However, depression

was not identified by the patients a

However, depression

was not. FGFR inhibitor identified by the patients as the most distressing symptom. A population-based study of 97 PD patients found that 36.1 % reported mild depressive symptoms, while another 10% reported moderate and severe symptoms.3 In a small, community-based New Zealand study, the prevalence of major Inhibitors,research,lifescience,medical depression was 2.7%; overall prevalence of mood and anxiety disorders was 6.8% in nondemented PD patients. The prevalence of mental illness for these PD patients did not. differ significantly from that of age-matched controls with no neurological disease, but similar disability:4 Rojo et al5 estimated the prevalence of depressive symptoms, as related to other clinical data, in a series of 350 PD patients over a 9-year period. Mild-to-moderate depressive symptoms and severe depressive symptoms were found in 40.2% and 16.7% of PD patients, respectively. Female gender, advanced disease, and poorer cognitive performance were Inhibitors,research,lifescience,medical significantly associated with depressive symptoms. On follow-up, 34% of patients remained stable, 35% showed an improvement in depressive symptoms, Inhibitors,research,lifescience,medical and 30.9% worsened. In addition to reactive mood changes due to loss of function, neurochemical

changes in PD probably contribute to the development of mood symptoms. Loss of the dopamine neurons in the ventral tegmental area, the origin of mesolimbic dopaminergic projection, is the most likely neuropathological cause of mood symptoms in PD, since changes in the serotonin and norepinephrine systems are not. as extensive. Although one earlier study found lower levels of serotonin metabolites in PD patients with major depression compared to those without,6 Inhibitors,research,lifescience,medical most, cerebral spinal fluid (CSF) studies did not concur with this result.7-9 However, positron emission tomography (PET) has shown hypermetabolism in caudate and inferior orbitofrontal cortex in depressed PD patients, possibly indicating damage to the dopaminergic system from the ventral tegmental region.10 Other blood flow studies of major Inhibitors,research,lifescience,medical depression in PD found changes in medial frontal cortex

and the anterior cingulate.“ These changes seen in very PD depression are similar to those seen in some studies of major depression. A study of major depression and dysthymia in 78 PD patients with classic PD (tremor plus rigidity and/or bradykinesia) compared with 34 akinetic-rigid variant PD patients found that the prevalence of dysthymia was similar in the two groups (31% versus 32%, respectively). However, the finding for major depression was significantly different, with akinetic-rigid variant patients showing a higher prevalence of major depression compared with the classic variant, patients (38% versus 15%, respectively). Bradykinesia was the motor symptom most highly correlated with severity of depression.

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