Pub Date : 1998-12-01DOI: 10.1016/S0013-4694(98)00125-4
{"title":"Index of Authors","authors":"","doi":"10.1016/S0013-4694(98)00125-4","DOIUrl":"https://doi.org/10.1016/S0013-4694(98)00125-4","url":null,"abstract":"","PeriodicalId":72888,"journal":{"name":"Electroencephalography and clinical neurophysiology","volume":"107 6","pages":"Pages 452-455"},"PeriodicalIF":0.0,"publicationDate":"1998-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0013-4694(98)00125-4","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"137163936","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1998-11-01DOI: 10.1016/S0013-4694(98)00074-1
A Cerullo, P Tinuper, F Provini, M Contin, A Rosati, C Marini, P Cortelli
Objectives: We describe two patients with hypothalamic hamartoma and gelastic seizures.
Methods: We performed ictal neurophysiological studies with polygraphic recordings of autonomic parameters and hormonal ictal plasma concentration measurements.
Results: Ictal recordings showed a stereotyped modification of autonomic parameters: increase in blood pressure and heart rate, peripheral vasoconstriction and modification of respiratory activity. At seizure onset, the norepinephrine plasma level was high and epinephrine unchanged, whereas prolactin and adrenocorticotropic hormone were increased in both cases. Growth hormone and cortisol plasma concentrations in each patient showed a different response to seizures.
Conclusions: These data provide evidence that gelastic seizures are accompanied by an abrupt sympathetic system activation, probably due to the direct paroxysmal activation of limbic and paralimbic structures or other autonomic centres of the hypothalamus and medulla.
{"title":"Autonomic and hormonal ictal changes in gelastic seizures from hypothalamic hamartomas1","authors":"A Cerullo, P Tinuper, F Provini, M Contin, A Rosati, C Marini, P Cortelli","doi":"10.1016/S0013-4694(98)00074-1","DOIUrl":"10.1016/S0013-4694(98)00074-1","url":null,"abstract":"<div><p><strong>Objectives:</strong> We describe two patients with hypothalamic hamartoma and gelastic seizures.</p><p><strong>Methods:</strong> We performed ictal neurophysiological studies with polygraphic recordings of autonomic parameters and hormonal ictal plasma concentration measurements.</p><p><strong>Results:</strong> Ictal recordings showed a stereotyped modification of autonomic parameters: increase in blood pressure and heart rate, peripheral vasoconstriction and modification of respiratory activity. At seizure onset, the norepinephrine plasma level was high and epinephrine unchanged, whereas prolactin and adrenocorticotropic hormone were increased in both cases. Growth hormone and cortisol plasma concentrations in each patient showed a different response to seizures.</p><p><strong>Conclusions:</strong> These data provide evidence that gelastic seizures are accompanied by an abrupt sympathetic system activation, probably due to the direct paroxysmal activation of limbic and paralimbic structures or other autonomic centres of the hypothalamus and medulla.</p></div>","PeriodicalId":72888,"journal":{"name":"Electroencephalography and clinical neurophysiology","volume":"107 5","pages":"Pages 317-322"},"PeriodicalIF":0.0,"publicationDate":"1998-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0013-4694(98)00074-1","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20780264","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Objective: To review the clinical and EEG manifestations of intrathecal baclofen overdose.
Methods: We identified one patient who had received an overdose of intrathecal baclofen. Information about the clinical course was obtained by reviewing the patient's medical record. EEGs were recorded with the use of the standard 10–20 electrode placement system.
Results: The patient received 30 mg baclofen intrathecally. Shortly after the injection he developed respiratory insufficiency and quadriparesis and later became comatose. The first EEG obtained 20 h after the injection showed very frequent quasiperiodic generalized epileptiform discharges. The patient gradually improved clinically and a second EEG obtained 24 h later showed only intermittent bursts of generalized slow wave activity. A repeat EEG study 1 week later was normal.
Conclusions: The EEG in intrathecal baclofen overdose can show quasiperiodic generalized epileptiform discharges. This does not necessarily indicate the presence of underlying potential epileptogenicity, and treatment with an antiepileptic medication is not necessary.
{"title":"EEG changes in intrathecal baclofen overdose: a case report and review of the literature","authors":"Toufic Fakhoury , Bassel Abou-Khalil , Bennett Blumenkopf","doi":"10.1016/S0013-4694(98)00085-6","DOIUrl":"10.1016/S0013-4694(98)00085-6","url":null,"abstract":"<div><p><strong>Objective</strong>: To review the clinical and EEG manifestations of intrathecal baclofen overdose.</p><p><strong>Methods</strong>: We identified one patient who had received an overdose of intrathecal baclofen. Information about the clinical course was obtained by reviewing the patient's medical record. EEGs were recorded with the use of the standard 10–20 electrode placement system.</p><p><strong>Results</strong>: The patient received 30 mg baclofen intrathecally. Shortly after the injection he developed respiratory insufficiency and quadriparesis and later became comatose. The first EEG obtained 20 h after the injection showed very frequent quasiperiodic generalized epileptiform discharges. The patient gradually improved clinically and a second EEG obtained 24 h later showed only intermittent bursts of generalized slow wave activity. A repeat EEG study 1 week later was normal.</p><p><strong>Conclusions</strong>: The EEG in intrathecal baclofen overdose can show quasiperiodic generalized epileptiform discharges. This does not necessarily indicate the presence of underlying potential epileptogenicity, and treatment with an antiepileptic medication is not necessary.</p></div>","PeriodicalId":72888,"journal":{"name":"Electroencephalography and clinical neurophysiology","volume":"107 5","pages":"Pages 339-342"},"PeriodicalIF":0.0,"publicationDate":"1998-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0013-4694(98)00085-6","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20780267","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1998-11-01DOI: 10.1016/S0013-4694(98)00091-1
U Kramer , L Carmant , M.A Mikati
We investigated the discharge morphology and propagation patterns of electroencephalographic seizures of temporal lobe onset in 21 children and young adults who underwent invasive long-term EEG monitoring (LTM). Of those, 15 subsequently underwent anterior temporal lobectomy. The onset was focal in 63%. The most frequent discharge morphology was low amplitude beta (30%) or rhythmic/semirhythmic theta discharge (30%). Thirteen patients displayed several sequences of propagation with different spreading stages along a fixed path. Initial spreading to the ipsilateral frontal lobe was associated with a higher frequency of secondary generalization than initial spreading to the contralateral temporal lobe (P=0.18). A comparison of 13 patients older than 18 years of age with 8 patients younger than 14 years showed a trend towards a lower rate of propagating from the temporal lobe (P=0.13) in the younger age group. Discharge morphology was not correlated with age, focality, or outcome of surgery.
{"title":"Electroencephalographic discharges of temporal lobe seizures in children and young adults","authors":"U Kramer , L Carmant , M.A Mikati","doi":"10.1016/S0013-4694(98)00091-1","DOIUrl":"10.1016/S0013-4694(98)00091-1","url":null,"abstract":"<div><p>We investigated the discharge morphology and propagation patterns of electroencephalographic seizures of temporal lobe onset in 21 children and young adults who underwent invasive long-term EEG monitoring (LTM). Of those, 15 subsequently underwent anterior temporal lobectomy. The onset was focal in 63%. The most frequent discharge morphology was low amplitude beta (30%) or rhythmic/semirhythmic theta discharge (30%). Thirteen patients displayed several sequences of propagation with different spreading stages along a fixed path. Initial spreading to the ipsilateral frontal lobe was associated with a higher frequency of secondary generalization than initial spreading to the contralateral temporal lobe (<em>P</em>=0.18). A comparison of 13 patients older than 18 years of age with 8 patients younger than 14 years showed a trend towards a lower rate of propagating from the temporal lobe (<em>P</em>=0.13) in the younger age group. Discharge morphology was not correlated with age, focality, or outcome of surgery.</p></div>","PeriodicalId":72888,"journal":{"name":"Electroencephalography and clinical neurophysiology","volume":"107 5","pages":"Pages 353-360"},"PeriodicalIF":0.0,"publicationDate":"1998-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0013-4694(98)00091-1","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20780269","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1998-11-01DOI: 10.1016/S0013-4694(98)00096-0
W Trojaborg
During the last 15 years new information about clinical, electrophysiological, immunological and histopathological features of acute and chronic inflammatory neuropathies have emerged. Thus, the Guillain–Barré syndrome (GBS) is no longer considered a simple entity. Subtypes of the disorder besides the typical predominant motor manifestation, are recognized, i.e. a cranial nerve variant with ophthalmoplegia, ataxia and areflexia, an immune-mediated primary motor axonal neuropathy (AMAN), and a motor-sensory syndrome (AMSAN). Also, the clinical pattern of GBS is related to preceding viral or bacterial infections. Two types of acute motor paralysis have been described, one with slow and incomplete recovery, another with recovery times identical with acute inflammatory demyelinating polyneuropathy (AIDP). Histologically, the first is characterized by Wallerian degeneration of motor roots and peripheral motor nerve fibres. In the latter anti-GM antibodies bind to the nodes of Ranvier producing a failure of impulse transmission. Motor-point biopsies have shown denervated neuromuscular junctions and a reduced number of intramuscular nerve fibres. Molecular mimicry has been postulated as a possible mechanism triggering GBS. Thus, in the cranial variant antibodies to ganglioside GQ1b recognizes similar epitopes on Campylobacter jejuni strains and similar observations apply to anti-GM1 antibodies. Chronic inflammatory demyelinating polyneuropathy (CIDP) also has several different clinical presentations such as a pure motor syndrome, a sensory ataxic variant, a mononeuritis multiplex pattern, relapsing GBS, and a paraparetic subtype. Each of the acute and the subtypes have different, more or less distinct, electrophysiologic and pathological findings. Instructive patient stories are presented together with there electrophysiologic and biopsy findings.
{"title":"Acute and chronic neuropathies: new aspects of Guillain–Barré syndrome and chronic inflammatory demyelinating polyneuropathy, an overview and an update","authors":"W Trojaborg","doi":"10.1016/S0013-4694(98)00096-0","DOIUrl":"10.1016/S0013-4694(98)00096-0","url":null,"abstract":"<div><p>During the last 15 years new information about clinical, electrophysiological, immunological and histopathological features of acute and chronic inflammatory neuropathies have emerged. Thus, the Guillain–Barré syndrome (GBS) is no longer considered a simple entity. Subtypes of the disorder besides the typical predominant motor manifestation, are recognized, i.e. a cranial nerve variant with ophthalmoplegia, ataxia and areflexia, an immune-mediated primary motor axonal neuropathy (AMAN), and a motor-sensory syndrome (AMSAN). Also, the clinical pattern of GBS is related to preceding viral or bacterial infections. Two types of acute motor paralysis have been described, one with slow and incomplete recovery, another with recovery times identical with acute inflammatory demyelinating polyneuropathy (AIDP). Histologically, the first is characterized by Wallerian degeneration of motor roots and peripheral motor nerve fibres. In the latter anti-GM antibodies bind to the nodes of Ranvier producing a failure of impulse transmission. Motor-point biopsies have shown denervated neuromuscular junctions and a reduced number of intramuscular nerve fibres. Molecular mimicry has been postulated as a possible mechanism triggering GBS. Thus, in the cranial variant antibodies to ganglioside GQ1b recognizes similar epitopes on <em>Campylobacter jejuni</em> strains and similar observations apply to anti-GM1 antibodies. Chronic inflammatory demyelinating polyneuropathy (CIDP) also has several different clinical presentations such as a pure motor syndrome, a sensory ataxic variant, a mononeuritis multiplex pattern, relapsing GBS, and a paraparetic subtype. Each of the acute and the subtypes have different, more or less distinct, electrophysiologic and pathological findings. Instructive patient stories are presented together with there electrophysiologic and biopsy findings.</p></div>","PeriodicalId":72888,"journal":{"name":"Electroencephalography and clinical neurophysiology","volume":"107 5","pages":"Pages 303-316"},"PeriodicalIF":0.0,"publicationDate":"1998-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0013-4694(98)00096-0","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20780263","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1998-11-01DOI: 10.1016/S0013-4694(98)00081-9
G Lantz , P Wahlberg , G Salomonsson , I Rosén
Objectives: In patients with epileptic seizures, localization of the source of interictal epileptiform activity is of interest. For correct source localization, a favorable signal to noise ratio is important, and to achieve this, averaging of several epileptiform potentials is often necessary. Before averaging, a careful categorization of epileptiform potentials with different potential distributions is crucial. The aim of this study was to investigate whether a hierarchic, graph-theoretic algorithm could be used for this categorization.
Methods: In 4 patients, 50–100 sharp waves with different surface distributions were categorized independently with the algorithm, and by visual inspection of the traces. As an independent evaluation of the algorithm, a dipole reconstruction was performed for each sharp wave, and the dipole results for the sharp waves from the different automatically obtained categories were compared.
Results: All patients showed a high degree of correspondence between the results of the automatic analysis and the visual estimation. There were clear differences in dipole results between the sharp waves of the different categories obtained from the automatic categorization.
Conclusion: The results indicate that the graph-theoretic categorization algorithm provides a reliable clustering of interictal epileptiform potentials, and that the method may become a useful tool in the pre-averaging categorization of interictal epileptiform potentials prior to source localization.
{"title":"Categorization of interictal epileptiform potentials using a graph-theoretic method","authors":"G Lantz , P Wahlberg , G Salomonsson , I Rosén","doi":"10.1016/S0013-4694(98)00081-9","DOIUrl":"10.1016/S0013-4694(98)00081-9","url":null,"abstract":"<div><p><strong>Objectives:</strong> In patients with epileptic seizures, localization of the source of interictal epileptiform activity is of interest. For correct source localization, a favorable signal to noise ratio is important, and to achieve this, averaging of several epileptiform potentials is often necessary. Before averaging, a careful categorization of epileptiform potentials with different potential distributions is crucial. The aim of this study was to investigate whether a hierarchic, graph-theoretic algorithm could be used for this categorization.</p><p><strong>Methods:</strong> In 4 patients, 50–100 sharp waves with different surface distributions were categorized independently with the algorithm, and by visual inspection of the traces. As an independent evaluation of the algorithm, a dipole reconstruction was performed for each sharp wave, and the dipole results for the sharp waves from the different automatically obtained categories were compared.</p><p><strong>Results:</strong> All patients showed a high degree of correspondence between the results of the automatic analysis and the visual estimation. There were clear differences in dipole results between the sharp waves of the different categories obtained from the automatic categorization.</p><p><strong>Conclusion:</strong> The results indicate that the graph-theoretic categorization algorithm provides a reliable clustering of interictal epileptiform potentials, and that the method may become a useful tool in the pre-averaging categorization of interictal epileptiform potentials prior to source localization.</p></div>","PeriodicalId":72888,"journal":{"name":"Electroencephalography and clinical neurophysiology","volume":"107 5","pages":"Pages 323-331"},"PeriodicalIF":0.0,"publicationDate":"1998-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0013-4694(98)00081-9","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20780265","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1998-11-01DOI: 10.1016/S0013-4694(98)00084-4
Zoltan J. Koles , Anthony C.K. Soong
Objectives: The spatio-temporal decomposition (STD) approach was used to localize the sources of simulated electroencephalograms (EEGs) to gain experience with the approach for analyzing real data.
Methods: The STD approach used is similar to the multiple signal classification method (MUSIC) in that it requires the signal subspace containing the sources of interest to be isolated in the EEG measurement space. It is different from MUSIC in that it allows more general methods of spatio-temporal decomposition to be used that may be better suited to the background EEG.
Results: If the EEG data matrix is not corrupted by noise, the STD approach can be used to locate multiple dipole sources of the EEG one at a time without a priori knowledge of the number of active sources in the signal space. In addition, the common-spatial-patterns method of spatio-temporal decomposition is superior to the eigenvector decomposition for localizing activity that is ictal in nature.
Conclusions: The STD approach appears to be able to provide a means of localizing the equivalent dipole sources of realistic brain sources and that, even under difficult noise conditions and only 2 or 3 s of available EEG, the precision of the localization can be as low as a few mm.
{"title":"EEG source localization: implementing the spatio-temporal decomposition approach","authors":"Zoltan J. Koles , Anthony C.K. Soong","doi":"10.1016/S0013-4694(98)00084-4","DOIUrl":"10.1016/S0013-4694(98)00084-4","url":null,"abstract":"<div><p><strong>Objectives</strong>: The spatio-temporal decomposition (STD) approach was used to localize the sources of simulated electroencephalograms (EEGs) to gain experience with the approach for analyzing real data.</p><p><strong>Methods</strong>: The STD approach used is similar to the multiple signal classification method (MUSIC) in that it requires the signal subspace containing the sources of interest to be isolated in the EEG measurement space. It is different from MUSIC in that it allows more general methods of spatio-temporal decomposition to be used that may be better suited to the background EEG.</p><p><strong>Results</strong>: If the EEG data matrix is not corrupted by noise, the STD approach can be used to locate multiple dipole sources of the EEG one at a time without a priori knowledge of the number of active sources in the signal space. In addition, the common-spatial-patterns method of spatio-temporal decomposition is superior to the eigenvector decomposition for localizing activity that is ictal in nature.</p><p><strong>Conclusions</strong>: The STD approach appears to be able to provide a means of localizing the equivalent dipole sources of realistic brain sources and that, even under difficult noise conditions and only 2 or 3 s of available EEG, the precision of the localization can be as low as a few mm.</p></div>","PeriodicalId":72888,"journal":{"name":"Electroencephalography and clinical neurophysiology","volume":"107 5","pages":"Pages 343-352"},"PeriodicalIF":0.0,"publicationDate":"1998-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0013-4694(98)00084-4","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20780268","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1998-11-01DOI: 10.1016/S0013-4694(98)00098-4
Jie Wu, Yoshio C Okada
Objective: The physiological bases of evoked magnetic fields were examined in a guinea-pig hippocampal slice preparation, motivated by new concepts in central nervous system (CNS) electrophysiology brought about by discoveries of active conductances in the dendrites and soma of neurons.
Methods: Their origins were elucidated by comparing them with intracellular and extracellular field potentials.
Results: With excitatory synaptic transmissions blocked, the magnetic signal elicited by an electrical stimulus applied to the pyramidal cell layer consisted of a spike and a depolarizing afterpotential-like waveform. With the excitatory synaptic transmissions intact, but with inhibitory synaptic transmissions blocked, the magnetic signal was bi- or triphasic depending on whether the cell layer or the apical dendrite area of the pyramidal cells was, respectively, depolarized. In both cases the signal consisted of a train of synchronized population spikes superimposed on a brief wave followed by a longer, slow wave. The spike train was correlated with synaptically mediated intracellular spikes. The underlying currents for the slow wave were directed from the apical to the basal side for both types of stimulation. It was most likely generated by depolarization of the apical dendrites, caused by recurrent excitatory synaptic activation.
Conclusions: This analysis illustrates how synaptic connections and intrinsic conductances in a disinhibited mammalian CNS structure can generate spikes and waves of the magnetic field and electrical potential.
{"title":"Physiological bases of the synchronized population spikes and slow wave of the magnetic field generated by a guinea-pig longitudinal CA3 slice preparation","authors":"Jie Wu, Yoshio C Okada","doi":"10.1016/S0013-4694(98)00098-4","DOIUrl":"10.1016/S0013-4694(98)00098-4","url":null,"abstract":"<div><p><strong>Objective</strong>: The physiological bases of evoked magnetic fields were examined in a guinea-pig hippocampal slice preparation, motivated by new concepts in central nervous system (CNS) electrophysiology brought about by discoveries of active conductances in the dendrites and soma of neurons.</p><p><strong>Methods</strong>: Their origins were elucidated by comparing them with intracellular and extracellular field potentials.</p><p><strong>Results</strong>: With excitatory synaptic transmissions blocked, the magnetic signal elicited by an electrical stimulus applied to the pyramidal cell layer consisted of a spike and a depolarizing afterpotential-like waveform. With the excitatory synaptic transmissions intact, but with inhibitory synaptic transmissions blocked, the magnetic signal was bi- or triphasic depending on whether the cell layer or the apical dendrite area of the pyramidal cells was, respectively, depolarized. In both cases the signal consisted of a train of synchronized population spikes superimposed on a brief wave followed by a longer, slow wave. The spike train was correlated with synaptically mediated intracellular spikes. The underlying currents for the slow wave were directed from the apical to the basal side for both types of stimulation. It was most likely generated by depolarization of the apical dendrites, caused by recurrent excitatory synaptic activation.</p><p><strong>Conclusions</strong>: This analysis illustrates how synaptic connections and intrinsic conductances in a disinhibited mammalian CNS structure can generate spikes and waves of the magnetic field and electrical potential.</p></div>","PeriodicalId":72888,"journal":{"name":"Electroencephalography and clinical neurophysiology","volume":"107 5","pages":"Pages 361-373"},"PeriodicalIF":0.0,"publicationDate":"1998-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0013-4694(98)00098-4","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20780270","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}