Psychotic and Depressive Symptoms in Parkinson's Disease a Study of the Growth Hormone Response to Apomorphine

• Published in: British journal of psychiatry 1995-10, Vol.167 (4), p.522-526
• Main Authors: Mellers, John D. C., Quinn, Niall P., Ron, Maria A.
• Format: Article
• Language: English
• Subjects: Aged; Apomorphine; Depression; Depressive Disorder - diagnosis; Depressive Disorder - physiopathology; Depressive Disorder - psychology; Dopamine receptors; Factors; Female; Growth Hormone - blood; Growth hormones; Hallucinations; Hallucinations - diagnosis; Hallucinations - physiopathology; Hallucinations - psychology; Humans; Male; Mental depression; Mental disorders; Middle Aged; Movement disorders; Neurocognitive Disorders - diagnosis; Neurocognitive Disorders - physiopathology; Neurocognitive Disorders - psychology; Neurodegenerative diseases; Parkinson Disease - diagnosis; Parkinson Disease - physiopathology; Parkinson Disease - psychology; Parkinson's disease; Patients; Psychoses; Psychosis; Psychotic symptoms; Receptor mechanisms; Receptors, Dopamine - drug effects; Receptors, Dopamine - physiology; Receptors, Serotonin - drug effects; Receptors, Serotonin - physiology; Reference Values; Relationship; Schizophrenia; Visual hallucinations
• ISSN: 0007-1250; 1472-1465
• DOI: 10.1192/bjp.167.4.522

The growth hormone (GH) response to apomorphine, thought to reflect central dopaminergic receptor sensitivity, has been reported as enhanced in acute schizophrenia. We investigated this response in relation to the psychotic episodes associated with Parkinson's disease (PD). The GH response to apomorphine was measured in three groups of patients with Parkinson's disease: those currently psychotic (n = 9), those with a past history of psychosis (n = 7) and those who had never been psychotic (n = 8). Apomorphine-induced GH response was not related to psychosis but was unexpectedly associated with measures of depression. Visual hallucinations were a prominent feature in the psychotic patients and the atypical nature of these psychoses might explain why we found no evidence of dopaminergic sensitivity. Serotonergic dysfunction would be in keeping with this. Dopaminergic mechanisms may contribute to the minor depressive symptomatology seen in PD.