Dynorphin A(1-17), an opioid peptide that is normally present in the hippocampal mossy fiber system, was localized immunocytochemically in the hippocampal formation of control autopsy and temporal lobe epilepsy (TLE) specimens. In control tissue, dynorphin-like immunoreactive (Dyn-IR) structures were confined to the mossy fiber path and were most highly concentrated in the polymorph (hilar) region of the dentate gyrus. Very few Dyn-IR structures were present in the molecular and granule cell layers of the dentate gyrus. In contrast, in all TLE specimens, Dyn-IR elements were present in these layers. The extent of aberrant staining varied among the TLE specimens, and 2 major patterns were observed. The first was a relatively wide band of reaction product in the inner one-third to one-fourth of the molecular layer (8 cases), and the second was a more limited distribution of immunoreactive fibers and presumptive terminals in the granule cell and immediately adjacent supragranular regions (2 cases). The extent of aberrant Dyn-IR structures appeared to be related to the amount of cell loss in the polymorph and CA3 fields and to dispersion of the granule cell somata. Specimens processed with the Timm's sulfide silver method for heavy metals provided independent evidence for the distribution of mossy fibers. In both control and TLE specimens, the patterns of labeling were virtually identical to those of dynorphin localization. These findings suggest that sprouting of mossy fibers or their axon collaterals has occurred in hippocampal epilepsy and that the reorganized fibers contain at least one of the neuropeptides that are normally present in this system. Such fibers could form recurrent excitatory circuits and contribute to synchronous firing and epileptiform activity, as suggested in studies of experimental models of 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.
Summary:Purpose: We performed this study to determine whether significant head trauma in human adults can result in hippocampal cell loss, particularly in hilar (polymorph) and CA3 neurons, similar to that observed in animal models of traumatic brain injury. We examined the incidence of hippocampal pathology and its relation to temporal neocortical pathology, neuronal reorganization, and other variables.Methods: Twenty-one of 200 sequential temporal lobectomies had only trauma as a risk factor for epilepsy. Tissue specimens from temporal neocortex and hippocampus were stained with glial fibrillary acidic protein (GFAP) and hematoxylin and eosin (H&E). Eleven hippocampal specimens had additional analysis of neuronal distributions by using cresyl violet and immunolabeling of a neuron-specific nuclear protein .Results: The median age at onset of trauma was 19 years, the median time between trauma and onset of seizures was 2 years, and the median epilepsy duration was 16 years. The length of the latent period was inversely related to the age at the time of trauma (r = 0.75; Spearman). The neocortex showed gliosis in all specimens, with hemosiderosis (n = 8) or heterotopias (n = 6) in some, a distribution differing from chance (p = 0.02; Fisher). Hippocampal neuronal loss was found in 94% of specimens, and all of these had cell loss in the polymorph (hilar) region of the dentate gyrus. Hilar cell loss ranged from mild, when cell loss was confined to the hilus, to severe, when cell loss extended into CA3 and CA1. Some degree of mossy fiber sprouting was found in the dentate gyrus of all 10 specimens in which it was evaluated. Granule cell dispersion (n = 4) was seen only in specimens with moderate to severe neuronal loss.Conclusions: Neocortical pathology was universally present after trauma. Neuronal loss in the hilar region was the most consistent finding in the hippocampal formation, similar to that found in the fluid-percussion model of traumatic head injury. These findings support the idea that head trauma can induce hippocampal epilepsy in humans in the absence of other known risk factors.
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