Abstract
Objectives: We investigated the role of stage of disease, motor status and dopaminergic treatment in cognitive impairment of Parkinson’s disease (PD) patients with visual hallucination (VH) and the presence of specific cognitive impairment patterns.
Method: We compared 33 PD patients with VH ( group 1 ) with 30 PD patients without VH (group 2) with regard to demographic characteristics and neuropsychological test scores.
Results: The group with VH demonstrated significantly worse Short Test of Mental Status scores; the cognitive impairment pattern presented in the form of frontal dysfunction and memory deterioration. There were significant differences in Stroop duration/error, verbal fluency, Wechsler Memory Scale and Sozel Bellek Surecleri Test (a Turkish verbal learning test) scores.
Conclusion: In PD patients with VH the main pattern of cognitive impairment is frontal dysfunction and memory deterioration. Because visual perceptive functions were not different between the two groups, such deterioration may not be a primary factor in the development of VH.
1. Introduction
Visual hallucinations ( VH ) may occur in up to 33% of patients undergoing long-term treatment for Parkinson’s disease (PD).1–3 Although VH had been reported in PD before the dopamine era,4,5 they were commonly reported as a side-effect of antiparkinsonian treatment.6,7 Goetz et al. reported in a prospective longitudinal study that the prevalence of VH reached 63% at the end of 48 months. The hallucinations in PD are a risk-factor for permanent nursing home placement with associated high mortality rate and control of hallucinations may be warranted.
However, the pathogenesis and pathophysiology of VH are not yet entirely understood. The effects of exogenous dopaminergic agents on the mesolimbic system have been implicated as the primary cause; however, recent data suggest that other factors such as stage and duration of disease, cognitive status and age, history of depression and sleep-wake cycle disturbances may contribute. Visual dysfunction may contribute to the development of VH.
While cognitive deterioration is one of the most common risk factors for the development of VH in PD, there is insufficient information on this cognitive impairment pattern. Understanding of the cognitive impairment patterns may aid in understanding of the nature of the VH.
This study aims to determine the role of duration of disease and stage, motor status and dopaminergic treatment on cognitive impairment of patients with VH and whether PD patients with VH present a specific cognitive impairment pattern.
2. Materials and methods
2.1. Subjects
After local ethics committee approval of the study, a total 63 PD patients were enrolled. Thirty-three of these with VH (group 1) were recruited consecutively from our out-patient clinic. These patients had experienced several episodes of definite VH in the past 3 months. VH were classified according to the Unified Parkinson’s disease rating scale (UPDRS) (0: none, 1: vivid dreams, 2: hallucinations with retained insight, 3: frequent hallucinations without retained insight, 4: psychotic process). The patients
with 2 and 3 points were assessed as the group with VH (n = 33) (group 1). A total of 30 patients with PD but without a history of VH were selected for the control group with similar demographic variables (group 2). Patients were evaluated while in the ‘on’ state but without hallucinations.
All patients were examined by a specialist in movement disorders and were diagnosed as PD according to the United Kingdom Parkinson’s Disease Society Brain Bank criteria.
Patients with dementia were not recruited into the study. Dementia was diagnosed according to the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) criteria. The use of DSM-IV criteria for dementia in patients with PD may be difficult, so not only patients with certain dementia, but also ones with suspected dementia and diffuse Lewy body disease were excluded.
Patients with pyramidal signs, cerebellar signs, clear gaze palsy or autonomic dysfunction or who had head trauma, encephalitis, cerebrovascular attacks or exposure to toxic agents were not included the study.
All patients were assessed according to clinical features, UPDRS total, motor and mental subscores and Hoehn-Yahr stages. They were also assessed according to dosage and duration of levodopa treatment.
Antiparkinsonian treatments were recorded and the total daily dose of levodopa was calculated for each patient.
For dopaminergic agonists we calculated the equivalent levodopa dosage as follows: 10 mg bromocriptine = 1 mg lisuride = 1 mg pergolide = 100 mg levodopa (with a dopa-decarboxylase inhibitor).
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02 22nd, 2008| 