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)

Fifteen inpatients (nine women, six men) aged 50-86 years with DSM-IIIR major depression were treated with electroconvulsive therapy (ECT). Electrode placement (unilateral versus bilateral) and total number of treatments were determined by the patients' own psychiatrists according to clinical indications. Prolactin (PRL) was determined after the 1st, 6th, 7th, 9th, 11th, and final ECT treatments. Subjects were rated with the Hamilton Depression Rating Scale (HDRS) at baseline, after the sixth ECT treatment, and upon completion of ECT. PRL response to unilateral ECT was consistent across treatment for each subject. Percentage PRL increase was significantly higher for bilateral than unilateral ECT (alpha = 0.05). Subjects with final HDRS of < 12 tended to have greater peak, increase, and percentage increase PRL at the first unilateral treatment than subjects with final HDRS of at least 12; these trends approached statistical significance (Kruskal-Wallis one-way analysis of variance; peak: p = 0.059, chi = 3.556, df = 1; increase: p = 0.099, chi = 2.722, df = 1; percentage increase: p = 0.099, chi = 2.722, df = 1). Decrease in HDRS after the sixth treatment failed to show a statistically significant relationship to any PRL parameter at the initial unilateral treatment. Further studies are needed to characterize the relationship between PRL response, seizure activity, and stimulus dosing.
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PMID:Prolactin release and clinical response to electroconvulsive therapy in depressed geriatric inpatients: a preliminary report. 779 64

Levels of prolactin (PRL) and cortisol were estimated to find out the acute effects of generalised tonic clonic seizures (GTCS), partial seizures and pseudoseizures in 60, 18 and 9 patients respectively. Prolactin levels were estimated at 20, 60 and 120 minutes whereas, cortisol was estimated at 20, 60, and 120 minutes postictally. Cortisol and PRL estimation was also done in 10 healthy controls and 11 patients of epilepsy during interictal phase. Serum PRL levels were elevated (> 25 ng/ml) in 68.33% of GTCS and 11.11% of partial seizure cases. The peak levels were achieved in first 30 minutes after the seizures with a gradual return to base line during subsequent one hour. None of the patients with pseudoseizure showed any rise in serum PRL levels. The interictal PRL levels were normal in all the epileptics. Plasma cortisol levels were elevated during 60 to 120 minute postictal period in 45% of GTCS, 55.55% of partial seizures and 66.66% of pseudoseizure patients. Cortisol appears to be non-selectively triggered by all stressful events but postictal PRL estimation can help in differentiating pseudoseizures from GTCS. While an elevated PRL indicates the occurrence of grandmal seizure, a normal postictal PRL level does not always exclude epileptic seizure, specially a partial seizure.
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PMID:Prolactin and cortisol levels in seizure disorders. 877 25

Sex steroid peripheral pattern, pulsatile luteinizing hormone (LH) secretion, gonadotropin and prolactin responses to LH-releasing hormone (LHRH) and thyrotropin-releasing hormone (TRH) were studied in 35 male epileptics treated with phenobarbital (PB), carbamazepine (CBZ), or phenytoin (PHT), and in age-matched healthy males. Idiopathic generalized epilepsy (IGE) was diagnosed in 12 cases and partial epilepsy (PE) in 23 cases. Patients were seizure-free and did not show EEG abnormalities at repeated controls in the last 5 years, so that interfering effects of seizures were possibly excluded. The aim of the study was to evaluate both the role of epileptic syndromes and of anti-epileptic drugs on the endocrine function. Changes in sex hormone binding globulin, total and free testosterone, dihydrotestosterone and delta 4-androstenedione were found to be independent of the epileptic syndrome type. The LH response to LHRH was lower in PB-treated PE than in IGE subjects on the same drug regimen. An impairment of LH pulsatility with respect to controls was found in PE but not in IGE patients taking PB. Among antiepileptic drugs, PHT is associated with higher sex hormone binding globulin and estradiol and lower free testosterone and dihydrotestosterone levels. PB and CBZ, but not PHT, blunt the LH response to exogenous LHRH in PE. Prolactin responses to TRH were consistently enhanced in PE subjects treated with CBZ or PHT.
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PMID:Sex hormones, gonadotropins and prolactin in male epileptic subjects in remission: role of the epileptic syndrome and of antiepileptic drugs. 796 56

Serum levels of prolactin may increase as a consequence of epileptic seizures. The hormone release is caused by the propagation of epileptic activity, usually from the temporal lobe to the hypothalamic-pituitary axis. Due to the intensity of the epileptic afterdischarge, a rise is seen in approximately 60% of complex partial seizures. Prolactin usually fails to rise after psychogenic seizures, therefore, postictal prolactin levels can be used to differentiate between epileptic and psychogenic seizures. However, a subclassification of epileptic seizures by means of prolactin measurement is not possible. In repetitive seizures, prolactin may show a decrease in its postictal release. This is more common in status epilepticus, probably as a result of a diminished propagation of ictal activity during the course of status epilepticus. The influence of chronic epileptic discharges and anticonvulsant medication on prolactin release is moderate.
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PMID:Epilepsy and prolactin in adults: a clinical review. 880 Jun 30

Prolactin (PRL) plasma levels rise several fold in response to electroconvulsive therapy (ECT). There is evidence that the magnitude of ECT-induced PRL release varies as a function of electrode placement with bilateral (BL) ECT, producing a larger PRL increase than does unilateral (UL) ECT. Although there is some evidence that the amount of PRL released by ECT may also vary as a function of stimulus intensity, the effect of stimulus intensity on the amount of PRL released by UL ECT has not been studied. This is an important question because it is with UL electrode placement that large differences in clinical efficacy as a function of stimulus intensity have been documented. We studied patients undergoing a course of UL ECT as the clinically indicated treatment for their illness. Subjects received low-dose (threshold) and high-dose (three times the threshold) ECT on two consecutive treatments. The order of low- and high-dose treatments was counterbalanced. Blood samples were drawn at 15-minute intervals before and for 1 hour after the administration of ECT and assayed for PRL and cortisol levels. Our results clearly indicate that the PRL and cortisol response to UL ECT-induced PRL release varies as a function of stimulus intensity. In fact, the amount of PRL released by high-dose UL ECT was nearly three times greater than that released by threshold stimulation. These results are consistent with the hypothesis advocating that the therapeutic advantage of high-intensity over low-intensity UL ECT is the result of greater seizure generalization and spread to subcortical regions and suggest that ECT-induced PRL release has the potential to distinguish a seizure induced by a therapeutic stimulus from a seizure induced by a stimulus known to have little therapeutic effect.
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PMID:Effect of stimulus intensity on prolactin and cortisol release induced by unilateral electroconvulsive therapy. 887 9

Virusencephalitis is characterised by clinical symptoms of a parenchymatous inflammation. In addition, early mental status changes often occur as a result of virusencephalitis, beside focal neurological deficiencies, epileptic seizures, cerebral compression, even coma. Other pathological manifestations of virusencephalitis are disturbances of the neurohumoral and the endocrine system, which are often recognised and treated too late. This case report describes symptoms, treatment, and complications of a 76 year old female in-patient, who was diagnosed with virusencephalitis. The number of lymphocytes in the cerebrospinal fluid was increased to 30 cells per microliter, liquor albumin was 1705 mg/l, liquor sugar was 53 mg/dl and liquor lactat was 1.9 mmol/l. IgM antibodies against herpes viruses were found in the cerebrospinal fluid and distinct contrasting foci were found near the mammillary bodies, hypothalamus, tractus opticus, hypophyseal stalk and right parahippocampal in the magnetic resonance imaging of the head, indicating a focal herpes simplex encephalitis. Within seven days, the following symptoms developed: akinetic parkinsonian syndrome, central diabetes insipidus with hypernatremia and polyuria (6 l/die), hypothyreosis, adrenal insufficiency with adynamia, sopor, hypotension and even hypophyseal coma. Panhypopituitarism was diagnosed after measuring the basal hormone levels (ACTH, TSH, FT3, FT4, Cortisol, Prolactin, LH, FSH, ADH) and conducting the pituitary stimulation test. The severeness of all symptoms was slightly improved after substitution with antidiuretic hormone at 0.4 microgram/die and administration of hydrocortisone at 50 mg/die. Administration of amantadine sulphate at 0.6 g/die and L-dopa at 187.5 mg/die for 14 days resulted in a complete regression of the parkinsonism. After administration of aciclovir at 2.25 g/die for 21 days a complete regression of the clinical symptoms could be reached in connection with a decrease of 90% in number and size of cerebral contrasting foci in the magnetic resonance imaging of the head. Three month after therapy, clinical examination and blood serum analysis revealed persistent panhypopituitarism. The present case report is the first description of a viral infection on of the central nervous system (CNS) in combination with parkinsonism, diabetes insipidus, persistent panhypopituitarism and hyperprolactinemia. Early treatment of viral infections of the brain can improve a patient's prognosis dramatically. Early determination and early treatment of a patient's neurohumoral parameters is therefore critical to prevent or reverse early mental status changes like attention disturbances, alterations of personality and behavior, apathy, and slowed cognition.
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PMID:[Virus encephalitis with symptomatic Parkinson syndrome, diabetes insipidus and panhypopituitarism]. 1059 69

Serum samples before and after electroconvulsive therapy (ECT) from eight women patients revealed that prolactin blood levels reached a peak about 11 min after the end of the seizure. On average, the peak elevation over baseline was 385%; this elevation correlated strongly (r = 0.6, p < 0.001) with baseline blood levels. Prolactin peaks after bilateral ECT were significantly (p < 10(-5)) higher than those after unilateral ECT, although seizure duration was not longer. Application of a mathematical model gave an estimate of 17.3 min for the half-life of prolactin elimination from the blood, close to published metabolic measurements. The rate of prolactin release into the blood was greater than the rate of its elimination from the blood.
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PMID:Time Course of Post-Electroconvulsive Therapy Prolactin Levels. 1194 Aug 11

Study of serum prolactin during electroconvulsive therapy (ECT) in depressive patients revealed a greater prolactin increase after bilateral than after unilateral ECT. A linear correlation between the two types of prolactin response was found for a group of 10 patients, a finding that suggests a quantitative rather than a qualitative difference between bilateral and unilateral ECT with regard to their prolactin-releasing properties. The magnitude of prolactin response did not differ between right and left unilateral ECT, nor in a systematically studied case of postictal dysphoric excitement that occurred after right, but not after left, unilateral ECT. In this case, maximal prolactin response occurred earlier with right than with left unilateral ECT. Prolactin increase after ECT was not correlated with such factors as severity of depression nor seizure duration.
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PMID:Electrode Placement and Prolactin Response to Electroconvulsive Therapy. 1194 Aug 52

Prolactin (PRL) plasma levels rise severalfold following spontaneous or electrically induced seizures. To assess the role of dopamine in this neuroendocrine response, we studied the effect of electroconvulsive therapy (ECT) on plasma PRL after maximal dopamine receptor blockade induced by intravenous metoclopramide. Six patients undergoing ECT received metoclopramide or placebo, in counterbalanced order, 30 min prior to application of the electrical stimulus. Blood samples were obtained at - 15 min, immediately before, and at 15 min intervals for 1 h after the treatment. Under placebo conditions, PRL plasma levels increased nearly sevenfold in response to ECT. The administration of metoclopramide produced a large increase in PRL plasma levels, with no further increase in PRL concentrations after ECT. The data suggest that the PRL plasma rise after ECT involves dopamine as it is not seen when the dopaminergic inhibitory tone, exerted by the hypothalamus on the pituitary lactotroph, has been removed.
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PMID:The Role of Dopamine in Seizure-Induced Prolactin Release in Humans. 1194 Nov 58

Prolactin releasing peptide (PrRP) is a recently identified neuropeptide that stimulates prolactin release from pituitary cells. The presence of its receptor outside the hypothalamic-pituitary axis suggests that it may have other functions. We present here evidence that PrRP can modulate the activity of the reticular thalamic nucleus, a brain region with prominent PrRP receptor expression that is critical for sleep regulation and the formation of non-convulsive absence seizures. Intracerebroventricular injection of PrRP (1-10 nmol) into sleeping animals significantly suppresses sleep oscillations and promotes rapid and prolonged awakening. Higher concentrations of PrRP (10-100 nmol) similarly suppress spike wave discharges seen during absence seizures in genetic absence epilepsy rats from Strasbourg, an animal model for this disorder. In concordance with these findings, PrRP suppressed evoked oscillatory burst activity in reticular thalamic slices in vitro. These results indicate that PrRP modulates reticular thalamic function and that activation of its receptor provides a new target for therapies directed at sleep disorders and absence seizures.
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PMID:Prolactin-releasing peptide (PrRP) promotes awakening and suppresses absence seizures. 1220 68


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