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)

We examined 348 patients who underwent thrombolytic treatment for acute myocardial infarction. Nine patients (2.58%) developed neurological complications related directly or indirectly to this procedure. Cerebral hemorrhage occurred in 3 patients; 2 patients had transient ischemic attacks, 1 had syncope, another had psychomotor agitation and 2 patients presented seizures during the infusion of the thrombolytic agent, without hemodynamic abnormalities. This latter feature had never been described before.
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PMID:Neurological complications after thrombolytic treatment for acute myocardial infarction: emphasis on unprecedented manifestations. 162 95

Nocturnal paroxysmal dystonia (NPD) and episodic nocturnal wanderings (ENWs) are complex motor attacks arising abruptly during sleep, especially nonrapid eye movement sleep. NPD is characterized by sudden arousal followed by motor agitation with dystonic posturing, and semipurposeful activity recurring several times per night. When short-lasting, NPD may respond favorably to carbamazepine. ENWs are unusual episodes of ambulation, with unintelligible speech, screaming, and complex, often violent, behavior that responds to anticonvulsants. In both short-lasting NPD and ENWs, electroencephalography may show some evidence of epilepsy; NPD is clinically similar to the frontal lobe seizures that arise mesially or in depth. Paroxysmal arousals (PAs) are even shorter episodes of arousal or awakening during nonrapid eye movement sleep, associated with transient dystonic posturing and related to the short-lasting NPD. PAs, short-lasting NPD, and ENWs probably represent a spectrum of peculiar sleep-related epileptic seizures.
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PMID:Nocturnal paroxysmal dystonia and nocturnal wandering. 163 Jun 41

The functional significance of the interaction between serotonergic and dopaminergic neurotransmission is still uncertain. To document this interaction further, specific behavioral responses of rats to tryptamine and apomorphine were studied. The sequential injection of these agonists, at time intervals with minimal direct behavioral interference, was used to observe response changes with respect to a single challenge. The antagonists haloperidol, ritanserin and risperidone, with known actions on serotonin-S2 (5-HT2) and dopamine-D2 (D2) receptors were used to evaluate effective antagonism of single and sequential challenges. When tryptamine was preceded by an apomorphine challenge the effective doses of the 5-HT2 antagonists ritanserin and risperidone for 50% inhibition of the seizures increased by a factor of 2.5. The dose-response curve of haloperidol remained virtually unchanged, apparently because of the potent dopamine-D2 antagonism associated with these doses which may block the potentiating effect of apomorphine. When apomorphine was preceded by a tryptamine challenge, the total agitation score of the control animals increased by 59% on the average. Haloperidol was equally effective against the enhanced as against the unenhanced apomorphine response. Ritanserin reduced agitation only by the part corresponding to the tryptamine enhancement. Risperidone's activity against the enhanced agitation started at very low doses and was complete at a dose still about 2.5 times lower than that required against the single apomorphine challenge. Mutual enhancement of tryptamine and apomorphine appears to occur even at a time when the behavioral effects of the first agonist are no longer manifest. The enhanced agitation remains largely dopamine-D2-specific and the enhanced seizures serotonin 5-HT2-specific.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Functional interaction between serotonin-S2 and dopamine-D2 neurotransmission as revealed by selective antagonism of hyper-reactivity to tryptamine and apomorphine. 169 23

The toxic effects of cocaine are becoming more widely recognized as the popularity of the drug increases. Although overdose is usually fatal, treatment is available for users who experience agitation, seizure, arrhythmias, severe hypertension, or other side effects. Hospital admission is often necessary to allow monitoring of the acute situation. Initial management involves standard life-support measures. Therapeutic agents are given, as appropriate, both to control acute reactions and to counteract continuing toxicity.
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PMID:Emergency management of cocaine intoxication. Counteracting the effects of today's 'favorite drug'. 172 70

Photosensitivity has proved to be a useful model to study the acute effects of experimental antiepileptic drugs (AEDs). The photosensitivity range is usually diminished or even abolished after administration of a known or experimental AED. An increase in photosensitivity, an unexpected reaction, was found in four photosensitive epileptic patients after oral ingestion of 500, 100, or 50 mg of Org 6370. Moreover, the three patients receiving doses of 100 and 500 mg reported nausea, dizziness, restlessness, and an increase in spontaneous epileptic seizures (myoclonus and in one patient a generalized tonic-clonic convulsion). The side effects coincided with peak Org 6370 serum levels. Our findings indicate that in the photosensitivity model experimental drugs with proven anticonvulsant properties in animals may increase rather than decrease the degree of patient photosensitivity. Photosensitive patients may represent a special subgroup of epileptic patients and therefore need to be classified as such.
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PMID:Preliminary assessment of the efficacy of Org 6370 in photosensitive epileptic patients: paradoxical enhancement of photosensitivity and provocation of myoclonic seizures. 173 47

There have been recent reports of rhabdomyolysis associated with cocaine abuse. The pathologic findings from these cases have not been described. Pathologic abnormalities in two fatalities with cocaine-associated rhabdomyolysis, including one with hyperpyrexia, acute renal failure, and disseminated intravascular coagulation, are discussed in detail. Skeletal muscle in both cases showed necrosis without evidence of vasculitis, polarizable foreign crystals, or other specific lesions. The individual with renal failure showed acute tubular necrosis with granular myoglobin casts in tubules. The mechanism of cocaine-associated rhabdomyolysis is unclear, but potentially includes ischemia due to vasoconstriction, direct toxicity, hyperpyrexia, and increased muscle activity from agitation or seizure. Adulterants may also play a role. In unexplained cases of rhabdomyolysis, toxicologic evidence of cocaine should be sought. In those cases of rhabdomyolysis associated with acute renal failure, the presence of cocaine in blood may be prolonged because of impaired renal clearance.
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PMID:Rhabdomyolysis associated with cocaine abuse. 174 98

A large number of opioids and nonopioids have been administered epidurally and intrathecally in the hope of providing segmental analgesia without serious adverse effects. However, neurotoxicity data are generally unavailable for many of these drugs. The present study evaluated the behavioral, motor, electroencephalographic, and histopathologic changes following intrathecal injection of large and small doses of butorphanol, sufentanil, and nalbuphine in sheep. Thirty-two sheep (20-32 kg) were anesthetized and catheters placed intrathecally after hemilaminectomy. The large doses of butorphanol, sufentanil and nalbuphine were 0.375 mg/kg (4.4-5.2 ml), 7.5 micrograms/kg (3.6-4.8 ml) and 0.75 mg/kg (1.5-2.4 ml), and the small doses were 0.075 mg/kg (0.9-1.1 ml), 1.5 micrograms/kg (0.7-0.9 ml) and 0.15 mg/kg (0.38-0.5 ml), respectively. The opioids were administered intrathecally every 6 h for 3 days and the above-mentioned parameters studied. Five sheep received intrathecal saline (1.1 or 5.2 ml) and served as controls. Histopathologic changes were evaluated by a neuropathologist blinded to the study protocol. Irrespective of dose, intrathecal injection of butorphanol was associated with severe behavioral responses such as agitation, rigidity, vocalization, and restlessness, as well as prolonged or irreversible hindlimb paralysis. Electroencephalography showed increased cortical activity or seizure activity. One sheep died because of severe respiratory depression that did not respond to naloxone. Spinal cord histologic changes consisted of suppurative meningitis and myelitis as well as neuronal changes such as spongiosis and chromatolysis. Large doses of intrathecal sufentanil were associated with similar though somewhat less severe responses. The behavioral and motor changes following the small dose of intrathecal sufentanil were of mild to moderate nature. Following intrathecal nalbuphine, the above-mentioned changes were similar to those seen in control animals. We conclude that butorphanol in doses of 0.075 and 0.375 mg/kg intrathecally and sufentanil 7.5 micrograms/kg intrathecally are neurotoxic in sheep.
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PMID:Behavioral and histopathologic effects following intrathecal administration of butorphanol, sufentanil, and nalbuphine in sheep. 138 69

In recent years, a differentiation has been made between two syndromes that are characterized by brief abnormal paroxysmal movements occurring principally at night: 1, hypnogenic paroxysmal dystonia (HPD), sometimes considered a particular form of dystonia similar to paroxysmal kinesigenic choreoathetosis, and 2, mesiofrontal epilepsy. Whether HPD is a distinct syndrome is not clear. Twenty-three patients, 11 men and 12 women, were hospitalized between 1985 and 1989 for examination of this type of abnormal paroxysmal movements (APM) occurring at night. In order to clarify the physiopathology of these abnormal nocturnal movement as focal epilepsy or a particular form of dystonia, we analyzed the personal and familial antecedents of all 23 patients, the polygraphic records during waking and sleep periods, and the results of neuroradiological examinations. Four patients were examined by positron emission tomography (PET) using i8F deoxyglucose. Symptoms first appeared between 3 and 28 years of age (M, 10.1) and developed over 1 to 20 years (M, 10.1). APM clearly occurred more commonly (greater than 90%) during sleep, usually during phases of slow-wave sleep. The sleeping patient opened his eyes and the motor signs then variously associated affective facial expression; axial postural modifications; tonic, dystonic or choreic postural movements of the limbs; pedalling; automatisms; disordered agitation and vocalization. The seizure was abruptly interrupted after 10 to 60 seconds. There was usually no postictal confusion. Thirteen patients clearly had clear epileptic antecedents: in 9, generalized tonic-clonic seizures; in 4, focal epileptic status. During nocturnal polygraphic recording, 6 patients presented a generalized seizure following a period of APM.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Postures and abnormal paroxysmal movements during sleep: hypnogenic paroxysmal dystonia or partial epilepsy?]. 190 68

Clonazepam is a potent, long-acting benzodiazepine approved for use in myoclonic and petit mal seizures. Initial reports have demonstrated encouraging results with clonazepam in the treatment of acute mania as well as a favorable side-effect profile. A trial of adjunctive clonazepam was initiated in a 41-year-old patient with chronic schizophrenia. Two weeks later, while on an 8-mg dosage, he became manic, developing pressured speech, euphoria, inflated esteem, agitation, and insomnia. Initiation of electroconvulsive therapy with gradual tapering and discontinuation of the clonazepam resulted in amelioration of the manic episode and a return to his previous clinical status. Clinicians should be alerted to the potential of clonazepam to cause manic-like behavior in susceptible patients.
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PMID:Mania associated with clonazepam. 194 70

Alcohol withdrawal reveals a condition of central nervous system (CNS) hyperexcitability opposite to that of the primary effect of the drug. Adaption to the decreased activity of the CNS during chronic ethanol ingestion may at least partly explain several of the symptoms of alcohol withdrawal. Benzodiazepines are therefore useful in the withdrawal state. The benzodiazepine loading dose technique, giving diazepam 20 mg every hour until the patient shows signs of clinical improvement and mild sedation, is the choice of treatment in cases of moderate to severe alcohol withdrawal. In general, neuroleptics should be avoided, because of increased risk of convulsions, but haloperidol can be used to control hallucinations and severe agitation. This treatment should then be combined with benzodiazepines. Most patients with mild withdrawal symptoms respond to non-pharmacological supportive care, except for those with a history of withdrawal seizures. These patients may need treatment with carbamazepine or diazepam.
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PMID:[Alcohol withdrawal--biological background, diagnosis and treatment]. 197 Nov 24


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