On August 25, 1953, the patient H.M., aged 27, underwent a bilateral surgical destruction of the inner aspect of his temporal lobes performed by William Beecher Scoville with the aim to control H.M.'s drug refractory epileptic seizures and alleviate their impact on his quality of life. Postoperatively, H.M. presented for 55 years a "striking and totally unexpected grave loss of recent memories". This paper reports what we know about H.M.'s epilepsy before and after surgery and puts forward arguments supporting the syndromic classification of his epilepsy. We attempted to elucidate what could have been the rationale, in 1953, of Scoville's decision to carry out a bilateral ablation of H.M.'s medial temporal lobe structures, and we examined whether there was any convincing argument published before 1953 suggesting that bilateral hippocampal ablation could result in a permanent and severe amnesia. Our a posteriori analysis of H.M.'s medical history suggested that he was most probably suffering from idiopathic generalized epilepsy with absences and generalized convulsive seizures worsened by high dosage phenytoin treatment, or less probably from cryptogenic frontal lobe epilepsy. Importantly, he did not have temporal lobe epilepsy. Scoville based his proposal of bilateral mesial temporal lobe ablation on his experience as a psychosurgeon and on the assumption that the threshold of generalized epileptic activity could be lowered by some kind of hippocampal dysfunction potentially epileptic in nature. Given the scanty information on the link between amnesia and medial temporal lobe lesions that was available in humans in 1953, one can understand why Scoville was so surprised by the "striking and totally unexpected" memory loss he observed in H.M. after the bilateral ablation of his mesial temporal lobe structures.
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http://dx.doi.org/10.1016/j.neurol.2015.01.002 | DOI Listing |
Cell Rep
January 2025
Nash Family Department of Neuroscience, The Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, NY, USA. Electronic address:
Temporal lobe epilepsy (TLE) causes pervasive and progressive memory impairments, yet the specific circuit changes that drive these deficits remain unclear. To investigate how hippocampal-entorhinal dysfunction contributes to progressive memory deficits in epilepsy, we performed simultaneous in vivo electrophysiology in the hippocampus (HPC) and medial entorhinal cortex (MEC) of control and epileptic mice 3 or 8 weeks after pilocarpine-induced status epilepticus (Pilo-SE). We found that HPC synchronization deficits (including reduced theta power, coherence, and altered interneuron spike timing) emerged within 3 weeks of Pilo-SE, aligning with early-onset, relatively subtle memory deficits.
View Article and Find Full Text PDFMed Sci (Basel)
January 2025
Department of Medical Genetics, Clinical Neurophysiology of Postgraduate Education, V.F. Voyno-Yasenetsky Krasnoyarsk State Medical University, Russian National Research, Krasnoyarsk 660022, Russia.
: Epilepsy is a group of disorders characterized by a cluster of clinical and EEG signs leading to the formation of abnormal synchronous excitation of neurons in the brain. It is one of the most common neurological disorders worldwide; and is characterized by aberrant expression patterns; both at the level of matrix transcripts and at the level of regulatory RNA sequences. Aberrant expression of a number of microRNAs can mark a particular epileptic syndrome; which will improve the quality of differential diagnosis.
View Article and Find Full Text PDFNeuroSci
January 2025
Department of Neuroscience "Rita Levi Montalcini", University of Turin, 10126 Turin, Italy.
Dementia, including Alzheimer's disease (AD) and frontotemporal dementia (FTD), presents critical challenges for correctional systems, particularly as global populations age. AD, affecting 60-80% of dementia cases, primarily impairs memory and cognition in individuals over 65. In contrast, FTD, rarer than AD but not uncommon in those under 65, affects the frontal and temporal brain regions, leading to deficits in social behavior, language, and impulse control, often resulting in antisocial actions and legal consequences.
View Article and Find Full Text PDFBrain Commun
January 2025
Department of Clinical Psychology and Psychobiology, Universidade de Santiago de Compostela (USC), Santiago de Compostela 15782, Spain.
Previous research has revealed patterns of brain atrophy in subjective cognitive decline, a potential preclinical stage of Alzheimer's disease. However, the involvement of myelin content and microstructural alterations in subjective cognitive decline has not previously been investigated. This study included three groups of participants recruited from the Compostela Aging Study project: 53 cognitively unimpaired adults, 16 individuals with subjective cognitive decline and hippocampal atrophy and 70 with subjective cognitive decline and no hippocampal atrophy.
View Article and Find Full Text PDFIBRO Neurosci Rep
June 2025
Department of Pharmacy, University of Mountains, P.O. Box 208, Bangangté, Cameroon.
Background And Aim: To date, there is no treatment to prevent the development of temporal lobe epilepsy, the most common form of drug-resistant epilepsy. A recent study revealed the antiepileptic-like effect of the aqueous extract of . Given the potential of this extract, the antiepileptogenic- and learning and memory-facilitating-like effects of the aqueous extract of were assessed using the kainate-induced post- model.
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