Robbert W K Borgemeester1, Andrew J Lees2, Teus van Laar3. 1. Department of Neurology, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands. 2. Reta Lila Weston Institute of Neurological Studies, UCL Institute of Neurology, London, UK. 3. Department of Neurology, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands. Electronic address: t.van.laar@umcg.nl.
Abstract
BACKGROUND: Visual hallucinations (VH) occur in the clinical course of Parkinson's disease (PD) and are predictive for PD dementia. The genesis of VH is related to impaired bottom-up and/or top-down visual processing which can be linked to cholinergic dysfunction and mono-amine imbalance. The risk of developing VH with oral dopamine agonists seems to increase with advancing disease, while in contrast some clinical studies suggest that apomorphine does not worsen VH, or might even improve VH. METHODS: The aim of this study is to review the current evidence of apomorphine and its effects on VH in PD patients. RESULTS: Apomorphine is well-tolerated in PD patients with VH, also in long-term follow-up studies. Apomorphine is also suggested to have the potential to alleviate VH. Some data suggest that the positive effect of apomorphine on VH is related to its piperidine moiety, part of many anti-psychotics. Irrespective this piperidine moiety, apomorphine has a high D1-like receptor affinity, and acts as a serotonin 5-HT2A receptor antagonist, which might explain the potential anti-hallucinogenic properties as well. CONCLUSION: The anecdotal evidence suggesting that apomorphine has a relatively low proclivity to induce VH in PD may be due to its capacity to reduce serotonergic activity in particular. Therefore apomorphine is still an option to consider in fluctuating PD patients with VH, if they are treated properly with respect to their cholinergic deficits and existing VH.
BACKGROUND:Visual hallucinations (VH) occur in the clinical course of Parkinson's disease (PD) and are predictive for PD dementia. The genesis of VH is related to impaired bottom-up and/or top-down visual processing which can be linked to cholinergic dysfunction and mono-amine imbalance. The risk of developing VH with oral dopamine agonists seems to increase with advancing disease, while in contrast some clinical studies suggest that apomorphine does not worsen VH, or might even improve VH. METHODS: The aim of this study is to review the current evidence of apomorphine and its effects on VH in PDpatients. RESULTS:Apomorphine is well-tolerated in PDpatients with VH, also in long-term follow-up studies. Apomorphine is also suggested to have the potential to alleviate VH. Some data suggest that the positive effect of apomorphine on VH is related to its piperidine moiety, part of many anti-psychotics. Irrespective this piperidine moiety, apomorphine has a high D1-like receptor affinity, and acts as a serotonin 5-HT2A receptor antagonist, which might explain the potential anti-hallucinogenic properties as well. CONCLUSION: The anecdotal evidence suggesting that apomorphine has a relatively low proclivity to induce VH in PD may be due to its capacity to reduce serotonergic activity in particular. Therefore apomorphine is still an option to consider in fluctuating PDpatients with VH, if they are treated properly with respect to their cholinergic deficits and existing VH.