Role of hippocampal formation in sensory-motor integration: evidence from a dual-pathology case study

Rationale: Dual pathology (DP) is defined as a combination of hippocampal and extrahippocamal lesion and it is often cause of intractable focal epilepsy. Seizures may arise from both hippocampal and extrahippocampal lesion. Sensory-motor integration refers to the capacity of a specific neural circuitry to provide continually update feedback from sensory system to voluntary motor system. Posterior Parietal Cortex (PPC) and Hippocampal Formation (HF) are integral part of Sensory-Motor Integration System and are supposed to have a crucial role in voluntary movement setting. Methods: We describe a dual pathology case with intractable seizures and a two year history of progressive left hand clumsiness. Results: Pure sensory and motor neurological deficit were excluded by neurophysiological evaluation. Neglect, apraxia, agnosia and somatoagnosia were excluded by an extensive neuropsychological evaluation performed during EEG recording. Memory and attention impairment, congruent with a right mesial temporal sclerosis was evident. Several EEGs showed continuous and prolonged sequences of epileptiform activity over the whole right hemisphere with predominant amplitude in fronto-temporal areas. This electrical activity was recorded for several days. Functional-MRI study discovered a normal bilateral activation sensory pattern. A MRI-diffusion study showed a hyperperfusion in right mesial temporal structures but not in the right parietal cortex. An ictal SPECT showed a hyperactivation in right mesial neocortical temporal, thalamic areas and hypoactivation in right frontal area. Ictal EEG pattern disappearance was not associated with a recovery of clumsiness. Conclusions: The overall data in our patient support the assumption of a relevant HF role in sensory-motor integration. Moreover, the persistence of clinical deficit after EEG normalization points to a neuronal loss rather than ictal pathogenensis.