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)

Although the diagnosis is rarely confirmed, enteroviruses are a common cause of meningitis. Coxsackie B is responsible for more than half of the cases of aseptic meningitis in infants less than 3 months old, but is less common as a cause of neurological disease in older persons. In addition to aseptic meningitis, Coxsackie B has been reported to cause a wide range of other neurological disorders, albeit rarely. The authors report a young adult with persistent Coxsackie B encephalitis that was heralded by focal seizures and evolved to intractable coma with multifocal myoclonus. The diagnosis was established by immunohistochemistry and reverse transcriptase-polymerase chain reaction (RT-PCR) on tissue obtained at brain biopsy. Cerebrospinal fluid (CSF) viral cultures and PCR were negative for enteroviruses. This case highlights unusual features of a persistent infection that could easily have been mistaken for a neurodegenerative or other noninfectious process. It also emphasizes the importance of performing brain biopsy on individuals with neurological disease of obscure nature.
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PMID:Persistent Coxsackie B encephalitis: Report of a case and review of the literature. 1716 66

The clinical features of subacute sclerosing panencephalitis (SSPE) include the following : stage I, behavioral changes; stage II, myoclonus and motor deterioration; stage III, mental and motor deterioration to coma; stage IV, a vegetative state. Anti-measles titers of serum and cerebrospinal fluid (CSF) are elevated in the patients with SSPE. CSF IgG levels and IgG index are also elevated in SSPE. The characteristic electroencephalography in stage II of SSPE shows periodic high voltage slow wave bursts. In the early stage, psychiatric diseases and epilepsy should be ruled out. Neurodegenerative diseases and other encephalitis/encephalopathy should be also excluded.
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PMID:[Clinical course and findings in and differential diagnosis of subacute sclerosing panencephalitis]. 1769 87

We describe a case of severe serotonin syndrome. The patient was simultaneously taking the atypical antidepressant olanzapine and a tricyclical antidepressant, clomipramine. Symptoms included altered mental state resulting in coma, myoclonus, hyperreflexia, diaphoresis, diarrhoea, disorientation and fever. After suspension of antidepressant drugs, intensive symptomatic treatment and administration of biperiden and cyproheptadine, the patient's condition improved.
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PMID:Serotonin syndrome caused by olanzapine and clomipramine. 1861 70

Tiagabine is an anticonvulsant acting by selective inhibition of neuronal and glial gamma-aminobutyric acid uptake, resulting in increased gamma-aminobutyric acid-mediated inhibition in the brain. Few reports in the literature describe the clinical course of severe tiagabine intoxication. A 44-year-old woman presented after deliberate self-poisoning with 100 tiagabine 15 mg tablets (1,500 mg; 25 mg/kg). Serum tiagabine level was 4,600 microg/L (1,725 mmol/L) at presentation, 20 times levels associated with therapeutic dosing. Intoxication was manifested by profuse vomiting, coma, myoclonus, generalized rigidity, bradycardia, hypertension, hypersalivation and generalized piloerection within 2 h of ingestion. The patient was intubated and management was supportive. Coma lasted until 10 h post-ingestion, but recovery was complicated by severe agitated delirium lasting 12 h. The patient recovered fully within 26 h of ingestion. Tiagabine deliberate self-poisoning was associated with the rapid onset of coma and an unusual toxidrome. Recovery, although complicated by agitated delirium, was complete within 26 h.
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PMID:Deliberate self-poisoning with tiagabine: an unusual toxidrome. 1878 11

Most patients who remain comatose for a few hours after a period of global cerebral ischemia have a poor prognosis. Early identification of these patients is desirable to reduce uncertainty about treatment and non-treatment decisions, and to improve relationships with the family. The absence of pupillary light response and corneal reflexes, absent or stereotyped extension motor response to noxious stimulation (3 days after insult); myoclonus status epilepticus; absence of cortical N20 response on somatosensory evoked potential studies; generalised suppression or burst-suppression EEG and serum neuron-specific enolase above 33 microg/L (sampled 1-3 days after insult) have been shown to predict poor outcome. We here propose an algorithm to help intensive care physicians' clinical decision making in post-anoxic coma.
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PMID:[Predicting prognosis in post-anoxic coma]. 1866 91

Hashimoto's encephalopathy (HE) is a rare, still not well understood, autoimmune disease with neurological and psychiatric manifestations. and elevated titers of antithyroid antibodies in serum and cerebrospinal fluid (CSF) as a hallmark of the disease. Patients are mostly women. Current diagnostic criteria include corticosteroide responsiveness, but it is the case in only 50% of patients with HE. In steroid non-responders other immunomodulatory therapies or plasmapheresis could be applied. Disease course can be acute, subacute, chronic or relapsing-remitting. Two distinct forms emerged from the reported cases: a vasculitic type characterized by multiple relapsing-remitting stroke-like episodes and mild cognitive impairment and a diffuse progressive type characterized by dementia and psychiatric symptoms. Both forms may be accompanied by depressed level of consciousness (stupor or coma), tremor, seizures, or myoclonus. We present two patients with two distinct forms of HE who had different clinical manifestations and response to therapy.
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PMID:Clinical manifestations, diagnostic criteria and therapy of Hashimoto's encephalopathy: report of two cases. 1984 19

A 16-year-old male started on isotretinoin 80 mg daily for acne developed persistent headache 3 weeks later, with myoclonus and confusion 10 weeks later. During initial hospital assessment his Glasgow Coma Scale score fell acutely to 8 and he required ventilation. Brain imaging and cerebrospinal fluid (CSF) analysis were normal and an electroencephalogram (EEG) showed features of encephalopathy. No cause was found. He was extubated after 24 hours and made a full recovery. This is the first report of a generalized encephalopathy thought likely to be due to isotretinoin.
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PMID:Isotretinoin-induced encephalopathy. 2005 67

Hashimoto encephalopathy is a steroid-responsive encephalopathy associated with elevated blood concentrations of antithyroid antibodies. The patients are usually euthyroid or mildly hypothyroid. The clinical picture is pleomorphic, presenting with variable symptoms ranging from behavioral and cognitive changes, myoclonus, seizures, pyramidal tract dysfunction, involuntary movements, and cerebellar signs to psychosis and coma, with relapsing and progressive course. The diagnosis is often overlooked at presentation but is crucial, given that this is a treatable disease. Described here, with a literature review, is the youngest patient reported to date with Hashimoto encephalopathy.
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PMID:Hashimoto encephalopathy in a preschool girl. 2011 54

Hypoxic-ischemic brain injury (HI-BI) after cardiac arrest commonly results in neurological injury and long term dysfunction, with outcomes ranging from coma and vegetative states to functional disability with various degrees of dependence. Increased rates of bystander CPR and cardiac defibrillation has led to a rapid increase in successful resuscitations. Patients who reach the hospital after cardiac arrest may develop various neurological deficits or clinical syndromes that may preclude recovery to their premorbid baseline. Consequently, clinicians are faced with not only predicting outcome regarding wakefulness and independence but also with long term therapeutic management. Several neurological syndromes have been reported as consequences of HI-BI. This review will describe some of the more common syndromes seen after HI-BI, including the various levels of arousal, seizures, myoclonus, movement disorders, cognitive impairments, and other specific neurological abnormalities.
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PMID:Neurological sequelae of hypoxic-ischemic brain injury. 2013 Mar 54

The cerebellum is one of the regions that contribute to urinary dysfunction in humans. A 43-year-old woman at age 35 had an acute onset of encephalitis that led to fever, generalized convulsion and coma. Six months after the disease onset, she regained consciousness and developed generalized myoclonus, cerebellar ataxia and overactive bladder, e.g., urinary urgency, daytime urinary frequency, and urinary incontinence. Eight years after the disease onset, she was revealed to have cerebellar atrophy on MRI, cerebellar hypoperfusion on SPECT, and detrusor overactivity on urodynamic study. Selective inflammation in the cerebellum seemed to produce cerebellar ataxia and overactive bladder in our case.
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PMID:Cerebellar Ataxia and Overactive Bladder after Encephalitis Affecting the Cerebellum. 2084 32


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