OBJECTIVE: The purpose of this review is to provide an update of the
research regarding depression in Parkinson's disease and to synthesize the
information into a neurobiological model relating the structural and
biochemical changes in this disorder to the behavioral manifestations.
METHOD: The author used a computer-based search of the literature,
augmented by extensive bibliography-guided article reviews, to find
information on depression and Parkinson's disease. FINDINGS: Depression
occurs in approximately 40% of patients with Parkinson's disease;
depression in Parkinson's disease is distinguished from other depressive
disorders by greater anxiety and less self-punitive ideation. Lower CSF
levels of 5-hydroxyindoleacetic acid, a past history of depression, and
greater functional disability are associated with a greater risk of
depression in Parkinson's disease. Female gender, early age at onset of
Parkinson's disease, and greater left brain involvement may also be risk
factors. Approximately half of depressed patients with Parkinson's disease
meet criteria for major depressive episodes; half have dysthymia.
Depression is more common in Parkinson's disease with prominent
bradykinesia and gait instability than in tremor-dominant syndromes.
Depressed patients with Parkinson's disease have greater frontal lobe
dysfunction and greater involvement of dopaminergic and noradrenergic
systems than nondepressed patients with the disease. Mood changes in
Parkinson's disease respond to treatment with conventional tricyclic
antidepressants or ECT. CONCLUSIONS: Neurobiological investigations suggest
that depression in Parkinson's disease may be mediated by dysfunction in
mesocortical/prefrontal reward, motivational, and stress-response systems.
Neuropsychological, metabolic, clinical, pharmacological, and anatomical
studies support the involvement of frontal dopaminergic projections in
patients with Parkinson's disease and depression.