Newly proposed investigations in the social cognition domain such

Newly proposed investigations in the social cognition domain such as TofM, but also metacognition87 or decision-making,104 may offer further opportunities for interpreting the nature of the behavioral manifestations

and their relationship to cognitive disorders. The correlation some authors have found between tasks exploring social cognition, primarily TofM, and standardized measures of behavioral impairment, has a potentially useful clinical application. Until now, detection and quantification Inhibitors,research,lifescience,medical of behavioral changes have relied almost exclusively on caregivers’ reports in structured questionnaires aimed toward defining specific symptoms or syndromes. Quantifying the severity of the social cognition disorder could provide a direct measure of the severity of the behavioral manifestation in dementia. This perspective should encourage the development of specific test batteries for investigating this area. Selected abbreviations and acronyms Inhibitors,research,lifescience,medical AD Alzheimer’s disease DLB dementia with Lewy bodies FTD frontotemporal dementia fv-FTD frontal

Inhibitors,research,lifescience,medical variant of frontotemporal dementia SD semantic dementia TofM theory of mind
Clinical neurologists and psychiatrists have long recognized the frequent occurrence of psychiatric conditions in the context of neurologic (brain) disease. Indeed, this frequent co-occurrence of psychiatric with neurologic symptoms should come as no surprise, since psychiatric disorders, such as schizophrenia and the mood disorders, can be induced by structural brain disease. Presumably, brain dysfunction from conditions that cause neurologic symptoms

– such as seizures, and impairments in movement, sensation, speech, or language – also affects areas of the brain that Inhibitors,research,lifescience,medical regulate mood, emotion, cognition, and perception. For the most part, this branch of psychiatry, neuropsychiatry,1 has lain relatively unexplored until experiencing resurgence in the last few decades. A major Inhibitors,research,lifescience,medical reason for this lack of exploration was the use of psychological explanations such as “reactions” to conceptualize why psychiatric symptoms occurred in the presence of neurologic symptoms. For example, it was asked, “How could Brefeldin_A a phase 3 person with hemiparesis not also feel depressed?” Or, “How could someone with aphasia not also be cognitively impaired?” More recently, it has been recognized that it is the diseased brain in many instances that causes the psychiatric symptoms. This appreciation has Imatinib Mesylate opened up new avenues for understanding of these symptoms, and by extension of brainbehavior relationships in this context. That is, the traditional “lesion approach” that so significantly advanced our understanding of neurologic disease is now being increasingly applied to the psychiatric conditions seen in patients with neurologic disease. Neuropsychiatry exists at the interface between neurology and psychiatry.

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