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PubMed2003

Lactic dehydrogenase isoenzyme in cerebrospinal fluid of children with febrile convulsions.

AIM: To study the lactic dehydrogenase isoenzyme values in children with simple and complex febrile convulsions. METHODS: Cerebrospinal fluid samples were collected from 115 children, 57 with simple febrile convulsions, 27 with complex febrile convulsions and 31 with no neurological or intracranial pathology (controls). Lactic dehydrogenase activity and isoenzyme levels were measured on a Hitachi analyser. RESULTS: Mean total lactic dehydrogenase activity was similar in the three groups. In the control group, lactic dehydrogenase-1 was the main fraction, followed by lactic dehydrogenase-2 and lactic dehydrogenase-3; only small percentages of lactic dehydrogenase-4 and lactic dehydrogenase-5 were detected. In the febrile convulsion group, the lactic dehydrogenase-1 fraction percentage was lower and lactic dehydrogenase-2, lactic dehydrogenase-3 percentages were higher than those in the control group; and the differences were statistically significant between the control and study groups (p < 0.01). Values of lactic dehydrogenase-4 and lactic dehydrogenase-5 were similar in all three groups. CONCLUSION: This is the first report on the lactic dehydrogenase isoenzyme pattern in the cerebrospinal fluid of patients with simple and complex febrile convulsions. The important finding that focal and general febrile convulsions are not associated with cell damage and changes in aerobic and anaerobic metabolism as lactic dehydrogenase remained unchanged. Analysis of cerebrospinal fluid lactic dehydrogenase isoenzyme levels can assist clinicians in differentiating febrile convulsions from clinical situations that might mimic them.

Child↗
PubMed1979

Rectal administration of diazepam in solution in the acute treatment of convulsions in infants and children.

In a prospective study 44 children, aged 6 months to 5 years, admitted to hospital with febrile convulsions or epilepsy, were treated with diazepam in solution administered rectally during 59 generalised attacks. Rectal administration of diazepam was effective in the acute treatment of convulsions in 80% of cases. In 10% the treatment failed, whereas diazepam administered intravenously had prompt effect; another 10% of the convulsions wer resistant to diazepam, irrespective of the route of administration. The therapeutic effect was significantly correlated with the duration of convulsions before treatment started. Early treatment (convulsions less than or equal to 15 minutes) had effect in 96%, and late treatment (convulsions greater than 15 minutes) in 57% of cases. A total of 317 children admitted with febrile convulsions were treated prophylactically with diazepam administered rectally whenever the temperature was greater than or equal to 38.5 degrees C. No case of significant respiratory depression or other serious side effects was observed. The rapid and reliable anticonvulsant effect of diazepam given rectally and the very few side effects makes this treatment a valuable alternative to IV administration in childhood.

Acute Disease↗
PubMed2005

Effect of fentanyl on lidocaine-induced convulsions in mice.

This study was undertaken to examine the effect of fentanyl on lidocaine-induced convulsions in mice. Seventy-five male mice were used and divided into five groups, 15 in each. Convulsions were obtained by lidocaine injection subcutaneously (150 mg/kg), in a dose volume of 0.1 ml/10 g body weight over the upper back. The five groups were: (a) control group: pretreated with normal saline; (b) F50 group: pretreated with fentanyl 50 microg/kg; (c) F100 group: pretreated with fentanyl 100 microg/kg; (d) F200 group: pretreated with fentanyl 200 microg/kg, and (e) F100+N group: pretreated with fentanyl 100 mug/kg plus naloxone 1 mg/kg. The pretreatments were given intraperitoneally (i.p.) 5 min prior to lidocaine injection. After lidocaine injection, the latency to the onset of generalized convulsions was observed for 12 min and recorded. The severity of convulsions was assessed and scored as 1 = mild, 2 = moderate, and 3 = severe. The recovery or death of the mice were also recorded. Student's t, Mann-Whitney U, and Fisher's exact tests were used to analyze the data. Compared with the control group (431.7 +/- 37.3 s), the latencies of onset of convulsions in the fentanyl groups were dose-dependently decreased (F50: 331.0 +/- 37.1 s; F100: 240.3 +/- 28.6 s, p < 0.001; F200: 188.7 +/- 19.4 s, p < 0.001), and the decreased latency was reversed by naloxone (F100+N: 412.9 +/- 34.1 s). Compared with the control group (1.13 +/- 0.19), the severities of convulsions in the fentanyl groups were also increased in a dose-dependent manner (F50: 1.47 +/- 0.19; F100: 1.93 +/- 0.21, p < 0.05; F200: 2.46 +/- 0.17, p < 0.001). Similarly, the increased severity was reversed by naloxone (F100+N: 1.33 +/- 0.16). There was no death in the control and naloxone-treated groups. The incidences of death were 2/15 in F50 group, 5/15 in F100 group, and 7/15 in the F200 group (p < 0.05). The results of this study demonstrated that fentanyl potentiates the lidocaine-induced convulsions in a dose-dependent manner in mice, and this effect may be mediated by an opioid mechanism.

Animals↗
PubMed2005

Community concepts of malaria-related illness with and without convulsions in southern Ghana.

BACKGROUND: Malaria, both with or without convulsions, is a serious hardship for people living in endemic areas, especially in sub-Saharan Africa. Community references to malaria, however, may encompass other conditions, which was collectively designated malaria-related illness (MRI). Inasmuch as the presence or absence of convulsions reportedly affects timely help-seeking for malaria, a local comparison of these conditions is needed to inform malaria control. METHODS: Vignette-based EMIC interviews (insider-perspective interviews) for MRI with convulsions (convulsion positive, MRI-CP) and without convulsions (convulsion negative, MRI-CN) were developed to study relevant features of MRI-related experience, meaning and behaviour in two rural communities in Ghana. These semi-structured interviews elicited both qualitative narrative and categorical codes for quantitative analysis. Interviews with 201 respondents were conducted. RESULTS: The conditions depicted in the vignettes were well recognized by respondents and named with various local terms. Both presentations were considered serious, but MRI-CP was more frequently regarded potentially fatal than MRI-CN. More than 90.0% of respondents in both groups acknowledged the need to seek outside help. However, significantly more respondents advised appropriate help-seeking within 24 (p = 0.01) and 48 (p = 0.01) hours for MRI-CP. Over 50.0% of respondents responding to questions about MRI-CP identified MRI-CN as a cause of convulsions. CONCLUSION: Local comparison of MRI-CP and MRI-CN based on vignettes found a similar profile of reported categories of perceived causes, patterns of distress, help-seeking and preventive measures for both presentations. This differs from previous findings in sub-Saharan Africa, which assert communities regard the two conditions to be unrelated. The perceived relationships should be acknowledged in formulating strategies to control malaria through timely help-seeking and treatment to reduce childhood mortality.

Adult↗
PubMed1996

Neurotoxic convulsions induced by theophylline and its metabolites in mice.

To evaluate the risk of neurotoxicity induced by theophylline and its main metabolites, 1-methylxanthine (1-MX), 3-methylxanthine (3-MX), 1,3-dimethyluric acid (1,3-DMUA) and 1-methyluric acid (1-MUA), we compared their convulsive potency to central nervous system (CNS) after intracerebral administration to mice. All compounds studied induced clonic convulsion in a dose-dependent manner, and the ED50 values for convulsion were 490, 546, 1107, 360 and 620 nmol/kg for theophylline, 1-MX, 3-MX, 1,3-DMUA and 1-MUA, respectively. These compounds were also administered intravenously to mice by constant rate infusion until the onset of convulsion. Clonic convulsion was induced by i.v. infusion of theophylline, 1-MX and 3-MX, while convulsion was not observed during 1,3-DMUA or 1-MUA infusion for 60 min. This finding may be due to the poor blood-brain barrier permeability of both 1-MUA and 1,3-DMUA as compared with theophylline, 1-MX and 3-MX. However, it may be also necessary to consider the possibility of 1,3-DMUA-induced-neurotoxicity judging from its intrinsic convulsive potency.

Animals↗
PubMed1979

Effect of antivitamin B6 on regional GABA metabolism in mouse brain and its relation to convulsions.

The effects of administration of DL-penicillamine (PeA), thiosemicarbazide (TSC), semicarbazide-HCl (SC) as convulsants and pyridoxine (PN) as anticonvulsant on gamma-aminobutyric acid (GABA) content, glutamic acid decarboxylase (GAD) and gamma-aminobutyric acid transaminase (GABA-T) activities in cerebral cortex, striatum, diencephalon, mesencephalon, cerebellum and pons/medulla were investigated. The onset of convulsions induced by these convulsants coincides with the fall in GABA content and GAD activity in the mesencephalon area, and in contrast, the cessation of the convulsions by PN supplement coincides with the recovery in both the parameters. Aminooxyacetic acid (AOAA), a potent GABA-elevating agent showed an anticonvulsant property against convulsion by TSC for several hours after the injection of AOAA, but lost this property 16 hr after the treatment. The TSC administration 16 hr after the AOAA pretreatment significantly decreased the GABA content in all the regions, particularly in the mesencephalon and diencephalon areas, which had been elevated by the AOAA pretreatment, together with its ability to induce convulsion. FRom the above results it may be postulated that the critical drop of GABA level from a plateau to another lower level following the decrease of GAD activity in the mesencephalon area is an important factor in the induction of convulsion.

4-Aminobutyrate Transaminase↗
PubMed1999

Anticonvulsant efficacy of N-methyl-D-aspartate antagonists against convulsions induced by cocaine.

Convulsions associated with cocaine abuse can be life threatening and resistant to standard emergency treatment. Cocaine (75 mg/kg, i. p.) produced clonic convulsions in approximately 90% of male, Swiss-Webster mice. A variety of clinically used antiepileptic agents did not significantly protect against cocaine convulsions (e. g., diazepam and phenobarbital). Anticonvulsants in clinical practice that did significantly protect against convulsion did so only at doses with significant sedative/ataxic effects (e.g., clonazepam and valproic acid). In contrast, functional N-methyl-D-aspartate (NMDA) antagonists all produced dose-dependent and significant protection against the convulsant effects of cocaine. Anticonvulsant efficacy was achieved by blockade of both competitive and noncompetitive modulatory sites on the NMDA receptor complex. Thus, competitive antagonists, ion-channel blockers, polyamine antagonists, and functional blockers of the strychnine-insensitive glycine modulatory site all prevented cocaine seizures. The role of NMDA receptors in the control of cocaine-induced convulsions was further strengthened by the positive correlation between the potencies of noncompetititve antagonists or competitive antagonists to block convulsions and their respective affinities for their specific binding sites on the NMDA receptor complex. Although some NMDA blockers produced profound behavioral side effects at efficacious doses (e.g., noncompetitive antagonists), others (e.g., some low-affinity channel blockers, some competitive antagonists, and glycine antagonists) demonstrated significant and favorable separation between their anticonvulsant and side effect profiles. The present results provide the most extensive evidence to date identifying NMDA receptor blockade as a potential strategy for the discovery of agents for clinical use in averting toxic sequelae from cocaine overdose. Given the literature suggesting a role for these drugs in other areas of drug abuse treatments, NMDA receptor antagonists sit in a unique position as potential therapeutic candidates.

Animals↗
PubMed2000

A transient increase in CCK mRNA levels in hippocampus following audiogenic convulsions in audiogenic seizure-prone rats.

AIM: To examine the effects of a single convulsion and multiple convulsions on cholecystokinin (CCK) mRNA expression in hippocampus of audiogenic seizure-prone rats (P77PMC). METHODS: Ringing (electric bell, 100 dB, 60 s) was used to induce convulsions, hippocampal CCK mRNA expression was exhibited by in situ hybridization. RESULTS: 1) The number of CCK mRNA-positive neurons in principal hippocampus of normal rats was 34 +/- 5, which elevated markedly after a single (155 +/- 7, P < 0.01) or multiple convulsions (95 +/- 8, P < 0.01). 2) CCK mRNA levels in multiple consecutive convulsion rats were lower than that in a single convulsion rats (P < 0.01). CONCLUSION: The increased number of CCK mRNA-positive neurons in hippocampus may have important functional consequences in convulsion-associated processes.

Acoustic Stimulation↗
PubMed2001

Clinical characteristics and risk factors for a complex first febrile convulsion.

OBJECTIVES: To determine the frequency of complex features in febrile convulsion, association of complex febrile convulsion with neurological findings and risk factors associated with complex febrile convulsion. METHODOLOGY: Retrospective review of clinical records of 379 patients admitted for their first febrile convulsion over a two-year period. RESULTS: Complex features occurred in 37.2% patients. Focal seizures tended to be prolonged as well. There was also significant association between prolonged or focal seizures with presence of neurological abnormalities. The longer the duration of the seizure, the higher was the likelihood of neurological abnormalities. Risk factors associated with a complex first febrile convulsion were: 1) Age of 15 months or less, 2) Birth weight of 2 kg or less and 3) initial temperature of 38 degrees C or less. CONCLUSIONS: Any acute febrile convulsion should be abbreviated soonest possible as neurological abnormalities, which may be signs of cerebral insult become more likely with increasing duration of seizures. The risk factors found associated with complex febrile convulsion underline the propensity of the immature, developing brain to abnormal seizure discharges in response to a lower temperature threshold.

Cerebral Cortex↗
PubMed2001

[Experimental pharmacodynamic study on the anti-convulsion effect of shenpu decoction].

OBJECTIVE: To observe the anti-convulsion effect of Shenpu Decoction (SPD). METHODS: Experiments were conducted in three acute convulsion models (cardiazol seizure, strychnine convulsion and maximal electrical shock). Models were divided into the control group (A, treated by normal saline), the high, middle and low dose SPD groups (B, C and D, treated with SPD 9 g/kg, 6 g/kg and 4 g/kg respectively), and the nitrazepam treated group (E). The anti-convulsion effect of SPD was evaluated by 50% convulsion dose (CD50) detected in each group. RESULTS: In cardiazol convulsion model, the CD50 detected in group A-E were 63.3 +/- 3.4 mg/kg, 116.2 +/- 3.4 mg/kg, 105.6 +/- 3.7 mg/kg, 74.0 +/- 3.7 mg/kg and 197.2 +/- 3.3 mg/kg respectively, while they were 0.71 +/- 0.04 mg/kg, 1.21 +/- 0.04 mg/kg, 1.19 +/- 0.04 mg/kg, 0.94 +/- 0.04 mg/kg and 1.16 +/- 0.04 mg/kg respectively in the strychnine convulsion model, and 67.1 +/- 2.6 V, > 140 V, 109.4 +/- 3.5 V, 84.4 +/- 3.1 V and 128.4 +/- 3.9 V in the maximal electrical shock model respectively. CONCLUSION: SPD has a good anticonvulsion effect.

Animals↗
PubMed1992

[The effect of acupuncture on high oxygen pressure-induced convulsion and its relationship to the brain GABA concentration in mice].

This paper reports the effect of acupuncturing "Renzhong" (GV26) and "Chengjiang" (GV24) points on OHP*-induced convulsion in mice. The results are as follows: 1. Convulsion induced by 6 ATA OHP were accompanied with a decrease in the brain GABA concentration. 2. When electro-acupuncture was applied for 15 minutes prior to exposure to hyperoxic chamber, the latency of convulsions was lengthened and the symptoms of seizures were alleviated. Besides, the brain GABA concentration was also elevated remarkably. 3. Administration of vitamin B6 enhanced the effect of acupuncture on convulsions and increased brain GABA concentration. 4. The latency of convulsions was well correlated with the GABA concentration of the brain (r = 0.9867). The above results indicate that acupuncture may elevate endogenous GABA levels in the brain and prevent the hyperbaric-oxygen-induced the decrease in the brain GABA content. Therefore. It is of protective effect against oxygen convulsions. Vitamin B6 may facilitate the effect of acupuncture by improving the GABA metabolism in the brain. In short, the effect of acupuncture against oxygen convulsions may be closely related to the increase in the brain GABA levels.

Acupuncture Therapy↗
PubMed2005

[Influence of acetazolamide given intraperitoneally on the latency to hyperbaric oxygen-induced convulsion of rats.].

The purpose of the present study was to explore the relation between the modulation of cerebral blood flow and the latency of hyperbaric oxygen-induced convulsion. There were two parts in this study. First, the effect of acetazolamide or (and) indomethacin on the latency of hyperbaric oxygen-induced convulsion was observed. Seventy Sprague-Dawley (SD) rats were randomly divided into 7 groups: the acetazolamide 200, 20, 10, 7.5, 5, 2.5 mg/kg body weight and normal saline (NS) group. Forty rats were divided into 5 groups: indomethacin 20, 10, 5, 2.5 mg/kg body weight and NS groups. Another 40 rats were divided into 5 groups which were administered with indomethacin in the dose of 0 mg/kg (NS), 0 mg/kg (NS), 5, 10 and 20 mg/kg body weight. Thirty min later the first group was given NS, and all the other four groups were given acetazolamide with a dose of 7.5 mg/kg body weight. The animals were given acetazolamide or (and) indomethacin intraperitoneally, and 20 min later they were exposed to the pressure of 6 ATA (absolute atmosphere) of pure oxygen. The time from exposure to the onset of seizure (clonic-tonic convulsion) was recorded for each animal according to behavioral observation. Second, the change of maleic dialdehyde (MDA) was measured after acetazolamide and (or) indomethacin treatment. Seventy-two SD rats were randomly divided into 9 groups: Control, 6 and 16 min respectively with NS, acetazolamide, indomethacin, and both acetazolamide and indomethacin group. The dose of acetazolamide was 7.5 mg/kg body weight and the dose of indomethacin was 20 mg/kg body weight. After injection of drugs, the animals were subjected to the pressure of 6 ATA of pure oxygen in respect to its time course group. Then the rats were decapitated and the cerebral cortex was dissected and homogenized. The content of MDA was determined. We found that (1) when the dose of acetazolamide is higher than 7.5 mg/kg, it shortened the latency to hyperbaric oxygen-induced convulsion significantly (P<0.05, P<0.01). There was no significant difference in the latency between every to hyperbaric oxygen-induced convulsion significantly (P<0.05, P<0.01). There was no significant difference in the latency between every two groups of rats treated with different doses of indomethacin. But when the rats were administered acetazolamide of 7.5 mg/kg body weight after being pretreated with indomethacin of 20 mg/kg body weight, the outbreak of convulsion was put off remarkably (P<0.05). (2) In comparison with the control, the content of MDA in the group treated with acetazolamide increased significantly (P<0.01), but when the rats were treated with both acetazolamide and indomethacin, the content of MDA was reduced significantly both in 6 and 16 min exposure time projects (P<0.05, P<0.01). These results suggest that acetazolamide which dilates the brain arterioles can obviously shorten the latency of hyperbaric oxygen-induced convulsion and aggravate the oxidation of the brain. Indomethacin can resist acetazolamideos effect on the latency and oxidation level when the animals were exposed to the hyperbaric oxygen. The activity of carbonic anhydrase correlates closely with the oxidation injury.

English Abstract↗
PubMed1990

[A study of the sequelae of perinatal hypoxia and convulsions in full-term newborn infants].

Perinatal hypoxia may result in neuromotor handicaps. The occurrence of convulsions after perinatal hypoxia is regarded as a bad prognostic sign. Thirty-two full-term babies with perinatal hypoxia were studied retrospectively. Post-hypoxic convulsions were seen in 20 newborns. In 26 out of 29 survivors follow-up assessments were made between 2 months and 2 years of age. Severe neuromotor abnormalities were demonstrated in 10 out of 19 patients with post-hypoxic convulsions, whereas no abnormalities were found in 7 patients without convulsions (p = 0.016, Fisher exact test). Although post-hypoxic convulsions are a bad prognostic sign, a number of infants with convulsions appear to develop normally. Further research on prognostic factors concerning neurodevelopment after perinatal hypoxia and convulsions appears indicated.

Child Development↗
PubMed1989

Opioids induce convulsions and wet dog shakes in rats: mediation by hippocampal mu, but not delta or kappa opioid receptors.

The opioid receptor subtypes and brain regions involved in eliciting convulsions and wet dog shakes (WDS) were studied by testing different opioid receptor selective agonists in unanesthetized rats. Selective mu agonists, [NMe-Phe3-D-Pro4]-morphiceptin (PL017) and [D-Ala2-N-methyl-Phe3-Gly5-ol]-enkephalin, induced convulsions and WDS when unilaterally injected into the ventral hippocampus. [D-Ala2,D-Leu5]-enkephalin (DADLE), a mixed mu and delta agonist, also elicited such behavioral changes, but its effect was less potent than the selective mu agonists. DADLE-induced WDS were dose dependent, and both convulsions and WDS were antagonized by the irreversible mu receptor antagonist, beta-funaltrexamine, but not by the selective delta receptor antagonist, ICI-174,864. Treatment with the selective delta agonist [D-Pen2,5]-enkephalin or the selective kappa agonists U-50,488H, dynorphin-A amide, or dynorphin-A(1-8) did not produce convulsions or WDS. The injection of a high dose of PL017 intraventricularly or into other brain regions such as the dorsal hippocampus, frontal cortex, striatum, and amygdala did not produce convulsions or WDS, therefore suggesting the ventral hippocampus is an important site for the expression of opioid-induced convulsions and WDS. These results suggest that opioid-induced convulsions and WDS are mediated exclusively by mu but not delta or kappa opioid receptors in the ventral hippocampus.

Animals↗
PubMed1979

Prospective study of convulsions in childhood.

One hundred and five children admitted to hospital with convulsions were studied prospectively. A convulsion was designated febrile if an axillary temperature of 38 degrees C or more occurred after the fit. Twenty-two children had an initial non-febrile convulsion and five of them (22.7 percent) have developed recurrent nonfebrile seizures. In the febrile group of 83 only two children (2.4 percent) have so far had non-febrile convulsions. Both their initial convulsions were uncomplicated. There was no difference between the groups of convulsion or EEG result. Investigations in hospital, including lumbar puncture, rarely revealed a diagnosis not clinically suspected. In previously healthy children with convulsions that are not prolonged, pyrexia is the only factor of prognostic significance by 12 months follow up.

Female↗
PubMedDate not supplied

The influence of auditory and lithium stimulation on blood and brain serotonin in the normal rat and in that susceptible to audiogenic convulsions.

Investigations were carried out in two groups of male rats: a group susceptible to audiogenic convulsions and a control group. The following parameters were determined under basal conditions and 24 and 48 hours after intraperitoneal administration of a single lithium carbonate dose (0.67 mEq/animal), before and after auditory stimulation: serotonin content in the blood and brain tissue (separately from the hypothalamus, rhinencephalon, midbrain and sensory-motor cerebral cortex) by fluorimetry: water-saline retention, renal potassium elimination, the dynamics of renal lithium elimination. The results showed that in the rats prone to audiogenic convulsions, blood serotonin concentrations are twice those in the controls, whereas serotonin levels in the brain are lower than in the controls. The administration of lithium is followed by a decrease in blood serotonin in the animals with audiogenic convulsions but does not influence the serotonin content in the brain. Acoustic stimulation does not influence the behaviour of the controls but induces convulsions in the animals sensitive to noise. After auditory stimulation under basal conditions or 48 hours after the administration of lithium a decrease takes place in cerebral serotonin and an increase in blood serotonin in the controls whereas in the rats sensitive to noise, cerebral serotonin increases and blood serotonin decreases on stimulation under basal conditions due to the convulsions and metabolic alterations induced by the latter. These findings suggest the existence of different mechanisms for the transport of serotonin in the blood of rats prone to audiogenic convulsions. These mechanisms may be influenced either by acid catabolites resulting from convulsive activity or by the administration of lithium. The latter may induce persistent alterations in the blood transporter, as appears to result from the observation at 48 hours after the administration of lithium.

Acoustic Stimulation↗
PubMed1987

Complex segregation analysis of febrile convulsions.

Complex segregation analysis was performed on 467 nuclear families ascertained through febrile-convulsion probands. The probands were identified as having their first febrile convulsion while residents of Rochester, MN, during the years 1935-64. Parents and first- and second-degree relatives of probands were identified through the Olmsted County, MN, record-linkage system. Diagnoses of convulsive activity were made from review of medical records. The genetic models investigated included both single-major-locus and polygenic models, with likelihoods computed jointly on children and parents as well as being conditioned on parental phenotype. Possible heterogeneity was investigated by means of analyses of frequency of febrile convulsions in the proband. Analyses of the entire data set indicated that the single-major-locus models could be rejected. The most parsimonious model for these data was the pure polygenic (or common familial environment) model with a large heritable component (68% +/- 7%). However, when families were partitioned on the basis of frequency of febrile convulsions in the proband, significant heterogeneity was present. Our results indicated that the polygenic model was strongly corroborated in families of probands with a single febrile convulsion. In families of probands with multiple febrile convulsions, evidence was consistent with a single-major-locus model with nearly dominant seizure susceptibility.

Child, Preschool↗
PubMed1983

Increase in brain prostaglandins during convulsions is due to increased neuronal activity and not to hypoxia.

The levels of prostaglandin D2 (PGD2) and prostaglandin F2 alpha (PGF2 alpha), being the major prostaglandins formed in mouse brain in vivo were determined using a radioimmunological technique. Under basal conditions, they were less than 8.49 ng/g for PGD2 and less than 3.76 ng/g for PGF2 alpha. During seizures, induced by the centrally acting convulsant pentylenetetrazol, cerebral concentrations of both prostaglandins were markedly enhanced as compared to basal conditions. The seizure evoked increase in brain prostaglandins could be attributed to the enhanced neuronal activity. If convulsions were induced with the spinal cord convulsant strychnine no increase in brain prostaglandins was seen although the occurring hypoxia was probably very similar. Therefore, hypoxia does not seem to play a significant role in the prostaglandin increase. The effect of pentylenetetrazol on cerebral prostaglandins was independent of the mechanical convulsions induced by the drug. Muscle relaxed mice showed the same increase in cerebral prostaglandins as convulsing mice. Muscle relaxation alone had no influence on prostaglandin formation in brain. These data indicate that the increased neuronal activity induced by centrally acting convulsants is likely to be the sole cause for the rise in cerebral prostaglandins. Brain hypoxia, another known stimulus of prostaglandin synthesis, does not seem to play an important role during convulsions.

Animals↗