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PubMed1988

Clinical spectrum and outcome of neonatal convulsions.

The clinical spectrum and outcome of neonatal convulsions within an obstetric hospital population were reviewed for the 5 years, 1978-82, inclusive. There were 156 convulsing neonates managed at the Mater Mothers Hospital (110 inborn, 46 outborn). The incidence of early neonatal convulsions for inborn babies was 3.0/1000 live births. Antenatal and perinatal risk factors were compared between the 156 convulsing infants and the 36,082 infants born during the same period who did not convulse. The leading risk factors for convulsions were prematurity, intra-uterine growth retardation, low 5 min Apgar score, pre-eclampsia, antepartum haemorrhage, twin pregnancy and breech presentation. The predominant seizure type was tonic in 28.6%, multifocal clonic in 27.2%, subtle in 18.4%, myoclonic in 15.0% and focal clonic in 8.8%. Mortality (31%) and long-term disability (43%) rates were high. Tonic seizures had the highest mortality and morbidity. Throughout the duration of the study period infants received increasingly thorough investigation. Causative factors were determined in 95% of convulsing infants, most frequent being hypoxic-ischaemic encephalopathy (40.3%) and cerebroventricular haemorrhage (30.5%). Follow-up data on 99 of the 107 survivors (93%) revealed severe disability in 25, moderate disability in eight and mild disability in 10. A poor long-term prognosis was associated with prolonged convulsions, tonic and multifocal clonic convulsions, convulsions due to asphyxia and cerebroventricular haemorrhage and an abnormal neurological examination at discharge.

Humans↗
PubMed1976

Clinical investigation of infantile convulsion.

We investigated 104 cases of infantile convulsions which occurred before two years of age. These cases had no detectable signs of acute brain disorders, and they had normal psychomotor development and normal EEG findings at onset. (1) Sex ratio was 1:1. (2) A positive family history of various types of convulsions was obtained in 30.8% (Febrile convulsion: 65.7%) (3) The incidence of perinatal anoxic brain damage was higher than that in the control group. This was probably related to the incidence of infantile convulsion. (4) More than half the cases (66.3%) had the first convulsion between three and eight months of age, and 95.6% of prospectively follow-up cases were shown free from attacks before two years of age. (5) Precipitating factors to convulsion were found in 45.1% of all cases. These factors were bathing and non-febrile infection. (6) The most common form of infantile convulsion is generalized tonic and/or clonic convulsion (78.8%) within 5 min. (82.7%). This convulsion reccurs frequently in a relatively short period. (7) The incidence of subsequent epilepsy seems to have been found among patients who had had an initial attack between three and five months of age, and had then experienced convulsion more than six times or in a prolonged state.

Adolescent↗
PubMed1978

Characterization of pinealectomy induced convulsions in the Mongolian gerbil (Meriones unguiculatus).

The Mongolian gerbil (Meriones unguiculatus) exhibits convulsions after pinealectomy (PX). Included in the convulsions are wild running, tonic-clonic activity, and occasionally death. This paper reports various parameters that influence the convulsions. Animals 60 and 90 days old have a shorter latency to onset of convulsions than do 30-day-old gerbils. Animals pinealectomized at the onset of light (0600) in an LD 14:10 photoperiod have a shorter latency to onset and greater number of convulsions than animals pinealectomized at other times. Modulation of the photoperiod to LD 20:4 and 4:20 does not affect the convulsions. Superior cervical ganglionectomy (SCGX) does not result in convulsions; subsequent PX of the SCGX animals does. Replacement of pineal extract does not prevent the convulsions. The PX induced convulsion in gerbils resembles the parathyroidectomy-pinealectomy induced convulsion in the rat in all aspects, but with a shorter latency to onset.

Age Factors↗
PubMed1998

Can convulsions alone cause retinal haemorrhages in infants?

AIM: To evaluate the likelihood that, in children under the age of 2 years, convulsions alone may cause retinal haemorrhages. METHODS: Children under the age of 2 years admitted to hospital following convulsions, were examined within 48 hours of admission. The convulsions were classified by a paediatric neurologist and detailed ocular examination, including indirect ophthalmoscopy, was performed by an ophthalmologist. Statistical analysis was undertaken using Hanley's rule of three. RESULTS: 32 consecutive children admitted with convulsions were examined; 10 of them were admitted following epileptic seizures and 22 following febrile convulsions. Two of the children with febrile convulsions were admitted in status epilepticus. None of these children had retinal haemorrhages. Therefore, using Hanley's rule of three, the upper limit of 95% confidence interval of retinal haemorrhages following convulsions in children under the age of 2 years, is less than 10/100. CONCLUSIONS: In children under the age of 2 years convulsions alone are unlikely to cause retinal haemorrhages. By combining the results of this study with those previously reported from this unit in older children, the upper limit of 95% confidence interval of retinal haemorrhages, following convulsions in children under the age of 14 years, is less than 5/100. Therefore, the finding of retinal haemorrhages in a child admitted with a history of convulsion should trigger a meticulous search for other causes of these haemorrhages, particularly non-accidental injury.

Epilepsy↗
PubMedDate not supplied

[Hypocalcemia and convulsive syndrome in alcoholics--an association frequently not diagnosed].

UNLABELLED: Hypocalcemia can be a contributory factor for epilepsy and previous studies showed that ethanol decreases plasma calcium. PURPOSE: To establish the prevalence of hypocalcemia in the general convulsive population and to ascertain if there was a specific group of risk for hypocalcemia. METHODS: A prospective study of plasma ionized calcium measurement in 78 consecutive patients admitted owing to seizures at the Emergency Department of Escola Paulista de Medicina was performed. 22% of these patients were alcoholics. The plasma ionized calcium in 44 ambulatory non-convulsive alcoholics was also measured. RESULTS: A high prevalence of hypocalcemia was found in the alcoholic convulsive population (32%), in contrast with the non-alcoholic convulsive group and the alcoholic non-convulsive group (no calcium disturbance in both groups). The alcoholic convulsive group had values of ionized calcium statistically lower than the non-alcoholic convulsive group using the Mann-Whitney test (p < 0.05) [median value = 1.20 mmol/L; range = 1.04-1.32 mmol/L/median value = 1.24 mmol/L; range = 1.16-1.29 mmol/L respectively]. The alcoholic non-convulsive group had values of ionized calcium between 1.17 and 1.32 mmol/L with median value of 1.26 mmol/L; these values were not different from those obtained with the non-alcoholic convulsive patients, however they were higher than the calcium levels in the alcoholic convulsive group (p < 0.05). PTH levels, liver function tests, phosphatemia and amylasemia were normal in all patients. CONCLUSION: This study emphasizes the importance of serum calcium measurement in alcoholic patients presenting seizures and suggests that hypocalcemia correction might be important in these patients.

Adolescent↗
PubMed2002

[Pathogenic factors of convulsion in neonates with hypoxic-ischemic encephalopathy].

OBJECTIVE: To explore the pathogenic factors of convulsion in neonates with mild to severe hypoxic-ischemic encephalopathy. METHODS: Altogether 70 neonates with mild to severe hypoxic-ischemic encephalopathy (HIE) were admitted into our hospital between Jan. 1988 and Jan. 2001. Serum calcium was dynamically monitored in all the patients, with cerebral ultrasonography performed. RESULTS: Convulsions occurred within the first and second days after birth in the neonates of convulsion group, whose serum calcium levels were significantly decreased during the third to sixth days in comparison with those of non-convulsion group (P<0.01). Cerebral ultrasonography showed that 1 to 3 d after birth, cerebral edema occurred in all the neonates of convulsion group (n=39), with 30 of them having diffuse edema. Cerebral edema was gradually alleviated in the fourth to seventh day after birth. In non-convulsion group (n=31), 14 patients suffered diffuse cerebral edema within 2 d after birth, an incidence significantly lower than that in convulsion group. Intracranial hemorrhage took place in 23 neonates in convulsion group (58.97 %), and the incidence in non-convulsion group was only 38.7 %. CONCLUSION: The principal causes of convulsions in neonates include hypoxia and cerebral edema, along with secondary causes such as birth trauma and hypocalcemia.

Calcium↗
PubMed1992

[The status of afebrile infantile convulsions within the epilepsy spectrum--a follow-up of 55 patients].

In an earlier study we observed 411 patients with cerebral convulsions, 118 of whom had the first convulsion during the 1 year of life. Among these 118 children we found 76 with afebrile convulsions. In this study we present the development and outcome in 55 patients with afebrile convulsions in the 1 year of life which could be observed for some years, most of them up to the present. In 25 infants the fits started in the newborn period, and in 30 infants after the 1 month; they were divided into groups with and without risk factors in the history. Benign neonatal convulsions were found in about one-third of children, with a good prognosis. These convulsions are divided into a dominantly inherited but rarely observed form and idiopathic benign neonatal convulsions. In contrast, among the newborns with risk factors in the history we found only half with a positive development. The results in the 30 infants with convulsions after the 1 month were similar with respect to risk factors in the history of risks. The 15 infants without risks had a good prognosis. Only 3 patients had oligoepilepsy. However, in the 15 patients with risks only 3 developed normally, 6 had no fits, but were neurologically or mentally handicapped, and 7 had fits and disability. We believe that afebrile convulsions without risk factors after the 1 month could be considered a late manifestation of benign newborn convulsions.(ABSTRACT TRUNCATED AT 250 WORDS)

Brain Damage, Chronic↗
PubMed2004

Investigation of central mechanism of insulin induced hypoglycemic convulsions in mice.

Insulin produces seizures in healthy and diabetic animals. Amongst suggested mechanisms, the role of neuromodulators and neurotransmitters is not clear. The present study explores the mechanisms involved in insulin-induced convulsions. Convulsions were induced in Swiss male albino mice with graded doses of insulin. Blood sugar levels were measured prior to and after the first convulsion. Drugs like 5-HTP (5-HT precursor), pCPA (5-HT depletor), ondansetron (5-HT3 antagonist), ketanserin (5-HT, antagonist), ketamine (NMDA antagonist), 1-dopa (dopamine precursor) and reserpine (amine depletor) were studied for interaction with convulsive behaviour induced by insulin. Insulin in 2 IU/kg dose did not produce convulsions while 4 and 8 IU/kg doses produced convulsions in 50% and 100% of animals respectively. 5-HTP, ondansetron, ketanserin, ketamine and l-dopa significantly protected/inhibited animals from convulsions at all studied doses of insulin. On the contrary, pCPA and reserpine potentiated insulin induced convulsions. Insulin caused mortality in 40 and 100% animals with 4 and 8 IU/kg doses respectively. pCPA and reserpine treatments caused mortality at all doses of insulin, while other drugs did not influence insulin induced mortality. Blood sugar levels were reduced in all groups irrespective of the presence or absence of convulsions. A definitive link of serotonergic, dopaminergic and excitatory amino acid pathways in mediating insulin-induced hypoglycemic convulsions is suggested.

5-Hydroxytryptophan↗
PubMed1990

[Febrile convulsion. A clinical study of 303 patients].

The clinical characteristics of 303 patients who had episodes of feverish convulsions (FC) were retrospectively reviewed. No preference was seen for either sex (1.3/1). In 75.3% of the cases, the convulsions occurred in children under two. There was some predominance of tonic-clonic crisis and generalized clonic-tonic convulsions (85.5%) with 21.8% of complex partial crisis. In 44.8% of the cases a perinatal history of high risk was noted. A comparative investigation was carried out in a subgroup of 244 children in who FC vs non-febrile convulsions (NFC) were during two years. In 35.2% of the patients neurological abnormalities were found associated, among them were language difficulties (27.4%) and psychomotor retardation (11.9%). In 36.4% of the cases, the EEG was found to be abnormal, and paroxysmal in 27%. The predominating perinatal pathological complications were perinatal hypoxia-anoxia and prematurity. In 84% of the patients, anti-convulsive medication was administered. Of the 244 patients, 62 (25.4) of them had NFC which were directly related to the number of risk factors and their characteristics. Among those risk factors were partial convulsions, neurological deficit, abnormal EEG, convulsions lasting over 10 minutes and a previous family history of epilepsy. It is noteworthy that 15.7% of the patients had no risk factors related to epilepsy. In those patients who suffered from convulsions from an early age, who had convulsions of a partial--complex type, which lasted over 20 minutes and repeated frequently--were seen to be the most likely to develop epilepsy. The medications prescribed prevented the occurrence of the FC but did not significantly diminish the development of epilepsy. Febrile convulsions; epilepsy; perinatal.

Adolescent↗
PubMed1995

Risk factors for subsequent epilepsy after febrile convulsions.

To evaluate the risk of subsequent epilepsy after febrile convulsions and the long-term prognosis of such patients, the risk factors for afebrile seizures following initial febrile convulsions were studied in 154 hospitalized children: 122 with simple febrile convulsions and 32 with complex features of febrile convulsions. The mean follow-up period was 7 years 2 months (range, 4 yr - 11 yr 2 mo). Nineteen patients (12.3%) developed subsequent epilepsy in the follow-up period. The seizure types in patients with subsequent epilepsy following febrile convulsions included generalized seizures in seven patients, complex partial seizures in five patients, partial seizures evolving to secondary generalized seizures in six patients and benign childhood epilepsy with centrotemporal spike in one patient. The occurrence of epilepsy was strongly associated with complex features of febrile convulsions, pre-existing neurodevelopmental abnormalities, family history of epilepsy, and abnormal electroencephalographic findings. However, the number of recurrences of febrile convulsions, sex, family history of febrile convulsions, age of onset and long-term prophylactic use of anticonvulsants for febrile convulsions were not significant factors for subsequent epilepsy. This study demonstrates the importance of identifying the risk factors for subsequent afebrile seizures after febrile convulsions.

Adolescent↗
PubMed1993

Anticonvulsant activity of delta-HCH, calcium channel blockers and calmodulin antagonists in seizures induced by lindane and other convulsant drugs.

The anticonvulsant activity of delta-HCH and of a calmodulin antagonist, W-7 were investigated on convulsions induced in mice by lindane (ED100 100 mg/kg), by GABAergic antagonists PTZ (ED100 60 mg/kg) and PTX(ED100 4 mg/kg), by calcium channel agonist BAY-K-8644 (ED100 5 mg/kg), by two agonists of excitatory amino acid receptors, kainic acid (ED100 80 mg/kg) and NMDA (ED100 160 mg/kg and by the atypical benzodiazepine Ro 5-4864 (ED100 40 mg/kg). The anticonvulsant activity of a voltage-dependent calcium channel antagonist, nifedipine was also investigated on convulsions induced by Ro 5-4864, BAY-K-8644, kainic acid and NMDA. delta-HCH antagonized lindane- and BAY-K-8644-induced convulsions (ED50 231 (172-309) mg/kg and 148 (142-154) mg/kg, respectively) and at concentrations up to 300 mg/kg failed to antagonize Ro 5-4864, kainic acid and NMDA convulsions. In contrast delta-HCH potentiated PTX-induced seizures. Nifedipine antagonized BAY-K-8644- and kainic acid-induced convulsions (ED50 6.5 (4.3-9.7) mg/kg and 30 (13-70) mg/kg but at concentrations up to 20 mg/kg failed to antagonize Ro 5-4864 and 25% of protection was observed on NMDA-induced convulsions at the highest dose (20 mg/kg). The ED50 of W-7 to antagonize convulsions induced by lindane and BAY-K-8644 were 12 (8-19) mg/kg and 49 (29-85) mg/kg, respectively. Some anticonvulsant effect was observed against PTZ and NMDA but without any dose-dependent anticonvulsant activity. W-7 did not protect against PTX and kainic acid convulsions and 30% of protection was observed against convulsions at the highest dose of W-7 (75 mg/kg).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Intracerebroventricular administration of kappa-agonists induces convulsions in mice.

Intracerebroventricular (ICV) administration of kappa-agonists (PD 117302, U-50488H and U-69593) induced convulsions in a dose-related manner in mice. The dose at which 50% of animals convulsed (CD50) was in nmol ranges for all opioids. Among the opioids used, PD 117302 was the most potent convulsant. ICV administration of either vehicle alone or U-53445E, a non-kappa-opioid (+) enantiomer of U-50488H did not induce convulsions. The convulsive response of kappa-agonists was differentially susceptible for antagonism by naloxone and/or MR 2266. Collectively, these findings support the view that convulsions induced by kappa-agonists in mice involve stereospecific opioid receptor mechanisms. Furthermore, the convulsant effect of kappa-agonists could not be modified by pretreatment with MK-801, ketamine, muscimol or baclofen. It is concluded that kappa-opioid but not NMDA or GABA receptor mechanisms are involved in convulsions induced by kappa-agonists. These results are the first experimental evidence implicating stereospecific kappa-receptor mechanisms in opioid-induced convulsions in mice.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗
PubMed1999

Reduction of pentylenetetrazol-induced convulsions by the octadecaneuropeptide ODN.

Intracerebroventricular injection of the octadecaneuropeptide ODN in mouse, at doses of 12.5-1000 ng, reduced the percentage of convulsing animals and increased the latency of convulsions elicited by pentylenetetrazol (50 mg/kg, intraperitoneal [i.p.]). ODN also reduced the percentage of mortality induced by pentylenetetrazol (100 mg/kg, i.p.). The COOH-terminal octapeptide fragment of ODN was approximately equally effective but acted more rapidly than ODN to reverse the convulsant effect of pentylenetetrazol. ODN (100 ng, intracerebroventricular [i.c.v.]) increased the convulsion latency and reduced the percentage of animals that convulsed after the administration of the inverse agonist of benzodiazepine receptors DMCM (13 mg/kg, i.p.), whereas the benzodiazepine receptor antagonist flumazenil (1 mg/kg, subcutaneously) abrogated the protective effect of ODN (100 ng, i.c.v.) on pentylenetetrazol-induced convulsions. ODN (100 ng, i.c.v.) also reduced the percentage of DBA/2J mice displaying audiogenic convulsions. In contrast, ODN did not reduce the percentage of mice displaying tonic or clonic convulsions when electrical interauricular stimulations were applied. It is concluded that ODN, or more likely a proteolytic fragment derived from ODN, reduces pentylenetetrazol-induced convulsions through activation of central-type benzodiazepine receptors.

Acoustic Stimulation↗
PubMed1992

Effects of flumazenil on intravenous lidocaine-induced convulsions and anticonvulsant property of diazepam in rats.

We investigated the effect of flumazenil on intravenous (IV) lidocaine-induced convulsions with and without diazepam pretreatment in rats. Wistar rats (200-250 g) were divided into four groups of seven each and were pretreated with IV diazepam or normal saline solution at 6 min and flumazenil or normal saline solution at 3 min before lidocaine infusion. The control group received normal saline solution; the diazepam group received 0.2 mg/kg of diazepam and normal saline solution; the diazepam+flumazenil group received 0.2 mg/kg of diazepam and 0.1 mg/kg of flumazenil; and the flumazenil group received normal saline solution and 0.1 mg/kg of flumazenil. After surgical preparation and recovery from anesthesia, all groups received a continuous IV infusion of lidocaine (15 mg/mL) at a rate of 4 mg.kg-1.min-1 until tonic/clonic convulsions occurred. The values of pH and blood gases were maintained within physiologic ranges. Heart rate was significantly decreased after 5 min of lidocaine infusion, but arterial blood pressure did not change until convulsions occurred in all groups. Pretreatment with diazepam alone increased both cumulative convulsant doses and plasma concentrations of lidocaine at the onset of convulsions. Flumazenil reversed these effects of diazepam. Pretreatment with flumazenil alone changed neither cumulative convulsant doses nor plasma concentrations of lidocaine at the onset of convulsions. Our data show that IV flumazenil reverses the anticonvulsant property of IV diazepam against lidocaine-induced convulsions and that flumazenil itself has no effect on lidocaine-induced convulsions in rats.

Animals↗
PubMed1991

The contribution of diffusion to the termination of penicillin-induced convulsive activity in the awake rat.

1. Experiments were performed to investigate the contribution of diffusion to the termination of PCN induced convulsive (epileptiform) activity in the awake rat. The basic question was whether convulsive activity terminates at the same critical concentration Ct of PCN independently of the concentration Co of PCN injected into the superficial layer of the foreleg field of the right motor cortex. Different concentrations Co were used, the lowest being 16 IU PCN/0.5 microliters saline, the largest 1000 IU PCN/0.5 microliters saline. The convulsive activity was recorded by means of the electroencephalogram (EEG). 2. Mathematical calculations concerning the diffusion of the substances were performed by using the diffusion equation with a PCN diffusion coefficient D = 3.52 x 10(-4) mm2/s and the tortuosity factor lambda = 1.62. 3. The lowest dose of PCN used was considered as a threshold dose for acute induction of convulsive activity because only 4 out of 9 rats treated with 16 IU PCN developed epileptiform activity. For the range of doses between 16 and 32 IU, the median frequency of convulsive potentials was dose-dependent, and increased from 7.9 to 13.8 pot./min, respectively. For higher doses covering the range between 63 and 1000 IU, there was only an insignificant increase from 19.2 to 22.7 pot./min, respectively. 4. The median period of convulsive activity increased significantly (p less than 0.05 or less than 0.01) and monotonically from 19.5 min in rats treated with 16 IU PCN to 267 min after treatment with 1000 IU PCN. 5. At the end of the convulsive activity, the median critical concentration Ct within the artificial focus ranged from 1.75 to 1.31 IU/0.5 microliters saline in rats treated with 16 to 125 IU PCN, while after induction of convulsive activity with doses of 250, 500 or 1000 IU PCN, Ct gradually increased to 2.01, 2.83, and 3.75 IU/0.5 microliters, respectively. This means that the brain became less sensitive for PCN the longer the epileptiform activity lasted. 6. It is concluded that during long-lasting convulsive activity, the brain takes advantage of its plastic properties by eliciting counteracting mechanisms. These self-protective factors may utilize neuronal networks which needs some time to become effective in the control of the cortical activity.

Administration, Topical↗
PubMed1996

The role of vasopressin, somatostatin and GABA in febrile convulsion in rat pups.

In order to further elucidate a possible role of neuropeptides and GABA in the pathogenesis of febrile convulsions, we studied changes of immunoreactive-arginine vasopressin (IR-AVP), IR-somatostatin (IR-SRIF) and gamma-aminobutyric acid (GABA) in the rat brain after febrile convulsions induced by ultra-red light (UR). Male Wistar rats at 16 days of age irradiated with UR developed generalized convulsions after 4.9 +/- 0.5 min irradiation. Six rats were killed by microwave irradiation 3 min after UR irradiation prior to convulsion development, and 29 rats were killed either 0 min, 2 h, 6 h, 24 h or 48 h after febrile convulsions. Non-irradiated rats served as controls. The rat brain was dissected into 4 regions; amygdala, hypothalamus, cortex and hippocampus, and subjected to radioimmunoassays. IR-AVP levels in hypothalamus were increased 3 min after UR and decreased at 2 h and 6 h after the convulsions. IR-SRIF levels were increased in cortex and hippocampus at 3 min after UR and 0 min after the convulsions. The GABA content increased in all regions tested at 2 h and 6 h after the convulsions. These results suggest that AVP, SRIF and GABA may be involved in the pathogenesis of febrile convulsions in different ways.

Animals↗
PubMed1990

Potentiation of malaoxon-induced convulsions by lithium: early neuronal injury, phosphoinositide signaling, and calcium.

Convulsions, neuronal morphology, brain phosphoinositide (PI) signaling, and calcium levels were studied in rats 1, 4, and 72 hr after malaoxon (MO; 26.2 or 39.2 mg/kg ip) subsequent to pretreatment with saline or LiCl (10 meq/kg ip). The high dose of MO induced convulsions in 60% of the rats whereas the low dose was ineffective. In nonconvulsing rats, MO transiently increased cerebral inositol 1-phosphate (Ins1P), an intermediate in PI cycle, but consistently elevated brain Ins1P in convulsing rats. LiCl did not induce convulsions, but elevated the resting level of Ins1P and decreased that of inositol. Lithium also increased the potential of MO to cause convulsions but attenuated MO-induced elevations of Ins1P. Moreover, total Ca2+ in cortex increased in LiCl-pretreated convulsing and nonconvulsing rats after MO. Astrocytic edema and cytoplasmic vacuolation and/or shrinkage of neurons in cortical layers 2-3 and in the hippocampus as well as in some subcortical structures occurred only in convulsing rats. These results suggest that PI signaling may be involved in convulsions and contribute to the early neuronal injury. Cerebral Ca2+ elevations seemed to precede permanent neuronal injury. A target other than the inhibition of the hydrolysis of inositol phosphates may be the site of lithium's action in cholinergic convulsions.

Animals↗
PubMed1990

The effects of dihydropyridine calcium channel modulators on pentylenetetrazole convulsions.

The effects of low doses of dihydropyridine (DHP) calcium channel antagonists nimodipine, nifedipine, (-)-R-202-791, and amlodipine, the DHP calcium channel agonist BAY K 8644 were investigated on clonic convulsions to pentylenetetrazole (PTZ) in mice. Nimodipine (2-20 mg/kg) produced a dose-dependent increase in the onset time for convulsions, but did not decrease the number of mice convulsing. Nifedipine, amlodipine (10 mg/kg) and BAY K 8644 (2 mg/kg) also produced an increase in the onset time for convulsions. (-)-R-202-791 (10 mg/kg) was without effect on clonic convulsions to PTZ. BAY K 8644 increased the number of mice dying from tonic-extension convulsions to PTZ. Nimodipine did not affect convulsions elicited by strychnine. Thus, low doses of DHP calcium antagonists possess anticonvulsant properties which are structurally dependent, while DHP calcium channel activators may act to promote convulsions. These observations suggest and support previous evidence that DHP receptors are important modulatory sites for the convulsive state.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗