Cortico-thalamic connections and temporal lobe epilepsy: an evolving story.

OBJECTIVE: Although experimental work has provided evidence that the thalamus is a crucial relay structure in temporal lobe epilepsy (TLE), the relation of the thalamus to neocortical pathology remains unclear. To assess thalamo-cortical network pathology in TLE, we mapped pointwise patterns of thalamic atrophy and statistically related them to neocortical thinning. METHODS: We studied cross-sectionally 36 patients with drug-resistant TLE and 19 age-and sex-matched healthy control subjects using high-resolution MRI. To localize thalamic pathology, we converted manual labels into surface meshes using the spherical harmonic description and calculated local deformations relative to a template. In addition, we measured cortical thickness by means of the constrained Laplacian anatomic segmentation using proximity algorithm. RESULTS: Compared with control subjects, patients with TLE showed ipsilateral thalamic atrophy that was located along the medial surface, encompassing anterior, medial, and posterior divisions. Unbiased analysis correlating the degree of medial thalamic atrophy with cortical thickness measurements mapped bilateral frontocentral, lateral temporal, and mesiotemporal cortices. These areas overlapped with those of cortical thinning found when patients were compared with control subjects. Thalamic atrophy intensified with a longer duration of epilepsy and was more severe in patients with a history of febrile convulsions. CONCLUSION: The degree and distribution of thalamic pathology relates to the topography and extent of neocortical atrophy, lending support to the concept that the thalamus is an important hub in the pathologic network of TLE. Commentary As an epilepsy community, we know temporal lobe epilepsy (TLE) very well. First, it is the most common type of focal epilepsy. Second, it is responsible for the majority of resec-tive surgeries performed for intractable epilepsy. Third, its exhaustively studied pathological substrates fall under the two major umbrellas of either hippocampal sclerosis with characteristic cell loss in the CA1 and CA3 hippocampal subfields, or various extrahippocampal epileptic pathologies such as vascular malformations, tumors, malformations of cortical development, and a growing minority of nonlesional cases with essentially normal structural neuroimaging and no pathological abnormalities on microscopic tissue examination, but with an electro-clinical picture that is highly consistent with a " TLE syndrome. " As such, our work-up of the full temporal lobe epilepsy spectrum, ranging from newly diagnosed to medically intractable disease, largely focuses on identifying signs of temporal lobe pathology. Yet, in the article chosen for this commentary , Bernhardt et al. used novel and elegant MRI processing techniques to demonstrate a pattern of bilateral thinning of the frontocentral, lateral …