Summary:Purpose: Decline in verbal memory as a surgical complication remains an unresolved problem in mesial temporal lobe epilepsy. Some areas in the temporal lobe associated with the language function, often including the basal temporal language area, have been removed or transected by conventional surgical procedures. The authors defined the basal temporal language area and removed only the epileptogenic zone with a subtemporal approach.Methods: The basal temporal language area was evaluated by using long-term subdural electrodes in five patients with language-dominant-side mesial temporal lobe epilepsy. While preserving this area, the hippocampus and the parahippocampal gyrus were removed by using a combined subtemporal, transventricular, transchoroidal fissure approach. Verbal memory performance was assessed with the Wechsler Memory Scale-Revised (WMS-R) before and after the operation.Results: The basal temporal language area, defined as a part of the inferior temporal gyrus, the fusiform gyrus, and the parahippocampal gyrus, was spared by entering the temporal horn via collateral sulcus. Verbal memory was significantly improved by 3 months and 1 year after the operation.Conclusions: In language-dominant-side mesial temporal lobe epilepsy, preserving the basal temporal language area would have potential to improve verbal memory outcomes after removal of the epileptogenic zone.

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We examined the quantitative and qualitative difference of the pattern with visuo-cognitive processing impairment in patients with early onset AD (EOAD) and late onset AD (LOAD). We use a visual attention task introduced by Navon (1977) to examine the function to integrate local visual stimuli into global image. Although the ability to identify solid digits ether of large and small size presented at the same exposure duration, EOAD performance was poor in the global perception especially at the short duration (20~msec). We provide evidence that this dysfunction is attribute to the AD pathology specific to early onset type.

The structural and functional abnormalities of the frontal lobes, the region implicated in social information processing, have been suspected to underlie social cognitive impairments in schizophrenia. However, multiple structures, including the limbic/paralimbic areas that are also important for social cognition, have been reported to be abnormal in schizophrenia. The aim of this study is to investigate the extent to which the frontal lobe dysfunction accounts for social cognitive impairments in schizophrenia by comparing with patients who have focal frontal lobe injuries. Social cognitive abilities, focusing on affective aspects, were examined by an emotion intensity recognition task, which is sensitive to the amygdala function, and the emotion attribution tasks, which rely mainly on the frontal lobe function. Individuals with schizophrenia were impaired on the emotion intensity recognition task as well as on the emotion attribution tasks as compared with healthy subjects. By contrast, the frontal lobe-damaged group was defective in the emotion attribution tasks but not in the emotion intensity recognition task. Our results indicated that social cognitive impairments observed in schizophrenia can be accounted for partly by their frontal lobe pathology. Other aspects of social cognitive impairments could also be associated with the extra-frontal pathology, such as the amygdala.

Reduplicative paramnesia (RP) is a well recognized neurological phenomenon, characterized by a false belief that a familiar person or place has been duplicated. In the development of RP, right-dominant frontal lesions are commonly observed. We report a 73-year-old woman who developed reduplication of people and places 3 months after the surgical removal of a large right frontotemporal meningioma. About 1 year after the surgery, her RP diminished after a small dose of risperidone. Neuropsychological evaluation was performed before surgery, after surgery when RP was present and again after recovery of RP. In accordance with the literature, the present case study suggests that a right hemispheric lesion is the essential neuroanatomical substrate in the development of RP. However, no single neuropsychological factor can fully explain the development and resolution of RP. Multiple factors, including neuroanatomical, cognitive and environmental factors seem to be dynamically involved.