Search PubMed⌕ Search

Biomedical subjects

J P Lieb

Publications and source records attributed to J P Lieb.

31 records · Page 2Linked to original sources
PubMed1977

Electrophysiological studies of long-term electrical stimulation of the cerebellum in monkeys.

Six rhesus monkeys were stimulated on the paravermal cortex for 205 hours (18 days) with different charge densities in order to determine the electrode performance and neural damage that may result from long-term cerebellar stimulation comparable to that being used in man. The electrode-tissue interface was relatively stable and no neural damage was found when the charge/phase (0.5 muC/ph) or charge density (7.4 muC/sq cm/ph) was very low. At all higher charge levels tested (2.4, 4.8, 10, and 22 muC/ph), changes in the electrode-tissue interface, meningeal encapsulation, and neural damage were directly related to the charge density delivered. Unstimulated electrodes on the opposite paravermal cortex exhibited mild tissue reactivity and cell damage, probably due to mechanical compression of the molecular layer and pial vessels. Motor cortex field potentials could be evoked by charges as low as 0.1 muC/ph delivered to paravermal cortex; for a given charge/phase longer pulses were more effective than short pulses. After neural damage resulting from 205 hours of 4.8 muC pulses at 10 per second (total charge 14.76 C), the threshold for the motor cortex evoked potential increased by a factor of four or more. With the charge held constant to different-sized electrodes placed bilaterally in the same monkey, damage was greater under the smaller electtrode. This finding suggests that the charge density to cerebellar cortex must be controlled to avoid neural damage.

Animals↗
PubMed1977

Tissue reactions to long-term electrical stimulation of the cerebellum in monkeys.

Light and electron microscopic analyses were carried out on the stimulated and unstimulated paravermal cortices of six rhesus monkeys that had electrodes implanted on their cerebella for 2 months. The electrodes and the stimulation regime (10 p.p.s.: 8 min on, 8 min off) were similar to those used to stimulate the human cerebellum for treatment of certain neurological disorders. Mere presence of the electrode array in the posterior fossa for 2 months resulted in some meningeal thickening, attenuation of the molecular layer, and loss of Purkinje cells immediately beneath the electrode array. There was no evidence of scarring. After 205 hours of stimulation (7.35 X 10(6) pulses) over 18 days, a charge of 0.5 muC/ph or estimated charge density of 7.4 muC/sq cm/ph resulted in no damage to the cerebellum attributable to electrical stimulation per se. Such a charge/phase is about five times the threshold for evocation of cerebellar efferent activity, and might be considered "safe" for stimulation of human cerebellum. Charge density/phase and charge/phase were directly related to increased cerebellar injury in the six other cerebellar cortices stimulated. Leptomeningeal thickening increased with increased charge density. Injury included severe molecular layer attenuation, ongoing destruction of Purkinje cells, gliosis, ongoing degeneration of myelinated axons, collagen intrusion, and increased levels of local polysaccharides. In all cases, even with damage that destroyed all conducting elements beneath the electrodes, there was no damage further than 1 to 2 mm from the edges of the electrode arrays.

Animals↗
PubMed1976

A comparison of EEG seizure patterns recorded with surface and depth electrodes in patients with temporal lobe epilepsy.

Surface and depth EEG seizure patterns were compared in 34 patients with intractable temporal lobe epilepsy in whom depth EEG electrodes had been chronically implanted in order to localize epileptogenic sites with a view to surgery. EEG records accompanied by clinical seizures, auras, no behavioral changes, as well as records for which no behavioral observations had been made, were judged with respect to the manner in which seizure activity originating unilaterally in the depth of one of the temporal lobes spread to the surface. For each EEG record, the onset of seizure activity in depth was classified as being focal or regional in form, and seizure activity was judged as: (1) not spreading to the surface, (2) spreading bilaterally and synchronously to the surface, (3) spreading initially to the surface ipsilateral to the depth site(s) in which the electrographic seizure first appeared, or (4) spreading initially to the surface contralateral to the depth site(s) in which the seizure activity initially occurred. EEG seizure activity was found to be less likely to propagate to the surface for those records that were either unaccompanied by behavior changes or accompanied only by auras than for those records accompanied by clinical seizures. In records accompanied by clinical seizures, seizure activity commonly propagated to the surface in a bilateral and synchronous fashion and was also found to spread initially to the ipsilateral but not to the contralateral surface. Anatomical and electrophysiological data accounting for the occurrence of ipsilateral spread were discussed. Diagnostic usefulness of surface recordings during clinical seizures in temporal lobe epilepsy was discussed.

Animals↗
PubMedDate not supplied

Interhemispheric propagation time of human hippocampal seizures. I. Relationship to surgical outcome.

This study evaluated ictal stereotaxic electroencephalogram (SEEG) records in 75 patients with complex partial seizures who later received anterior temporal lobectomy and were evaluated for long-term seizure relief. The time required for seizures to propagate from the putatively epileptogenic hippocampal formation to the contralateral hippocampal formation was measured from 615 ictal SEEG records. These interhemispheric propagation times were then compared with the degree of post-lobectomy seizure relief. Poor postsurgical seizure relief was associated with seizure propagation times of less than or equal to 5 s. Relief or reduction of seizures after surgery was associated with seizure propagation times greater than 50 s. These relationships were also found to occur in a subset of 56 patients who did not exhibit interhemispheric propagation times of less than 0.5 s, thus indicating that interhemispheric propagation times in the range of 0.5-5 s is a negative prognostic sign even in the absence of "bilaterally synchronous" ictal SEEG onsets. The finding of longer interhemispheric propagation times in patients who were improved by surgery may be accounted for by the greatly reduced size, or absence, of the hippocampal commissure in humans and suggests that the corpus callosum is a major, albeit indirect, route by which hippocampal foci may propagate seizure activity contralaterally. The finding of shorter interhemispheric propagation times in patients who did poorly after surgery may be accounted for by the existence of foci outside the region of excision with more direct access to callosal pathways or, alternatively, by the presence of damage in a more seizure-prone contralateral hippocampus.

Electroencephalography↗
PubMedDate not supplied

Interhemispheric propagation time of human hippocampal seizures: II. Relationship to pathology and cell density.

The time required for hippocampal seizure activity to propagate to the contralateral hippocampal formation was evaluated in 57 patients with complex partial seizures and related to histological findings following temporal lobectomy. Interhemispheric propagation times were found to be significantly longer (greater than 20 s) in those patients diagnosed as having hippocampal sclerosis than in those patients without hippocampal sclerosis. Quantitative analysis of cell densities was made in 28 patients. Dentate fascia granule densities and hippocampal pyramidal cell densities were found to be lower in those patients with longer interhemispheric propagation times. However, this relationship was not observed when only patients with hippocampal sclerosis were considered. Thus, a tendency for hippocampal seizures to exhibit interhemispheric propagation times greater than 20 s is suggestive of underlying hippocampal sclerosis. However, information about interhemispheric propagation time does not appear useful for estimating the actual degree of cell loss within the sclerotic hippocampus. The association of longer interhemispheric propagation times with hippocampal sclerosis supports the hypothesis that direct commissural connections between the hippocampal formations in humans are either unimportant or missing.

Electroencephalography↗
PubMedDate not supplied

Prognostic significance of independent auras in temporal lobe seizures.

We performed a retrospective study of auras that occurred independently of complex partial seizures in patients undergoing continuous EEG monitoring with stereotactically implanted depth electrodes placed in mesiotemporal structures. Forty of 54 patients had a history of independent auras, and 32 of these individuals had independent auras while being monitored. Two hundred ninety-two independent auras were recorded, and EEG characteristics and subjective symptoms were analyzed with regard to surgical outcome. Most patients had ictal EEG changes with all or some of their auras. Four patients had nonlocalized or multifocal complex partial seizures despite the presence of well-localized auras, indicating that if intracranial ictal recording is used as a gold standard for localization, complex partial seizures must be recorded. Presence or absence of EEG change with auras did not affect prognosis nor did variability of ictal EEG pattern, spatial extent of initial field potential, aura duration, or character of symptoms correlate with prognosis or postoperative persistence of auras.

Electroencephalography↗
PubMedDate not supplied

Quantitative comparison of cell loss and thiopental-induced EEG changes in human epileptic hippocampus.

Thiopental-induced EEG beta activity recorded from mesial and lateral temporal lobe sites was analyzed both visually and by computer in 30 patients with complex partial seizures. All patients later received anterior temporal lobectomy. Volumetric cell densities and percentage of principal cell loss relative to normal controls were determined in several different areas of each resected temporal lobe. The percentage of drug-induced beta activity was then compared with the percentage of cell loss by (a) making precise topographic correlations between induced beta and cell loss, (b) relating the overall degree of left/right beta asymmetry to cell loss averaged over wide regions, and (c) comparing the likelihood of left/right beta asymmetries in patients with and without extreme cell loss. The results obtained were consistently negative and were unaffected by whether EEG data were analyzed by computer or visual inspection. These results indicate that the well-known loss of drug-induced beta activity found in epileptogenic regions is not an indicator of the degree of cell loss or sclerosis. The underlying focal dysfunction measured by EEG beta activity remains unknown, and factors such as focal hypoperfusion, hypometabolism, and the microanatomic features of the cells remaining in the focus should be investigated.

Beta Rhythm↗
PubMedDate not supplied

Role of the frontal lobes in the propagation of mesial temporal lobe seizures.

The depth ictal electroencephalographic (EEG) propagation sequence accompanying 78 complex partial seizures of mesial temporal origin was reviewed in 24 patients (15 from the University of Pittsburgh Epilepsy Center and 9 from UCLA). All patients were monitored with bilateral mesial frontal and mesial temporal depth electrodes and later received anterior temporal lobectomy. Ictal EEG records were categorized according to sequence of spread from the temporal focus to the other regions. Although propagation patterns varied both within and between patients, certain features were notable: (a) It was very common for seizure activity to spread initially to the ipsilateral frontal lobe (observed in 22 of 24 patients). (b) The most common mode of spread (15 of 24 patients) was initiating temporal lobe----ipsilateral frontal lobe----contralateral frontal lobe----contralateral temporal lobe. (c) Occasionally, seizure discharges invaded the frontal lobes but failed to invade the contralateral temporal lobe (2 of 24 patients). (d) Seizure activity occasionally invaded the contralateral temporal lobe prior to invading the frontal lobes (2 of 24 patients). Other notable features included (i) a clear tendency for mesial temporal seizure discharges initially to invade orbitofrontal (as opposed to anterior cingulate) cortex and (ii) the emergence of a period of clear asymmetry in the frontal lobes during which high-amplitude, rapid discharges were present on the side ipsilateral to the initiating temporal lobe. These results suggest that the prefrontal region, especially the orbitofrontal cortex, is strongly influenced by mesial temporal ictal activity. This region appears to be frequently involved in the propagation of seizures initiated in the mesial temporal lobe and may play a role in the interhemispheric propagation of mesial temporal seizures.

Brain Mapping↗