Convulsive State Research Articles

Cephalic tetanus: report of case

Tetanus is an acute, often fatal, neurological disease that is characterised by increased muscle tone and spasms caused by tetanospasmin, which is a protein toxin elaborated by Clostridium tetani; this is an obligate anaerobic, motile Gram-positive rod found in the soil, in animal and occasionally in human faeces, and in house dust, hospitals, and operating theatres.1–3 The incubation period is about seven days and the mortality is high.1 Spores may survive for years and are resistant to various disinfectants and to boiling for 20 minutes.1 Muscles of the jaw, face, and head are involved first because the toxin has to travel along shorter axonal pathways.2 Infection is independent of the size of the wound provided that the blood supply and the oxygenation are compromised.2 Clinical tetanus comprises four symptomatic types: generalised, local, cephalic, and neonatal.2,4,5 Local tetanus is uncommon with a reasonable prognosis.3 Cephalic tetanus is a rare variant of local tetanus that involves 1–3% of all reported cases and several cranial nerves are involved.5 It may follow an injury such as laceration, abrasion, or puncture wound.1 It may be associated with a head injury or middle ear infection. It may follow traditional practices like ear piercing, circumcision, and tattooing, or the mouth may be the point of entry.6 Two-thirds of cases of cephalic tetanus progress to generalised disease that can involve the limb muscles and trunk progressively.3,7 The commonest presenting symptom is trismus. Other manifestations include dysfunction of one or more cranial nerves (often the seventh nerve), facial pain, dysphagia, dysarthria, risus sardonicus (spasms of the face and jaw), stiffness of the neck and back (opisthotonos – an arched back with the body resting on the heels and occiput), spasms, voiding difficulties, abdominal pain and gastrointestinal problems, and mental and emotional problems.5,7 Other presenting symptoms may be fever, nystagmus, diplopia, cardiac disorders and malaise.1,2,7 Episodes of hypotension and bradycardia have been attributed to either withdrawal of sympathetic activity or increased parasympathetic activity. Episodes of hypertension and tachycardia have also been recorded and are thought to be the result of sympathetic stimulation. Spasms may be mild, infrequent and brief, or severe, painful, and exhausting. They can cause cyanosis that threatens ventilation, occur repetitively, and may be spontaneous or provoked by even the slightest auditory, visual or emotional stimulation. They may also be protracted, the patient seeming to be in a state of perpetual convulsion. Spasm of the pharyngeal muscles prevents swallowing of saliva that may be aspirated and cause atelectasis and aspiration pneumonia. Laryngeal spasm may lead to sudden death from asphyxia. The diagnosis of tetanus is based entirely on clinical findings.1,2 The activity of creatine phosphokinase (CPK) may be increased in some cases, but it is not pathognomonic.1 It is of interest that C. tetani can be isolated from wounds of patients without tetanus and often cannot be recovered from wounds of those with tetanus.

Epileptic nystagmus in a patient with nonconvulsive status epilepticus

Epileptic nystagmus (EN) is a rare form of rhythmic eye oscillations occurring during seizure activity. Not only convulsive states, but also nonconvulsive status may represent with EN and this phenomenon may be the only motor manifestation of seizure activity. Epileptic activation of a cortical saccade region may be distinguished from activation of a cortical pursuit region clinically as activation of pursuit regions results in nystagmus slow phases that bring the eyes across the midline. Horizontal EN results most commonly from seizure activity involving the occipital cortex. In this report, horizontal EN in a patient with nonconvulsive status epilepticus (NCSE) is described with clinical, radiological and electrophysiological findings that occur probably due to posterior leukoencephalopathy syndrome.

Prolonged exposure to hypobaric hypoxia transiently reduces GABA A receptor number in mice cerebral cortex

The central nervous system is severely affected by hypoxic conditions, which produce alterations in neural cytoarchitecture and neurotransmission, resulting in a variety of neuropathological conditions such as convulsive states, neurobehavioral impairment and motor CNS alterations. Some of the neuropathologies observed in hypobaric hypoxia, corresponding to high altitude conditions, have been correlated with a loss of balance between excitatory and inhibitory neurotransmission, produced by alterations in glutamatergic and GABAergic receptors. In the present work, we have studied the effect of chronic hypobaric hypoxia (506 hPa, 18 h/day×21 days) applied to adult male mice on GABA A receptors from cerebral cortex, to determine whether hypoxic exposure may irreversibly affect central inhibitory neurotransmission. Saturation curves for [ 3H]GABA specifically bound to GABA A receptors in isolated synaptic membranes showed a 30% decrease in maximal binding capacity after hypoxic exposure ( B max control, 4.70±0.19, hypoxic, 3.33±0.10 pmol/mg protein), with no effect on GABA binding sites affinity ( K d control: 159.3±13.3 nM, hypoxic: 164.2±15.1 nM). Decreased B max values were observed up to the 10th post-hypoxic day, returning to control values by the 15th post-hypoxic day. Pharmacological properties of GABA A receptor were also affected by hypoxic exposure, with a 45 to 51% increase in the maximal effect by positive allosteric modulators (pentobarbital and 5α-pregnan-3α-ol-20-one). We conclude that long-term hypoxia produces a significant but reversible reduction on GABA binding to GABA A receptor sites in cerebral cortex, which may reflect an adaptive response to this sustained pathophysiological state.

Pharmacological reminders of emotional state facilitate the retrieval of traces from amnesiac memory.

The experiments reported here show that animals with different levels of acquisition of a conditioned passive avoidance reflex retrieved the reflex differently on systematic testing over a period of 28 days. Animals with the highest and high levels of training reproduced the reflex stably. Animals with an intermediate level of training reproduced the reflex with significant variation. Convulsions induced by pentylenetetrazole (75 and 50 mg/kg. i.p.) resulted in amnesia. The amnestic effect of pentylenetetrazole convulsions depended on the ratio of the intensity of training and the intensity of the induction of convulsions. Reminding, provided by presentation of an unconditioned stimulus, removed the amnestic effect of the convulsive state. Training led to significant decreases in the parameters determining the severity of the convulsive state. The convulsive state was a dissociative state, as subconvulsive doses of pentylenetetrazole (30 mg/kg, i.p.) removed the amnestic effect of convulsive doses. The dissociated state was reproduced by pharmacological reminding of the state of anxiety and fear which was formed during training. A subcataleptic dose of haloperidol (0.25 mg/kg, i.p.) induced a state of fear and removed the amnestic effect of the convulsive state. The same dose of haloperidol improved retrieval of the reflex in animals with low levels of training, i.e., those in which retrieval hardly occurred in normal conditions.

Anticonvulsant effects of the 3-hydroxyanthranilic acid dioxygenase inhibitor NCR-631

The kynurenine pathway intermediate 3-hydroxyanthranilic acid (3-HANA) is converted by 3-HANA 3,4-dioxygenase (3-HAO) to the pro-convulsive excitotoxin quinolinic acid. In the present study, the anticonvulsant effect of the 3-HAO inhibitor NCR-631 was investigated in models of chemically- and sound-induced seizures. Administration of NCR-631 i.c.v. at a dose of 300nmol in Sprague-Dawley rats was found to prolong the latency of occurrence of pentylenetetrazole (PTZ)-induced seizures. Also systemic pre-treatment with NCR-631 s.c. in N.M.R.I. mice subjected to PTZ-induced seizures provided an increase in the latency until onset of seizures, concomitant with a reduction in the severity of the seizures. However, the anticonvulsant effect of NCR-631 was short lasting (15-30min), and only observed at a dose of 250 mg/kg. A similar dose- and time-dependent anticonvulsant effect of NCR-631 was found in seizure-prone DBA/2J mice following sound-induced convulsions. Hence, the findings show that NCR-631 has anticonvulsant properties against generalized tonic-clonic seizures of different origin, suggesting that it may constitute a useful tool to study the role of kynurenines in various convulsive states.

Correlation between brain glycogen and convulsive state in mice submitted to methionine sulfoximine

It is now well established that in epileptic patients, hypometabolic foci appear during interictal periods. The meaning and the mechanism of such an hypometabolism are as yet unclear. The aim of the present investigation was to look for a putative relationship between glucose metabolism in the brain and the genesis of seizures in mice using administration of the convulsant, methionine sulfoximine. Besides its epileptic action, methionine sulfoximine is a powerful glycogenic agent. We analyzed the epileptogenic and glycogenic effects of methionine sulfoximine in two inbred mouse strains with different susceptibility towards the convulsant. CBA/J mice displayed high response to methionine sulfoximine. The tonic convulsions appeared 5–6 h after MSO administration, without brain glycogen content variations during the preconvulsive period. These mice died of status epilepticus during the first seizure(s). Conversely, C57BL/6J mice displayed low response to MSO. The tonic and clonic seizures appeared 8 to 14 h after MSO administration with only 2% mortality. The seizures were preceded by an increase in brain glycogen content during the preconvulsive period. Moreover, during seizures, C57BL/6J mice were able to mobilize this accumulated brain glycogen, that returned to high value after seizures. The epileptic and glycogenic responses of the parental strains were also observed in mice of the F2 generation. The F2 mice that convulsed early (16%) did not utilize their small increase in brain glycogen content, and resembled CBA/J mice; while the F2 mice that seized tardily (24%) increased their brain glycogen content before convulsion, utilized it during convulsions, and resembled C57BL/6J mice. Sixty percent of the F2 mice presented an intermediate pattern in epileptogenic responses to the convulsant. These data suggest a possible genetic link between the two MSO effects, epileptiform seizures and increase in brain glycogen content. The increase in brain glycogen content and the capability of its mobilization during seizures could delay the seizure's onset and could be considered a “resistance factor” against the seizures.

Dissociation of mossy fiber sprouting and electrically-induced seizure sensitivity: rapid kindling versus adaptation.

It has been shown that massed stimulation (MS) of the amygdala or hippocampus does not result in seizure progression but in the 'phenomenon of adaptation', whereas alternate day rapid kindling (ADRK) produces reliable kindling (Lothman, E.W., Williamson, J.M., 1994. Brain Res. 649, 71-84). The goal of the present experiment was to determine if the two different effects are due to differences in mossy fiber sprouting and/or different seizure and postictal spike propagation patterns. Nine rats underwent MS (66-70 stimulations separated by 5-min interstimulus interval), six were exposed to ADRK (12 stimulations/day, every 30 min, with 4 stimulus days, each separated by 1 stimulus-free day), five rats served as control. All rats had electrodes implanted bilaterally in dorsal and ventral hippocampi (VH) and 14 of them had additional electrodes in the piriform cortex. Animals were stimulated in the left VH at afterdischarge threshold. There was no potentiation in seizure response 4-7 weeks after MS. In contrast, ADRK produced not only kindling but also ongoing epileptogenesis resulting 4-7 weeks later in spontaneous seizures and development of a prolonged convulsive state in response to the initially subconvulsive stimulus. Epileptiform activity during MS was mostly restricted to VH, whereas during ADRK it spread widely among studied structures including piriform cortex. Afterdischarges during MS were elicited frequently but seizures did not progress beyond stage 2-3. During ADRK, afterdischarges were evoked less frequently but seizures reached stage 4-7 by the end of the 3rd and 4th stimulus days. The fully kindled state was not reached at this time, but epileptogenic changes continued to progress. Seven weeks after the initial stimulation, both groups demonstrated mossy fiber sprouting of similar intensity in VH. We suggest, (1) frequent but predominantly local hippocampal afterdischarges induce mossy fiber sprouting, but this is not sufficient to produce significant enhancement in seizure susceptibility, and (2) the involvement of extra-hippocampal structures, possibly piriform cortex, and formation of an aberrant hippocampal-para-hippocampal circuit is required to result in a condition of progressive epileptogenesis.

New approaches for the detection and analysis of electroencephalographic burst-suppression patterns in patients under sedation.

An automatic EEG pattern detection unit was developed and tested for the recognition of burst-suppression periods and for the separation of burst from suppression patterns. The median, standard deviation and the 95% edge frequency were computed from single channels of the EEG within a moving window and completed by the continuous computation of frequency band power via an adapted Hilbert resonance filter. These parameters were given to the inputs of two hierarchically arranged artificial neural networks (NNs). The output signals of NNs indicate the suppression and burst phases. The burst recognition was focused on the precise recognition of the burst onset. In subsequent processing steps the time course of percentages of burst patterns within their corresponding burst-suppression-phases was calculated and the time locations of burst onsets can be used to trigger an averaging for a burst-related analysis. The data for our investigations were derived from the routine EEG derivations of 12 patients with various neurosurgical diseases. A group-related training of the NNs was realized. For the group-related trained NNs EEG data for 6 patients were used for training and the data of 6 other patients for testing the classification performance of the pattern recognition units. Additionally, the reliability of the detection algorithm was tested with data of two patients with convulsive state, resistant to treatment, and burst-suppression like pattern EEC.

New principle of search for compounds possessing anticonvulsive properties

One method of creating new drugs is to synthesize compounds containing a specific fragment (pharmacophore) found as a result of the statistical processing of a large data file for the known compounds possessing the desired type of pharmacological activity. In recent years, various mathematical techniques and computer simulation methods have been extensively used in drug design [I 6 ] . The formalized analysis of a large volume of statistical ~ t a and the derivation of semiempirical rules are most expedient in cases where it is difficult to elaborate a unified hypothesis concerning the neurocbemical mechanisms of a disease for which the potential drugs have to be synthesized. In particular, this approach may be promising in the search for new anticonvulsive preparations, since the convulsive states are usually heterogeneous and involve various neurochemical systems of the brain. Below we propose a new principle of the pre-experimental search for the compounds possessing anticonvulsive (AC) properties with the aid of two "filters." The first is based on the originally formulated "5-rule" capable of selecting potential structures possessing, in principle, the AC activity. The second stage consists in the computer-aided analysis of the pre-selected structures using the PASS program package, providing selection of a narrow circle of potential AC agents offering maximum efficacy at a minimum level of side effects (including minimum toxicity). The class of AC compounds contains substances either suppressing the CNS excitation processes (for example," lamotrigine inhibits the secretion of glutamate-a salt of exciting amino acid, EAA) or potentiating the inhibition processes in CNS (for example, tiagabine decreases the back capture of G A B A the major CNS inhibition mediator, while vigabatrin produces irreversible blocking of GABA-transaminase) [7]. The main disadvantage of GABA as a potential

Delayed development of spontaneous seizures and prolonged convulsive state in rats after massed stimulation of the anterior piriform cortex

We studied the short- and long-term epileptogenic effects of massed stimulation (MS) of the piriform cortex. Sprague–Dawley rats with electrodes implanted bilaterally in the anterior piriform cortex and the dorsal and ventral hippocampi underwent MS: electrical stimulation of the left piriform cortex every 5 min for 6 h (afterdischarge threshold, 60 Hz, 1 ms, 1 s). Animals were retested (5 stimulations) 3–4 times later at different time points to check for the kindled state. Our data showed that MS resulted in delayed development of severe epilepsy. The interval between MS and the first appearance of convulsive response (2 weeks) was characterized by deep refractoriness to seizure (silent period). Unexpectedly, dramatic seizure activity occurred 4–7 weeks after MS. This was manifested by (1) generalized tonic-clonic convulsions with multiple fallings, which were elicited repeatedly during retest; (2) frequent progression of elicited generalized convulsions into a prolonged (>8 min) postictal convulsive state expressed mainly by continuous partial seizures and even new bouts of generalized seizures, and (3) development of mild spontaneous seizures. We found that epileptiform activity predominated in the ventral hippocampus. Mossy fiber sprouting was also most pronounced in this area. We propose that the MS resulted in formation of pathological circuits which involve both piriform cortex and ventral hippocampus and lead to severe epilepsy. © 1997 Elsevier Science B.V. All rights reserved.

F303. The change of blood rheology during the baby rabbit's continual state of convulsion

F303. The change of blood rheology during the baby rabbit's continual state of convulsion

Functional mapping of the late stages of status epilepticus in the lithium-pilocarpine model in rat: a 14C-2-deoxyglucose study.

Pilocarpine administration to lithium chloride-pretreated rats results initially in discrete convulsive seizures, each behaviorally and electroencephalographically terminated, which then progress to convulsive activity with waxing-and-waning behavioral and electrographic severity; finally, a continuous convulsive state ensues, associated electrographically with continuous fast spiking. This stage does not last indefinitely but is followed by a dramatic electrographic change to periodic epileptiform discharges. The purpose of the present study was to determine with the 14C-2-deoxyglucose functional mapping technique what changes occur in the seizure anatomic substrate during and after this transition, in order to enable inferences about underlying mechanisms. Behavior associated with early and late continuous fast spiking consisted of head twitching; corresponding deoxyglucose autoradiographs displayed seizure-induced intense glucose utilization in most forebrain areas; extranigral brainstem was normal. At 2-3 h of status, fast spiking became interrupted by flat periods; periodic complexes soon dominated the electroencephalogram. Behaviorally, convulsive severity increased. Despite this dramatic electrographic evolution, little change in generalized forebrain metabolic hyperactivation occurred, except that the zona incerta/pretectal/superior colliculus complex displayed markedly increased activity. Deoxyglucose studies in late stages of periodic epileptiform discharges established a sequence of further changes. In late periodic discharges with clonic jerks, at 4 h after status entry, generalized forebrain hyperactivation still prevailed, but to a lesser degree than in early periodic discharges with clonic jerks. At a still later stage, late periodic discharges, subtle convulsive, autoradiographs revealed constriction of the seizure-activated anatomic substrate: hyperactivation was lost in most of neocortex and thalamus, and in caudal olfactory structures, cortical amygdala, and entorhinal areas, but retained in deep occipital cortex and many limbic areas. In the last stage, late periodic discharges, electrical, not associated with convulsive behavior, autoradiographs revealed residual activation in only Ammon's horn; in contrast, much of the forebrain displayed below-normal glucose utilization. These results demonstrate that in the later stages of status epilepticus, the transition from fast spiking to periodic complexes is not associated with a reduction in the seizure anatomic substrate. The electrographic entity of periodic epileptiform discharges is not anatomically or behaviorally homogeneous, but proceeds through successive stages characterized initially by a reduction of glucose utilization within generalized seizure-activated forebrain, then a contraction of the seizure anatomic substrate. Possible mechanisms underlying the transition to periodic complexes are discussed.

P193 ontogenetic aspects of pyridoxal enzyme activities in experimental convulsive states induced by glutamate decarboxylase inhibitors

P193 ontogenetic aspects of pyridoxal enzyme activities in experimental convulsive states induced by glutamate decarboxylase inhibitors

Effects of diltiazem in convulsive states differ from those previously reported for dihydropyridine calcium channel antagonists.

Unlike the dihydropyridine calcium channel antagonists studied previously, the benzothiazepine calcium channel antagonist, diltiazem, increased the incidence of convulsions caused by bicuculline, N-methyl-DL-aspartate or 4-aminopyridine. However, the latencies to convulsions were also increased. Diltiazem increased the ratings of convulsive behaviour on handling after intraperitoneal administration of bicuculline, or pentylenetetrazol and after the calcium channel activator, Bay K 8644, administered ICV. When the binding of the dihydropyridine, [3H]-nitrendipine in the CNS was measured in vivo, this was increased by diltiazem. This compound therefore showed a different pattern of interaction with convulsant drugs then that previously demonstrated for other calcium channel antagonists, appearing to possess both pro- and anticonvulsant actions, and a different pattern of interaction with the dihydropyridine receptor complex.

Histamine release from basophils in childhood: age dependency and inhibition by pertussis infection and pertussis toxin.

The influence of childhood pertussis infection and of purified pertussis toxin on histamine release from human basophil leucocytes was investigated. Three different stimuli, the peptide N-formyl-Met-Phe (NFMP), anti-IgE, and the calciumionophore A23187 were used to challenge the cells. When NFMP was the stimulus, histamine release in the control group (age 0.5-17 years) increased in an age-dependent fashion, whereas anti-IgE and A23187 stimulated release did not vary with age. During the convulsive state of pertussis infection there was a significant reduction of histamine release in response to 10 microM NFMP (from 9.5 +/- 1.4 [n = 21] to 6.7 +/- 1.5 [n = 19], P < 0.05) and in response to 800 and 80 U/ml anti-IgE (from 28.5 +/- 5 [n = 19] to 16.3 +/- 5 [n = 13], P < 0.05, and from 6.9 +/- 1.7 [n = 16] to 2 +/- 0.8 [n = 13], P < 0.01), whereas histamine release stimulated by A23187 was unchanged compared to release in control children. In vitro pretreatment of basophils from healthy children and adults with pertussis toxin also inhibited histamine release. When NFMP was the stimulus, release was completely blocked by pertussis toxin with an IC50 of about 11 ng/ml, whereas anti-IgE stimulated release was only inhibited by 20%-30% and release induced by A23187 was reduced to 40%-50% by toxin treatment. In conclusion we have demonstrated a functional impairment of histamine release during the convulsive state of pertussis and that this inhibition is likely to be mediated by pertussis toxin.

Aggravation of Penicillin-Induced Epilepsy in Rats with Locus Ceruleus Lesions

The rate and pattern of development of seizures induced by penicillin injected intraperitoneally were determined in rats that had been depleted of brain norepinephrine (NE) by bilateral injections of the neurotoxin 6-OH dopamine into the locus ceruleus. Behavioral observations and scalp electrographic recordings were made after injection and the efficacy of NE depletion was determined by high performance liquid chromatography measurement of cortical levels of NE and its metabolites. We found that in comparison to sham-operated control rats, NE-depleted rats had a significantly shorter latency to first observable myoclonic jerk, the first epileptic discharge, the first convulsion with sustained epileptic discharges, and a longer duration of convulsions. We observed a similar electrographic pattern of multifocal spikes with bilateral synchrony in both groups. However, more of the control rats (six of 12) had convulsions as compared to the lesioned rats (four of 12). These findings are consistent with previous evidence that depletion of neocortical NE facilitates the development of epileptiform activity in the CNS; however, a convulsive state was not induced by NE depletion.

Some Correlations between Local Anesthetic-Induced Convulsions and .GAMMA.-Aminobutyric Acid in Rat Spinal Cord.

The effects of local anesthetics (procaine and lidocaine) on the gamma-aminobutyric acid (GABA) and L-glutamic acid (Glu) levels in rat spinal cord were studied during the convulsive process. The present study also investigated the influence of central GABA manipulations on the local anesthetic-induced convulsions. An increase in spinal GABA levels was observed at the preconvulsive and convulsive states after administration of procaine (170 mg/kg, i.p.) or lidocaine (120 mg/kg, i.p.), which induced clonic convulsions; in the depressive state, GABA levels returned to normal; in all states, Glu levels were unchanged. Semicarbazide (25-100 mg/kg, i.p.), a glutamic acid decarboxylase inhibitor, produced a decrease in spinal GABA content and strongly enhanced both local anesthetic-induced convulsions as shown by a shortening of the latency and an increase in the mortality. Aminooxyacetic acid (AOAA; 10-40 mg-kg, i.p.), a GABA transaminase inhibitor, dose-dependently increased spinal GABA content and markedly suppressed procaine-induced convulsions. However, lidocaine-induced convulsions were enhanced by AOAA. These results suggest that the spinal GABA neuron may respond to the convulsions induced by local anesthetics. Furthermore, there is a clear relationship between spinal GABA content and procaine-induced, but not lidocaine-induced, convulsions.

Electroencephalographic and behavioural correlates of seizures development in rats in response to hyperbaric exposure

Electroencephalographic (EEG) activity was continuously monitored from the hippocampus, amygdala, reticular formation and frontal cortex in freely moving Sprague-Dawley rats exposed to 91 atmosphere absolute pressure (ATA) using compression rates of 1 or 3 ATA/min. Videotape recordings were made for subsequent behavioural analysis. Tremor, myoclonic jerks and tonic extensions of the tail were observed in all animals but did not appear to correlate with epileptiform activity. Convulsions occurred between 66.5 and 91 ATA in all subjects compressed at 3 ATA/min, but in only 1 rat (at 91 ATA) in the 1 ATA/min group. Tonic-clonic motor seizures developed explosively and involved the entire body. EEG records showed continuous spiking at all sites during the generalized convulsive state. There was no evidence of differential susceptibility of the various brain regions examined to the epileptogenic effects of high pressure. The behavioural and EEG data indicate that hyperbarically induced seizures differ from the classical limbic type.

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.

An outbreak of rotavirus infections in newborns — New aspects?

In the context of a prospective study for detection of rotavirus infections, an outbreak in neonates was observed in April 1986 at the Schweizerische Pflegerinnenschule in Zurich. Altogether, 103 neonates were investigated by means of genome gel electrophoresis for rotaviruses (HRV, human rotavirus) in the feces in the course of April 1986. Of these 103 neonates, 51 (49%) were HRV-positive and 52 (51%) were HRV-negative. Of the 51 HRV-positive neonates, 42 (82%) showed clinical symptoms, especially a typically altered pathological quality of the feces and an increased frequency of fecal passage. Vomiting and fever were observed less frequently. The pathological quality of the feces proved to be significantly correlated with the infection of rotaviruses in the neonate at risk. Besides this, reduced feeding behavior, circulatory signs and in one neonate a convulsive state of unclear etiology were also observed. This has only been rarely described up to now in rotavirus infections in neonates. This study confirms that rotavirus may cause frequently slight symptoms in neonates, but sometimes also symptoms of a clinically significant extent.