The insular cortex has been considered to be the neural base of visceral sensation for many years. Previous studies in psychology and cognitive neuroscience have accumulated evidence indicating that interoception is an essential factor in the subjective feeling of emotion. Recent neuroimaging studies have demonstrated that anterior insular cortex activation is associated with accessing interoceptive information and underpinning the subjective experience of emotional state. Only a small number of studies have focused on the influence of insular damage on emotion processing and interoceptive awareness. Moreover, disparate hypotheses have been proposed for the alteration of emotion processing by insular lesions. Some studies show that insular lesions yield an inability for understanding and representing disgust exclusively, but other studies suggest that such lesions modulate arousal and valence judgments for both positive and negative emotions. In this study, we examined the alteration in emotion recognition in three right insular and adjacent area damaged cases with well-preserved higher cognitive function. Participants performed an experimental task using morphed photos that ranged between neutral and emotional facial expressions (i.e., anger, sadness, disgust, and happiness). Recognition rates of particular emotions were calculated to measure emotional sensitivity. In addition, they performed heartbeat perception task for measuring interoceptive accuracy. The cases identified emotions that have high arousal level (e.g., anger) as less aroused emotions (e.g., sadness) and a case showed remarkably low interoceptive accuracy. The current results show that insular lesions lead to attenuated emotional sensitivity across emotions, rather than category-specific impairments such as to disgust. Despite the small number of cases, our findings suggest that the insular cortex modulates recognition of emotional saliency and mediates interoceptive and emotional awareness.

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The aim of this study was to assess the cognitive functions of patients with spinocerebellar ataxia type 6 (SCA6). We examined 13 patients with genetically confirmed SCA6 and 13 healthy control subjects matched for age, years of education, global cognitive status, and intellectual ability. We administered verbal memory (word recall and word recognition), executive function (digit span, category and letter fluency, Frontal Assessment Battery, and Trail Making Test-A and B), and visuospatial construction (figure copying) tests. We found that the patients with SCA6 had significantly lower scores on the demanding word recall and letter fluency tests compared to the control subjects, while word recognition was well preserved in the patients with SCA6. The other executive functions tested, as well as visuospatial construction, were preserved in the SCA6 group. However, although memory encoding and storage processes were preserved, the retrieval of memorized information concerning frontal function might be selectively affected in patients with SCA6 compared to in control subjects. The impaired word recall and letter fluency noted in patients with SCA6 were interpreted as being related to a word-retrieval disability. Such dysfunctions may be attributed to damage in the frontal-cerebellum circuit owing to SCA6.

Time estimation in patients with prefrontal cortex (PFC) damage is often inaccurate. The relationship between PFC and estimation of short time intervals has been examined. However, it remains unclear whether PFC damage affects estimation of longer time intervals. Here, we investigated the ability of patients and healthy subjects to verbally estimate a period of 30 min, using a method easily applied in clinical settings. In 99 patients with brain damage, we compared under and normal ranges of time in patients with PFC damage or damage to other brain areas with the chi-squared test. Subsequently, we conducted a discriminant analysis and a multiple linear regression analysis to identify specific brain areas affecting time estimation. We observed a significantly larger number of patients who overestimated 30 min in the group with bilateral PFC damage compared to patients with damage to other regions. Discriminant analysis revealed that damage of right lateral PFC and left medial PFC contributed to discrimination between the normal range and overestimation groups. Multiple linear regression analysis indicated that right lateral PFC damage strongly affected overestimation of a 30-min interval. Neuropsychological test results revealed lower general cognitive function scores and orientation scores in overestimation group. The length of estimated time and the score of delayed word recall were negatively correlated. We propose that these may require encoding, maintenance, and updating of memory and are indirectly related to contextual memory. We discuss hypotheses on contextual memory segmentation and reconstruction to clarify the mechanism of impaired time overestimation in PFC-damaged patients.