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 report a 1-year and 9-month old girl with a pachygyria in the left cerebral hemisphere who showed intractable seizures mimicking severe myoclonic epilepsy in infancy (SMEI) treated with TRH-T. The patient has been admitted to our department 3 times and then treated with intramuscular TRH-T (0.5-1.0 mg daily) successfully. Seizures had been controlled with TRH-T in 21, 10 and 5 days, and thereafter ad-on therapy with peroral TRH-T (1-4 mg daily) has been continued. The drop of plasma prolactin level after TRH-T treatment suggests a possible participation of the inhibitory action of dopaminergic neurons in seizure control. Pachygyria is known to have microdysgenesis of the cerebral cortex, which can be the epileptic focus of the case. The TRH-T can be beneficial in the treatment of intractable seizures mimicking SMEI seen in patients with pacygyria.
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PMID:[A case of intractable epilepsy with pachygyria: the effect of TRH-T treatment]. 839 38

Increasing experience with intensive monitoring of patients with intractable seizures has shown that a significant number of patients presents with pseudoseizures (psychogenic seizures). While in a majority of the patients differential diagnosis should be obvious, in some patients diagnostic error may occur. This is the case if the physician is unfamiliar with uncommon seizures, if the patient presents with atypical or bizarre attacks, and if interictal and/or ictal EEG are normal. Comparative studies of patients with true convulsive seizures and patients with pseudoseizures have revealed some 'typical' ictal features of pseudoseizures. Of these, longer ictal duration, less stereotypy, asynchronous extremity movements, atypical vocalization, alternating head movements and pelvic thrusting are the most characteristic. Many exceptions exist, however, since many patients with complex partial seizures (mostly of frontal origin) may present with similar ictal features. The final diagnosis of pseudoseizures is based upon integration of numerous data including careful seizure history, results of intensive video EEG monitoring and electroclinical correlation by experienced observers. Psychiatric and personality examination, different techniques of suggestion and determination of serum prolactin may provide additional diagnostic evidence.
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PMID:The diagnosis of pseudoseizures. 845 10

The introduction of clozapine has given clinicians a unique agent for treating patients with schizophrenia that is refractory to other neuroleptics. Despite its efficacy, the drug continues to be prescribed with trepidation due to the incidence of agranulocytosis. This article reviews the pharmacokinetic and pharmacological properties of clozapine and the clinical implications for monitoring plasma concentrations. Various assays have been developed for clozapine that include gas-liquid chromatography, radioimmunoassay and high performance liquid chromatography. Only a few studies have examined the pharmacokinetics of clozapine in patients with schizophrenia. These studies have revealed a wide interpatient variability in pharmacokinetic parameters that include: time to reach peak plasma concentrations 1.1 to 3.6h; elimination half-life 9.1 to 17.4h; clearance 8.7 to 53.3 L/h; and a volume of distribution of 1.6 to 7.3 L/kg. Clozapine is metabolised via the hepatic microsomal enzyme system into 2 principle metabolites: demethyl-clozapine and clozapine N-oxide. Urine samples have reported the ratio of clozapine:demethyl:N-oxide to be 1:1:2. The clozapine N-oxide binding affinity with 3H-haloperidol was 4 times lower than clozapine and its conversion back to clozapine is hypothesised. Although the exact pharmacological mechanism of action of clozapine is not fully understood, the drug does possess significant binding affinity for different dopamine receptors, with recent evidence supporting binding to the D4 receptor subtype. Clozapine transiently increases serum prolactin levels with minimal changes in homovanillic acid plasma levels. Limited studies investigating the relationship between clinical response and plasma clozapine concentrations have investigated the range between 100 and 800 micrograms/L. In the treatment of patients with refractory schizophrenia, a minimum concentration of 350 micrograms/L was suggested as needed. The occurrence of agranulocytosis could have a genetic basis and patients should be rigorously monitored during treatment. The incidence of tardive dyskinesia and extrapyramidal side effects is minimal. Clozapine can lower the seizure threshold in a dose- and time-dependent manner. Careful patient selection and monitoring are required when clozapine therapy is used in patients with schizophrenia.
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PMID:Pharmacokinetics and pharmacodynamics of clozapine. 845 23

The effect of pindolol, a beta-receptor blocker with potent 5-HT1 receptor antagonistic properties, on the prolactin (PRL) and thyrotropin (TSH) responses to electroconvulsive therapy (ECT) was systematically studied in 12 female depressed patients. In a balanced order, crossover design, the patients were given placebo or pindolol 5 mg orally, 1 h prior to bilateral ECT. The last five patients were additionally tested with 10 mg pindolol during the third ECT. Plasma levels of PRL and TSH increased in all three trials, but no consistent effect of pindolol on these hormonal responses could be demonstrated. Pindolol tended to attenuate seizure duration, especially at the 10 mg dose. The participation of 5-HT1 receptor activity in the secretion of PRL and TSH during ECT remains uncertain.
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PMID:Prolactin and thyrotropin responses to ECT after pindolol administration. A placebo controlled study. 847 32

Numerous investigators have found that serum prolactin levels increase after tonic-clonic and partial complex seizures, but the effect of syncope on prolactin levels has been studied little. Serum prolactin levels were measured following unexpected syncopal attacks in patients seeking emergency treatment in a community hospital. Levels sampled 18 to 60 minutes after syncopal episodes were increased in 8 of 11 cases. Follow-up prolactin levels, measured 17 to 222 days later, were normal in all eight cases in which they were initially increased. Most subjects had concurrent illness. Although the current study does not clarify whether it was the syncope, the concurrent illness, or both that caused the prolactin elevations, it implies that measurement of this hormone will not help the clinician in distinguishing between seizures and syncopal attacks.
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PMID:Increases in serum prolactin levels associated with syncopal attacks. 848 72

Transient hyperprolactinaemia has been reported to follow unprovoked seizures, a finding proposed to be useful in the differential diagnosis of epilepsy. There is also evidence that patients with unprovoked seizures may have high baseline prolactin levels, which could be of value in detecting those predisposed to epilepsy after a first convulsive attack. The purpose of this study was to examine whether prolactin levels are elevated: (1) postictally in febrile seizures and (2) interictally in afebrile seizures. In 17 children with simple febrile seizures, mean postictal prolactin value (370 +/- 160 mU/l, mean +/- SD) was significantly higher (approximately 0.001) than the mean baseline value of 18 seizure-free controls (202 +/- 136 mU/l). The mean baseline prolactin values were not significantly different: (1) in ten children with afebrile versus ten seizure-free controls and (2) in 18 children with febrile seizures associated with high risk for subsequent afebrile seizures versus 23 children with febrile seizures but unlikely to suffer from afebrile seizures. CONCLUSION. Postictal prolactin levels may be a useful marker of recent febrile seizures, while baseline prolactin levels do not appear to have any prognostic significance in afebrile seizures.
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PMID:Prolactin levels in febrile and afebrile seizures. 858 8

Postictal serum prolactin and cortisol levels were measured in 37 children having either epilepsy, febrile seizure or syncopal attack and in 37 normal controls. Blood samples were obtained within 1.5 h following the seizure episode. All serum levels were compared between each group and the control groups. Significantly higher (P < 0.005) prolactin levels (56.64 +/- 34.78 ng/mL) were found in the epileptic group, compared to the levels in children with febrile seizures (21.72 +/- 12.92 ng/mL), syncope attacks (13.88 +/- 5.27 ng/mL) and the control group (14.32 +/- 5.05 ng/mL). In contrast, serum cortisol levels were non-specifically elevated in children with epilepsy, febrile seizures and syncopal attacks. Cortisol secretion appears to be non-specifically elevated in all stressful events. Elevated prolactin levels may be helpful in differentiating epilepsy from febrile seizures and syncope.
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PMID:Serum cortisol and prolactin levels in childhood paroxysmal disorders. 867 85

The effects of thyrotropin-releasing hormone (TRH) administration on electroconvulsive therapy (ECT)-induced prolactin (PRL) secretion and the duration of the seizure were studied in 14 depressed women. In a balanced order crossover design the patients were given 0.4 mg TRH or placebo intravenously 20 min before ECT during the first two sessions. In the third ECT session TRH was given just prior to ECT. ECT elicited the expected PRL response when given alone and when given 20 min after TRH when PRL plasma levels were high. During the coadministration design (third ECT session) PRL levels were raised not as a sum of the two stimuli but even significantly more. TRH failed to modify the duration of the seizure induced by ECT. Therefore, if TRH is involved in seizure modulation during ECT, our findings suggest a postictal rather than ictal role for TRH.
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PMID:Effects of thyrotropin-releasing hormone administration on the electroconvulsive therapy induced prolactin responses and seizure time. 867 90

The distinction between syncope and epileptic seizures is a common clinical diagnostic problem. Elevated serum prolactin (PRL) concentrations are used to help differentiate epileptic from nonepileptic attacks such as pseudoseizures. Reports of PRL concentrations following syncope have been variable. To determine whether PRL rises after syncope, we measured serum PRL concentrations during a 45-minute passive 60-degree head-up tilt in 21 patients with a history of near-fainting or syncope. Head-up tilt triggered hypotension (mean arterial pressure 51 mm Hg, 95% CI = 45-57) with syncope in 11 patients. PRL concentrations were elevated ( > 19 ng/mL) and reached a maximum within the first 30 minutes after tilt-induced syncope in nine patients (PRL supine: 11 ng/mL, 95% CI = 7-15, vs. PRL after syncope: 52 ng/mL, 95% CI = 36-67; a greater than fourfold rise), while they remained unchanged in 10 patients who had a normal response to head-up tilt (PRL supine: 6 ng/mL, 95% CI = 5-8, vs. maximum PRL while upright: 8 ng/mL, 95% CI = 6-10). The findings indicate that elevated PRL concentrations are present after hypotensive syncope and are of little use in differentiating such syncope from epileptic seizures.
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PMID:Serum prolactin concentrations are elevated after syncope. 915 12

An abnormal circadian pattern of melatonin was found in a group of young adults with an extreme autism syndrome. Although not out of phase, the serum melatonin levels differed from normal in amplitude and mesor. Marginal changes in diurnal rhythms of serum TSH and possibly prolactin were also recorded. Subjects with seizures tended to have an abnormal pattern of melatonin correlated with EEG changes. In others, a parallel was evidenced between thyroid function and impairment in verbal communication. There appears to be a tendency for various types of neuroendocrinological abnormalities in autistics, and melatonin, as well as possibly TSH and perhaps prolactin, could serve as biochemical variables of the biological parameters of the disease.
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PMID:Brief report: circadian melatonin, thyroid-stimulating hormone, prolactin, and cortisol levels in serum of young adults with autism. 872 32


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