A controlled study, involving EEG recordings from the scalp and chronically implanted electrodes in the cortex (ECoG), as well as from selected subcortical nuclei, was undertaken to investigate the neurophysiologic effects on rhesus monkeys following experimental whiplash (hyperextension of the head and neck). Sixteen animals, equally divided into four groups, were studied through the following protocol: (1) two animals within each group were whiplashed and then electrodes were implanted into the brain of one; (2) the second two animals were implanted with deep electrodes and then one was whiplashed. Weekly EEG follow-ups showed hippocampal spiking in three of the four whiplashed and then electrode-implanted animals and in one of implanted and then whiplashed animals 6 to 8 weeks postwhiplash. Several results deserve attention. (1) The "whiplash syndrome" owes part of its symptoms to EEG disturbances in the brain. (2) Prior to the onset of spiking, ie, 6 to 8 weeks postwhiplash, practically all scalp, cortical, and subcortical EEG recordings were normal. (3) When hippocampal EEG spiking did take place, only normal and mildly abnormal changes were seen in either the electrocorticogram (ECoG) or scalp electroencephalogram (EEG). (4) The growth and development of this trauma-induced hippocampal spiking followed the classic sequence for the spread of an epileptogenic focus. (5) This apparent subclinical form of posttraumatic epilepsy may be due to the combined effects of the whiplash plus the subcortical electrode placements further decreasing the already well-known, low-spiking threshold of the hippocampi.

Animals↗

PubMedDate not supplied

[Cortico-subcortical electrophysiological study during the effects of benzodiazepines in patients with panic disorders].

INTRODUCTION: Tribute to Robert Heath, M.D. a pioneer in human implanted corticosubcortical microelectrodes. OBJECTIVES: We evaluate retrospective electroencephalography (EEG), local evoked potentials (LEP) and extracellular unitary activity (EUA) of patients with diagnosis of panic disorder in association of simple partial seizures. These patients had presences or absence of agoraphobia. They received treatment with clonazepam or diazepam. PATIENTS AND METHODS: Ten patients with implanted corticosubcortical were divided in two groups. The five patients of group A were treated with clonazepam and the five patients of group B with diazepam. RESULTS: Panic attacks showed EEG thetha activity, increased amplitude of the negative phase of LEP, and an increase in the frequency of EUA in cortico-subcortical organizations. This changes occurred in all organizations with exception of the inhibitory reticular substance. Panic disorder produced abundance of repetitive epileptiform discharges that could precipitate convulsive crisis. Both benzodiazepines were efficacious although results with clonazepam were observed earlier: at 7 to 14 days. Benzodiazepines increased corticosubcortical EEG beta activity, decreased amplitude of negative phase of LEP, and diminution in the frequency of EUA. This changes occurred with exception on the inhibitory reticular system. We postulate: a) That panic disorder hyperexcitability at the cortico-subcortical neuronal level may be the result of gabergic dysfunction, or alteration in neuroinhibitory mechanism through GABAA receptors, and through GABAB neuromodulator receptors, and b) That there is a direct correlation between GABA inhibitory basic mechanism and electroencephalographic beta activity. CONCLUSIONS: Panic disorder produces neuronal hyperexcitability by gabergic dysfunction both benzodiazepines were efficacious in treatment.

Adult↗

PubMedDate not supplied

Neural substrate for emotion: relationship of feelings, sensory perception, and memory.

Explore the source record for details and available documents.

Animals↗