In their study of 62 patients, all four SSRI treatment groups showed significant improvement in depressive symptoms without worsening motor symptoms.

Bupropion, an antidepressant, with dopamine agonist, effects, has received little study in PD to date. It produced dose-limiting side effects in some subjects in the limited investigations that, have been conducted with PD patients.22 There are currently no studies on the efficacy of psychotherapy for treatment of depression in PD. Anxiety disorders Anxiety disorders (including generalized anxiety, social phobia, obsessive-compulsive disorder, and panic disorder) are probably increased in PD, although Inhibitors,research,lifescience,medical there has been little research Inhibitors,research,lifescience,medical in this area. Many PD learn more patients have anxiety symptoms due to legitimate concern about their chronic, progressive illness. In the small studies that have been conducted to date, PD patients also had higher rates of anxiety disorders compared with other neurological23-24 and medical illnesses.25 One study found actual anxiety disorders, separate from simple anxiety symptoms, interfered Inhibitors,research,lifescience,medical with normal function in 40% of patients with PD.26 Anxiety disorders are often seen in conjunction with

depression in PD, a common comorbidity in the general population.27 Anxiety symptoms may occur with “on-off fluctuations in medication treatment of motor symptoms.28, 29 There is some evidence that anxiety disorders in PD are linked to the underlying neurobiology of the illness. Noradrenergic dysfunction is implicated most strongly

in studies of anxiety disorders in the general population, and noradrenergic dysfunction may play a role in development, of anxiety symptoms Inhibitors,research,lifescience,medical in PD. Neuropathological changes in the noradrenergic system, including cell loss in the locus ceruleus, have been seen in PD brain autopsy studies.30 In a preliminary yohimbine challenge study, Richard et al31 administered oral yohimbine, an a2-adrenergic autorcccptor blocker, to 6 PD patients with anxiety or depression, 2 PD patients Inhibitors,research,lifescience,medical with no psychiatric symptoms, and 2 normal Edoxaban controls. The patients with a history of anxiety showed precipitation of panic attacks following the challenge at a rate similar to that, seen in anxiety disorder patients given yohimbine. All the PD patients showed increased sensitivity to development, of somatic symptoms following yohimbine challenge. This study, while too small to offer any conclusive evidence, does suggest that there are noradrenergic system alterations in PD mimicking those thought to occur in primary anxiety disorders. Further work is obviously needed to investigate noradrenergic dysfunction in PD. Deficits in both the serotonergic and GABAergic (GABA, y-aminobutyric acid) systems have also been implicated in the development of anxiety disorders, and PD has been reported to affect both systems.