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The paper by Bonilha et al in this issue (pp 1627–1630) represents yet another step in clarifying the significance of atrophy of mesial temporal structures beyond the hippocampus.1
One of the major advances in the imaging of patients with temporal lobe epilepsy was recognition of hippocampal atrophy, now visible and quantifiable, based on high quality magnetic resonance imaging.2 Measurements of the amygdala volume, carried out in addition to volumetric studies of the hippocampus, provided insights into the significance of the clinical symptom presentation in patients who turned out to have prominent amygdaloid atrophy. Much less clear is the significance of amygdaloid enlargement present in some patients. This does not correspond to a clear neoplastic process and is still awaiting pathological correlation. The issue of enlargement of the amygdala correlating with various behavioural states such as anxiety, depression, or an aura of fear is receiving increasing attention.
Recent studies have also focused on the volume of the entorhinal cortex, the parahippocampal cortex, the perirhinal cortex and the temporopolar cortex. The latter, coupled with an abnormal signal in the anterior temporal lobe, has been the object of recent studies by the French and Australian schools, but the role of the temporal pole in mesial temporal epilepsy is still not fully clarified.
The study by Bonilha et al,1 in an attempt to resolve the differences between the results of the Montreal3 and the Kuopio schools,4 concludes that there is significant reduction in the volume of cortical structures closest to the hippocampus, for example, the entorhinal and perirhinal cortices, whereas the parahippocampal and temporopolar cortices are less affected. They suggest that this volumetric information may strengthen the conclusions of studies of the hippocampus and amygdala and confirm lateralisation of seizures in patients with unilateral ictal onsets.
Despite the growing body of data describing mesial temporal atrophy, many neurosurgeons, neuroradiologists, and neurologists have not been converted to recognising the value of quantitative volumetric studies, and continue to rely solely on their visual impression of atrophy. This, in addition to signal abnormalities, is often quite clear. Volumetric studies, however, have been shown to greatly improve the yield and to provide valuable evidence for lateralisation and localisation. They also improve recognition of dual pathology—that is, mesial atrophy associated with an additional lesion. These studies require validation by correlation with the surgical results.
Hopefully, increased use of automated methods will lead to greater utilisation of volumetric studies, which together with optimal EEG and SEEG will provide improved presurgical evaluation and surgical treatment of patients with intractable temporal lobe epilepsy. There will always remain some uncertainty in prognosis based on the effect of disconnection v resection, and last but far from least, on the extent of resection as well as the experience and skill of the surgeon.
Patients with mesial temporal sclerosis and atrophy are still over-represented among individuals with intractable epilepsy. Frequently, because of residual prejudice and other reasons they are deprived of the benefits of surgical therapy, which is increasingly successful in the treatment of this form of epilepsy.
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