شناسایی عبارات هیجان صورتی در بیماری پارکینسون
|کد مقاله||سال انتشار||مقاله انگلیسی||ترجمه فارسی||تعداد کلمات|
|31075||2008||14 صفحه PDF||سفارش دهید||11073 کلمه|
Publisher : Elsevier - Science Direct (الزویر - ساینس دایرکت)
Journal : European Neuropsychopharmacology, Volume 18, Issue 11, November 2008, Pages 835–848
A limited number of studies in Parkinson's Disease (PD) suggest a disturbance of recognition of facial emotion expressions. In particular, disgust recognition impairment has been reported in unmedicated and medicated PD patients. However, the results are rather inconclusive in the definition of the degree and the selectivity of emotion recognition impairment, and an associated impairment of almost all basic facial emotions in PD is also described. Few studies have investigated the relationship with neuropsychiatric and neuropsychological symptoms with mainly negative results. This inconsistency may be due to many different problems, such as emotion assessment, perception deficit, cognitive impairment, behavioral symptoms, illness severity and antiparkinsonian therapy. Here we review the clinical characteristics and neural structures involved in the recognition of specific facial emotion expressions, and the plausible role of dopamine transmission and dopamine replacement therapy in these processes. It is clear that future studies should be directed to clarify all these issues.
Parkinson's disease (PD) is a neurodegenerative disorder clinically characterized by motor symptoms, such as bradykinesia, rigidity, and rest tremor, which usually arise unilaterally, and spread to the opposite side of the body and the axial muscles with disease progression. These symptoms depend mostly on the degeneration of the dopamine-containing neurons in the substantia nigra pars compacta in the mesencephalon (Hughes et al., 1992), where cytoplasmic inclusions of ubiquinated proteins, the Lewy bodies, have been identified. Recent neuropathological data, however, indicate that the Lewy bodies can be found in a number of brainstem structures, including the olfactory nuclei, the dorsal motor nucleus of the vagus, the locus coeruleus, the raphe nuclei, and the reticular formation, and in several cortical regions (Braak et al., 2003 and Braak et al., 2004). Therefore, the original description of PD as due to the selective damage of the dopaminergic neurons in the mesencephalon should be updated into the concept of a more severe and multisystemic neurodegenerative disorder, whose clinical symptoms reflect the progression of the pathological damage from the medulla oblongata to neocortical areas. Thus, PD patients frequently experience non-motor symptoms, including autonomic, behavioral, and cognitive dysfunctions, and one of the most intriguing aspects of the studies by Braak et al., 2003 and Braak et al., 2004 is that neuropathological alterations outside the substantia nigra are soundly correlated with some of these non-motor symptoms of PD. Depression is a neuropsychiatric symptom frequently observed in PD patients, occurring in up to 45% of cases (Burns, 2002). Depression in PD is not necessarily related to the severity of motor impairment, and it is often misdiagnosed since hypomimia and reduction of voluntary movements are common to both PD and functional depression. Therefore, the identification of depression in PD patients is essentially based upon subjective perception of depressive symptoms, such as the feeling of incapability, the reduced reaction to emotional stimuli, and the impairment to experience pleasure from things or events (anhedonia). Also, cognitive impairment is frequent in PD and is usually characterized by ‘frontal’ cortical dysfunction, including visual–perceptual and executive deficits, whereas episodic memory and verbal fluency are generally spared (Levin and Katzen, 1995). However, in the late stages of PD, severe cognitive impairment may be observed, giving rise to the PD-dementia complex. Because of the frequent involvement of these behavioral and cognitive manifestations, in recent years interest is growing on the characterization of the possible impairment of the processing of facial emotion expressions in PD. In an evolutionary perspective, emotions play a significant role for the adaptation of a subject and for the establishment of relationships within a community. Moreover, emotions have a regulatory function on the mechanisms of motivation, on promoting transgeneration relationships, and on modulating individual behavior as to increase the chances of survival. Thus, this aspect is of more than a theoretical importance. Patients suffering from PD may have alteration in areas strategic for the identification of specific facial expressions, such as the insula, the amygdala, the ventral striatum, the inferior orbitofrontal cortex, and the anterior cingulate cortex.