Depression and Parkinson's disease: a review.
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.


METHODS
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.


RESULTS
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.
Department of Neurology, University of California, School of Medicine, Los Angeles.
J L
JL
Cummings
D015415:Biomarkers; D003866:Depressive Disorder / Q000175:diagnosis / Q000209:etiology* / Q000503:physiopathology; D004298:Dopamine / Q000502:physiology; D005260:Female; D005625:Frontal Lobe / Q000503:physiopathology; D007839:Functional Laterality / Q000502:physiology; D006801:Humans; D006897:Hydroxyindoleacetic Acid / Q000134:cerebrospinal fluid; D008297:Male; D008959:Models, Neurological; D008960:Models, Psychological; D009638:Norepinephrine / Q000502:physiology; D010300:Parkinson Disease / Q000150:complications* / Q000175:diagnosis / Q000503:physiopathology; D012720:Severity of Illness Index
D015415:Biomarkers; D006897:Hydroxyindoleacetic Acid; D004298:Dopamine; D009638:Norepinephrine