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Query: UMLS:C0036572 (seizures)
80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Changes in plasma glucose, nonesterified fatty acids, insulin, glucagon, cortisol, growth hormone, and prolactin have been studied in baboons during the course of generalized epileptic seizures induced by intravenous bicuculline. Plasma glucose rose to a peak at 25 min but fell to hypoglycemic levels after 60 min of seizure activity. This hypoglycemia was accompanied by a marked elevation in plasma insulin. Plasma glucagon rose to a peak at 14 min, then returned to normal. Plasma growth hormone levels were elevated after 60 min of seizure activity. Plasma prolactin and cortisol levels also rose during the seizure. These changes result from sequential interaction of (1) autonomic activation at seizure onset, (2) spread of neuronal activity to the hypothalamus leading to the liberation of releasing factors, and (3) indirect physiologic consequences of seizure activity.
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PMID:Endocrine factors and glucose metabolism during prolonged seizures in baboons. 11 9

The studies included 64 children with newly diagnosed epilepsy, aged from 6 to 15 years of life. In 25 children with partial and secondary generalized seizures monotherapy with carbamazepine was introduced; in 19 children with primary generalized seizures--with phenobarbital, and in patients with both types of seizures--with primidone. Monotherapy was controlled by means of blood serum drug concentration level monitoring; the therapy was successful in all the children. The group did not include patients with mental retardation, and epilepsy was idiopathic. Prior to the institution of treatment, a single determination of blood serum triiodothyronine, thyroxine, TSH, prolactin, cortisol, LH and testosterone was made. Psychological test were carried out employing Wechsler's scale, Bender-Santucci test, rhythmic structures developed by Mira Stambak and test of manual dexterity (card display). In order to evaluate short-term effects of the employed drugs upon the blood serum concentration values of the studied hormones, a repeated determination was made one month after the initiation of therapy. The third determination was made one year after the onset of treatment in order to assess the long-term effects. The effect of drugs upon their cognitive functions was assessed in a follow-up psychological testing performed after one year of therapy. The studies combined with statistical analysis led to a conclusion that after one month of monotherapy there occurred a significant drop in thyroxine concentration levels, still augmented after one year. Patients treated with carbamazepine showed a significant decrease of T3 levels after one month and one year, whereas treatment with phenobarbital and primidone did not result in significant changes of T3 concentration. Yet, T3 and T4 concentration values did not exceed normal limits. No type of monotherapy resulted in significant long-term changes of TSH concentration levels. No clinical signs of hypothyroidism nor goiter were observed in the studied children. After one month of monotherapy with carbamazepine and phenobarbital there was observed a significant increase of prolactin and cortisol levels, which was absent after one year. The values observed did lie within normal limits. No significant changes were observed with respect to the effect of the studied drugs upon blood serum LH and testosterone levels. After a one-year monotherapy with primidone the children revealed a significant improvement of results measured on performance scale and by means of a full Wechsler scale. Carbamazepine and phenobarbital did not affect the intelligence quotient of the studied children.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[The effect of monotherapy on concentration of selected blood serum hormones and upon cognitive function of children with epilepsy]. 134 59

This study measures whether there is a rise in the secretion of nocturnal prolactin and growth hormone (GH), during the delta phase of the first sleep cycle in children who are suffering from either complex partial or generalized tonic-clonic seizures. The findings are compared with those obtained in the control group of patients which is made up who suffer from pseudoseizures. There is a moderate but significant rise in the nocturnal prolactin plasma level in both types of infantile seizures. No significant difference was found in the GH.
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PMID:Nocturnal prolactin and growth hormone levels in children with complex partial and generalized tonic-clonic seizures. 141 23

In 20 healthy subjects (10 female and 10 male) and 17 patients undergoing presurgical epilepsy evaluation with intracranial EEG electrodes, circadian variations of serum prolactin (PRL) were measured. A comparison between the peak values found in normals with the postictal rises in patients, led us to consider 700 microU/ml to be the threshold of diagnostic value and the observed rises above this level to be all induced by seizures. In order to assess the clinical value of this threshold, PRL was measured postictally in a further 30 patients with epilepsy and in 11 patients with psychogenic seizures. In none of the latter group did PRL rises exceed 700 microU/ml, while they did so in 39% of the complex partial seizures and in 80% of the tonic-clonic seizures. There was no significant difference with respect to sex (a rise over 700 microU/ml in 42% in male and in 55% in female patients). Based on the findings in 17 patients investigated by means of intracranial electrodes, we were not able to establish different criteria for different focus localisations: in 66% of both temporal as well as frontal lobe seizures the 700 microU/ml level was exceeded. As a trend, in the period preceding an epileptic seizure we found a slightly decreasing PRL level, whereas in healthy persons the PRL concentrations gradually increased in the 40 minutes before the maximum spontaneous peak was reached.
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PMID:Serum prolactin concentrations and epilepsy. A study which compares healthy subjects with a group of patients in presurgical evaluation and circadian variations with those related to seizures. 150 14

Transient elevation of serum prolactin frequently follows generalised tonic-clonic and complex partial seizures. However, the levels of prolactin during status epilepticus are not increased above the normal range. Exhaustion of central prolactin supplies has been proposed as a possible mechanism for the absence of prolactin increase during status epilepticus. To test this hypothesis we injected intravenous metoclopramide (10 mg) in eight consecutive patients with status epilepticus. One patient had generalised tonic-clonic status epilepticus. Seven patients had EEG-verified non-convulsive status epilepticus, consisting of one typical absence status, one atypical absence status and five complex partial status epilepticus. Metoclopramide raised the mean (SD) prolactin levels at least five-fold in all patients, from 5.8 (8.0) micrograms/l to 87.0 (39.0) micrograms/l, within 60 minutes after the injection. Thus the mechanism for low prolactin values in status epilepticus is not cellular depletion of stored prolactin, but more likely an altered regulation, presumably induced by prolonged seizure activity.
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PMID:Serum prolactin response to metoclopramide during status epilepticus. 152 38

The acute effects of partial (focal) epileptic seizures on serum prolactin levels were studied in two groups of patients: (1) 10 with temporal lobe seizures and (2) 11 with seizures that arose from the frontal lobes, recorded on cable video-electroencephalographic telemetry. Six of the eight complex partial seizures of temporal lobe origin were associated with a marked rise in prolactin levels at 10 minutes after onset (rise in levels, from a mean of 279 to 534 mU/L), compared with a rise in only one of the eight frontal lobe complex partial seizures. None of the five simple partial seizures (two of temporal and three of frontal lobe origin) was associated with a marked rise in prolactin levels. This difference in prolactin response following complex partial seizures of frontal and temporal lobe origin may help in the clinical differentiation of these seizures. A failure of prolactin levels to rise does not, however, exclude a diagnosis of complex partial seizures; thus, this measurement will not help in the clinical differentiation of frontal lobe complex partial seizures from psychogenic attacks.
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PMID:Comparison of the effects of frontal and temporal lobe partial seizures on prolactin levels. 801 35

Intensive neurodiagnostic monitoring is useful in the diagnosis and classification of epileptic seizures and other paroxysmal disorders. The correlation of clinical/behavioral data, EEG events, and serum prolactin levels may clarify the type(s) of epileptic seizures and may distinguish epileptic seizures from non-epileptic events. Serial determinations of AED's may assist in the detection of problems with AED compliance and with drug interactions which complicate the patient's management.
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PMID:Intensive neurodiagnostic monitoring. 160 49

Prolactin levels were measured immediately after the seizure in some, and 15 to 20 minutes later in all of 67 children aged between 6 months and 17 years. Values were determined after grand mal, complex partial and petit mal seizures and psychogen seizures. A more than 2 to 3 fold prolactin increase over the baseline value occurred almost always after grand mal and regularly after complex partial seizures. No hyperprolactinaemia was observed after petit mal seizures. Also after psychogenic seizures a rise in serum prolactin failed. The neurophysiological basis underlying this phenomenon is a decrease of gaba- und dopaminergic systems associated with the seizure. The described method is useful in the differential diagnosis of epileptogenic versus psychogenic seizures.
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PMID:[Serum prolactin after cerebral and psychogenic seizures in childhood and adolescence--an additional useful method for differentiating the two forms of seizure]. 161 80

Serum prolactin (HPR) levels are influenced by waking and sleep states, as reflected by surges in serum concentrations during daytime naps and nocturnal sleep. Other physiological causes of hyperprolactinemia include sexual activity, pregnancy, and lactation. Drugs may stimulate or inhibit HPR secretion. Pathological causes for HPR secretion include destructive lesions of the hypothalamus, prolactin-secreting neoplasms of the pituitary gland, lesions of the spinal cord, and occasionally Parkinson's disease. The most predictable postictal changes are increased serum cortisol levels and hyperprolactinemia. Serum HPR rises after virtually all generalized tonic-clonic seizures, most complex partial seizures, and some simple partial seizures. Absence and myoclonic seizures do not affect serum HPR levels. Repeated epileptic seizures and electroconvulsive therapy treatments produce successively less marked rises in serum HPR. The postictal elevation of serum cortisol has a longer latency than for HPR and follows an earlier rise in serum ACTH. Other postictal hormonal changes are much more variable. Because of the normal diurnal variation in serum cortisol levels and the relative delay in the postictal elevation of serum cortisol, HPR is more useful as a diagnostic measure of epileptic seizures. This application of HPR requires an understanding of other factors that influence serum HPR and the use of baseline serum HPR levels for comparison. HPR data must be correlated with behavioral and electroencephalographic events.
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PMID:The effect of seizures on hormones. 165 82

The potential of transcranial magnetic stimulation (TMS) to cause undesired or unexpected effects on cognition and other cerebral functions has received only limited study, although extensive clinical use has suggested that obvious problems are unlikely. Evidence so far accumulated suggests that exposure to TMS in the expected clinical situations will have no persistent effects on the electroencephalogram (EEG) or on cognitive function, although transient effects may occur. The absence of increases in either prolactin or adrenocorticotropic hormone (ACTH) in subjects undergoing TMS indicates that seizure-like events do not routinely occur, although recent evidence suggests that TMS may cause seizures or enhance the occurrence of epileptiform abnormalities in circumstances of heightened susceptibility. Despite these observations, treated seizure patients are unlikely to experience seizures with TMS. The technique is generally safe, but not entirely free from unwanted effects, and further study to define those effects is warranted.
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PMID:The safety of transcranial magnetic stimulation reconsidered: evidence regarding cognitive and other cerebral effects. 166 48


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