Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cerebral dyspraxia associated with hemodialysis is a progressive, fatal syndrome. Patients suffer from a combination of psychiatric and neurological signs and symptoms. Psychiatric manifestations include anxiety, depression, paranoid ideation, and a progressive dementia with impaired concentration, decreased memory, personality changes, and hallucinations. Neurological findings include deliberate speech, stuttering, dysarthria, dyspraxia of speech and movement, tremulousness, myoclonic activity, asterixis, and seizures. These symptoms are aggravated during and immediately following dialysis. Patients usually die within 6 months of its onset. The etiology is unknown. Treatment efforts have failed to reverse its course. Recognition of this syndrome is highlighted so that informed, critical decisions can be made as to whether to continue dialysis therapy.
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PMID:Clinical and psychological test findings in cerebral dyspraxia associated with hemodialysis. 125 51

Acquired stuttering subsequent to subcortical pathology of mesothalamus was observed in four neurosurgical subjects. The patients suffered from chronic pain, seizures, and somatosensory disorders. They also exhibited unpredictable and uncontrollable speech, spasmodic blocks which were devoid of accessory features, and adaptation effect. Therapeutic mesothalamic stimulation, used as a treatment of last resort to relieve the pain and associated symptoms, also had an ameliorating effect on the stuttering. Spontaneously occurring focal abnormal EEG discharges were anatomically delineated and used as a guide for therapeutic stimulation electrode placement. Attentuation of the abnormal discharges was followed by alleviation of symptoms. This investigation examines the clinical characteristics of stuttering in four neurosurgical patients and suggests an electropathologic basis for their mesothalamic-generated speech dysfluencies. The cooccurrence of pain, seizures, somatosensory disorders, and stuttering, and their concurrent amelioration, suggests that both chronic pain and stuttering may be implicated by similar or related reticular electropathologic generators, couched in overlapping reticular networks extending from the brain stem to the thalamus, and that the acquired stuttering may be recruited as one component of a larger syndrome complex.
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PMID:Stuttering acquired from subcortical pathologies and its alleviation from thalamic perturbation. 161 65

A case is presented in which adult onset stuttering and focal seizures appear to be linked. The EEG showed left anterior and mid-temporal sharp waves. The patient responded well to combined therapy with phenytoin, fluency exercises, and stress reduction. The association between stuttering and seizures in adults and children, as well as treatment with anticonvulsants, are discussed.
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PMID:Adult onset stuttering and seizures. 309 Dec 95

A patient had seizures triggered by spontaneous blinking associated with the act of beginning to speak. Diffuse paroxysmal discharges in the EEG appeared when the patient was blinking in darkness or in bright light. Closing the eyes voluntarily, on command, or as a reflex reaction produced this response very infrequently. During intermittent photic stimulation the epileptic discharges were accompanied by myoclonic jerks. The act of beginning to speak was linked with spontaneous blinking and EEG changes and was accompanied consistently by seizures. These were characterized by a peculiar stuttering and an absencelike impairment of consciousness. Seizures have been controlled well using clonazepam and valproic acid.
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PMID:Seizures triggered by blinking when beginning to speak. 682 38

Marked asterixis occurred in two patients following metrizamide myelography. One also suffered generalized seizures and the other had severe stuttering speech for seven days. The spectrum of toxic manifestations of metrizamide is reviewed with emphasis on the unusual lethargy and other depressive effects seen with this relatively safe agent. The hypothesis that metrizamide exerts a ouabain-like effect on the cortical surface was tested. Metrizamide in concentrations as high as 20 mM had no inhibitory effect on rat cerebral K+-para-nitrophenylphosphatase, a partial reaction of (Na+K+)-adenosine triphosphatase. Because metrizamide is a 2-deoxyglucose analogue, a competitive inhibition of hexokinase at the first step in glycolysis was also postulated. Metrizamide was found to competitively inhibit commercial (microbial) hexokinase. The Michaelis constant for glucose rises from 0.13 to 0.25 to 0.33 to 0.91 mM in the presence of 0, 0.4, 1.0, and 2.0 mM metrizamide, respectively. Since the concentration of metrizamide over the cerebral cortex after routine myelography may be approximately 50 mM compared with a glucose concentration of only 3.6 mM (65 mg/dl), it is postulated that impaired brain glucose metabolism may be responsible for some of the toxic effects of metrizamide.
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PMID:Asterixis and encephalopathy following metrizamide myelography: investigations into possible mechanisms and review of the literature. 722 1

Alteration of speech is a rare but distressing complication of orthotopic liver transplantation (OLT). We describe a characteristic speech disorder identified in a large series of consecutive patients undergoing OLT. Between 1988 and 1993, 525 adults underwent OLT. For all recipients with neurologic complications, we reviewed clinical findings, imaging and electrophysiologic test results, and perioperative laboratory data. Five patients (ages 23-52; UNOS status 3-4) exhibited a characteristic pattern of stuttering dysarthria, leading to complete loss of speech production, occasionally with elements of aphasia. In four of the five patients, right-sided focal seizures were subsequently noted. All cases presented within the first 10 postoperative days and improved with 1 month of cessation of cyclosporin (CyA), although halting, monotonous speech was evident to some degree in all five for up to 1 year. There was no correlation between onset of symptoms and CyA levels. None of the patients has clinical or radiologic findings suggestive of central pontine myelinolysis or akinetic mutism. EEGs and Spect scan results were consistent with dysfunction in the left frontotemporoparietal regions of the brain. A characteristic speech disorder, which may be described as cortical dysarthria or speech apraxia, occurs in approximately 1% of adults undergoing OLT. Prompt recognition of this syndrome and temporary cessation of CyA therapy may favorable affect the course.
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PMID:Loss of speech after orthotopic liver transplantation. 762 86

This overview summarizes the major and minor side effects and drug interactions of fluoxetine. The adverse reactions include the "serotonin syndrome", cardiovascular complications, extrapyramidal side effects such as akathisia, dyskinesias, and parkinsonian-like syndromes and an apparently increased risk of suicidality. Fluoxetine-induced mania and hypomania, seizures and sexual disorders are evaluated along with minor symptoms of allergic reactions, stuttering, hematological changes, psoriasis, and inappropriate secretion of the antidiuretic hormone. The major fluoxetine-drug interactions involve the amino acids L-dopa and L-tryptophan, anorexiants, anticonvulsants, antidepressants, anxiolytics, calcium channel blockers, cyproheptadine, lithium salts, and drugs of abuse. The underlying mechanism and the paradoxical effects of fluoxetine are addressed.
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PMID:Fluoxetine: adverse effects and drug-drug interactions. 825 2

Controversy exists over the pathophysiology of Tourette syndrome (TS). The case reported is a 37-year-old unmarried man suffering from both TS and complex partial epilepsy (CPE). He began to have seizures at 2-3 months of age. The CPE featured dark vision, dizziness, followed by unresponsiveness, a blank stare, occasional loss of posture control, and occasional automatism consisting of going to the toilet to urinate. TS gradually began to develop when he was 3-4 years of age. The tics were characterized by stereotypic stuttering, vocalization, hiccups, grimacing, snorting, and jerky supination of both forearms. EEG sharp waves with phase reversal at the left frontotemporal region were present but they were not related to the tics. Magnetic resonance imaging revealed atrophy of the left temporal and frontal lobes, as well as absence of normal asymmetry of basal ganglia. This case supports the theory that TS is related to the left frontal lobe, limbic system, and basal ganglia, but contradicts the hypothesis that the tics are ictal events.
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PMID:Tourette syndrome and complex partial epilepsy--a case report. 875 47

We report on a patient with a left frontal lesion who, many years after an injury, developed non-fluent aphasia and facial myoclonic jerks triggered by speaking and listening to spoken language. At age 57, the patient first noted that he would begin to stutter when delivering lectures at conferences. The stuttering would worsen if he continued talking. The video-polygraphic EEG recording shows brief paroxysms of spikes and polyspikes, followed by a slow wave, more evident in the left fronto-temporal region. The myoclonic jerks originating from the submental area correlate with EEG abnormalities. Clinically, these jerks determined a form of stuttering. The triggering factors were reading, speaking and listening to spoken language. This case had several characteristic features: facial myoclonus was the only seizure type experienced by the patient; the seizures and language impairment had a very late onset--about 50 years after the traumatic event that produced a dramatic lesion in the left fronto-polar region. (Published with videosequences.)
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PMID:Symptomatic epilepsy with facial myoclonus triggered by language. 1167 6

Landau-Kleffner syndrome is marked by an acquired aphasia in children who have had normal language and motor development. A 3.5-year-old girl was referred to our clinic with stuttering. She was diagnosed as having benign myoclonic epilepsy of infancy at 3.5 months of age and treated with valproic acid. Her electroencephalogram (EEG) returned to normal at the end of the first year. The therapy was stopped after a 2-year seizure-free period. She started to stutter prominently 3 months after the discontinuation of antiepilepsy drugs. She had no verbal agnosia. Her EEG revealed multiple spike and wave discharges. She was diagnosed as having Landau-Kleffner syndrome. Her previous epilepsy history had contributed to her having obtained an EEG in the early period. We suggest that if a child with normal language function starts to stutter, Landau-Kleffner syndrome must be considered in the differential diagnosis.
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PMID:Landau-Kleffner syndrome beginning with stuttering: case report. 1254 39


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