Because of its relatively mild extrapyramidal side effect profile and the lack of a monitoring requirement, quetiapine is a common first choice in treating PD psychosis

Because of its relatively mild extrapyramidal side effect profile and the lack of a monitoring requirement, quetiapine is a common first choice in treating PD psychosis. Cost About $160 for 25 mg (60 tablets), $290 for 100 mg (60 tablets), $538 for 200 mg (60 tablets). Risperidone Standard dosage 1 to 3 mg/d. Contraindications Use with caution in elderly patients and those with seizure history, cardiovascular disease, dementia, diabetes mellitus, hepatic impairment, or suicide risk. Main drug interactions Avoid with triptorelin, haloperidol, sodium oxybate, or ziprasidone. Main side effects Extrapyramidal symptoms, including neuroleptic malignant-like syndrome and tardive syndromes, hyperprolactinemia, gastrointestinal hypomotility, weight gain, diabetes mellitus or hyperglycemia. treatment strategies in PD psychosis. Introduction Psychotic symptoms have long been recognized as possible side effects of dopaminergic medication for the treatment of the motor features of Parkinsons disease (PD), but more recently they have been linked to processes inherent in the disease itself [1?]. Approximately 20% to 40% of PD patients will develop psychosis [2], and management presents a unique clinical challenge, as many antipsychotic brokers are known to induce parkinsonism in individuals without PD and to exacerbate parkinsonism in many PD patients. Thus, management must be considered within the context of an individual patients unique profile of motor and nonmotor symptoms. In PD, psychotic features typically arise late in the disease course (10 or more years after initial diagnosis) and usually present first in the context of a obvious sensorium and retained Lox insight [3]. PD psychosis most commonly takes para-iodoHoechst 33258 the form of visual hallucinations and minor sensory disturbances such as illusions or passage and sense of presence hallucinations, but it also para-iodoHoechst 33258 may be characterized by paranoid delusions. Symptoms tend to recur and worsen over time, and insight is usually ultimately lost. Indeed, psychosis can be prognostic of cognitive decline in PD [4]. Some experts previously conceptualized a continuum of PD psychosis marked first by minor experiences such as vivid dreaming and misperceptions, followed by more frank hallucinations and delusions, and ultimately florid psychosis and dementia [5]. However, more recent evidence does not support such a chronology [6]. Despite our lack of a clear understanding of its natural course, we know that psychotic features in PD, once present, are persistent and distressing. Psychosis in PD has been independently linked with unfavorable end result variables such as caregiver distress, nursing home placement, and mortality [7,8]. Use of dopaminergic medication was the first risk factor considered to be implicated in the development of PD psychosis, and many authors have indicated that dopamine agonists put patients at higher risk than levodopa [9]. However, there are reports of hallucinations in PD patients prior to the introduction of levodopa [10], and it is now generally accepted that dopaminergic medications are neither necessary nor sufficient to account for psychosis. Indeed, there is no obvious relationship between medication dosage and occurrence or severity of psychosis in PD, and nondopaminergic brokers such as anticholinergics and amantadine have also been linked with psychotic symptoms [1?]. Thus, it is likely that intrinsic processes combined with iatrogenic variables produce psychotic symptoms. Important areas of contemporary research around the complex pathophysiology of PD psychosis include visual para-iodoHoechst 33258 processing abnormalities, sleep dysfunction, and specific neurochemical changes (involving, for example, dopamine, serotonin, and acetylcholine [ACh]). The most appropriate first-line treatment for PD psychosis entails simplification of the patients anti-PD medication regimen. However, if distressing symptoms persist despite reduction of PD medications to the lowest tolerable dosages, addition of a pharmacologic agent should be considered. Choice of an atypical antipsychotic (AA) is based largely on each drugs unique side effect profile. Currently, clozapine and quetiapine are the most commonly used AAs. Fueled in part by the black box warning issued by the US Food and Drug Administration (FDA) regarding higher mortality risk with AAs in elderly patients with dementia, recent clinical studies have turned to alternate agents for the treatment of PD psychosis, including cholinesterase inhibitors (eg, rivastigmine) and memantine. para-iodoHoechst 33258 Because antipsychotic medications can worsen motor functioning and psychotic symptoms tend to persist in PD despite aggressive pharmacologic treatment, behavioral intervention represents an important, albeit understudied, strategy for optimizing psychosis management. Although most studies of cognitive behavioral therapy for psychosis have been conducted in the schizophrenia populace, PD patients have been reported to benefit from self-driven coping strategies to manage psychotic symptoms. Thus, structured psychological interventions may be a valid avenue for new research. Treatment Pharmacologic treatment Drug therapy for the treatment of PD psychosis aims to reduce the frequency and severity of psychotic symptoms with minimal worsening of PD motor symptoms. Early treatment with antipsychotic medications may also reduce the risk of later deterioration to psychosis.