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PubMed1992

Brain neuropeptides: changes by treatment with the convulsants pentylenetetrazole and bicuculline.

1. The effects of chemically induced convulsions, clinically similar to those elicited by electroconvulsive treatment (ECT), on brain regional distribution of neuropeptide Y-, neurokinin A-, substance P- and neurotensin-like immunoreactivities were studied in the rat. 2. Pentylenetetrazole (PTZ) and bicuculline (BIC) were used to induce grand mal seizures. Rats were divided into three groups receiving one of the following treatments: Saline, PTZ (45 mg/kg) or BIC (1.5 mg/kg). 3. After sacrifice by focused microwave irradiation, brains were dissected, peptides extracted and measured by specific radioimmunoassays. 4. Repeated grand mal convulsions induced by PTZ, in similarity to ECT, markedly increased NPY-LI concentrations in frontal cortex and hippocampus. In contrast to ECT, no changes in NKA- or SP-LI levels were seen. NT-LI was lowered in striatum. 5. Bicuculline effects were more circumscribed: some animals developed grand mal and died while convulsing (peptides not measured), others did not develop generalized seizures and were sacrificed after the fourth treatment. 6. The results demonstrate a similar effect of PTZ and ECT on regional NPY-LI concentrations and raise the possibility that grand mal, regardless of etiology, is necessary for effects on peptides.

Animals↗
PubMed1992

Nerve growth factor (NGF) in rat brain following long-term barbital treatment: relation to convulsions and cognitive function.

Nerve growth factor (NGF) protein has been implicated in alterations of cognitive function either following brain damage, selective lesions or aging. Groups of rats were given long-term (48 weeks) oral barbital treatment or tap water and following an extended period of abstinence (14 weeks) were tested for spatial learning ability in the Morris swim maze. Following the maze test, they were sacrificed and the NGF content of hippocampal and cortical brain regions were analyzed. Barbital treated rats were divided into convulsing and non-convulsing groups. It was found that there was a slight, significant increase (12%) in NGF content of the hippocampus in convulsing rats. Correlations between maze learning performance, brain weight and NGF in the cortex indicated a significant negative relationship between (a) performance and brain weight on day 1 of testing and (b) NGF content and performance on day 2. These data indicate some involvement of NGF in functions derived from a considerably different animal model to those applied previously.

Animals↗
PubMed1993

Increases in brain polyamine concentrations in chemical kindling and single convulsion induced by pentylenetetrazol in rats.

Concentrations of the polyamines, putrescine, spermidine and spermine were investigated in rat brains, in which chemical kindling or single convulsion had been induced by intraperitoneal injection of pentylenetetrazol (PTZ). A single injection of 60 mg/kg of PTZ produced tonic-clonic convulsion and increased the putrescine concentration 8 h after the injection. At lower doses of PTZ (10 and 30 mg/kg), neither marked behavioral seizure nor significant change in any polyamine concentration was observed. On the other hand, repeated injections of 30 mg/kg of PTZ eventually resulted in intense motor seizures (PTZ kindling) and increased the concentrations of all three polyamines. The most marked increase was detected in putrescine 1-48 h after the intense seizures. The increase in putrescine was clearly higher in PTZ kindling than in single convulsion. These results suggest that increases in polyamine concentrations are involved in neuronal excitability in the epileptic brain.

Animals↗
PubMed1984

Differential effects of picrotoxin- and pentylenetetrazol-induced convulsions on the secretion of luteinizing hormone and follicle-stimulating hormone in rats.

A single subcutaneous (sc) injection of picrotoxin in a dose ranging from 3 to 40 mg/kg to proestrous female rats produced sustained clonic-tonic convulsions and resulted in a significant elevation of serum LH levels. FSH release was not stimulated. Serum calcium levels increased, with a positive correlation with the increment of serum LH increase in these animals. Similarly, 5 mg/kg of picrotoxin was effective in inducing an increase in serum LH and calcium, but not FSH, in adult male rats. Pentylenetetrazol in a dose of 120 mg/kg induced sustained clonic-tonic convulsions and stimulated the release of LH, but not of FSH, in both adult male and female rats. An increase in serum calcium levels also was evident. These results suggest that sustained convulsions induce overall excitation of the central nervous system and result in the enhancement of LH release from the pituitary. The mechanism responsible for the differential stimulation of LH and FSH release remains to be clarified.

Animals↗
PubMed1990

Hypozincemia during fever may trigger febrile convulsion.

Febrile convulsions are generally thought to be induced by metabolic changes during the rise-phase of body temperature. The mechanism by which convulsions are induced, however, is not fully elucidated. In this article, we propose a new hypothesis about the induction mechanism of febrile convulsions that takes into account the hypozincemia during fever. This hypozincemia activates the NMDA receptor, one of the glutamate family of receptors, which may play an important role in the induction of epileptic discharge.

Child↗
PubMed1988

The role of vasopressin as an antipyretic in the ventral septal area and its possible involvement in convulsive disorders.

Perfusion of the peptide, arginine vasopressin (AVP), within the ventral septal area (VSA) of the brain of a number of species reduces fever but not normal body temperature. This antipyretic response appears to be mediated by AVP receptors of the V1 subtype. Lesions of the VSA with kainic acid are associated with prolonged and enhanced fevers in rats. A role for endogenous AVP in fever suppression within the VSA comes from several types of experiments: (1) AVP release within the VSA is inversely correlated to fever height; (2) AVP antagonists or antiserum injected into the VSA prolong fever; (3) animals lacking endogenous AVP in the VSA (Brattleboro rat, long-term castrated rat) develop enhanced fevers. Electrical stimulation of the AVP-containing cell bodies of the bed nucleus of the stria terminalis (BST) orthodromically inhibits VSA neurons and also suppresses fever; the latter effect can be abolished with application of a V1 antagonist to the VSA. Iontophoretic studies indicate that AVP inhibits glutamate-stimulated activity of thermoresponsive and other VSA neurons. AVP can also act in the VSA to cause severe motor disturbances; this action is receptor mediated and increases in severity upon sequential exposure to AVP. Because sites of action of the antipyretic and convulsive action of AVP are similar, and because animals lacking brain AVP display reduced convulsive activity, it is possible that AVP, released during fever, could be involved in the genesis of convulsive activity.

Action Potentials↗
PubMed1987

Convulsions as the etiology of lactic acidosis in acute diazinon toxicity in rats.

Diazinon, in acute doses (40 mg/kg, i.p.) in rats produced tremors and convulsions with lactic acidosis which was accompanied by depletion of glycogen and activation of glycogen phosphorylase activity in triceps and diaphragm muscles, 2 h after its administration. Prevention of convulsions with phenobarbitone administered immediately before diazinon, resulted in neither the development of lactic acidosis nor mobilization of muscle glycogen or activation of glycogen phosphorylase. Lactic acidosis was due to depletion of glycogen through enhanced activity of glycogen phosphorylase in muscles on account of tremors and convulsions induced by diazinon in rats.

Acidosis, Lactic↗
PubMed1993

Protective effect of calmodulin inhibitors against acute cyanide-induced lethality and convulsions in mice.

The ED50 value of cyanide as measured by induction of convulsions (tonic seizure) was significantly increased by 80% or 69% when trifluoperazine (TFP) or chlorpromazine (CHP), a specific calmodulin inhibitor was preinjected intracerebroventricularly (i.v.t.) at a dose of 0.09 mumol/body of mice. However, the ED50 of cyanide was not significantly changed by the same dose of promethazine (PMZ), another calmodulin inhibitor. Since it is known that the inhibitory effect of TFP or CHP against calmodulin-dependent enzymes such as phosphodiesterase is 100-400-fold higher compared to PMZ, it is speculated that the inhibitory effect of TFP or CHP against cyanide-induced convulsions may be based on its strong inhibitory properties into calmodulin-dependent enzymes. On the other hand, the LD50 value of cyanide was significantly increased by i.v.t. preadministration of TFP or CHP (0.045 mumol/body). Furthermore, the LD50 value of cyanide was also significantly increased by the same dose of PMZ. These results suggest that there is no positive correlation between mortality and convulsions induced by cyanide.

Animals↗
PubMedDate not supplied

Prenatal alcohol exposure attenuates pentylenetetrazol-induced convulsions in rats.

Female rats prenatally exposed to alcohol were tested at 35 days of age for susceptibility to pentylenetetrazol (PTZ)-induced convulsions. There was a significant dose-response effect of PTZ. Contrary to expectations, alcohol-exposed females were slightly but still significantly less convulsion-prone than pair-fed controls. These results suggest prenatal alcohol exposure reduces the susceptibility to convulsions in rats.

Animals↗
PubMedDate not supplied

Determination of the threshold for convulsions by direct cortical stimulation.

In this study we investigated whether determination of the convulsion threshold by electrical stimulation of the cortex could be used as a simple test for measuring anticonvulsant drug activity in unrestrained, unanaesthetized rats. Pulse trains delivered to electrodes implanted in the frontoparietal cortex elicited convulsions, similar to those seen in the classical electroshock tests. The threshold could be determined rapidly with pulse trains which increased in strength in a ramp-shaped fashion (bipolar pulses of 2 msec, 50 pulses/sec, increment 1.3 microA/pulse). The threshold was defined as the current needed to elicit forelimb clonus. Upon repeated stimulation the threshold declined from a value of about 600 microA to about 350 microA in 20 sessions. Thereafter, continued testing did not result in considerable changes in threshold. After stabilization, the convulsion threshold could be determined repeatedly with intervals as short as 5 min. Following i.p. injection of 5 mg/kg of diazepam an elevation of the threshold of 30% was observed 0.5 h after injection. After 5 daily injections, evidence for the development of complete tolerance was obtained. After i.v. injection of 8 mg/kg oxazepam, the threshold increase reached a peak level of 75% after 20 min. The changes in threshold followed arterial blood concentration of oxazepam, which was maximally 4.8 micrograms/ml immediately after injection. The threshold returned to baseline in approximately 6 h. The results of the present study show that with our procedure anticonvulsant drug activity can be accurately, rapidly and repeatedly determined in individual animals, both in acute and chronic experiments.

Animals↗
PubMedDate not supplied

Transection of the pineal stalk produces convulsions in male Mongolian gerbils (Meriones unguiculatus).

The pineal gland has been implicated in the regulation of epileptic-like seizures in gerbils. Pinealectomy of gerbils results in seizures which affect approximately 80% of the gerbils. Telencephalic catecholamine levels are depressed by pinealectomy in gerbils and it has been suggested that the reduced norepinephrine (NE) levels are responsible for initiating or facilitating these seizures. The present study found that pineal stalk transection produced convulsions in gerbils which were indistinguishable from pinealectomy-induced convulsions. Stalk transection also produced a depression (38%) in parietal cortex NE levels which was similar to a depression observed in pinealectomized gerbils (52%). These depressions in cortical NE levels were not observed in other brain regions, specifically the hippocampus or the amygdala. However, a decline (25%) in hypothalamic NE levels was observed after stalk transection. These results suggest that the signals responsible for pinealectomy-induced convulsions are carried by the pineal stalk and that pinealectomy produces regional, not global, reductions in NE content.

Animals↗
PubMed1990

Recurrence of febrile convulsions in a population-based cohort.

The risk of recurrence after an initial febrile seizure was 25% in a population-based cohort of 639 children followed from their first febrile seizure. Prognostic factors were an increasing risk of recurrence with younger age at first febrile seizure, a first degree relative with febrile seizures and complex features of the first febrile seizure. The effect of complex features was modified by age at first febrile seizure and family history in that complex features alone did not increase risk of recurrence but further increased the risk for children under 18 months at first seizure and/or with a positive family history. The prognostic factors for all febrile convulsions recurrences were also prognostic for having subsequent complex febrile convulsions. Children with none of the prognostic factors had only a 3% risk of a future complex febrile seizure while children under 18 months at first febrile convulsion and a positive family history or complex features had about a 20% risk of a subsequent complex febrile seizure.

Child, Preschool↗
PubMedDate not supplied

A progressive sequence of electroencephalographic changes during generalized convulsive status epilepticus.

Review of 60 electroencephalograms recorded during episodes of generalized convulsive status epilepticus suggested that there are 5 identifiable EEG patterns which occur in a predictable sequence during the course of generalized convulsive status epilepticus in man: (1) discrete seizures; (2) merging seizures with waxing and waning amplitude and frequency of EEG rhythms; (3) continuous ictal activity; (4) continuous ictal activity punctuated by low voltage 'flat periods'; and (5) periodic epileptiform discharges on a 'flat' background. We confirmed our hypothesis that this sequence represents the natural history of electroencephalographic changes in untreated generalized convulsive status epilepticus by observing the same sequence in the EEGs of rats in which status epilepticus had been induced by 3 different methods: (1) systemic administration of kainic acid, (2) injection of homocysteine thiolactone to cobalt-lesioned rats; and (3) injection of lithium chloride followed 24 h later by injection of pilocarpine.

Adult↗
PubMed1993

Quantitative MRI hippocampal volumes: association with onset and duration of epilepsy, and febrile convulsions in temporal lobectomy patients.

The relationships between preoperatively acquired MRI-based hippocampal volumes (HV), seizure disorder onset and duration, and early childhood febrile convulsions were investigated retrospectively with data from 72 left and 56 right temporal lobectomy patients. Patients with lesional pathology and heterotopic abnormalities were excluded. Age at development of spontaneous seizures unprovoked by an acute illness defined age of seizure disorder onset. Age of onset was subtracted from age at neurosurgery to determine duration. MRI variables included in this study were the right and left HV divided by total intracranial volume (RAHV, LAHV), and the right-left hippocampal difference (DHF). Partial correlations were used to better isolate relationships with onset of recurrent seizures corrected for age at surgery, and age at neurosurgery corrected for age of recurrent seizure onset. Partial correlations between age at neurosurgery and volume were not significant in either group. LAHV (r = 0.42, P < 0.0003) and DHF (r = -0.49, P < 0.0001) were correlated with age of onset in the left lobectomy group. Correlations in the right lobectomy group were not significant. The presence of a febrile convulsion was associated with smaller LAHV (F(1,70) = 10.54, P < 0.002) and larger DHF (F(1,70) = 11.36, P < 0.002) in left temporal lobectomy patients. The presence of a febrile convulsion in the right temporal group was associated with a slightly smaller DHF (F(1,56) = 5.90, P < 0.02), and slightly smaller RAHV (F(1,56) = 4.49, P < 0.04). These data suggest that hippocampal atrophy remains stable over the duration of temporal lobe onset seizure disorders, and is associated with early onset of recurrent seizures in left temporal patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1994

A new, non-pharmacologic model of convulsive status epilepticus induced by electrical stimulation: behavioral/electroencephalographic observations and response to phenytoin and phenobarbital.

Much remains to be learned about mechanisms underlying entry into, and temporal progression of, status epilepticus (SE). This report describes a non-pharmacologic model of generalized convulsive SE in rat. Pulsed trains of suprathreshold electric current, were administered bilaterally to either of four rostral forebrain sites: orbital cortex, medial precentral cortex, deep prepiriform cortex, or rostral caudate-putamen (n = 8 per site). This induction method resulted in 30/32 animals attaining limb-clonic convulsive SE within a mean of 30-35 min for each forebrain site, with no differences between sites. Subsequent SE proceeded without further interventions, permitting observation of the natural course of progression. A stereotyped behavioral/electrographic sequence occurred, characterized by devolution. Behaviorally, animals progressed from predominantly limb clonus to head clonus, then to subtle twitching, and finally to electrical SE before cessation of spikes. The corresponding electrographic progression was from fast and slow spiking to periodic epileptiform discharges (PEDs). In 20 animals surviving to 48 h, pathologic damage affected mainly limbic sites; damage was related to total convulsive time rather than to clonic activity. High-dose phenobarbital but not phenytoin suppressed SE when given during orbital cortex-induced limb-clonic SE. These findings are compatible with human observations and indicate that this model will enable investigations of generalized SE mechanisms and evaluation of new therapeutic agents for refractory SE.

Animals↗
PubMedDate not supplied

Modification of tonic-clonic convulsions by atracurium in multiple-monitored electroconvulsive therapy.

STUDY OBJECTIVE: To determine the effect of two different doses of atracurium on the modification of tonic-clonic convulsions in multiple-monitored electroconvulsive therapy (MMECT). To compare recovery time and adverse reactions of these doses. DESIGN: Clinical study. Anesthesiologist was blinded in the evaluation of post-electroconvulsive therapy (ECT) myalgia and other side effects. SETTING: University-affiliated veterans general hospital. PATIENTS: Two groups of twelve psychiatric inpatients who suffered from major depression or catatonic-type schizophrenia that failed to respond to tricyclic antidepressant therapy. INTERVENTIONS: Under single-channel, prefrontal electroencephalographic (EEG) monitoring, patients were given either 0.3 mg/kg or 0.5 mg/kg of atracurium intravenously (IV) after anesthetic induction with methohexital 1 mg/kg i.v. MEASUREMENTS AND MAIN RESULTS: Evoked electromyographic responses of the adductor pollicis muscle was obtained by train-of-four stimulation of the ulnar nerve at the wrist every 20 seconds. The first twitch depression (T1) of neuromuscular blockade was maintained within 11% to 25% (atracurium 0.3 mg/kg) or 0% to 10% (atracurium 0.5 mg/kg) of control during the entire session of MMECT. Patients pretreated with atracurium 0.5 mg/kg had significantly fewer ECT-induced moderate and vigorous convulsions when compared with patients receiving atracurium 0.3 mg/kg (16.7% vs. 78.4%, moderate; 0% vs. 8.3%, vigorous). However, patients pretreated with atracurium 0.5 mg/kg took a longer time to attain a T4 ratio of 0.5 than did patients receiving atracurium 0.3 mg/kg (9.2 +/- 0.8 minutes vs. 4.3 +/- 0.4 minutes). There was no significant difference between the two groups with respect to cumulative seizure duration or frequency of bradycardia, sialorrhea, postseizure myalgia, nausea, headache, or confusion. No patient in either group recalled any event concerning electroconvulsive shock. CONCLUSIONS: Whereas full neuromuscular blockade by atracurium 0.5 mg/kg i.v. is very effective in the modification of tonic-clonic convulsions induced by ECT, we suggest that a lower dose of atracurium (0.3 mg/kg i.v.) be used if one needs to ascertain the occurrence of ECT-induced seizures as indicated by minimum peripheral muscle activity at the time of EEG recording during MMECT.

Adolescent↗
PubMed1996

Abnormal theta response to nociceptive stimuli during sleep EEG in children with febrile convulsions and control children.

Nociceptive stimuli were tested in 373 sleep EEG from 349 children with febrile convulsions and 50 control children (mean age: 2.54 and 2.05 years, respectively). Stimuli consisted of light pecks on each limb with a beveled cut plastic straw or a toothpick. Responses were deemed abnormal if frontal theta episodes would repeat three times without awakening. These abnormal responses appeared in 232 (62%) out of the 373 children of the febrile convulsive group, and in only 4 (8%) out of the 50 children in the normal control group: confidence interval significant at 95%. During sleep recording without stimulation, this sign is directly related to spontaneous theta bursts and inversely related to focal activity, but bears no relationship with sleep induction agents, generalized spike and waves, or delta discharges. In 24 repeat recordings, it begins to disappear at 3.7 years of age. Such responses to nociceptive stimuli should be considered characteristic of febrile convulsions.

Case-Control Studies↗
PubMed2006

Ictal EEG in patients with convulsions with mild gastroenteritis.

The aim of this study is to reveal detailed clinical manifestations and an evolution of ictal EEG discharges of convulsions with mild gastroenteritis (CwG). We recorded ictal EEGs of six patients with CwG. Clinical manifestations included loss of responsiveness, motion arrest, cyanosis, lateral eye deviation, and hemifacial convulsion. Automatism was not observed in any patients. A generalized tonic-clonic convulsion was observed in five of six patients. Ictal EEGs demonstrated that all seizures were of focal onset that evolved into a secondarily generalized seizure. The region of the onset of ictal discharge was the occipital area in three patients, parietal in one, central in one, and frontal in one, respectively. The seizure of patients with CwG is likely to be a partial seizure with secondary generalization.

Age Factors↗