Cerebral Metabolic and Circulatory Responses to Induced Convulsions in Animals

Plum, Fred; Posner, Jerome B.; Troy, Bart L.

doi:10.1001/archneur.1968.00470310015001

Cited by 298 publications

(86 citation statements)

References 15 publications

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“…Convulsant drugs such as pentylenetrazol produce an increase in cerebral blood flow secondarily to an increase in both oxygen consumption and cerebral activity (Schmidt et al, 1945;Fujita, 1956;Ingvar, Lubbers & Siesjo, 1962;Plum, Posner & Troy, 1968). In the present study, pentylenetetrazol and bemegride each produced an increase in the cerebral blood flow associated with an increase in the cerebral oxygen consumption of the brain.…”

Section: X2supporting

confidence: 54%

Effects of drugs on the cerebral circulation of the dog in relation to the cerebral oxygen consumption

Chin

Imai

Nakano

et al. 1983

British J Pharmacology

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1Drug effects were studied on the cerebral circulation by measuring the sagittal sinus outflow in the anaesthetized dog following the method of Michenfelder and by monitoring cerebral oxygen consumption. Systemic aortic pressure, heart rate and spinal fluid pressure were also studied. 2 Since dilatation of cerebral vessels was observed in nearly all the preparations after inhalation of C02, it was thought that gross extracerebral contamination was virtually eliminated in this preparation. A close correlation was observed between the oxygen consumption of the brain as a whole and the sagittal sinus outflow (r= 0.93, P< 0.001); therefore it became feasible to differentiate the direct effects of drugs on cerebral blood vessels from indirect ones attributable to changes in the cerebral oxidative metabolism. 3 Sodium pentobarbitone (5 mg kg-1, i.v.), reduced the cerebral venous outflow and caused a decrease in the oxygen consumption. Pentylenetetrazol (30 mg kg -i.v.) and bemegride (5 mg kg-1 i.v.) produced an increase in the blood flow and a corresponding increase in the cerebral oxygen consumption. Thus, it was concluded these substances had no direct effects on the cerebral blood vessels. 4 Acetazolamide (10mgkg-1, i.v.), a carbonic anhydrase inhibitor, produced a marked and sustained vasodilatation after a latent period of 0.5-1 min. There was no increase in the cerebral oxygen consumption. A similar pattern was seen after CO2 had been inhaled. Methylergometrine and dihydroergotamine (20 jig kg-1 i.v.) induced a prolonged vasoconstriction of the cerebral vascular bed without any changes in the oxygen consumption of the brain. Therefore this method can discriminate between indirect or direct effects of drugs on cerebral vascular outflow.

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Section: X2supporting

confidence: 54%

Effects of drugs on the cerebral circulation of the dog in relation to the cerebral oxygen consumption

Chin

Imai

Nakano

et al. 1983

British J Pharmacology

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“…Many observations in epilepsy patients (19)(20)(21)(22)(23)(24), confirmed by animal studies (25)(26)(27)(28), demonstrated that SE provokes transient BBB breakdown and vasogenic edema in the area of the seizure focus. It is commonly proposed that local (relative hypoxia secondary to increased ictal metabolism with an increase in local PCO 2 and lactate) and systemic (increase in blood pressure and decrease in blood pH) physiologic changes induce a vasodilatation, resulting in increased regional blood flow and BBB breakdown (25,26,29).…”

Section: Role Of the Bbb Breakdown In The Genesis Of The Lesionsmentioning

confidence: 87%

“…It is commonly proposed that local (relative hypoxia secondary to increased ictal metabolism with an increase in local PCO 2 and lactate) and systemic (increase in blood pressure and decrease in blood pH) physiologic changes induce a vasodilatation, resulting in increased regional blood flow and BBB breakdown (25,26,29).…”

Section: Role Of the Bbb Breakdown In The Genesis Of The Lesionsmentioning

confidence: 99%

Magnetic Resonance Imaging in the Study of the Lithium–Pilocarpine Model of Temporal Lobe Epilepsy in Adult Rats

et al. 2002

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Summary:Purpose: In temporal lobe epilepsy, it remains to be clarified whether hippocampal sclerosis is the cause or the consequence of epilepsy. We studied the temporal evolution of the lesions in the lithium-pilocarpine model of epilepsy in the rat with magnetic resonance imaging (MRI) to determine the progressive morphologic changes occurring before the appearance of chronic epilepsy.Methods: MRI was performed on an MR scanner operating at 4.7 T. We followed the evolution of lesions using T 2 -and T 1 -weighted sequences before and after the injection of gadolinium from 2 h to 9 weeks.Results: At 2 h after status epilepticus (SE), a blood-brain barrier breakdown could be observed only in the thalamus; it had disappeared by 6 h. At 24 h after SE, edema was present in the amygdala and the piriform and entorhinal cortices together with extensive neuronal loss; it disappeared progressively over a 5-day period. During the chronic phase, a cortical signal reappeared in all animals; this signal corresponded to gliosis, which appeared on glial fibrillary acidic protein (GFAP) immunohistochemically stained sections as hypertrophic astrocytes with thickened processes. In the hippocampus, the correlation between histopathology and T 2 -weighted signal underscored the progressive constitution of atrophy and sclerosis, starting 2 days after SE.Conclusions: These data show the reactivity of the cortex that characterizes the initial step leading to the development of epilepsy and the late gliosis that could result from the spontaneous seizures. Moreover, it appears that hippocampal sclerosis progressively worsened and could be both the cause and the consequence of epileptic activity.

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“…A grand mal epileptic seizure causes marked acute cardiovascular changes both in humans [5] and in experimental animals [6,8]. In the brain the blood flow increases considerably during an epileptic seizure [6] but veiy little is known about the placental blood flow during maternal seizures.…”

Section: Discussionmentioning

confidence: 99%

“…In the brain the blood flow increases considerably during an epileptic seizure [6] but veiy little is known about the placental blood flow during maternal seizures. Case no.…”

Section: Discussionmentioning

confidence: 99%

Fetal heart rate during a maternal grand mal epileptic seizure

Teramo¹,

Hiilesmaa²,

Bardy³

et al. 1979

Journal of Perinatal Medicine

136

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An increased rate of malformations, particularly oral clefts, of newborn infants born to epileptic mothers has been reported in several studies [1,2,3,4,7]. Although maternal Ingestion of antiepileptic drugs is strongly suspected of causing congenital defects, the effect of epilepsy itself or a combined effect of drug intake and epilepsy have not been excluded äs etiological factors. Very little is known about fetal oxygenation during a maternal grand mal seizure. We describe here two cases in which fetal heart rate (FHR) was recorded during a maternal epileptic seizure during the first stageof labor. Caseno. 1.The patient was a 28-year old primipara whose own birth weight had been 1600 g. A small cleft palate was closed operatively when she was 2 years of age. She had three grand mal seizures since the age of 25. The last seizure occurred 9 months before the onset of her pregnancy. Her medication was diphenylhydantoin 100 mg daily before the pregnancy. The same dose was continued unchanged during the pregnancy. The patient attended an outpatient clinic for pregnant epileptics regularly during her pregnancy, which progressed uneventfully until term. Serial determination of 24-hour urinary excretion of estriol and human placental lactogen of the maternal serum gave normal values during the last weeks of pregnancy. FHR showed normal patterns during weekly cardiotocographic recordings during the last month of pregnancy. Labor started spontaneously at term. The membranes were ruptured and a spiral electrode was attached to the fetal scalp for recording of FHR when the cervix was 4 cm dilated 4.5 hours before delivery. 43 minutes before delivery when the cervix was 6 cm dilated the patient unexpectedly suffered a grand mal epileptic seizure, which lasted 2.5 minutes (Fig. 1) a periGyneand 10 mg intramuscularly. Fig. l shows FHR before, during and after the grand mal seizure of the mother. FHR decelerated below 120 beats/minfor over 13 minutes. The short-term variability of FHR decreased during the deceleration period, after which there was a phase of tachycaidia up to 165 beats/min with decreased shortterm and long-term variability. The mother's blood pressure was normal during the fetal bradycardia. 29 minutes after the beginning of the seizure a late deceleration bradycardia wave is seen. The fetus was delivered by cesarean section 43 minutes after the beginning of the seizure. The cesarean section was performed under general anesthesia with nitrous oxide/oxygen and succinyl choline Infusion after induction with thiobarbitone. The male infant weighed 3630 g and received an APGAR score of 8 at the age of one minute. The condition of the newborn infant was good during the following days except for slightly reduced muscular tone. The mother recovered from the Operation uneventfully. At delivery the concentration of diphenylhydantoin in maternal venous blood was only 0.9 Mg/ml. The patient assured having taken her medication regularly. The mother and the infant were discharged in good condition 9 days after the delivery.

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Cerebral Metabolic and Circulatory Responses to Induced Convulsions in Animals

Abstract: C O N V U L S I O N S place

Cited by 298 publications

References 15 publications

Effects of drugs on the cerebral circulation of the dog in relation to the cerebral oxygen consumption

Effects of drugs on the cerebral circulation of the dog in relation to the cerebral oxygen consumption

Magnetic Resonance Imaging in the Study of the Lithium–Pilocarpine Model of Temporal Lobe Epilepsy in Adult Rats

Fetal heart rate during a maternal grand mal epileptic seizure

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