Seminars in neurology
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Neurological dysfunction is a common side effect of many chemotherapy drugs. For several agents neurotoxicity is common, severe, and can be dose-limiting. This is a review of the clinical features of chemotherapy-induced syndromes involving the central and peripheral nervous systems.
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Seminars in neurology · Sep 2004
ReviewThe restless legs syndrome and periodic limb movement disorder: a review of management.
The restless legs syndrome (RLS) and periodic limb movement disorder (PLMD) are distinguishable but overlapping disorders. Both feature nocturnal involuntary limb movements (periodic limb movements) that can cause sleep disruption, but each has distinct clinical features that are relevant to the diagnosis and management of the patient. The diagnosis of RLS is made by meeting established clinical criteria, not from discovery of periodic limb movements of sleep (PLMS) on a sleep study. ⋯ Anticonvulsants, opioids, and sedative/hypnotics also have a role. A treatment algorithm is provided to assist with the management of RLS. Treatment of PLMD relies on many of the same medications, but is generally more straightforward and places a greater reliance on levodopa compounds and sedative-hypnotics.
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Tick paralysis results from inoculation of a toxin from tick salivary glands during a blood meal. It is a relatively uncommon neuromuscular disease with a higher prevalence among young girls, although older men who get exposed to ticks may also be affected. It typically presents as an acute ascending paralysis occurring a few days after tick attachment and may result in respiratory failure and death. ⋯ These appear to result from a failure of acetylcholine release at the motor nerve terminal level. There may be subtle abnormalities of motor nerve conduction velocity and sensory action potentials. Removal of the tick results in the very rapid reversal of clinical and physiologic deficits, quicker with North American ticks than with the Ixodes species seen in Australia.
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Congenital myasthenic syndromes are genetic disorders of neuromuscular transmission that should be considered in the differential diagnosis of seronegative myasthenia gravis and other neuromuscular disorders. They are present at birth but may not manifest until childhood or adult life. ⋯ Some types of congenital myasthenia (e.g., slow-channel and fast-channel syndrome, acetylcholinesterase deficiency, and choline acetyltransferase deficiency) can be identified by clinical features, response to cholinesterase inhibitors, and standard electrodiagnostic studies. The molecular genetics, pathogenesis, clinical features, differential diagnosis, natural history, and treatment of well-characterized congenital myasthenic syndromes are discussed.
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Seminars in neurology · Mar 2004
ReviewMyasthenia gravis: management of myasthenic crisis and perioperative care.
Myasthenic crisis may be defined as respiratory failure or delayed postoperative extubation for more than 24 hours resulting from myasthenic weakness. Myasthenic crisis results from weakness of upper airway muscles leading to obstruction and aspiration, weakness of respiratory muscles leading to reduced tidal volumes, or from weakness of both muscle groups. About one-fifth of patients with myasthenia gravis experience crisis, usually within the first year of illness. ⋯ Common precipitating factors for myasthenic crisis include respiratory infections, aspiration, sepsis, surgical procedures, rapid tapering of immune modulation, beginning treatment with corticosteroids, exposure to drugs that may increase myasthenic weakness, and pregnancy. Myasthenic crisis should not be fatal, as long as patients receive timely respiratory support and appropriate immunotherapy to reduce myasthenic weakness of the upper airway and respiratory muscles. Myasthenic patients with oropharyngeal or respiratory muscle weakness should receive preoperative plasma exchange or intravenous immunoglobulin therapy to a minimal level of weakness to prevent postoperative complications.