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J Gotman

Publications and source records attributed to J Gotman.

At least 19 recordsLinked to original sources
PubMed1992

State dependent spike detection: validation.

We present a formal validation of the method of state dependent spike detection; its principle and initial results were given in Gotman and Wang (1991). The method utilizes different procedures for elimination of non-epileptic transients according to state (active or quiet wakefulness, sleep stages); it also varies detection sensitivity according to state. Twenty new 100 min recordings were obtained from 20 unselected patients, covering active wakefulness, quiet wakefulness and various sleep stages. Results indicated that, while the total number of detections was reduced by 15%, true detections increased by 39% and false detections decreased by 60%. This significant improvement is due to the fact that wave morphology is now considered within its spatial context and particularly within a wide temporal context.

Adolescent↗
PubMed1992

Intracranial EEG study of brain structures affected by internal carotid injection of amobarbital.

Hippocampal function, considered critical in memory processing, is supposedly tested in the intracarotid sodium amobarbital (ISA) procedure; however, since the hippocampus is not completely irrigated by the internal carotid artery, some believe the procedure may be invalid for memory testing. We quantified delta activity in intracerebral EEGs during ISA tests. There was increased delta in ipsilateral structures as follows: amygdala (6.4 minutes), anterior hippocampus (7.2), middle hippocampus (7.4), temporal neocortex (9.1), frontal lobe (8.4), central/parietal area (11.0), and occipital lobe (9.7). Contralateral structures usually (> 64%) showed increased delta lasting 4 to 5 minutes. The ipsilateral hippocampus had delta waves in over 90% of injections. We conclude that the hippocampus is clearly affected by the ISA injection. We argue that the slow waves may not be caused by a direct effect of the drug, but rather by a functional deafferentation due to the profound inactivation of structures surrounding the hippocampus. Similarly, slow waves contralateral to injection may be caused by sudden removal of neuronal input from the regions receiving the amobarbital.

Amobarbital↗
PubMed1991

State-dependent spike detection: concepts and preliminary results.

In traditional methods of spike detection, spikes are defined in absolute terms (duration, amplitude) or relative to a few seconds of background. These methods result in many false positive detections during long-term epilepsy monitoring because of numerous artefacts and non-epileptic transients. To reduce significantly false detection, we propose to render spike detection sensitive to the state of the EEG. We thus defined 5 states (active wakefulness, quiet wakefulness, desynchronized EEG, phasic EEG and slow EEG) and designed a method for automatic state classification. We then designed procedures for identification of non-epileptic transients (eye blinks, EMG, alpha, spindles, vertex sharp waves). These procedures are to be applied only in the state in which they are likely to occur (e.g., eye blinks in wakefulness). We present preliminary results from 14 recordings each lasting 100 min, which indicate a state classification reliability of 85-90%, reduction in false detection of 65-90% if state classification were perfect; true spikes lost as a result of these procedures were under 5%. These results are encouraging and validate the concept of a spike detection system which analyses a wide temporal and spatial context before deciding the significance of a wave form.

Blinking↗
PubMed1991

Effects of seizures and carbamazepine on interictal spiking in amygdala kindled cats.

We examined the influence of seizures and carbamazepine (CBZ) on spiking rates in kindled cats. In the first experiment, spiking rates were measured before and after seizures, with and without CBZ. CBZ was administered immediately after seizures in order not to affect them. Spiking rates were measured over 9 h during the different sleep stages. In a second experiment, CBZ was administered before and after seizures so as to affect seizure strength and thus measure its effect on spiking. Results confirmed earlier findings of a large increase in spiking following a stage 6 seizure in fully kindled animals. We also established that: (1) repeated daily seizures caused a further increase in spiking until a ceiling was reached; (2) increased spiking was not a direct effect of postictal alterations in sleep stages; (3) CBZ, despite its effectiveness as an anticonvulsant, did not reduce spiking but rather increased it; (4) postictal increases in spiking were related to seizure 'strength'. These findings support the hypothesis that spiking rates are primarily influenced by seizure occurrence, as was found in patients with temporal lobe seizures, and that anticonvulsants act differently on seizures and spikes. This emphasizes the possibility of distinct pathophysiological mechanisms for interictal spikes and seizures.

Action Potentials↗
PubMed1991

Relationships between interictal spiking and seizures: human and experimental evidence.

Epileptic seizures of focal origin often occur unpredictably as do interictal spikes. It is often assumed that spikes increase prior to seizures of focal origin and that antiepileptic medication affects spikes and seizures in a parallel fashion. We review evidence that this assumption is invalid and that there is a clear dissociation between spikes and seizures: increases in spiking before seizures have not been clearly documented; decreases in antiepileptic medication do not result directly in increased spiking; seizures are often followed by long-lasting increases in spiking; finally, seizures are no more likely when spikes are frequent than when spikes are rare. It therefore appears that spikes and seizures are two quite distinct phenomena, both originating in the epileptic focus but varying over time differently from what is most often believed.

Anticonvulsants↗
PubMed1991

Interictal spiking during wakefulness and sleep and the localization of foci in temporal lobe epilepsy.

We examined variations in interictal spiking during sleep and wakefulness to assess differences in reliability for localizing epileptic foci. Forty patients were studied prospectively. Spikes were assessed for rates, field, and appearance of new foci. Final localization was determined by surgery, electrocorticography, and seizure onset. Comparison of interictal EEG foci with final localization was made. In 39 patients, slow-wave sleep activated spiking compared with wakefulness. Most patients showed maximal spiking in sleep stages 3 or 4. Restriction of field in rapid eye movement (REM) sleep and wakefulness, and extension of field in slow-wave sleep occurred. New foci appeared in non-rapid eye movement sleep in 53% of patients. Similar but not identical spiking rates, foci, and field distributions were seen in wakefulness and REM sleep. All REM foci were unilateral. Our findings suggest that localization of the primary epileptogenic area is more reliable in REM sleep than in wakefulness, and in wakefulness more than in slow-wave sleep.

Action Potentials↗
PubMed1990

Automatic seizure detection: improvements and evaluation.

Improvements to an existing automatic seizure detection program are described. They are aimed at taking into account a larger temporal context and thus improving the specificity of the detections. Results were evaluated on 293 recordings from 49 patients, totaling 5303 h of 16-channel recording. They showed that 24% of the 244 seizures recorded were missed by the automatic detection; in 41% of the seizures, the patient alarm was not pressed but the computer made detections. The false detection rate was of the order of 1 false detection per hour of recording. Conclusions are: (1) automatic seizure detection must be used in conjunction with a patient alarm button since some seizures, having poorly defined EEG activity, are not detected; (2) the automatic detection allowed capture of many seizures, clinical and subclinical, for which the alarm was not pressed; (3) the low false detection rate indicates that lower detection threshold could be used, yielding better seizure detection.

Adolescent↗
PubMed1990

Quantitative EEG analysis of carbamazepine effects on amygdaloid kindled seizures in cats.

We studied the effects of carbamazepine (CBZ) on seizure behaviour and electroencephalographic (EEG) activity in 6 amygdala kindled cats. CBZ reduced the behavioural severity of kindled seizures and prolonged the earlier seizure stages (latency to stage 4). These effects were not always paralleled by a reduction in the duration of seizure activity. EEG activity paradoxically increased in amplitude during early and mid-seizure, then fell in late seizure after CBZ. CBZ also caused an overall decrease in EEG coherence during mid and late seizure. These observations represent a first attempt to use quantitative EEG analysis to investigate the effects of anticonvulsants on electrographic seizure activity. The duration of postictal EEG suppression was reduced after CBZ treatment. The results support the view that CBZ has a major effect on limiting the spread of seizure discharges.

Administration, Oral↗
PubMed1990

Can slow waves in the electrocorticogram (ECoG) help localize epileptic foci?

In patients operated for medically refractory epilepsy, ECoGs are often performed to help further localize the epileptogenic focus. During the necessarily short recording, spikes may be rare or absent, or may be only a partial representation of the epileptic activity. The usefulness of background abnormality in localizing the focus in ECoGs was therefore determined. The relationships of MRI, CT, and pathological findings with ECoG background were also noted. The ECoGs of 40 patients were recorded. Delta activity was evaluated by spectral analysis. In 22 ECoGs, maximum delta activity coincided spatially with maximum spiking or was adjacent to it. The region of maximum delta activity rarely coincided with CT, MRI and pathological findings. Although the relationship between delta activity and spiking was much stronger than expected by chance, it may not be sufficient to allow the use of delta activity to localize a focus in individual cases.

Action Potentials↗
PubMed1990

Asymmetry in delta activity in patients with focal epilepsy.

The localization of epileptogenic foci usually relies on multiple factors. The validity of background EEG abnormalities in lateralizing or localizing the focus was examined. Asymmetries in delta activity were measured by comparing EEGs of epileptic subjects to that of control subjects. The relationships of MRI, CT and pathological findings with delta asymmetries were also noted. In only 2 of 22 patients, delta activity showed no asymmetry. In 17 patients, delta asymmetries correlated with the side of the focus, and in the remaining 3 patients, predominant delta activity was observed in the hemisphere contralateral to the focus. The analysis of the relationship between delta activity and lesions observed on the CT scan was inconclusive. The area exhibiting predominant delta activity frequently coincided with the regions showing solitary discrete lesions on MRI scans. The results suggest that slow wave abnormalities, when measured by comparison to a control population, can be useful in lateralizing the epileptogenic focus.

Adult↗
PubMed1990

Changes in seizure activity following anticonvulsant drug withdrawal.

We retrospectively studied the effects of changing antiepileptic drug levels on patterns of seizure discharge in 8 patients investigated with intracerebral electrodes during presurgical evaluation. We compared seizures recorded at high levels of medication to seizures recorded at low levels for changes in seizure duration, duration from unilateral onset to contralateral spread, inter- and intrahemispheric coherence, and morphology of EEG discharges. Seizures were more frequent with low medication, as was secondary generalization. Reduction in medication did not affect the morphology of discharges at onset, duration to contralateral spread, and coherence between EEG discharges. Seizures of similar type (eg, complex partial seizures without secondary generalization) were not longer with low than with high medication. Whereas medication clearly affects seizure frequency and generalization, it has little effect on the pattern of early parts of seizures. In particular, we found no evidence that seizure discharges become bilateral or generalized more quickly when medication is reduced.

Anticonvulsants↗
PubMed1989

Interictal spiking increases after seizures but does not after decrease in medication.

In patients with focal epilepsy, EEG spike rate fluctuates considerably over time. We had previously shown that seizure occurrence played an important role in these fluctuations. We undertook this study to confirm this finding with better control of critical variables such as state of alertness and spike quantification, and to assess the spatial extent of the changes. Background activity changes and antiepileptic drug levels were also examined in relation to spiking. Spike discharge rate increased in the hours and days following seizures in widespread brain regions including, but not restricted to, the seizure focus. Spike rate did not change systematically before seizures. Postictal changes in background activity did not parallel spike fluctuations. Decreased antiepileptic drug levels did not cause increased spike rate. These results indicate that, following seizures, there is activation of interictal spiking which is not paralleled by changes in background activity. It is most often widespread and not necessarily most prominent at the site of seizure onset.

Adult↗
PubMed1988

Excitatory amino acids are elevated in human epileptic cerebral cortex.

We used intraoperative electrocorticography to identify and compare specimens from two groups of patients undergoing temporal lobectomy: (1) spiking cortex (12 patients)--epileptic activity recorded over much of the temporal convexity; and (2) nonspiking cortex (9 patients)--temporal convexity free of interictal spiking, epileptic activity confined to the hippocampus and/or amygdala. Comparative amino acid levels were (mumol/g protein, mean +/- SEM): glutamate--spiking 109.8 +/- 1.8, nonspiking 87.4 +/- 2.0 (p less than 0.001); aspartate--spiking 15.2 +/- 0.9, nonspiking 12.2 +/- 0.5 (p less than 0.05); GABA--spiking 15.0 +/- 1.0, nonspiking 13.9 +/- 1.4 (NS); taurine--spiking 14.5 +/- 0.8, nonspiking 12.2 +/- 0.8 (NS); and glycine--spiking 11.5 +/- 0.8, nonspiking 7.4 +/- 0.6 (p less than 0.01). Cortical epileptic activity appears to be associated with elevated concentrations of glutamate, aspartate, and glycine, but not GABA and taurine, perhaps indicating a relative imbalance between putative excitatory and inhibitory amino acid neurotransmitters.

Adolescent↗
PubMed1987

Interhemispheric interactions in seizures of focal onset: data from human intracranial recordings.

Interactions between the two hemispheres were studied during seizures recorded in 8 epileptic patients having chronic intracranial electrodes. Seven had temporal lobe foci and one a fronto-central focus. Strength of interaction was measured by the coherence between the EEGs from symmetrical contralateral locations. Time delays of a few milliseconds between discharges were computed by the coherence and phase method. The evolution of interactions was followed from the time a seizure of focal onset had become bilateral to its end. It was found that interhemispheric coherence was generally low throughout seizures, highest values being reached early in the seizure at the time of spread, or at the very end. Time delays most often indicated a lead from the side of onset, whether they were measured early or late in the seizure. Exceptions to these results were found in 2 of 3 patients with bilateral independent onsets: interhemispheric coherence was higher and time leads were always from the same side, independently of the side of onset. If it is assumed that high interhemispheric coherence is mediated by direct connections such as corpus callosum and anterior commissure, then these results can be interpreted as follows: the major commissures do not play an important role in contralateral spread of temporal lobe seizures although they are sometimes active, particularly at initial spread and at seizure end. Time leads from the side of onset indicate that the focus retains an influence over the contralateral discharge throughout the seizure. A different situation may exist with independent bitemporal foci.

Brain↗
PubMed1986

Structural determinants of electroencephalographic findings in acute hemispheric lesions.

We studied electroencephalograms and computed tomographic scans of 54 patients with acute hemispheric strokes. Electrographic parameters evaluated included field, amplitude, frequency, persistence, and reactivity of focal or lateralized slow-wave activity. Ipsilateral and contralateral background activity were also assessed. Structural and clinical features studied were lesion size, density, mass effect, location, tissue involvement, deep structure involvement, level of consciousness, and outcome. The data were analyzed using computer sorting and the chi 2 test. The field, amplitude, and frequency of focal slow-wave abnormalities generally failed to show a specific association with structural details. Continuous focal abnormalities correlated with large lesions (p less than 0.05), mass effect (p less than 0.05), and altered state of consciousness (p less than 0.05). Reactive focal abnormalities were associated with small lesions (p less than 0.05) and the absence of mass effect (p less than 0.02). Ipsilateral background activity abnormalities correlated with lesion size (p less than 0.001) and mass effect (p less than 0.01). Attenuation of ipsilateral background activity was more important than irregularity. Abnormal background activity contralateral to the lesion side was associated with alteration of consciousness (p less than 0.05).

Adult↗