دانلود مقاله ISI انگلیسی شماره 34408
ترجمه فارسی عنوان مقاله

ابعاد کنترل روانشناختی والدین: ارتباطات با پرخاشگری فیزیکی و رابطه پیش دبستانی در روسیه

عنوان انگلیسی
Mania caused by a diencephalic lesion
کد مقاله سال انتشار تعداد صفحات مقاله انگلیسی
34408 2002 8 صفحه PDF
منبع

Publisher : Elsevier - Science Direct (الزویر - ساینس دایرکت)

Journal : Neuropsychologia, Volume 40, Issue 3, 2002, Pages 245–252

ترجمه کلمات کلیدی
کلمات کلیدی انگلیسی
Mania; Thalamus; Fronto-subcortical circuits; Orbitofrontal area; Dorsolateral prefrontal region
پیش نمایش مقاله
پیش نمایش مقاله  ابعاد کنترل روانشناختی والدین: ارتباطات با پرخاشگری فیزیکی و رابطه پیش دبستانی در روسیه

چکیده انگلیسی

We describe the case of a young male patient, SN, who suffered a MR-documented ischaemic lesion of both dorsomedial thalami and presented with a transient maniform syndrome. SN's neuropsychological, structural and functional imaging findings are compared with similar reported cases and are discussed in the framework of fronto-subcortical circuits and their proposed behavioural disorders. SN's mania was characterized by restlessness, mood elevation, a tendency for pleasurable activities, inflated self-esteem and loss of disease awareness. Other symptoms were sexual disinhibition, tactlessness, abnormal discourse, and reduced need for food and sleep. His neuropsychological assessment revealed an anterograde amnesia, and an impairment of frontal-executive functions. A SPECT-study showed diaschisis-related areas of hypoperfusion in both prefrontal regions which were interpreted as equivalents of SN's frontal-dysexecutive syndrome. In addition, there was a perfusion deficit in the right orbitofrontal cortex, which was taken as the imaging correlate of SN's secondary mania and personality disorder. These findings suggest that SN's mania and his other symptoms result from the twofold disruption of fronto-subcortical connections, namely of the right orbitofrontal loop which is concerned with mood regulation and socially appropriate behaviour, and of the dorsolateral prefrontal loop which mediates executive cognitive functions.

مقدمه انگلیسی

The core behavioural abnormalities of the acute bilateral paramedian thalamic infarct (BPTI) comprise a state of somnolence and abulia accompanied by amnesia and a ‘frontal brain’ syndrome [38]. The disorder of vigilance often starts with a transient coma, followed by a gradually remitting stupor or hypersomnia during which patients present slow, apathetic and emotionally impoverished. During this state of ‘psychic akinesia’ spontaneous activity is decreased and patients require repeated and vigorous external stimulation during conversation or psychometric testing. With recovery of consciousness, behavioural and neuropsychological abnormalities become evident, mostly encompassing diencephalic amnesia [7], [27], [29] and [39], and frontal-executive dysfunction [10] and [33]. In addition to these standard findings, some case studies have described mood changes, such as cheerfulness, depression, lability with sudden switches from sadness to irritability, and outbursts of anger coupled with physical aggression [7], [10], [14], [15] and [27]. Other forms of reported behavioural changes include sexual disinhibition and uncontrolled eating behaviour [8] and [15]. At present, no conclusive evidence exists as to exact origin of mood disorders following thalamic lesions. We report on a patient who suffered an acute manic episode due to a BPTI. The patient's findings are compared with similar, previously published cases in order to specify ‘diencephalic mania’ in greater detail, and an attempt is made to propose a neurological background hypothesis for the abnormalities of mood and cognitive behaviour following lesions of the diencephalon. Since it is known from experimental and clinical case studies that the frontal lobes are part of a complex neural network responsible for mood regulation and social behaviour [28], the approach adopted in this study will focus on the functional relationship between the diencephalon and frontal brain areas, and on the consequences of a focal diencephalic lesion on this network.