Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0013362 (dysarthria)
 3,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Clonazepam, a benzodiazepine with anticonvulsant properties, has recently been found to be effective in the control of acute mania. Its use in combination with lithium has been advocated. Here 5 cases are presented in which the combination of clonazepam (2 mg-16 mg) plus lithium (900 mg-2400 mg) produced a neurotoxic syndrome with ataxia and dysarthria. In all cases the syndrome was reversible.
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PMID:Clonazepam and lithium--a toxic combination in the treatment of mania? 279 69

The antimanic effect of zotepine was investigated in 16 patients with manic-depressive psychosis or manic schizoaffective psychosis. Zotepine markedly improved manic symptoms in 75% and afforded at least slight improvement in all patients studied. However, in 50%, zotepine caused conversion from mania to depression. The most frequent side effects were dysarthria in 50%, parkinsonian symptoms in 33%, dry mouth in 28%, and sleepiness in 28%. EEG abnormalities were noted in 22% of patients. The antimanic effect of zotepine was enhanced by lithium carbonate; however, concomitant use of zotepine and lithium possibly increased the incidence of EEG abnormalities. The conversion-to-depression effect of zotepine was not inhibited by lithium. Overall, the concomitant use of zotepine and lithium may be important in the treatment of manic psychoses.
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PMID:Antimanic effect of zotepine. 308 26

A case of acute mania in a 50-year-old woman who had received hemodialysis treatment for 2 1/2 years is described. The patient's presentation with secondary manic and associated psychotic features was the initial symptom of the syndrome of progressive dialysis encephalopathy (PDE). Shortly thereafter, an abnormal EEG tracing was obtained. Several months later she developed dysarthria and muscular twitchings and EEG changes persisted, a symptom complex characteristic of PDE. The appearance of psychiatric symptoms among patients receiving chronic dialysis treatment may herald the onset of PDE.
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PMID:Secondary mania as a presentation of progressive dialysis encephalopathy. 682 59

A woman with mania who had been treated with lithium carbonate since 69 years of age presented mild tremulousness of both hands at the age of 76 years. She subsequently developed dysphagia, dysarthria, unsteady gait and progressive deterioration of the higher cortical function over 1.5 months. Her tremulousness deteriorated until it resembled myoclonus. EEG showed periodic sharp wave complexes appearing predominantly over the bilateral parieto-occipital areas. Although the EEG abnormality was not identical with that usually observed in the fully developed stage of Creutzfeldt-Jakob disease (CJD), it was reminiscent of that seen in the early stage of CJD. Thus, her clinical symptoms and signs were considered to resemble those of CJD. The plasma concentration of lithium, however, was found to be over the therapeutic range. Reduction of the dose of lithium carbonate almost completely resolved her symptoms within 3 weeks. Consequently, her clinical condition was considered lithium intoxication. Antidepressant and bismuth as well as lithium have been reported to induce a Creutzfeldt-Jakob like syndrome. Awareness of drug-induced Creutzfeldt-Jakob like syndrome is clinically important because of its excellent prognosis as opposed to the ominous prognosis of CJD.
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PMID:[Creutzfeldt-Jakob like syndrome due to lithium intoxication--a case report]. 924 46

Twenty-two patients with PD received bilateral implants for high frequency stimulation of the subthalamic nucleus. The patients were treated for more than 1 year (up to 36 months). At the last visit, the Unified Parkinson Disease Rating Scale (UPDRS) motor score without medication improved by 50.2% (p < 0.001) and the UPDRS activities of daily living score improved by 68.4% (p < 0.001). The most common long-lasting adverse events were hypophonia and dysarthria; transient events were increased sexuality and mania. The surgical procedure induced transient intraoperative psychosis in seven patients.
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PMID:Long-term follow up of subthalamic nucleus stimulation in Parkinson's disease. 1203 98

Late-onset Tay-Sachs (LOTS) disease is a chronic, progressive, lysosomal storage disorder caused by a partial deficiency of beta-hexosaminidase A (HEXA) activity. Deficient levels of HEXA result in the intracellular accumulation of GM2-ganglioside, resulting in toxicity to nerve cells. Clinical manifestations primarily involve the central nervous system (CNS) and lower motor neurons, and include ataxia, weakness, spasticity, dysarthria, dysphagia, dystonia, seizures, psychosis, mania, depression, and cognitive decline. The prevalence of peripheral nervous system (PNS) involvement in LOTS has not been well documented, but it has traditionally been thought to be very low. We examined a cohort of 30 patients with LOTS who underwent clinical and electrophysiologic examination, and found evidence of a predominantly axon loss polyneuropathy affecting distal nerve segments in the lower and upper extremities in eight patients (27%).
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PMID:Late-onset Tay-Sachs disease: the spectrum of peripheral neuropathy in 30 affected patients. 1864 77

The development of extrapyramidal syndrome characterised by rigidity, bradykinesia, dysphagia and dysarthria in a male individual with four distinct episodes of (mania like) behavioural disturbances with fairly good remission in a time frame of five years, in a male individual, was suspected to develop the neurological manifestations of Wilson's disease and was investigated. In the absence of Kayser-Fleischer ring by slit-lamp examination and with normal copper and ceruloplasmin serum levels, the diagnosis was possible because of the positive findings of the magnetic resonance imaging (MRI) studies and increased 24 hours urinary copper levels with the penicillamine challenge test. The findings and its implications are highlighted and discussed.
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PMID:Wilson's disease--a rare psychiatric presentation. 2011 50

This study characterizes psychiatric manifestations as a primary symptom of neurosyphilis (NS). Fifty-two of the 169 NS patients presented with psychiatric manifestations, many patients had characteristics of more than one syndrome, including cognitive impairment, personality disorders, delirium, hostility, dysarthria, confusion, disruption of their sleep-wake cycle, fecal and urinary incontinence, dysphoria, paranoia, hallucinations, expansive mood, and mania. Fifty-two patients had positive sera RPR and T. pallidum particle agglutination (TPPA), 75% had positive CSF RPR, 96.2% had positive CSF TPPA, 44.2% had CSF pleocytosis and elevated CSF proteins, and 70.0% had nonspecific, abnormal brain MRIs. These results indicate that NS mimics almost all psychiatric disorders.
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PMID:Psychiatric manifestations as primary symptom of neurosyphilis among HIV-negative patients. 2473 21

Lithium is widely used in the treatment of bipolar disorder. Here we describe the syndrome of irreversible lithium-effectuated neurotoxicity in a patient within therapeutic doses and levels, which persisted after discontinuation of Lithium. A 50-year-old gentleman with Bipolar disorder presented with symptoms of Mania following drug default. Lithium was initiated as a mood stabilizer. On day 4, the patient developed abdominal pain, itching, and sore throat. On day 5, lithium levels were 0.9 mEq/L. Subsequently, the patient was noted to have slurring of speech, dysarthria, past pointing, and dysdiadochokinesis. Lithium was withdrawn on day 7. When lithium was re-introduced at a lower dose, the neurological symptoms re-appeared after 2 days and lithium was discontinued. Mild degree of slurring of speech persisted at 2-month follow-up. The patient had no history of side effects with antipsychotics in the past or current episode. In the absence of predisposing factors, Lithium has resulted in neurotoxicity at therapeutic doses and levels. Slurring of speech persisted despite adequate dose of anticholinergics. In addition to presumed neuroprotective effects of lithium, it can produce neurotoxic symptoms at therapeutic doses and levels.
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PMID:Resurrecting the discussion on neurotoxicity of lithium at therapeutic levels. 3313 60