, increased mortality, and persistent disability are the main problems associated with ICUAW. ⋯ The approach to the diagnosis and the yield of various techniques (mainly electrophysiological and histological) is discussed. Possible therapeutic interventions of this condition that modify the course of this deleterious situation and lead to better rehabilitation are discussed. The current postulated mechanisms associated with ICUAW (mainly the more frequent critical illness neuropathy and myopathy) are reviewed.
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Narrowing of the spinal canal or foramina is a common finding in spine imaging of the elderly. Only when symptoms of neurogenic claudication and/or cervical myelopathy are present is a spinal stenosis diagnosis made, either of the lumbar spine, cervical spine or both (only very rarely is the thoracic spine involved). Epidemiological data suggest an incidence of 1 case per 100 000 for cervical spine stenosis and 5 cases per 100 000 for lumbar spine stenosis. ⋯ Surgical strategy consists mainly of decompression (depending on the anatomical level and type of narrowing: laminectomy, foraminotomy, discectomy, corporectomy) with additional instrumentation should spinal stability and sagittal balance be at risk. For cervical spine stenosis the main objective of surgery is to halt disease progression. There is class 1b evidence that surgery is of benefit for lumbar stenosis at least in the short term.
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Bacterial meningitis is a neurologic emergency. Vaccination against common pathogens has decreased the burden of disease. Early diagnosis and rapid initiation of empiric antimicrobial and adjunctive therapy are vital. ⋯ Dexamethasone therapy has been implemented as adjunctive treatment of adults with pneumococcal meningitis. Adequate and prompt treatment of bacterial meningitis is critical to outcome. In this chapter we review the epidemiology, pathophysiology, and management of bacterial meningitis.
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Reversible cerebral vasoconstriction syndrome is characterized by severe headaches with or without focal neurologic deficits and/or seizures, and segmental constriction of cerebral arteries that resolves within 3 months. This increasingly recognized syndrome is supposedly due to a transient disturbance in the control of cerebral vascular tone with sympathetic overactivity. It can cause stroke in the young. ⋯ Convexity subarachnoid hemorrhage or stroke may occur a few days after initial normal imaging, and cerebral vasoconstriction is maximal on angiography 2-3 weeks after clinical onset. Symptomatic treatment includes rest and removal of vasoactive substances. Nimodipine has been proposed to reduce thunderclap headaches within 48 hours, but has no proven effect on the hemorrhagic and ischemic complications.