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Year : 2011  |  Volume : 14  |  Issue : 5  |  Page : 16-17
 

Psychosis in Parkinson's disease



Date of Web Publication21-Jul-2011

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PMID: 21847320

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How to cite this article:
. Psychosis in Parkinson's disease. Ann Indian Acad Neurol 2011;14, Suppl S1:16-7

How to cite this URL:
. Psychosis in Parkinson's disease. Ann Indian Acad Neurol [serial online] 2011 [cited 2019 May 24];14, Suppl S1:16-7. Available from: http://www.annalsofian.org/text.asp?2011/14/5/16/83090


Psychosis in Parkinson's disease (PD) appears in the later stages of the disease. It affects 5-8% of the treated patients, [1] more often as the disease advances. The clinical features include prominent visual hallucinations with clear sensorium and retained insight. The risk factors for the development of psychosis in PD are anti-PD medications (particularly, dopamine receptor agonists), duration of disease, older age, disease severity, sleep disturbance, cognitive impairment, dementia and/or depression.M

The pathophysiology of PD psychosis is now known to involve an interaction between extrinsic, drug-related and intrinsic, disease-related components. The most important extrinsic factor is use of dopaminergic medication, which plays a prominent role in PD psychosis. Intrinsic factors seen in PD patients with hallucination consist of duration of illness, old age, visual processing deficits such as lower visual acuity, difficulty in recognizing color and contrast, ocular pathology and functional brain abnormalities. Sleep disturbances are reported early and include fragmentation of sleep and vivid dreams. The intrinsic factors include altered neurochemicals (dopamine, serotonin, acetylcholine, etc.) and structural abnormalities involving Lewy body deposition in specific regions of brain. Genetic predisposition such as presence of apolipoprotein E epsilon 4 allele and tau H1H1 genotype may also play a role. Deep brain stimulation surgery resulted in reduction of anti-PD medication, but this failed to improve psychosis, thus leading to some insights to the intrinsic factors where reduction in anti-PD medications to the lowest tolerated dose did not improve psychosis. Initial manifestation of chronic dopaminergic medication may be sleep disturbances in the form of dreams, night terrors. Dreams are vivid, real, featuring people and events from past and nightmares, where the patient screams and thrashes. The patient is commonly unaware of these symptoms but disturbs the spouse or companion sharing the bed. Visual hallucinations in PD psychosis take form of people, friends and relatives from past. Solitary figures are seen repeatedly but do not speak. Animals running across floor appearing through closed window or door are seen. Inanimate objects grow legs and walk. Miniature people are seen. Ceiling and floors appear to be in motion. Often hallucinations are benign and nonthreatening. They occur in the evening hours and commonly are visual, rarely auditory, thus differentiating them from other causes such as schizophrenia. Paranoid delusions are common. Anticholinergic drugs produce toxic delirium, confusion, agitation, and are associated with tachycardia, unformed hallucination and lack a theme.

Other behavior manifestations in patients with PD include delusions, punding, hypersexuality, gambling, obsessive-compulsive disorders, euphoria, anxiety, anticholinergics - toxic confusional state.


   Treatment of Psychosis Top


Papapetropoulos et al. concluded that virtually all anti-Parkinsonian drugs are able to induce psychotic symptoms. [2] It is controversial that some of the dopaminergic drugs do have a higher potential to induce psychosis than others. In a study by Aarsland et al., the authors found no correlation at all between anti-Parkinsonian drugs (levodopa and dopamine agonist (DA)) and hallucinations. [3] Possible correlations between dopaminergic treatment with different drugs and the risk for PD patients to develop psychosis were analyzed. In randomized, double-blind trials investigating different DAs, the incidence of hallucinations was 8.1% for priribedil, 2.8% for bromocriptine, 4% for rotigotine, 5% for ropinirole, 7-9.3% for pramipexole, 4.8% for cabergoline, 3.4% for pergolide, and 0-4.4% for levodopa. All DAs are effective D2 agonists and, to a lower extent, D3 agonists. These drugs also have D4 receptor affinity which may play a role. Levodopa - the drug with the lowest risk for psychosis in the present investigation - has only low affinity to D4 receptors. Dopamine agonists with α2 receptor affinity, such as pergolide, may have higher incidence of psychosis. Cabergoline behaves as a strong antagonist at α2 receptors, whereas ropinirole and pramipexole are mostly inactive. Thus, the treatment of psychosis is focused on withdrawing the drugs which have higher incidence of inducing psychosis and less antiparkinsonian effect. Thus, the following order of withdrawing the offending drugs is suggested, that is tapering and stopping, if necessary, the drugs with the highest risk-to-benefit ratio first. Anticholinergics are stopped first, followed by selegiline, dopamine agonists, amantadine, and finally catechol-O-methyltransferase (COMT) inhibitors, which have no psychotomimetic action of their own. Finally, levodopa is reduced. If the hallucinations still persist on withdrawing the offending drugs and further reduction in dopaminergic drugs is not possible without hampering the mobility of the patient, then only addition of atypical antipychotic is considered.

Several atypical antipsychotic agents (i.e. clozapine, olanzapine) have been shown to be efficacious in reducing psychotic symptoms in PD; however, use of clozapine requires regular monitoring due to the side effects such as agranulocytosis, worsening of confusion, tachycardia, dizziness, sweating. Regular WBC monitoring every 2 weeks is required. Olanzepinein in smaller doses may help but also has the side effects such as worsening of confusion, somnolence, balance impairment, lipid abnormalities, weight gain, impaired sugar control in diabetics. Caution in warranted in glaucoma, prostatic hypertrophy, seizure disorder, hypovolemia and dehydration. This drug leads to motor worsening in higher doses. Ziprasidone and aripiprazole are proven to be efficacious in open-label trials and have shown limited efficacy. Quetiapine is a common first-line treatment for PD psychosis because of its tolerability, ease of use although it has failed to demonstrate its efficacy in double-blind trials. A common side effect in the elderly is sedation. Cholinesterase inhibitors may prove to be more beneficial than antipsychotics. Donepezil has not shown significant reductions in psychotic symptoms, perhaps due to methodological limitations. However, results from an open-label study and a double-blind, placebo-controlled trial involving PD patients with hallucinations support the efficacy of rivastigmine. Non-pharmacological interventions such as electroconvulsive therapy in isolated case reports have shown the potential to reduce psychotic symptoms and may be considered in cases involving concurrent depression and/or medication-refractory psychosis. Antidepressants (i.e. clomipramine and citalopram) may improve psychosis in some depressed patients.

 
   References Top

1.Freidman JH. Stewart Factor Atypical antipsychotics in the treatment of drug induced psychosis in Parkinsons disease. Mov Disord 2000;15:201-11.  Back to cited text no. 1
    
2.Papapetropoulos S, Mash DC. Psychotic symptoms in Parkinsons disease: From description to etiology. J Neurol 2005;252:753-64.  Back to cited text no. 2
    
3.Aarsland D, Bronnick K, Ehrt U, De Deyn PP, Tekin S, Emre M, et al. Neuropsychiatric symptoms in patients with Parkinsons disease and dementia: Frequency, profile and associated care giver stress. J Neurol Neurosurg Psychiatry 2007;78:36-42.  Back to cited text no. 3
    




 

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