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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Previous anatomical investigations have reported a direct projection from substantia nigra pars lateralis to the dorsal midbrain anticonvulsant zone. The present study tested the hypothesis that the anticonvulsant properties of nigral inhibition previously attributed to substantia nigra pars reticulata were, in fact, due to the suppression of neural activity in the adjacent pars lateralis. Using the electroshock model of epilepsy, a systematic map of the anticonvulsant effects of bilateral injections of muscimol (60 ng/0.5 mu l per side) into different parts of substantia nigra was constructed. Electroshock (1 s of 40 mA 50 Hz AC) was administered via ear-clip electrodes 5 or 60 min following injections of muscimol, or 60 min after control injections of saline. To provide insight into the functional mechanisms whereby nigral inhibition might suppress tonic seizures the behavioural effects elicited by muscimol were also noted. No evidence supporting the experimental prediction was found. The most sensitive region of substantia nigra for suppressing tonic hindlimb extension was caudal pars reticulata. These data indicate a serious mismatch between the results of microinjection mapping studies and underlying patterns of anatomical connectivity. The behavioural reaction most closely associated with tonic seizure suppression was stereotyped locomotion; both were obtained maximally from caudal pars reticulata. Rostral substantia nigra was associated more with oral stereotypy, while a raised head position was observed at lateral injection sites and a lowered positioning of the head at medial locations. These data suggest that the rat substantia nigra may contain a functional organization based on a form of somatomotor topography. This organization may influence which part of the substantia nigra is most effective in suppressing seizures expressed by different muscle groups of the body.
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PMID:Regional distribution of the anticonvulsant and behavioural effects of muscimol injected into the substantia nigra of rats. 908 26

The effects of [arginine8, glycine-OH9]-vasopressin (AGV), alone and in combination with adrenaline, on pentylenetetrazol (PTZ) seizure threshold by timed intravenous infusion in tall vein and intensity by subcutaneous (s.c.) PTZ test (85 mg/kg) were studied in male albino mice. AGV was administered intracerebroventricularly (i.c.v.) at doses of 0.001, 0.01, 0.1, 1.0 and 5.0 ng/mouse 5, 15 and 30 min prior to PTZ AGV induced decrease of seizure threshold at middle doses (0.01 and 0.1) 5 and 15 min prior to PTZ (75 and 67% respectively vs. controls). Adrenaline (1 mg/kg, i.p.) potentiated the effect of AGV on seizure threshold. AGV also induced increase of seizure intensity at doses of 0.01 and 1.0 ng and decrease of latency of the first tonic seizure. Adrenaline (1.0 mg/kg, i.p.) enhanced the effects of AGV suggesting interactions of vasopressin with adrenergic neurotransmission in the CNS.
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PMID:Effects of [arginine8, glycine-OH9]-vasopressin on pentylenetetrazol seizures in mice. Interaction with adrenaline. 920 63

Seizures in genetically epilepsy-prone rats (GEPRs) may result from hypoactivity of locus coeruleus (LC) neurons during seizures. This study examined Fos-like-immunoreactivity (FLI) in the LC following audiogenic seizures in two strains of GEPRs (GEPR-9s and -3s), and following pentylenetetrazol (PTZ) or maximal electroshock seizures (MES) in normal rats. After tonic seizure, GEPR-9s showed an identical LC-FLI response to that of normal rats following tonic seizures induced by either PTZ or MES. GEPR-3s, having clonic seizures, had less FLI in the LC. Therefore, stimulus-transcription coupling in the GEPR LC is apparently normo-typic in its FLI response to seizure and thus is not likely the root cause of NE abnormalities in this seizure model.
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PMID:Fos in locus coeruleus neurons following audiogenic seizure in the genetically epilepsy-prone rat: comparison to electroshock and pentylenetetrazol seizure models. 932 30

1. Contribution of nitric oxide to the convulsive seizures induced by fluoroquinolones (FQs) coadministered with 4-biphenyl acetic acid (BPAA), the active metabolite of fenbufen, was assessed in mice. 2. Enoxacin + 4-biphenyl acetic acid caused clonic seizures in all treated mice, followed by tonic seizures and death. These events were associated with a significant increase in intracerebellar cyclic GMP. 3. Pretreatment with the nitric oxide synthase (NOS) inhibitor, NG-nitro-L-arginine methylester (L-NAME), but not with D-NAME, significantly reduced the incidence of convulsions and lethality, as well as the increase in cyclic GMP. 4. Pretreatment with N-methyl-D-aspartic acid (NMDA)-receptor antagonist, MK-801, inhibited only the transition of clonic seizure to tonic seizure without affecting the incidence of clonic seizure and lethality. 5. These findings suggest that FQs + BPAA exert convulsions by activating NOS partly through the mediation of the NMDA receptor in the brain cells.
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PMID:Role of nitric oxide in the convulsive seizures induced by fluoroquinolones coadministered with 4-biphenyl acetic acid. 934 23

Previous experimental work has established that activation of sites in the dorsal midbrain can suppress tonic hindlimb extension in the electroshock model of epilepsy. The most sensitive region for this effect is centred on the intercollicular area and is referred to as the dorsal midbrain anticonvulsant zone (DMAZ). Subsequent experiments have shown that the ipsilateral descending projection from this region to the ventrolateral pons is critically involved in mediating its tonic seizure-suppressing properties. The purpose of the present investigation was to test whether direct anticonvulsant effects in the electroshock model could be obtained from selective manipulation of DMAZ target regions in the ventrolateral pons. Animals were prepared with chronically implanted guide cannulae through which microinjections could be made directly into the lateral pontine reticular formation. Animals received injections of saline or bicuculline (25-100 pmol) administered either bilaterally or unilaterally. The effects of these injections on the animals' behaviour were determined in an open arena, after which maximal electroshock (1 s, 40 mA, 50 Hz AC) was administered via ear-clip electrodes and the duration of tonic hindlimb extension was recorded. Bilateral injections of bicuculline (100 pmol) suppressed tonic seizures at a significantly higher proportion of sites centred on DMAZ target regions of the ventrolateral pons than surrounding areas. For injections centred on this region the suppressive effects of bicuculline were dose-related in the range 25-100 pmol. Unilateral injections of bicuculline into the ventrolateral pons also effectively suppressed tonic seizures in the electroshock model. Within the ventral pons there was a significant association between the behavioural and anticonvulsant effects of bicuculline; injections suppressing tonic seizures were associated with the induction of fast continuous locomotor activity. These data confirm that the DMAZ recipient region of the ventrolateral pontine reticular formation is part of a circuit which can suppress the manifestation of tonic hindlimb extension in the electroshock model. Whether this property is related to the participation of this region in normal locomotion and posture remains to be determined.
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PMID:Regional distribution of the anticonvulsant and behavioural effects of bicuculline injected into the pontine reticular formation of rats. 938 10

Previous microinjection mapping studies in the mesencephalon established a significant association between the induction of locomotor activation and the suppression of tonic seizures in the electroshock model of epilepsy. The purpose of the present study was to see if this relationship also applies in an area of the brainstem commonly known as the mesencephalic locomotor region (MLR). The principal findings were the following. (i) Activation of extensive areas of the dorsal midbrain and tegmentum, including the MLR, by unilateral injections of the GABA antagonist bicuculline induced leg movements and suppressed the tonic component of electroshock-induced seizures. (ii) A highly significant correlation was observed between these two variables. (iii) In some cases, however, the induction of phasic leg movements was neither sufficient nor necessary for tonic seizure suppression. It is possible, therefore, that injection-elicited changes in tonic aspects of limb control may be more directly related to the suppression of tonic motor seizures in the electroshock model of epilepsy.
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PMID:Anticonvulsant and behavioural effects of bicuculline injected into the mesencephalic locomoter region of rats. 945 59

The ventrolateral periaqueductal gray is implicated as a component of the neuronal network for audiogenic seizure. This implication is based on immunocytochemical labeling of the proto-oncogene, c-fos, and microinjection studies in the severe substrain of genetically epilepsy-prone rats that exhibits tonic seizures. The present study examines changes in acoustically evoked neuronal responses within the periaqueductal gray in the awake and behaving genetically epilepsy-prone rat as compared to normal Sprague Dawley rats. Two populations of neuronal response were observed in the periaqueductal gray of both genetically epilepsy-prone and normal rats. Most of the neurons exhibited long latencies (>10 ms) and lower thresholds, and were more responsive to the acoustic stimulus. The remainder of the periaqueductal gray neurons exhibited short latencies (<10 ms) and higher thresholds, and exhibited minimal responsiveness to the acoustic stimulus. The mean threshold of periaqueductal gray acoustically evoked neuronal firing of short-latency neurons was significantly higher than normal in the genetically epilepsy-prone rat. The number of acoustically evoked action potentials was significantly elevated in the genetically epilepsy-prone rat, particularly at the highest acoustic intensity and at a repetition rate of 1/2 s. In the genetically epilepsy-prone rat, the number of action potentials exhibited adaptation (habituation) at 1/s as compared to 1/2 s across stimulus intensities. Habituation in normal rats was observed primarily at high intensities (95 dB sound pressure level or above). During wild running and tonic seizures in the genetically epilepsy-prone rat, periaqueductal gray neurons. which had diminished firing rates due to habituation, exhibited a tonic firing pattern. Just (1-5 s) prior to the onset of tonic convulsive behaviors, an increase in the rate of periaqueductal gray tonic firing was observed. These patterns of abnormal neuronal firing suggest that periaqueductal gray neurons may be involved in generation of the tonic seizure behavioral component of audiogenic seizure in the genetically epilepsy-prone rat, which will need confirmation in other audiogenic seizure models.
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PMID:Periaqueductal gray neurons exhibit increased responsiveness associated with audiogenic seizures in the genetically epilepsy-prone rat. 953 30

We have recently demonstrated that eight, daily flurothyl-induced generalized clonic seizures, followed by a four week stimulus-free interval, results in a long-lasting reduction in generalized seizure threshold and a change in the type of seizure expressed in response to flurothyl from clonic to tonic. There is a progressive increase in the probability that a mouse will express a tonic seizure during the four week interval, suggesting that prior flurothyl seizures initiate a proepileptogenic process that requires time to develop. In this study, the immunohistochemical detection of the c-fos protein (Fos) was used to evaluate whether seizure-induced epileptogenesis resulted in regional differences in the degree of neuronal activation. Fos immunoreactivity was examined 1.5 h following either a single generalized seizure, the last of eight consecutive daily seizures or a retest seizure evoked two weeks after the last of eight seizures. In each condition, generalized seizure behaviours were elicited in C57BL/6 mice using flurothyl and classified as either "forebrain" (face and forelimb clonus) or "brainstem" (running/bouncing, treading, tonic extension). The spatial distribution of Fos induction was compared on the basis of the seizure phenotype and the seizure history. The predominant differences in Fos distribution were found to be related to the type of seizure expressed regardless of the seizure history. Furthermore, the different motor components that make up a "brainstem" seizure could not be distinguished by the pattern of Fos labelling suggesting that multiple convulsive behaviours are mediated by one anatomical system. Finally, Fos induction in the ventromedial hypothalamic nucleus preceded and predicted the change in seizure type from "forebrain" to "brainstem". These data support the concept that separate anatomical systems mediate the expression of the two generalized seizure phenotypes. In addition, the ventromedial nucleus of the hypothalamus may be a point of interaction between the systems and may play a role in seizure-induced neural reorganization.
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PMID:Regional analysis of the spatial patterns of Fos induction in brain following flurothyl kindling. 957 7

Midazolam infusion was tried as the treatment for 48 episodes of refractory status epilepticus or a cluster of seizures in 16 children. The mean age of patients was 3.5 years (range, 1 month to 18 years). Nine children had epilepsy, one purulent meningitis, one encephalitis, one acute cerebral infarction, and the remaining four had acute phase of hypoxic ischemic encephalopathy. The type of the seizure was a generalized tonic clonic seizure (including a partial seizure secondarily generalized) in 41 episodes, a tonic seizure in 3, an atypical absence in 1, and a complex partial seizure in 3, respectively. All patients received intravenous midazolam at 0.15 mg/kg as bolus, followed by a continuous infusion at 0.1-0.15 mg/kg/hr initially. The dose was increased gradually up to 0.3 mg/kg/hr until the complete control of seizures was achieved. Fourty-one of the 48 episodes of seizures were controlled within 30 minutes after the initiation of midazolam therapy. The mean infusion rate of midazolam required was 0.22 mg/kg/hr. The mean duration of the treatment was 4.1 days. None of the patients had serious changes in the blood pressure or respiratory status attributable to the use of midazolam. In conclusion, midazolam infusion is an effective and safe therapeutic approach for the management of childhood status epilepticus.
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PMID:[Efficacy of continuous intravenous infusion of midazolam in the treatment of status epilepticus in children]. 969 22

3-Nitropropionic acid, a potent inhibitor of succinate dehydrogenase which thus compromises cellular energy metabolism, evoked convulsions in mice in a dose-dependent manner. CD50 for clonic seizures was 158.5 (144.1-174.3) mg/kg. Tonic seizures were not observed. Broad-spectrum anticonvulsants, namely diazepam, phenobarbital and valproate, prevented the occurrence of 3-nitropropionic acid-induced seizures with ED50 of 4.9 (3.1-7.6), 33.1 (17.9-61.0) and 389.7 (351.2-432.3) mg/kg, respectively. Diphenylhydantoin-like drugs (diphenylhydantoin, and carbamazepine), anti-absence drugs (trimethadione and ethosuximide) and acetazolamide were ineffective. The characteristics of 3-nitropropionic acid-induced seizures resembled those of convulsions evoked by another mitochondrial toxin, aminooxyacetic acid.
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PMID:Mitochondrial toxin 3-nitropropionic acid evokes seizures in mice. 983 Dec 93


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