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T L Babb

Publications and source records attributed to T L Babb.

At least 109 records · Page 6Linked to original sources
PubMed1978

Human hippocampal formation EEG desynchronizes during attentiveness and movement.

The relation of the hippocampal EEG to behavior and to the neocortical EEG is being studied in psychomotor epileptics. Hippocampal recordings displaying only rare epileptiform spikes and slow waves are found to follow grossly the simultaneously recorded neocortical EEG, becoming desynchronized during wakefulness and paradoxical sleep (PS), and displaying large irregular slow waves during slow-wave sleep. In the one patient reported in this clinical note, strong rhythmic 5--6 c/sec waves dominated the neocortical and hippocampal EEG during quiet wakefulness. These slow waves were replaced by desynchronized activity during PS and during difficult tasks, suggesting a further desynchronizing influence. The findings in all patients suggest that the rhythmic slow activity ('theta') found in rats and cats during specific behaviors is not observed in the human hippocampal formation during the homologous behaviors.

Adult↗
PubMed1977

Post-EEG seizure depression of human limbic neurons is not determined by their response to probable hypoxia.

A subclinical EEG seizure occurred in each of 2 patients during a test that repeatedly evoked probable mild cerebral hypoxia. The firing rate of the neurons was unaffected until the EEG seizure had been ongoing for over a minute. After the EEG seizures, all neurons were profoundly depressed regardless of whether their responses to hypoxia had been an increase, decrease, or no change in firing rate. These observations indicate that the mechanism responsible for post-EEG seizure depression of neuronal firing is probably not cerebral hypoxia.

Action Potentials↗
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

Epileptogenesis of human limbic neurons in psychomotor epileptics.

Different stages of epileptogenesis of neurons in deep temporal lobe structures have been studied with fine wire microelectrodes chronically implanted in patients with drug-refractory psychomotor epilepsy. The interictal firing patterns of single neurons ipsilateral to the focus (identified by EEG seizure onset and/or neuropathology studies and seizure reduction following anterior temporal lobectomy) often exhibited burst when contralateral neurons did not. The intraburst sequence of action potentials was not organized or reliable except in one focal hippocampal neuron. Bursts of action potentials often occurred in the absence of regional sharp waves recorded with the same microelectrode; however, sharp waves with fast rise times were almost always associated with action potentials from nearby neurons. During sub-clinical EEG seizures, when EEG abnormalities did not propagate contralaterally, neurons were activated in rough proportion to the intensity of EEG activation and extent of spread of seizure activity to ipsilateral temporal lobe structures. During clinical seizures, involving both hemispheres, firing rates of neurons near the focus increased during the small amplitude high-frequency EEG phase and decreased as this high-frequency rhythmical waveform increased in amplitude. Variable firing rates followed until the clonic EEG phase, where a reliable excitation of neurons occurred during the sharp waves and strong inhibition during the following slow waves. Between these sharp--slow wave events many neurons were inhibited, but to a lesser degree and for longer than the post-excitation inhibition. These neurophysiological phenomena are discussed in relation to the literature on cellular mechanisms of epileptogenesis in experimental epilepsy.

Action Potentials↗
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↗
PubMed1975

Limbic neuronal firing rates in man during administration of nitrous oxide--oxygen or sodium thiopental.

Electroencephalographic activity and extracellular discharges from neurons in deep temporal lobe structures were recorded from fine wire microelectrodes chronically implanted in seven psychomotor epileptic patients for diagnostic localization of seizure foci. In four patients, inhalation of 80 per cent nitrous oxide resulted in loss of consciousness without change in firing rates of temporal lobe neurons (n = 22). In all seven patients, thiopental (400 or 200 mg, iv) decreased limbic neuronal firing rates (n = 38) until the return of wakefulness. In only three of these patients, however, did the firing rates of the neurons (n = 19) decrease significantly (P less than .05). Thiopental suppression of unit activity was not related to systemic hypoxia. This study demonstrates that anesthetic induction with nitrous oxide-oxygen does not significantly affect the firing of neurons in various regions of the human limbic system, which may explain the incidence of patient awareness reported when nitrous oxide-oxygen is administered alone. Thiopental depresses the firing of limbic neurons, and this may account in part for the temporary confusion and amnesia often manifested by patients recovering from the effects of thiopental.

Adolescent↗
PubMedDate not supplied

Kainic acid induced hippocampal seizures in rats: comparisons of acute and chronic seizures using intrahippocampal versus systemic injections.

Hyppocampal epilepsy is a recently defined syndrome occurring in 65% of all temporal lobe epilepsies as defined by: 1) electrographic (EEG) onset in the hippocampus (HC) prior to EEG seizures elsewhere, 2) post-resection hippocampal sclerosis and mossy fiber synaptic reorganizations and 3) relief of typical complex partial seizures after surgical resection of the hyppocampus. We used intrahippocampal kainic acid injections V2 in rats at different developmental ages (postnatal 7 through adult) to develop long term spontaneous HC EEG spikes, EEG seizures, and behavioral seizures. Split-screen video/EEG monitoring demonstrated that this intrahippocampal kainic acid model produced progressive development of: 1) ipsilateral interictal spikes, 2) later polyspike complexes, 3) bilaterally-asynchronous EEG spiking, 4) unilateral HC EEG seizure onsets with occasional secondarily generalized spread to apposite HC and motor cortex to elicit complex partial seizures, and 5) in all seizing rats there was mossy fiber synaptic reorganization, even when injected at age 7 days. These results indicate that the intrahippocampal kainic acid injection model is similar to human hippocampal epilepsy.

Action Potentials↗
PubMedDate not supplied

Granule cell mRNA levels for BDNF, NGF, and NT-3 correlate with neuron losses or supragranular mossy fiber sprouting in the chronically damaged and epileptic human hippocampus.

This study determined in temporal lobe epilepsy patients if there were correlations among hippocampal granule cell expression of neurotrophin mRNAs, aberrant supragranular mossy fiber sprouting, and neuron losses. Consecutive surgically resected hippocampi (n = 9) and comparison tissue from autopsies (n = 3) were studied for: 1. Granule cell mRNA levels using in situ hybridization for brain-derived neurotrophic factor (BDNF), nerve growth factor (NGF), and neurotrophin-3 (NT-3); 2. neo-Timm supragranular mossy fiber sprouting; and 3. Ammon's horn neuron densities. Clinically, patients were classified into those with hippocampal sclerosis (HS; n = 7) and non-HS cases (i.e., mass lesions and autopsies; n = 5). Results showed that compared to non-HS cases, HS patients showed increased granule cell mRNA levels for BDNF, NGF, and NT-3 (p = 0.035, p = 0.04, p = 0.045 respectively; one-tail directional test). Moreover, granule cell BDNF mRNA levels correlated inversely with Ammon's horn neuron densities (p = 0.02) and correlated positively with greater supragranular mossy fiber sprouting (p = 0.02). NGF mRNA levels correlated inversely with Ammon's horn neuron densities (p = 0.02), and NT-3 mRNA levels correlated inversely with age at surgery (p = 0.04) and correlated positively with greater mossy fiber sprouting (p = 0.026). These results indicate in the chronically damaged human hippocampus that granule cells express neurotrophin mRNAs, and mRNA levels correlate with either hippocampal neuron losses or aberrant supragranular mossy fiber sprouting. These data support the hypothesis that in the epileptic human hippocampus, there may be pathophysiologic associations among mossy fiber synaptic plasticity, hippocampal neuron damage, and granule cell mRNA neurotrophin levels.

Analysis of Variance↗