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Chronic exposure to stress can lead to a variety of mental disorders such as depression. There are many treatment-resistant patients who do not respond adequately to the standard pharmacological treatments. Therefore, the development of novel therapeutic agents is highly expected. In rodents, socially defeated animals that were exposed to repeated physical aggression from other individuals are widely used in this field of research. The social defeat is considered as a stress that mimics human social stress. On the other hand, emotional stress, but not physical stress, is likely to contribute to the pathogenesis and etiology of depression in human. Therefore, there is a gap between the process of pathogenesis and the animal models, and this is one of the reasons why the development of new psychotropic drugs to treat depression has been difficult. Recently, a novel stress model has been introduced, in which mice are subjected to emotional stress without physical distress by witnessing social defeat scenes of their conspecifics. We have investigated the mechanisms by which emotional stress is transmitted by witnessing social defeat in mice, focusing on the insular cortex. In this article, we summarize and discuss the recent advancements in the neural basis of behavioral changes induced by emotional stress. [ABSTRACT FROM AUTHOR]

The mechanisms of neuropathic pain have been explored by multiple approaches including electrophysiology, immunohistochemistry, neuroimaging, and molecular biology. Recent studies have demonstrated a part of mechanisms that contribute to the development of a new treatment for neuropathic pain. In this review, we first overview the basic anatomical and physiological evidence of orofacial pain mechanisms, and second, we introduce our recent pharmacological findings in terms of orofacial neuropathic pain obtained by using optical imaging techniques. [ABSTRACT FROM AUTHOR]

The “taste” of foods is perceived as a flavor formed from integrating multimodal information such as olfaction, temperature of foods and the sense of touch on the oral mucosa, with gustation. However, the mechanisms for the flavor information processing are still controversial. In this review, it will be described where and how the taste and odor information are integrated into the flavor in the brain on the basis of recent our knowledge. As part of the review, I will also introduce recent our research for this issue. We observed the cortical responses for the taste and/or odor stimulation in the experimental rats and mouse brain under the anesthetized condition using in vivo flavin protein autofluorescence imaging technique. When the animals were stimulated by odor alone, corresponding responses were observed only in the piriform cortex （PC）. Similarly, taste-alone stimulation elicited the responses in the gustatory area（ GC） in the insular cortex（ IC）. Interestingly, simultaneous stimulation by odor and taste induced the additional response in the agranular insular cortex （AI）. Moreover, in mice trained to learn the association between a taste and an odor, the response area evoked by stimulation with odor or taste alone was altered. In these mice we observed that the odor-alone stimulation evoked the responses not only in the PC but also in the GC, and that taste-alone stimulation evoked the responses in the PC in addition to the GC. These results suggest that the PC, IC including the AI, and surrounding brain region are involved in the formation of associative learning of taste and odor, as “the flavor formation”, and in the representation of the flavor in the brain. [ABSTRACT FROM AUTHOR]

An 86-year-old man was admitted for the abrupt onset of right hemiparesis and aphasia. DWI revealed the high intensity legion in the left insular cortex, and MRA demonstrated the left middle cerebral artery occlusion. Recanalization of the artery was not achieved after mechanical thrombectomy. The diagnosis of infective endocarditis was made as Enterococcus faecalis was cultured from the blood, and mobile vegetation was detected at the aortic valve by transthoracic echocardiography. The patient died from multiple organ failure at 19 days. Autopsy findings revealed fibrin-rich thrombus in the left middle cerebral artery containing neutrophils and bacteria. At the occluded site, neutrophils had intensively infiltrated into the vessel wall, and endothelial cells had partially disappeared. Moreover, disrupted internal elastic lamina was discovered. These findings could indicate that the thrombus had adhered to the vessel wall. The adhesion of the thrombus and vessel wall could be associated with unsuccessful recanalization after endovascular thrombectomy in patients with ischemic stroke due to infective endocarditis.

A 70-year-old man visited our hospital with a chief complaint of involuntary movements, diagnosed as chorea, involving the right upper and lower limbs. Brain MRI showed acute cerebral infarctions involving the left insular and parietal cortices. Chorea is usually due to dysfunction of components of the basal ganglia pathways, such as the caudate nucleus or subthalamic nucleus, and is rarely caused by lesions of the insular or parietal cortex. Here, we describe a case of cerebral infarctions in the left insular and parietal cortices and chorea of the right limbs, and discuss the relationship between the mechanism of chorea and insular and parietal cortical lesions.

A 79-year-old woman developed consciousness disturbance, left eye deviation, right hemiplegia and aphasia with hypoxemia. Chest X-ray showed bilateral pulmonary edema. MRI revealed the left internal carotid artery occlusion and entire left middle cerebral artery infarct including insular cortex. We performed mechanical thrombectomy therapy and TICI3 recanalization was obtained. During operation, the respiratory condition deteriorated and the ventilator was started after mechanical thrombectomy therapy. Chest X-ray showed butterfly shadow, which indicated pulmonary edema. Pulmonary edema improved on the 2nd day of onset, and disappeared on the 3rd day. There was no heart diseases such as Takotsubo myocardiopathy, acute cardiac failure and cardiomyopathy on echocardiography and electrocardiography. Therefore, we diagnosed her as having neurogenic pulmonary edema due to cerebral infarction including insular cortex. We consider that left insular cortex infarction was a trigger of neurogenic pulmonary edema. If hypoxemia associated with infarction including the insular cortex, neurogenic pulmonary edema should be considered for medical treatment.