المؤلفون: Westin K; NatMEG, Department of Clinical Neuroscience, Karolinska Institute, Stockholm, Sweden; Clinical Neurophysiology, Karolinska University Hospital, Stockholm, Sweden. Electronic address: karin.westin@ki.se., Pfeiffer C; Department of Microtechnology and Nanoscience - MC2, Chalmers University of Technology, Gothenburg, Sweden., Andersen LM; Center of Functionally Integrative Neuroscience (CFIN), Aarhus University, Aarhus, Denmark; NatMEG, Department of Clinical Neuroscience, Karolinska Institute, Stockholm, Sweden., Ruffieux S; Department of Microtechnology and Nanoscience - MC2, Chalmers University of Technology, Gothenburg, Sweden., Cooray G; NatMEG, Department of Clinical Neuroscience, Karolinska Institute, Stockholm, Sweden; Clinical Neurophysiology, Karolinska University Hospital, Stockholm, Sweden., Kalaboukhov A; Department of Microtechnology and Nanoscience - MC2, Chalmers University of Technology, Gothenburg, Sweden., Winkler D; Department of Microtechnology and Nanoscience - MC2, Chalmers University of Technology, Gothenburg, Sweden., Ingvar M; NatMEG, Department of Clinical Neuroscience, Karolinska Institute, Stockholm, Sweden., Schneiderman J; MedTech West and the Institute for Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden., Lundqvist D; NatMEG, Department of Clinical Neuroscience, Karolinska Institute, Stockholm, Sweden.

المصدر: Clinical neurophysiology : official journal of the International Federation of Clinical Neurophysiology [Clin Neurophysiol] 2020 Aug; Vol. 131 (8), pp. 1711-1720. Date of Electronic Publication: 2020 May 11.

نوع المنشور: Comparative Study; Journal Article

بيانات الدورية: Publisher: Elsevier Country of Publication: Netherlands NLM ID: 100883319 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1872-8952 (Electronic) Linking ISSN: 13882457 NLM ISO Abbreviation: Clin Neurophysiol Subsets: MEDLINE

مواضيع طبية MeSH: Brain/*physiopathology , Brain Waves/*physiology , Epilepsy/*physiopathology , Magnetoencephalography/*methods , Seizures/*physiopathology, Electroencephalography/instrumentation ; Electroencephalography/methods ; Female ; Humans ; Magnetoencephalography/instrumentation ; Middle Aged ; Scalp/physiopathology

مستخلص: Objective: Conventional MEG provides an unsurpassed ability to, non-invasively, detect epileptic activity. However, highly resolved information on small neuronal populations required in epilepsy diagnostics is lost and can be detected only intracranially. Next-generation on-scalp magnetencephalography (MEG) sensors aim to retrieve information unavailable to conventional non-invasive brain imaging techniques. To evaluate the benefits of on-scalp MEG in epilepsy, we performed the first-ever such measurement on an epilepsy patient.
Methods: Conducted as a benchmarking study focusing on interictal epileptiform discharge (IED) detectability, an on-scalp high-temperature superconducting quantum interference device magnetometer (high-Tc SQUID) system was compared to a conventional, low-temperature SQUID system. Co-registration of electroencephalopraphy (EEG) was performed. A novel machine learning-based IED-detection algorithm was developed to aid identification of on-scalp MEG unique IEDs.
Results: Conventional MEG contained 24 IEDs. On-scalp MEG revealed 47 IEDs (16 co-registered by EEG, 31 unique to the on-scalp MEG recording).
Conclusion: Our results indicate that on-scalp MEG might capture IEDs not seen by other non-invasive modalities.
Significance: On-scalp MEG has the potential of improving non-invasive epilepsy evaluation.
Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
(Copyright © 2020 International Federation of Clinical Neurophysiology. Published by Elsevier B.V. All rights reserved.)

المؤلفون: Bettini L; Department of Clinical Neurosciences, Lausanne University Hospital and University of Lausanne, Switzerland., Croquelois A; Department of Clinical Neurosciences, Lausanne University Hospital and University of Lausanne, Switzerland., Maeder-Ingvar M; Department of Clinical Neurosciences, Lausanne University Hospital and University of Lausanne, Switzerland; Institution de Lavigny, Switzerland., Rossetti AO; Department of Clinical Neurosciences, Lausanne University Hospital and University of Lausanne, Switzerland. Electronic address: andrea.rossetti@chuv.ch.

المصدر: Epilepsy & behavior : E&B [Epilepsy Behav] 2014 Oct; Vol. 39, pp. 55-8. Date of Electronic Publication: 2014 Sep 07.

نوع المنشور: Journal Article

بيانات الدورية: Publisher: Academic Press Country of Publication: United States NLM ID: 100892858 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1525-5069 (Electronic) Linking ISSN: 15255050 NLM ISO Abbreviation: Epilepsy Behav Subsets: MEDLINE

مواضيع طبية MeSH: Diagnostic Techniques, Neurological/*standards , Electroencephalography/*methods , Epilepsy/*diagnosis , Psychophysiologic Disorders/*diagnosis , Seizures/*diagnosis, Adolescent ; Adult ; Europe ; Female ; Humans ; Male ; Middle Aged ; Time Factors ; Video Recording ; Young Adult

مستخلص: Introduction: Although long-term video-EEG monitoring (LVEM) is routinely used to investigate paroxysmal events, short-term video-EEG monitoring (SVEM) lasting <24 h is increasingly recognized as a cost-effective tool. Since, however, relatively few studies addressed the yield of SVEM among different diagnostic groups, we undertook the present study to investigate this aspect.
Methods: We retrospectively analyzed 226 consecutive SVEM recordings over 6 years. All patients were referred because routine EEGs were inconclusive. Patients were classified into 3 suspected diagnostic groups: (1) group with epileptic seizures, (2) group with psychogenic nonepileptic seizures (PNESs), and (3) group with other or undetermined diagnoses. We assessed recording lengths, interictal epileptiform discharges, epileptic seizures, PNESs, and the definitive diagnoses obtained after SVEM.
Results: The mean age was 34 (±18.7) years, and the median recording length was 18.6 h. Among the 226 patients, 127 referred for suspected epilepsy - 73 had a diagnosis of epilepsy, none had a diagnosis of PNESs, and 54 had other or undetermined diagnoses post-SVEM. Of the 24 patients with pre-SVEM suspected PNESs, 1 had epilepsy, 12 had PNESs, and 11 had other or undetermined diagnoses. Of the 75 patients with other diagnoses pre-SVEM, 17 had epilepsy, 11 had PNESs, and 47 had other or undetermined diagnoses. After SVEM, 15 patients had definite diagnoses other than epilepsy or PNESs, while in 96 patients, diagnosis remained unclear. Overall, a definitive diagnosis could be reached in 129/226 (57%) patients.
Conclusions: This study demonstrates that in nearly 3/5 patients without a definitive diagnosis after routine EEG, SVEM allowed us to reach a diagnosis. This procedure should be encouraged in this setting, given its time-effectiveness compared with LVEM.
(Copyright © 2014 Elsevier Inc. All rights reserved.)

المؤلفون: Lundgren J; Department of Neurobiology, University of Lund, Sweden., Ingvar M, Smith ML, Siesjö BK

المصدر: Experimental brain research [Exp Brain Res] 1992; Vol. 88 (2), pp. 355-60.

نوع المنشور: Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.

بيانات الدورية: Publisher: Springer Verlag Country of Publication: Germany NLM ID: 0043312 Publication Model: Print Cited Medium: Print ISSN: 0014-4819 (Print) Linking ISSN: 00144819 NLM ISO Abbreviation: Exp Brain Res Subsets: MEDLINE

مواضيع طبية MeSH: Brain Ischemia/*physiopathology , Frontal Lobe/*physiology , Hyperglycemia/*physiopathology , Seizures/*physiopathology , Substantia Nigra/*physiopathology, Amino Acids/physiology ; Animals ; Behavior, Animal/physiology ; Brain Ischemia/psychology ; Histocytochemistry ; Hyperglycemia/psychology ; Male ; Rats ; Rats, Inbred Strains

مستخلص: Preischemic hyperglycemia worsens brain damage after ischemia, and characteristically leads to post-ischemic seizures and a pan-necrotic lesion in substantia nigra pars reticulata (SNPR). The excitatory input to SNPR could contribute to the damage observed. By performing a unilateral frontal cortex lesion 6-19 days prior to the ischemia, we wanted to explore whether a decrease in excitatory input to the ipsilateral SNPR ameliorate the seizures or alter the light microscopical damage in SNPR. Our results demonstrate that unilateral frontal cortex lesion did not alter the development of fatal post-ischemic seizures after 10 min of ischemia in hyperglycemic subjects. Thus, 7/8 animals developed seizures and died within 20 h of recovery. This study also failed to show any difference between the left and right side in post-ischemic SNPR damage after 15 h of recovery in animals with preischemic unilateral frontal cortex lesion. Furthermore, no side difference was observed in any other brain region evaluated. The results thus suggest that the pan-necrotic lesion in SNPR after hyperglycemic ischemia is not caused by excessive excitatory input from frontal cortex. A decrease in the GABA-ergic inhibitory input from caudoputamen to SNPR may be a more important mechanism for the ensuing excitotoxic post-ischemic SNPR damage, and for seizure development.

المؤلفون: Ingvar M; Department of Histology and Neurobiology, Karolinska Institute, Stockholm, Sweden., Eriksdotter-Nilsson M, Henschen A, Olson L

المصدر: Experimental brain research [Exp Brain Res] 1990; Vol. 81 (2), pp. 279-82.

نوع المنشور: Journal Article; Research Support, Non-U.S. Gov't

بيانات الدورية: Publisher: Springer Verlag Country of Publication: Germany NLM ID: 0043312 Publication Model: Print Cited Medium: Print ISSN: 0014-4819 (Print) Linking ISSN: 00144819 NLM ISO Abbreviation: Exp Brain Res Subsets: MEDLINE

مواضيع طبية MeSH: Cerebral Cortex/*transplantation , Seizures/*physiopathology , Substantia Nigra/*physiopathology, Animals ; Cerebral Cortex/pathology ; Cerebral Cortex/physiopathology ; Eye ; Female ; Fetus ; Necrosis ; Rats ; Rats, Inbred Strains ; Reference Values ; Substantia Nigra/pathology ; Transplantation, Heterotopic

مستخلص: We have developed a model system in which the mechanisms of neuronal damage due to hyperexcitation can be studied in isolation and where extended observation periods can be used. Substantia nigra pars reticulata (SNPR) develops a hypermetabolic necrosis following status epilepticus (Nevander et al. 1985; Auer et al. 1986). We transplanted rat fetal nigral area alone or together with fetal frontal neocortex to the anterior chamber of the eye in adult rats. Following 3 months of transplant maturation the hosts were subjected to status epilepticus for 60 min. In single nigral transplants no sign of structural damage was found. In the double transplants of frontal cortex and the substantia nigra a tissue necrosis had developed in the nigral part. This was demonstrated by a total loss of glial fibrillary acidic protein (GFA) immunoreactivity within a circumscribed necrotic region in the nigral part of the double transplant. Such a loss of GFA immunofluorescence had also developed in the host SNPR, as we have earlier shown (Eriksdotter-Nilsson et al. 1987). Thus, intraocular brain tissue transplants provide a unique model for studies on the development of neuronal damage and functional dependence between different neuronal structures for the development of such damage.

المؤلفون: Eriksdotter-Nilsson M; Department of Histology, Karolinska Institutet, Stockholm, Sweden., Björklund H, Dahl D, Olson L, Ingvar M

المصدر: Experimental brain research [Exp Brain Res] 1987; Vol. 69 (1), pp. 155-66.

نوع المنشور: Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.

بيانات الدورية: Publisher: Springer Verlag Country of Publication: Germany NLM ID: 0043312 Publication Model: Print Cited Medium: Print ISSN: 0014-4819 (Print) Linking ISSN: 00144819 NLM ISO Abbreviation: Exp Brain Res Subsets: MEDLINE

مواضيع طبية MeSH: Brain/*metabolism , Glial Fibrillary Acidic Protein/*metabolism , Intermediate Filament Proteins/*metabolism , Laminin/*metabolism , Seizures/*metabolism, Animals ; Brain/pathology ; Globus Pallidus/metabolism ; Globus Pallidus/pathology ; Immunohistochemistry ; Male ; Neurofilament Proteins ; Rats ; Rats, Inbred Strains ; Seizures/chemically induced ; Seizures/pathology ; Substantia Nigra/metabolism ; Substantia Nigra/pathology ; Thalamus/metabolism ; Thalamus/pathology

مستخلص: Sustained experimental seizures in rats have previously been shown to cause an extensive necrosis in pars reticulata of substantia nigra (SNPR) and globus pallidus (GP). In the present paper we have studied the effects of hexafluorodiethyl ether-induced seizures on the immunoreactivity seen with antibodies directed against glial fibrillary acidic protein, GFA, used to visualize astrocytes, antibodies to the glycoprotein laminin as a marker for blood vessel walls and neurofilament (NF) antibodies to monitor neuronal disturbances. Already 12 h after a 20-min seizure period a reduction in GFA immunofluorescence intensity was observed in SNPR. After 3 days, marked lesions were noted in SNPR and GP as seen with cresyl violet staining. The lesions contained almost no GFA-positive structures. In the proximity of the lesions, an increase in GFA-immunoreactivity was noted. Such an increase, although less pronounced, was also seen in the major projection areas of SNPR. Two months post-seizure, the gliotic reaction had disappeared, and only a thin and elongated gliotic scar was observed. In spite of the development of a profound central necrosis especially evident in SNPR, both laminin- and NF-immunoreactivity was slightly increased within the lesioned areas. NF-immunoreactivity was also increased in the superior colliculus and in the reticular formation. Two months post-experiment NF-immunofluorescence was normalized but the former lesion sites showed signs of hypervascularization. We conclude that hexafluorodiethyl ether-induced 20-min seizures lead to rapid, localized glial and neuronal changes in the rat brain as evidenced by GFA and NF immunohistochemistry, while the vascular network remains intact.

المؤلفون: Ingvar M, Lindvall O, Folbergrová J, Siesjö BK

المصدر: Brain research [Brain Res] 1983 Apr 04; Vol. 264 (2), pp. 225-31.

نوع المنشور: Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.

بيانات الدورية: Publisher: Elsevier/North-Holland Biomedical Press Country of Publication: Netherlands NLM ID: 0045503 Publication Model: Print Cited Medium: Print ISSN: 0006-8993 (Print) Linking ISSN: 00068993 NLM ISO Abbreviation: Brain Res Subsets: MEDLINE

مواضيع طبية MeSH: Brain/*metabolism , Locus Coeruleus/*physiology , Norepinephrine/*physiology , Seizures/*metabolism, Animals ; Bicuculline ; Brain Chemistry ; Cyclic AMP/analysis ; Cyclic GMP/analysis ; Fatty Acids, Nonesterified/analysis ; Glycolysis ; Male ; Rats ; Rats, Inbred Strains ; Seizures/chemically induced

مستخلص: The objective of the present study was to explore if lesions of the ascending noradrenergic pathways, originating in the locus coeruleus, modulate the cerebral metabolic response to bicuculline-induced seizures in rats. Bilateral noradrenergic lesions were performed by 6-hydroxydopamine injections in the caudal mesencephalon, 12-22 days before seizures were induced in animals ventilated on N2O:O2 (75:25). After 5 min of seizures the brain was frozen in situ and cerebral cortex and hippocampus were sampled for analysis. Labile phosphates, glycolytic metabolites, cyclic nucleotides, and free fatty acids were measured. In another series, lesioned animals were used for measurements of cerebral oxygen consumption. The noradrenergic lesions neither modified the electroencephalographically recorded seizure discharge, nor did they alter cerebral oxygen consumption or cerebral energy state. However, when compared to sham-operated animals, those with noradrenergic lesions had significantly higher (115% and 68%) glycogen concentrations and lower (50% and 52%) cyclic AMP concentrations in cerebral cortex and hippocampus, respectively, demonstrating the marked influence of noradrenergic activity on adenylate cyclase activity and glycogenolysis. The lesions failed to modulate the rise in free fatty acids in the cerebral cortex, or the cyclic GMP concentrations in the cerebral cortex and hippocampus. Thus, increased noradrenergic activity during status epilepticus does not seem responsible for lipolysis or for activation of guanylate cyclase.

المؤلفون: Siesjö BK, von Hanwehr R, Nergelius G, Nevander G, Ingvar M

المصدر: Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism [J Cereb Blood Flow Metab] 1985 Mar; Vol. 5 (1), pp. 47-57.

نوع المنشور: Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.

بيانات الدورية: Publisher: SAGE Publications Country of Publication: United States NLM ID: 8112566 Publication Model: Print Cited Medium: Print ISSN: 0271-678X (Print) Linking ISSN: 0271678X NLM ISO Abbreviation: J Cereb Blood Flow Metab Subsets: MEDLINE

مواضيع طبية MeSH: Osmolar Concentration*, Brain/*metabolism , Seizures/*metabolism, Acid-Base Equilibrium ; Acidosis/metabolism ; Animals ; Brain/physiology ; Extracellular Space/metabolism ; Flurothyl ; Hypoxia/metabolism ; Intracellular Fluid/metabolism ; Lactates/metabolism ; Male ; Rats ; Rats, Inbred Strains ; Seizures/chemically induced

مستخلص: The objective of the study was to estimate changes in extracellular pH (pHe) and intracellular pH (pHi) during seizures and in the recovery period following the arrest of seizure activity. Seizures of 5- and 20-min duration were induced in rats by fluorothyl added to the insufflated gas mixture, and recovery for 5, 15, and 45 min was instituted by withdrawal of the fluorothyl supply following 20 min of continuous seizures. Changes in pHe were measured by double-barreled, liquid ion-exchange pH microelectrodes, and in pHi by the CO2 method, following estimation of tissue PCO2 and extracellular fluid (ECF) volume. The animals were either normoxic or rendered moderately hypoxic (arterial PO2 40-50 mm Hg). Upon induction of seizures in normoxic animals, pHe decreased by a mean of 0.36 unit, the values being identical at 5 and 20 min. In moderate hypoxia, seizures sustained for 20 min were accompanied by a further fall in pHe (mean decrease 0.51 unit). The changes in pHe seemed mainly to reflect the nonionic diffusion of lactic acid from cells to the ECF (tissue lactate levels approximately 10 and 15 mumol g-1 during seizures in normoxic and hypoxic animals, respectively). However, the gradual fall in pHe attributable able to lactic acid production was preceded by rapid acidification, sometimes exceeding the steady-state values subsequently attained. This acidification was interpreted to reflect spreading depression and fast transcellular Na+/H+ exchange. Following cessation of seizure discharge, pHe normalized at a surprisingly slow rate, with some acidosis persisting even after 45 min. The difference between cerebrovenous and arterial PCO2 was reduced during seizures and increased in the recovery period, probably reflecting alterations in the blood flow/metabolic rate coupling. Impedance changes were slight, indicating only minor changes in ECF volume. Changes in pHi after 5 min of seizures ranged from 0.20 (normoxic animals) to 0.32 (hypoxic animals) unit, the pHi values after 20 min being 0.07-0.08 unit higher. The results suggest the regulation of pHi during ongoing seizures. Upon arrest of seizure activity, pHi rapidly increased to normal and subsequently to supranormal values. Postepileptic intracellular alkalosis occurred at a time when pHe was still reduced and in spite of the fact that tissue lactate values had not normalized. It is concluded that the rapid normalization of pHi and overt alkalosis were caused by the simultaneously occurring oxidation of lactate, with the removal of a stoichiometrical amount of H+, and the extrusion of H+ from cells, possibly via a Na+/H+ exchanger, the latter probably delaying normalization of pHe.

المؤلفون: Ingvar M, Shapiro HM

المصدر: Anesthesiology [Anesthesiology] 1981 Jan; Vol. 54 (1), pp. 33-7.

نوع المنشور: Journal Article

بيانات الدورية: Publisher: Lippincott Williams & Wilkins Country of Publication: United States NLM ID: 1300217 Publication Model: Print Cited Medium: Print ISSN: 0003-3022 (Print) Linking ISSN: 00033022 NLM ISO Abbreviation: Anesthesiology Subsets: MEDLINE

مواضيع طبية MeSH: Lidocaine*, Glucose/*metabolism , Hippocampus/*metabolism , Seizures/*metabolism, Animals ; Autoradiography ; Brain/metabolism ; Carbon Radioisotopes ; Deoxyglucose/metabolism ; Electroencephalography ; Female ; Male ; Rats ; Seizures/chemically induced

مستخلص: Neurophysiologic studies indicate that local anesthetic-induced seizures are generated in subcortical brain structures. The authors utilized a quantitative autoradiographic technique to measure cerebral metabolism during lidocaine-induced seizure activity in rats anesthetized with nitrous oxide. Local cerebral metabolic rate for glucose (l-CMRg) was determined when lidocaine infusion resulted in sustained electroencephalographic patterns consisting of approximately 100--125-mu volt discharges with a frequency of about 9 Hz, lasting 1-2 sec, and superimposed upon almost isoelectric periods lasting 1-3 sec. Significant reductions in 1-CMRg (30-70 per cent decreases) occurred in 19 of 26 regions surveyed. All areas of cerebral cortex had decreased glucose uptake following lidocaine administration. The hippocampus developed a striking increase in 1-CMRg of 237 per cent, while the amygdala and other related nuclei sustained metabolic rates similar to those present before lidocaine was given. This study demonstrates a coupling of metabolic activity with functional activity in subcortical structures recognized to be involved in the generation of local anesthetic seizure activity. Additionally, it reveals a heterogeneous response of cerebral metabolism to lidocaine infusion in the presence of subcortically localized seizures.

المؤلفون: Folbergrová J, Ingvar M, Siesjö BK

المصدر: Journal of neurochemistry [J Neurochem] 1981 Nov; Vol. 37 (5), pp. 1228-38.

نوع المنشور: Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.

بيانات الدورية: Publisher: Wiley on behalf of the International Society for Neurochemistry Country of Publication: England NLM ID: 2985190R Publication Model: Print Cited Medium: Print ISSN: 0022-3042 (Print) Linking ISSN: 00223042 NLM ISO Abbreviation: J Neurochem Subsets: MEDLINE

مواضيع طبية MeSH: Bicuculline/*pharmacology , Cerebellum/*metabolism , Cerebral Cortex/*metabolism , Hippocampus/*metabolism , Seizures/*metabolism, Animals ; Blood Pressure/drug effects ; Body Temperature/drug effects ; Cerebellum/drug effects ; Cerebral Cortex/drug effects ; Energy Metabolism/drug effects ; Glucose/metabolism ; Hippocampus/drug effects ; Male ; Rats ; Rats, Inbred Strains ; Seizures/chemically induced

مستخلص: The objective of the present experiments was to study metabolic correlates to the localization of neuronal lesions during sustained seizures. To that end, status epilepticus was induced by i.v. administration of bicuculline in immobilized and artificially ventilated rats, since this model is known to cause neuronal cell damage in cerebral cortex and hippocampus but not in the cerebellum. After 20 or 120 min of continuous seizure activity, brain tissue was frozen in situ through the skull bone, and samples of cerebral cortex, hippocampus, and cerebellum were collected for analysis of glycolytic metabolites, phosphocreatine (PCr), ATP, ADP, AMP, and cyclic nucleotides. After 20 min of seizure activity, the two "vulnerable" structures (cerebral cortex and hippocampus) and the "resistant" one (cerebellum) showed similar changes in cerebral metabolic state, characterized by decreased tissue concentrations of PCr, ATP, and glycogen, and increased lactate concentrations and lactate/pyruvate ratios. In all structures, though, the adenylate energy charge remained close to control. At the end of a 2-h period of status epilepticus, a clear deterioration of the energy state was observed in the cerebral cortex and the hippocampus, but not in the cerebellum. The reduction in adenylate energy charge in the cortex and hippocampus was associated with a seemingly paradoxical decrease in tissue lactate levels and with failure of glycogen resynthesis (cerebral cortex). Experiments with infusion of glucose during the second hour of a 2-h period of status epilepticus verified that the deterioration of tissue energy state was partly due to reduced substrate supply; however, even in animals with adequate tissue glucose concentrations, the energy charge of the two structures was significantly lowered. The cyclic nucleotides (cAMP and cGMP) behaved differently. Thus, whereas cAMP concentrations were either close to control (hippocampus and cerebellum) or moderately increased (cerebral cortex), the cGMP concentrations remained markedly elevated throughout the seizure period, the largest change being observed in the cerebellum. It is concluded that although the localization of neuronal damage and perturbation of cerebral energy state seem to correlate, the results cannot be taken as evidence that cellular energy failure is the cause of the damage. Thus, it appears equally probable that the pathologically enhanced neuronal activity (and metabolic rate) underlies both the cell damage and the perturbed metabolic state. The observed changes in cyclic nucleotides do not appear to bear a causal relationship to the mechanisms of damage.

المؤلفون: Siesjö BK, Ingvar M, Westerberg E

المصدر: Journal of neurochemistry [J Neurochem] 1982 Sep; Vol. 39 (3), pp. 796-802.

نوع المنشور: Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.

بيانات الدورية: Publisher: Wiley on behalf of the International Society for Neurochemistry Country of Publication: England NLM ID: 2985190R Publication Model: Print Cited Medium: Print ISSN: 0022-3042 (Print) Linking ISSN: 00223042 NLM ISO Abbreviation: J Neurochem Subsets: MEDLINE

مواضيع طبية MeSH: Bicuculline/*pharmacology , Cerebellum/*metabolism , Cerebral Cortex/*metabolism , Fatty Acids, Nonesterified/*metabolism , Hippocampus/*metabolism , Seizures/*metabolism, Animals ; Cerebellum/drug effects ; Cerebral Cortex/drug effects ; Hippocampus/drug effects ; Kinetics ; Male ; Organ Specificity ; Rats ; Rats, Inbred Strains ; Seizures/chemically induced

مستخلص: Using ventilated rats maintained on N2O-O2 (70:30, vol/vol) we induced continuous seizures with i.v. bicuculline and analysed free fatty acids (FFA) in cerebral cortex, hippocampus, and cerebellum after seizures durations of 1-120 min. In the cerebral cortex, peak FFA concentrations were observed after 5 min, with a threefold increase in total FFA content. The values then remained unchanged for the next 15-20 min, but decreased thereafter. At 60 and 120 min, total FFA contents were only moderately increased above control. In the initial period, arachidonic acid increased about 10-fold and stearic acid 2- to 3-fold, with little change in palmitic acid and linoleic acid concentrations. At all times, the docosahexenoic acid concentration was markedly increased. Following its massive accumulation at 1 min, arachidonic acid gradually decreased in concentration. Pretreatment of animals with indomethacin did not alter this behaviour. After 20 and 120 min of seizure activity, changes in total and individual FFA concentrations in the hippocampus were similar to those observed in the cerebral cortex. The cerebellum behaved differently. Thus, at 20 min the only significant change was a 5- to 10-fold increase in arachidonic acid concentration and, after 120 min, total and individual FFA concentrations were similar to control values. Furthermore, since the control values for arachidonic acid were much lower in the cerebellum, the 20-min values were only about 20% of those observed in the cerebral cortex and the hippocampus.