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)

Carbromal is metabolized extensively in humans. The major metabolites known to date are bromoethylbutyramide, ethylbutyrylurea and inorganic bromide. After ingestion of a therapeutic dose of 1.0 g carbromal (4.2 mmoles) by four healthy volunteers highest concentrations in serum were found to be for carbromal 30 mumoles/l, for bromoethylbutyramide up to 20 mumoles/l and for ethylbutyrylurea 2--3 mumoles/l. In patients acutely poisoned by carbromal-containing sedatives serum concentrations measured were in the range of 200 mumoles/l carbromal, 350 mumoles/l bromoethylbutyramide and 50 mumoles/l ethylbutyrylurea. These patients were comatose, apneic, had isoelectric encephalographic records and decreased body temperature. The degree of central nervous depression as judged by clinical signs was found to correlate with the serum concentrations of carbromal and of bromoethylbutyramide. Pharmacological activity and acute toxicity of carbromal and its two metabolites were examined in rats and compared with the activity of phenobarbitone. For intraperitoneal injection LD-50 values were found to be for carbromal 1.8 mmoles/kg, for bromoethylbutyramide 1.5 mmoles/kg, for ethylbutyrylurea 5.0 mmoles/kg and for phenobarbitone 0.9 mmoles/kg. Carbromal and bromoethylbutyramide severely decreased body temperature. The relative narcotic activity was estimated to be for carbromal = 100; bromoethylbutyramide = 66; ethylbutyrylurea = 33; phenobarbitone = 100. The anticonvulsive activity against pentetrazol-induced generalized seizures was nearly identical for carbromal, bromoethylbutyramide and phenobarbitone. Anticonvulsant activity of ethylbutyrylurea was two to three times less than that of carbromal. Inorganic bromide was found to increase the narcotic activity of carbromal and of bromoethylbutyramide. The findings show that the clinical signs of central nervous system depression seen in patients acutely poisoned with carbromal are caused mainly by unchanged carbromal and by its metabolite bromoethylbutyramide.
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PMID:[On the toxicology of carbromal. III. Role of active metabolites in humans acutely poisoned with carbromal-containing sedatives (author's transl)]. 2 10

The steady rise in the promiscuous use of phencyclidine (PCP) as a "recreational" drug has recently gained nationwide attention because of the numerous violent and/or bizarre incidents caused by the use of this drug. Because the media often exaggerate reports of bizarre and violent behavior to make a "good" story, the potential PCP user may be tempted to ignore the media warnings. In the case of PCP, however exaggerated the story, a real danger does exist. So, despite numerous newspaper, radio and television warnings about the possible consequences of PCP use and abuse, the incidence of toxic reactions continues to climb. In many cases PCP is sold as other drugs, particularly THC, and in various colored capsules, tablets, liquids and crystals which may explain the increased usage despite the numerous warnings against its use. The advances in laboratory techniques and chemical processess have enabled the clandestine chemist to prepare relatively pure PCP and thus eliminate many of the toxic side effects due to impurities in the drug. In addition, 30 or more psychoactive PCP analogues have been developed and are starting to make an appearance on the street. PCP is perhaps the most potent psychotomimetic compound known at the present time and is capable of inducing a psychosis which is clinically indistinguishable from schizophrenia. The psychosis-producing effects of PCP are the most common toxic effects seen in hospital emergency rooms; but as the amount of PCP taken and/or the simultaneous involvement of other drugs, particularly barbiturates, occurs, severe medical problems (e.g., coma, seizures, respiratory arrest) begin to appear. Death from high doses of PCP or PCP plus other drugs does occur, but the principal cause of death from PCP abuse is due to trauma, homicide or suicide (usually of the bizarre or violent form). Young adult males, persons predisposed to mental illness and naive drug users appear to be the most susceptible to the adverse effects of PCP. The fact that chronic PCP users are starting to increase in number is mute testimony that not all users experience "bad trips" with PCP. Unfortunately for the user, however, this does not guarantee that the next trip will not be a bad one. The effects of chronic use seem to be twofold: severe depression with suicidal thoughts and numerous violent, agitated behavioral patterns. Neither seems to be a suitable alternative. At the present time there is not specific antidote for toxic PCP reactions and the prolonged psychosis induced in some cases does not appear to respond to the standard antipsychotic medications as quickly as do the functional psychoses. The major improvement from a medical standpoint is the development of more sensitive laboratory techniques to confirm the presence of PCP in body fluids. This advance has undoubtedly led to the apparent increase in the number of PCP cases reported by hospitals and to the accuracy of clinical diagnosis by medical, drug or law enforcement communities...
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PMID:PCP (phencyclidine): an update. 4 8

A 40 year old man developed seizures, intermittent fever, and progressive dementia ending in coma and death after four years. The cerebrospinal fluid showed variable pleocytosis and occasional elevation of protein. The necropsy revealed many lesions characteristic of Whipple's disease confined to the grey matter of the brain. The pathological changes were studied with the light and electron microscope. The findings permitted an understanding of the temporal sequence of changes in the lesions. Involvement of the brain in this condition is rare, but the disease is treatable and the diagnosis can be made by brain biopsy.
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PMID:Whipple's disease confined to the brain: a case studied clinically and pathologically. 7 5

Nonketotic hyperglycemia has a definite convulsive effect, which may manifest itself in generalized or focal seizures. This report deals specifically with focal convulsive phenomena. Two patients with nonketotic hyperglycemia focal seizures are described. Focal seizures are of motor Jackson, aphasic, adversive or of the 'epilepsia partialis continua' type. Different types of focal seizures may appear in one and the same patient. Focal epilepsy can be the first manifestation of a diabetic disorder. Focal epileptic seizures are linked with moderate nonketotic hyperglycemia with values of 360 mg% sugar and 310 osm. Higher values lead to generalized seizures and coma. The mechanisms are discussed and pertinent literature is reviewed.
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PMID:Moderate nonketotic hyperglycemia--a cause of focal epilepsy. Report of two cases and review of literature. 9 31

A case report of survival after severe ingestion of phenol is described. The patient developed coma, respiratory arrest 30 minutes postingestion, hypotension, ventricular arrhythmias, metabolic acidosis, seizures, selective elevation of uric acid and gastrointestinal disturbances. Treatment consisted of gastric lavage, olive oil, activated charcoal and supportive therapy. The exact amount of ingested substance was known, and ventricular arrhythmias specifically related to phenol, not its derivatives, could be described.
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PMID:Phenol poisoning. 10 93

The authors present the results of a long-term follow up of 52 juvenile head-injured patients who showed early epileptic seizures. The purpose of this study is to stress the role of long-term prognosis in the early seizures and to determine in which cases a treatment preventing late seizures is eligible. They consider long-term prognosis as to be favourable. Late epilepsy occurred in 15.3% of the cases and responded favourably to anticonvulsive therapy. They suggest prophylaptic treatment in those patients who had loss of consciousness immediately after trauma, recurring seizures, coma and/or surgery.
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PMID:Long-term prognosis of early epilepsy in juvenile head-injured patients (preliminary results). 11 40

Clinically evident epileptic seizures were observed in 145 patients during the first week of traumatic coma. They frequently occurred during the first day in young subjects in reactive coma, and were often isolated attacks. When ssen at a later stage they are more common in adults with non-reactive coma. The partial or generalised nature of the seizures, the depth of the coma, and the chronological order in which the seizures appear have no bearing on the etiology; the only positive finding was that recurrent seizures were more frequent in patients with intracranial hematoma (18,6% of the patients). The early appearance of seizures does not worsen the prognosis of reactive coma or non-reactive coma in young people. Critical discharges without clinical manifestations were present in 37 patients with traumatic coma during the first week. The average age of these injured patients was higher, and the prognosis for non-reactive coma worse in this group. The comatous state does not modify the clinical aspects or the etiological significance of these early post-traumatic discharges.
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PMID:[Significance of epileptic seizures occurring during the first week of traumatic coma (author's transl)]. 11 88

This is the first reported case of a major overdose of Lioresal (baclofen or CIBA BA-346467). A 29-year-old woman with known Huntington's disease took from 900 to 970 mg of Lioresal, a cogener of gamma amino butyric acid (GABA) used experimentally to treat muscle spasm. She was admitted in deep coma with absent brain stem reflexes and without spontaneous respiration, and she required cardiovascular support. Her pupils were fixed at 3 mm and unreactive for 48 hours. She continued to require intensive support for a total of 72 hours and had one seizure during the recovery phase. Her eventual recovery was complete. No specific antidotes are currently available for overdose of Lioresal and supportive care is the only method of treatment for overdose.
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PMID:Overdose of lioresal. 13 33

Serologic responses, physical findings, and survival were studied in 51 cases of proved (14 patients) or presumptive (37 patients) herpes simplex encephalitis occurring in North America between 1965 and 1972. On the basis of a statistical analysis of 16 serological parameters tested in both groups, presumptive cases are likely similar to definitive cases. Using this assumption, the following tentatives conclusions are possible. Complement-fixing antibodies may be more sensitive measures of rises in anti-herpes simplex virus antibodies than are conventional or complement-requiring neutralizing or passive hemagglutinating antibodies. Mortality in herpes simplex virus encephalitis may vary from 0 to 80% and may be predictable depending upon the occurrence of seizures, paralysis and coma. Coma seems to dictate the dour prognosis. When 51 cases of herpes simplex virus encephalitis reported in the literature by others between 1944 and 1972 were analyzed by this method, a comparably varied mortality was obtained. It did not appear that treatment with idoxuridine increased the likelihood of survival.
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PMID:An estimate of the course of herpes simplex virus encephalitis. 17 51

A 62-year-old woman developed neurologic deficits 7 months after pulmonary lobectomy for alveolar cell carcinoma of the lung. CT scan of the head demonstrated two metastases with marked peritumoral edema. Administration of Decadron, chemotherapy and 3,000 rad cranial radiation resulted in dramatic improvement of dysphasia and right hand paresis. Almost 2 months later, rhythmic, involuntary movements of the left hand developed. There was progression to multifocal seizures, grand mal seizures, postictal depression, status epilepticus, and coma, with death 9 days after onset of the movement disorder. Bronchoalveolar carcinoma was widely disseminated in lungs and bones, and as three metastases in brain. Bland "ischemic" necrosis in a pseudolaminar pattern was present in the neocortex. Innumerable Cowdry type A intranuclear inclusion bodies were seen in neurons, astrocytes, and oligodenodroglia. Immunofluorescence demonstrated Herpes simplex virus type 2 antigen and electron microscopy revealed virions with the morphology of the Herpes group. The case is significant for (1) the concurrence of intracranial metastases and Herpes simplex encephalitis, and (2) the causal agent, Herpes simplex virus type 2. The implication for the clinical neurocientist is the potential in a patient with systemic cancer, for the causation of neurologic complications by more than one factor or mechanism.
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PMID:Herpes simplex type 2 encephalitis concurrent with known cerebral metastases. 22 22


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