Complex visual hallucinations and hallucinosis occurs frequently (5-40%) in patients with Parkinson’s disease, especially after many years of treatment with dopaminergic drugs. Duration and severity of the disease, the presence of depression, sleep problems and cognitive decline are predisposing factors.
Visual hallucination (frequently blurry) arrive with the open eyes, are usually brief (few seconds) and move for short periods. They consists of object but more often of animals or people, unknown or known by the patient. Sometimes, the hallucination is a dead relative. Many patient try to interact with the hallucinations although most of them appear to know that it is just an illusion. Thus, insight is variably impaired. The semiology is quite similar to hallucinations, which occur with the Charles-Bonnet Syndrome (hallucinosis or visual hallucinations in patients with blindness or severe reduction of visual acuity).
Antiparkinsonian agents (especially dopamine-agonists), are probably the most powerful trigger factor in patients with Parkinson. Several mechanisms should interact with dopaminergic stimulation for the occurrence of hallucinations.
These mechanisms are related to the excitability or to release phenomena in higher visual center (secondary visual associative areas), to defective central or peripheral visual processing and to brainstem modulation of thalamocortical projections. Lewy body deposits in Parkinson’s disease and Lewy Body Disease are prominent in brainstem and primary and secondary visual areas.
However, the phenomenon is quite complex and still mysterious as sensory, cognitive, emotional, attentional factors intervene together with default of reality-checking processes.
Dopaminergic drugs should be carefully assessed to reduce hallucinations. Comorbidities should be treated. Atypical neuroleptics (Clozapine more than Quetiapine) and Rivastigmine are drugs that could be helpful. The effects of behavioral and cognitive interventions have not been adequately studied.
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