Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027066 (myoclonus)
 4,275 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The clinical pattern of typhoid fever is changing, and in particular the incidence of neuro-psychiartic manifestations is on the increase. In 246 cases of enteric fever we found 124 with confusional states, delirium, coma, generalized myoclonus, Parkinsonian rigidity or psychoses. We further distinguished two major sub-groups with an acute and an insidious onset. The apparent increase in the frequency of neuro-psychiatric complications of typhoid could represent a change in the pathogenicity of S. typhi or the increasing recognition of a biochemical defect caused by a bacterial endotoxins and provoked by poor nutrition.
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PMID:Neuro-psychiatric manifestations of typhoid. 59 55

Although there is evidence that the delirium, stupor, coma, and seizure-like activity seen in overdosage with tricyclic antidepressants and antiparkinson drugs are due to the central anticholinergic activity of these agents, patients with overdosage of these drugs are still frequently misdiagnosed. The authors present a case of reversal of anticholinergic-drug-induced prolonged coma, myoclonus, and choreoathetosis by physostigmine. This report supports the anticholinergic basis of the clinical manifestations of such overdosages, provides information on the role of acetylcholine and dopamine in psychiatric and movement disorders, and illustrates dramatically the need for accurate diagnosis and treatment.
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PMID:Reversal of tricyclic-overdosage-induced central anticholinergic syndrome by physostigmine. 96 21

The authors review the literature describing the neural symptoms induced by tricyclic antidepressants, especially tremor, seizures, akathisia, myoclonus, dyskinesia and delirium. Sedation, modifications of sleep, memory and appetite are also described. Tremor and myoclonus are the most frequent drug-induced neural symptoms. Delirium is most often caused by high-dosage treatments. The pathophysiology of akathisia and dyskinesia raises important questions concerning the mode of action of antidepressants.
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PMID:Neural symptoms induced by tricyclic antidepressants: phenomenology and pathophysiology. 131 56

An autopsy case of ataxic form of Creutzfeldt-Jakob disease (Brownell and Oppenheimer, 1965) was reported. The patient, a 71-year-old male, noticed ataxic gait at the beginning of June in 1988, and was admitted to the Hiroshima City Hospital for the neurological examination at the end of June. He showed ataxia of the left arm and legs and diplopia. Gradually he became delirious at night. On July 16, tremor-like involuntary movement of the left hand was noticed. On July 20, he became somnolent and doubly incontinent. Myoclonus and paratonic rigidity were also observed. The EEG showed periodic synchronous discharge on July 25. The brain CT and MRI were normal. He became apallic gradually and died on October 28. The duration of illness was 5 months. At autopsy, brain weighed 1000gr. Cerebral atrophy and slight enlargement of the ventricles were observed. The cerebellum was also slightly atrophic. Histologically, the destruction of the cerebral cortical layer, slight sieve-like spongy state of the neuropil, slight neuronal loss of the thalamus and sieve-like spongy state of the striatum were observed. The cerebellar lesion was the most severe, where granular cell loss and gliosis of the cortex were observed.
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PMID:[An autopsy case of ataxic form of Creutzfeldt-Jakob disease]. 156 39

A case of sporadic shigellosis is reported. A 30 year old woman, presented neurologic dysfunction, mild watery diarrhea and fever which had started one week before her admission. Abdominal tenderness, confusion, delirium, impairment of orientation and of recent memory were found. Abnormal motor activity with rigidity, tremors, myoclonus around the mouth also existed. There were neither focal signs nor signs of meningeal irritation. Computed tomography and nuclear magnetic resonance of the brain were normal. Laboratory analyses did not explain the anomalies. Several deep ulcers were disclosed by colonoscopy and a S. flexneri was isolated from the material extracted by endoscopy. Nonspecific colitis was informed by pathology. The patient was treated with 400 mg ciprofloxacin for 14 days, with improvement of the clinical picture. The most prominent aspect in this case was the clinical presentation with predominant neurologic symptoms creating the impression of a primary nervous system disease. Admission diagnosis was viral encephalitis. We believe that all of the anomalies present in our patient, the diarrhea and encephalopathy, were produced by the same etiologic agent, S. flexneri and by its toxins.
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PMID:[Encephalopathy in an adult with Shigella]. 192 94

We describe a 37-year-old man with a 30-month history of progressive dementia, myoclonus and prominent ataxia with the additional clinical features of dysautonomia and delirious psychomotor excitement and with relatively preserved verbal responses. The pathological changes include 1) severe neuronal loss and gliosis without spongiform change of the thalamus and inferior olives associated with gliosis of the midbrain tegmentum, and demyelination and gliosis of the central tegmental tract, olivo-cerebellar fibers and spino-olivary tract, and 2) mild spongiform encephalopathy of the cerebral cortex. Although the latter implies that the present case may be an example of the rare thalamic form of Creutzfeld-Jakob disease, the preferential and severe involvement of the thalamus and inferior olives without spongiform change as well as the clinical features are quite reminiscent of primary thalamic degeneration [Stern 1939]. This case draws further attention to the relationship between spongiform encephalopathy and degeneration without spongiform change of the thalamus and olivary system.
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PMID:Degeneration of the thalamus and inferior olives associated with spongiform encephalopathy of the cerebral cortex. 329 94

A case of episodic delirium with incapacitating myoclonus associated with therapeutic doses of phenelzine is described. No evidence of epilepsy was found. The delirium and the myoclonus remitted rapidly after phenelzine was stopped and treatment with a benzodiazepine was started. No previous reports of the association of phenelzine with myoclonus and delirium have been found. The possible neurophysiology of the association is explored. Treatment with phenelzine should be reviewed if myoclonus occurs.
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PMID:Myoclonus and episodic delirium associated with phenelzine: a case report. 361 Oct 37

Irrespective of the etiology, a water and electrolyte imbalance provoking a hypo- or hyperosmolar state causes metabolic encephalopathy, as may occur with any metabolic disturbance. The pathophysiology of metabolic encephalopathy relies on a diffuse neuronal dysfunction which occasionally shows a focal maximum. To the clinician it presents in the form of nonspecific symptoms or signs, such as altered level of alertness or awareness of the environment, or impaired attention, cognition or orientation. When the onset of hypo- or hyperosmolality is rapid, delirium may develop or the level of consciousness can decrease to the point of coma. Myoclonic jerks, gait disturbance and focal or generalized fits are additional nonspecific signs. When the water and electrolyte imbalance coincides with or is caused by brain disease, the signs of the two conditions are added. On the other hand, complicating hemorrhages, sinus thrombosis, or brainstem herniation or compression may be taken for a primary structural brain lesion, and the water and electrolyte imbalance may easily be overlooked. Pathophysiology, symptoms and signs, and therapy of hypo- and hyperosmolar states are discussed. Central pontine myelinolysis is considered separately.
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PMID:[Neurologic manifestations of osmolality disorders]. 389 13

Among patients with renal failure, there have been impressive modifications of both the duration and quality of life as a result of dialysis, renal transplantation, and improved medical management. However, patients who have renal failure continue to manifest a variety of neurologic disorders. Patients with chronic renal failure who have not yet received dialytic therapy may develop a symptom complex progressing from mild sensorial clouding to delirium and coma, with tremor, asterixis, multifocal myoclonus, and seizures. Even after the institution of otherwise adequate maintenance dialysis therapy, patients may continue to be afflicted with more subtle nervous system dysfunction, including impaired mentation, generalized weakness, and peripheral neuropathy. The central nervous system disorders of both untreated renal failure and that persisting despite dialysis are referred to as uremic encephalopathy. The dialytic treatment of end stage renal disease has itself been associated with the emergence of two distinct, new disorders of the central nervous system: Dialysis dysequilibrium and dialysis dementia. The dialysis disequilibrium syndrome consists of headache, nausea, muscle cramps, obtundation and seizures, and is a consequence of the initiation of dialysis therapy in some patients. Dialysis dementia is a progressive, generally fatal encephalopathy which affects patients on chronic hemodialysis. This disease also appears to be a complication of the therapy for renal failure.
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PMID:Pathogenesis of dialysis encephalopathy. 636 3

Patients with renal failure may manifest a variety of neurologic disorders. Patients with chronic renal failure who have not yet received dialytic therapy may develop a symptom complex progressing from mild sensorial clouding to delirium and coma, with tremor, asterixis, multifocal myoclonus, and seizures. After the institution of adequate maintenance dialysis therapy, patients may continue to be afflicted with more subtle nervous dysfunction, including impaired mentation, generalized weakness, and peripheral neuropathy. These central nervous system disorders are referred to as uremic encephalopathy. The dialytic treatment of end-stage renal disease has itself been associated with the emergence of two distinct, new disorders of the central nervous system; dialysis dysequilibrium and dialysis dementia. The dialysis disequilibrium syndrome consists of headache, nausea, muscle cramps, obtundation, and seizures, and is a consequence of the initiation of dialysis therapy in some patients. Dialysis dementia is a progressive, generally fatal encephalopathy which affects patients on chronic hemodialysis. There are at least three different forms of dialysis encephalopathy: sporadic, epidemic; and that associated with renal disease in children. In addition to the foregoing neurologic diseases which are specifically related to uremia and/or dialysis, a number of other neurologic disorders occur with increased frequency in patients with end-stage renal disease on chronic hemodialysis. These include subdural hematoma, electrolyte disorders, vitamin deficiencies, drug intoxication, hypertensive encephalopathy, and acute trace element intoxication. Renal transplantation is associated with a variety of central nervous system infections, reticulum cell sarcoma, and central pontine myelinosis. The present manuscript will review the clinical, structural, and biochemical components of those neurologic disorders which are peculiar to the uremic state and its treatment with dialysis.
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PMID:Uremic encephalopathies: clinical, biochemical, and experimental features. 675 30


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