Why do herpes simplex encephalitis and semantic dementia show a different pattern of semantic impairment in spite of their main common involvement within the anterior temporal lobes?

What is it about?

I tried to check the factors that could explain these different patterns of semantic disruption by making a separate survey of anatomo-clinical investigations and of activation studies relevant to this issue and taking into account the following factors: (a) laterality of lesions; (b) disease aetiology; (c), kind of brain pathology and (d) locus of damage within the temporal lobes.

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Why is it important?

Locus of damage within the temporal lobes and kind of brain pathology seemed to play the most important role, because in HSE patients and in category-specific semantic disorder for biological entities the lesions prevailed in the anteromedial temporal lobes. Furthermore, in HSE patients the neuropathology concerned both the anterior temporal cortices and the white matter pathways connecting these areas with the posterior visual areas, whereas in SD the inferior longitudinal fasciculus involvement was restricted to the rostral temporal lobes and did not extend into the cortically uninvolved occipital lobes. The massive white matter lesions observed in HSE patients could disconnect the anteromedial temporal lobes by the visual information playing a critical role in the organization of the biological categories

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