James Parkinson's original 1817 description of PD focussed on the motor symptoms, but it is now recognised that non-motor features are a significant feature of both PD and its treatment. Psychotic symptoms have a prevalence of 20-70% depending on disease stage.
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The high prevalence rate reflects in part the broad definition of psychosis used. This encompasses both illusions and brief hallucinations with retained insight at the one end of the spectrum to delusional and more complex psychotic states at the other.
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Diagnostic criteria for Parkinson's Disease psychosis (PDP): 1 of (illusions, false sense of presence, hallucinations, delusions), UK Brain Bank criteria for PD, Symptoms onset after PD onset, Recurrent or continuous symptoms>1 month. Not better accounted for by another cause.
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PDP symptoms: illusions (real objects transformed into other shapes), simple hallucinations (animals, people & objects), passage hallucinations (objects/dots of light passing into visual field), presence hallucinations (sense of nearby person/animal)(3)
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Pareidolia (faces & objects seen in formless visual stimuli eg clouds, patterned curtains), Charles-Bonnet (VH's occuring due to occular or visual pathway disease), Capgras (familiar person replaced by impostor), reduplicative paramnesia (belief that room/place was duplicated)(3)
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Othello syndrome (delusion of partner infidelity), complex delusional and psychotic states without insight. Delusional themes include sin, religion, guilt, theft etc (3)
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Risk factors: old age, REM sleep disorder, long duration of PD, cogntive impairment, depression, drugs (amantadine, selegiline, DA agonists, COMT inhibitors, anticholinergics, L-Dopa), deep brain stimulation (STN), genetic susceptibility.
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Pathogenesis: Degeneration of presynaptic 5HT neurons with compensatory upregulation of postsynaptic 5HT-2A receptors & overstimualation of postsynaptic serotonergic neurons + normal DA-ergic mechanisms.
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Treatment: 1) Rule out delirium, alcohol & substance misuse, primary psychiatric disorder, 2) sleep hygiene, avoid excessively patterned furniture, reduce sensory overload/deprivation, 3) reduce anti-parkinsonian medication (amantadine, anticholinergics & selegiline first (2)...
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then DA agonists, COMT inhibitors and L-Dopa, 4) Medication used to treat PDP includes antipsychotics, 5HT-2A receptor antagonists, 5HT-3 receptor antagonists, and acetylcholinesterase inhibitors. ECT may also have a role (2).
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Antipsychotics (start low go slow): Quetiapine (12.5-150mg/d) commonly used, well tolerated but not always effective. Clozapine (usual dose in PD 12.5-150mg/d) is the 'gold standard' and doesn't worsen motor symptoms. Neutropenia risk 1%, not dose related, needs registration.
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Doses used in PD are much lower than those used in schizoprhenia. Avoid first generation antipsychotics, olanzapine and risperidone. Antipsychotic treatment has been associated with improved prognosis.
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Pimavanserin: 5HT-2A inverse agonist licensed in US for PDP but not in Europe. Dose 34mg/d in divided doses. Takes 2-4 weeks to work. Reduce dose with CYP3A4 inhibitors.
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Ondansetron: 5HT-3A antagonist (looks like pimavanserin), appears to reduce VH's and paranoid ideas but RCT's needed. Rivastigmine may be useful in patient with PDP with and without dementia.
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ECT has not been systematically tested but may reduce psychosis and improve motor symptoms. Cannabidiol is currently the subject of a UK phase 2 clinical trial for PDP.
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Source material and further reading: 1) https://doi.org/10.1038/nrneurol.2016.200 … 2) http://dx.doi.org/10.1136/pgmj.2004.032029 … 3)https://doi.org/10.1155/2017/3256542 …
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Thank you for taking the time to read this tweetorial. I hope it is helpful. Please feel free to correct any errors. If you have any suggestions how I might make these more useful eg for trainees/medical students please do let me know.
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