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)

Cerebrospinal fluid (CSF) from 6 cases of asymptomatic infantile spasms (IS) (mean age, 6.1 months) was collected before and after treatment with adrenocorticotropic hormone (ACTH). The concentration of CSF tryptophan (TRP) metabolites was analyzed using HPLC and compared to the metabolite concentration in CSF from 10 age-matched controls (mean age, 6.7 months). Levels of CSF serotonin (5-HT), 5-hydroxyindoleacetic acid (5-HIAA), and kynurenine (KYN) at pretreatment were significantly lower in IS patients compared to controls (p < 0.05). In contrast, the levels of CSF 3-hydroxykynurenine (3-OHKY) before ACTH treatment were significantly higher in IS patients than in controls (p < 0.05). After the treatment, significant increases in 5-HIAA and decreases in KYN and 3-OHKY levels (p < 0.05) were observed in CSF of infants whose seizures were eliminated by ACTH. These findings suggested that the presence of seizures in IS was associated with a significant decrease in serotonergic activity, or that the turnover in the direction of 3-OHKY was altered. The possibility that elimination of seizures by ACTH might be related to decreased production of kynurenine metabolites was discussed.
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PMID:[Changes in CSF tryptophan metabolite levels in infantile spasms]. 141 65

Induced microseizures (IMS) were observed in a 5-month-old girl with symptomatic West syndrome. The seizures occurred following the suppression of infantile spasms with adrenocorticotropic hormone therapy and disappeared following the cessation of clonazepam administration. The ictal manifestations consisted of periods of irregular respiration, and respiratory arrest lasting for several seconds which often involved opening of the eyes and mild extension of the neck corresponding with the diffuse fast wave bursts in EEG activity observed during sleep. These seizures were thought to be equivalent to the IMS in Lennox-Gastaut syndrome, which have never been reported before in patients with West syndrome.
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PMID:Induced microseizures in West syndrome. 165 8

Among the 257 pediatric patients examined, 104 were classified as having drug-resistant epilepsy (DRE). In all of them genetic, metabolic, chromosomal and infectious causes were investigated, and brain imaging with computed tomography scans and nuclear magnetic resonance were obtained. Since treatment with gammaglobulins (GGs) has been reported to be useful in pediatric cases of epilepsy, informed consent for GGs treatment was obtained in 43 patients with DRE. The etiology or evidence of brain lesions was identified in 16 of them. In 31 of these patients, neither conventional drug treatment, nor a trial with adrenocorticotropic hormone was successful. Intact monomeric GGs, 400 mg/kg, were given intravenously. A second dose was given after 15 days and, thereafter, every 21 days for a maximum of ten injections (protocol A), or every 2nd day for a maximum of five doses (protocol B). In every patient, the type of epilepsy was identified according to the classification of the International League Against Epilepsy. The frequency of seizures was recorded for a period beginning at least 6 months before the administration of GGs. Immunological evaluation was also performed before and after the treatment with GGs. A transient decrease of the seizure frequency was noted in 12 subjects. In another patient with infantile idiopathic myoclonic epilepsy, seizures disappeared for 30 months. In 1 case a persistent 80% reduction in the number of seizures was observed. A persistent disappearance of seizures was noted in a subject with complex partial seizures (CPS) that followed an idiopathic infantile spasm syndrome.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Use of intravenous immunoglobulins in drug-resistant epilepsy. 166 50

Cerebrospinal fluid (CSF) from 7 patients with infantile spasms (mean age: 6.7 months) was collected before and after treatment with adrenocorticotropic hormone (ACTH). The concentration of neurotransmitter metabolites was analyzed using high-performance liquid chromatography and compared to the metabolite concentration in the CSF from 7 age-matched controls (mean age: 6.1 months). Pretreatment levels of CSF 5-hydroxyindoleacetic acid (5-HIAA), homovanillic acid, 3-methoxy-4-hydroxyphenyl glycol (MHPG), and kynurenine were significantly lower in infantile spasm patients compared to controls. Following treatment, marked increases in 5-HIAA and decreases in kynurenine levels were observed in the CSF of the 5 infants whose seizures were eliminated or reduced by ACTH. In the 2 nonresponders 5-HIAA levels decreased. The level of MHPG was reduced slightly in 5 infants, including the 2 nonresponders, and was increased in 2 responders. CSF homovanillic acid levels increased in 4 infantile spasm infants and decreased in 3 following ACTH. These data demonstrate that the presence of seizures in infantile spasms is associated with a significant decrease in serotonergic activity and that elimination of seizures by ACTH is accompanied by increased serotonin turnover. The simultaneous increase of 5-HIAA and decrease of kynurenine, an alternate metabolite of tryptophan, suggests an underlying disturbance of tryptophan metabolism in infantile spasms. The possibility that elimination of seizures by ACTH may be related to decreased production of certain kynurenine metabolites, particularly quinolinic acid, is discussed.
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PMID:Changes in CSF neurotransmitters in infantile spasms. 172 2

We report seizures induced by adrenocorticotropic hormone (ACTH), which were demonstrated clinically and electro-encephalographically, in a severely handicapped 7-month-old infant with West syndrome due to perinatal hypoxicischemic encephalopathy. Although tonic spasms (original seizures) decreased soon after starting ACTH treatment, new brief tonic seizures, somewhat more slowly motioned than the original tonic spasms, frequently appeared only during sleep after consecutive ACTH injections for 11 days, in place of the tonic spasms seen in the waking state. After discontinuation of ACTH therapy with the last injection on the 16th day, the brief tonic seizures began to decrease and finally disappeared in 8 days. Ictal EEG of new brief tonic seizures revealed diffuse fast spiky wave bursts, 50-150 microV and 10-20 c/s, with a duration of 0.5-4 seconds, which were different from attenuation associated with low voltage rhythmic fast activity corresponding to tonic spasms, the original seizures. Therefore, we considered that the new brief tonic seizures, which appeared only during sleep in the course of ACTH therapy, were ACTH-induced seizures.
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PMID:ACTH-induced seizures in an infant with West syndrome. 255 40

Recurrent seizures are a significant cause of childhood morbidity. Often the underlying pathogenesis is unknown. Studies from several laboratories have suggested a relationship between perturbations of humoral immunity and clinical epilepsy. Brain-specific antigens have been observed in the systemic circulation after brain injury. This can be followed by the appearance of antibodies to neuronal tissues in both serum and cerebrospinal fluid. Moreover, there appears to be disproportionate representation of persons with coexisting humoral immune deficiencies among patients with chronic epilepsy. Interestingly, a potent immunosuppressant, adrenocorticotropic hormone, has long been the principal treatment for infantile spasms. Given this body of information associating humoral immunity with recurrent seizures, several investigators have recently attempted to treat intractable childhood epilepsy with high-dose intravenous immune globulin. Although the number of patients treated is small and it is not possible to make comparisons between individual studies, nevertheless the results have been encouraging. Five patients with intractable seizures who failed to respond to conventional therapy were treated with an outpatient regimen of intravenous immune globulin (1 gm/kg/day) for 2 days. Two patients showed significant clinical improvement while a third had an equivocal response. Immunologic analysis of these patients before therapy revealed a surprisingly high incidence of immune abnormalities. We conclude that intravenous immune globulin may be useful in the treatment of selected patients with chronic epilepsy unresponsive to anticonvulsants.
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PMID:Use of intravenous immune globulin in the treatment of seizure disorders. 279 1

Suppression of an adrenocorticotropic hormone (ACTH) response to insulin hypoglycemia has been reported in ACTH-treated adults. There are no guidelines for withdrawal of ACTH treatment in children. After observing suppressed morning cortisol in several children, insulin tolerance tests were performed in five children within 48 hours after tapered withdrawal of ACTH treatment for myoclonic seizures. ACTH response, as determined by cortisol and beta-endorphin radioimmunoassay, was adequate in four of the children. One child showed low basal levels and minimal elevation during hypoglycemia for both beta-endorphin (0 to 3 pg/ml) and cortisol (3.6 to 4.4 micrograms/dL) on initial testing, but normal responses six weeks later. Measurement of beta-endorphin response supported a central basis for suppression in the child, who had had an adrenal hemorrhage during gram-negative sepsis while on ACTH. ACTH release is transiently suppressed in some children after exogenous ACTH treatment. Tapered withdrawal and stress coverage is recommended.
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PMID:Suppressed pituitary ACTH response after ACTH treatment of infantile spasms. 303 33

Infantile spasms constitute a severe seizure disorder unresponsive to standard anticonvulsants. Both prednisone and adrenocorticotropic hormone (ACTH) have produced remission of seizures in some patients. The mechanisms of action of these hormones are not known. Eight infants with infantile spasms were treated with prednisone for 2 weeks. This controlled the seizures in two patients. In the remaining six patients, prednisone was continued and ACTH was added. This treatment produced cessation of spasms in four patients. Serum prednisone and cortisol were measured at a number of points during treatment. In infants receiving prednisone and then prednisone plus ACTH, serum cortisol was suppressed to about one-quarter of baseline levels with the initiation of prednisone, and remained suppressed during ACTH administration. We conclude that ACTH can exert its effect on infantile spasms in the setting of adrenal suppression, and can act without stimulating endogenous cortisol production. A CNS site of action is suggested and should be sought.
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PMID:Adrenocorticotropic hormone controls infantile spasms independently of cortisol stimulation. 609 Jan 11

As more small peptidergic components of the central nervous system are isolated, their role in disease states is being investigated. Several of these neuropeptides, especially the opioidlike peptides, adrenocorticotropic hormone, and some hypothalamic releasing factors, have been found to alter neuronal excitability. This finding has led to the proposal that these peptides may play a role in the pathogenesis of the epilepsies. We tested this hypothesis in a genetic model of epilepsy. At nontoxic doses, several exogenously administered peptides had anticonvulsant properties, while others were proconvulsant. The most potent anticonvulsant was the opioidlike peptide beta-endorphin. Its effect was similar to that of the opioid alkaloids. Using the potent antagonist naloxone hydrochloride to block possible endogenous opioid-like peptides, we found no effects on seizures in naive animals. Naloxone did alter postictal events, however, by partially blocking the postictal refractoriness to further seizures. We speculate that one possible role for the endogenous opioid peptides may be to limit the spread of seizures or to modulate postictal susceptibility to further seizures. Naloxone was effective in this model only after stressful situations occurred that modified the seizures and presumably induced a release of endogenous opioidlike peptides. Support for this hypothesis from other epilepsy models is discussed. Other peptidergic systems may also be active in various epileptic models, and the current understanding of their roles is reviewed.
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PMID:Neuropeptides: a role as endogenous mediators or modulators of epileptic phenomena. 609 40

ACTH and cortisol were measured simultaneously in plasma samples obtained every 5 min from subjects at two different diurnal times. In the first study adrenocorticotropic hormone (ACTH) mean concentration and secretory rate were elevated in anticonvulsant drug-treated temporal lobe epileptic patients in comparison to anticonvulsant drug-treated patients with pseudoseizures. Cortisol mean concentrations and secretory rate were similar in these groups of subjects. In the second study, mean ACTH concentration and secretory rate were higher in temporal lobe epileptic patients than in normal controls. Both measures of ACTH secretion were similar in post-temporal lobectomy patients and normal controls. Mean cortisol concentration and secretory rates were highest in the temporal lobe epileptic patients, lowest in normal controls, and intermediate in post-temporal lobectomy patients. We conclude that ACTH and cortisol secretion is abnormal in temporal lobe epileptic patients. Temporal lobectomy restores abnormal ACTH secretion to normal whether or not seizures are controlled. The absence of ACTH changes in the pseudoseizure patients suggests that these changes are not drug induced. Cortisol secretion is similar in temporal lobe epileptic patients and pseudoseizure patients, suggesting a direct effect of the drugs upon the adrenal cortex.
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PMID:Pituitary and adrenal function in epileptic patients. 609 18


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