Hippocampal sclerosis is now one of the best-known structural pathologies associated with drug-resistant mesial temporal lobe epilepsy, but clinicians recognised the abnormality long before MRI made it visible during life.
The earliest observations
In 1825 Bouchet and Cazauvieilh described hardened and shrunken hippocampal tissue in post-mortem brains of people who had epilepsy. The significance of the finding was uncertain.
Sommer’s 1880 description
Wilhelm Sommer described a characteristic pattern of neuronal loss in Ammon’s horn. The especially vulnerable CA1 region later became known as Sommer’s sector.
Cause or consequence?
Neuropathologists debated whether hippocampal damage caused epilepsy or whether repeated severe seizures damaged the hippocampus. Modern evidence suggests hippocampal sclerosis is heterogeneous and cannot be reduced to one pathway.
Surgery changes the evidence
The expansion of temporal-lobe surgery in the 1950s provided surgical specimens that could be correlated with clinical history, EEG and seizure semiology. Falconer’s Maudsley programme was particularly important.
MRI brings pathology into life
High-resolution MRI made hippocampal atrophy and signal abnormality visible before surgery, profoundly changing presurgical assessment.
Modern classification
Contemporary neuropathology recognises different patterns of hippocampal sclerosis according to the distribution of neuronal loss. Imaging, genetics and molecular pathology continue to investigate why apparently similar lesions arise through different pathways.
Related reading
Sources and further reading
- Hippocampal sclerosis: progress since Sommer
- Hippocampal sclerosis — origins and imaging
- Clinical neuropathology of the epilepsies
Evidence checked: September 2026.