Cognitive Function In Parkinson's Disease Research Articles

Correlation of Sleep Disturbance and Cognitive Impairment in Patients with Parkinson’s Disease

ObjectiveCognitive impairment is a common nonmotor symptom of Parkinson’s disease (PD) and is associated with high mortality, caregiver distress, and nursing home placement. The risk factors for cognitive decline in PD patients include advanced age, longer disease duration, rapid eye movement sleep behavior disorder, hallucinations, excessive daytime sleepiness, and nontremor symptoms including bradykinesia, rigidity, postural instability, and gait disturbance. We conducted a cross-sectional study to determine which types of sleep disturbances are related to cognitive function in PD patients.MethodsA total of 71 PD patients (29 males, mean age 66.46 ± 8.87 years) were recruited. All patients underwent the Mini- Mental State Examination (MMSE) and the Korean Version of the Montreal Cognitive Assessments (MoCA-K) to assess global cognitive function. Sleep disorders were evaluated with the Stanford Sleepiness Scale, Epworth Sleepiness Scale, Insomnia Severity Index (ISI), Pittsburg Sleep Quality Index, and Parkinson’s Disease Sleep Scale in Korea (PDSS).ResultsThe ISI was correlated with the MMSE, and total PDSS scores were correlated with the MMSE and the MoCA-K. In each item of the PDSS, nocturnal restlessness, vivid dreams, hallucinations, and nocturnal motor symptoms were positively correlated with the MMSE, and nocturnal restlessness and vivid dreams were significantly related to the MoCA-K. Vivid dreams and nocturnal restlessness are considered the most powerful correlation factors with global cognitive function, because they commonly had significant correlation to cognition assessed with both the MMSE and the MoCA-K.ConclusionsWe found a correlation between global cognitive function and sleep disturbances, including vivid dreams and nocturnal restlessness, in PD patients.

Structural Changes on the Brain MRI and Cognitive Function in Parkinson Disease

Purpose: Cognitive impairment in Parkinson disease (PD) related with the fronto-striatal dysfunction as one cause of subcortical dementia. However, cognitive impairment in PD might be associated with medial temporal lobe atrophy in recent studies. We carried out this study to know whether structural changes on brain MRI are responsible for cognitive dysfunction in PD. Materials and Methods: We recruited 183 patients who were newly diagnosed with PD from January, 2007 to February, 2012. All patients were undertaken brain MRI and neuropsychological assessment. Structural changes of the brain images were evaluated with visual rating scales. We analyzed clinical and neuro-imaging data to assess a relation between cognitive function and brain structural changes in the total patients and did subanalysis with PD-cognitively declined (PD-CD) and PD-cognitively preserved (PD-CP) subgroup. Results: Total scores of the MMSE and 3MS was worsened as havingsevere white matter change (WMC), ventricular enlargement (VE), medial temporal lobe atrophy (MTA), and cortical atrophy in PD patients. PD-CD showed more severe WMC, VE and MTA than those in PD-CP patients even after adjustment of age and durations of education. Degree of the MTA among the brain structural changes was the most relevant factor for cognitive dysfunction in PD patients. Conclusions: Although cognitive dysfunction in PD is suggestive of subcortical origin, medial temporal structure also may have an important role for cognition in PD. Therefore, clinicians need thorough evaluation of the structural changes in the brain MRI as well as neuropsychological assessment to define cognitive function in PD. Keywords: Parkinson disease, dementia, cognitive function, brain magnetic resonance imaging, atrophy. Read more →

Neuropsychological outcomes after psychosocial intervention for depression in Parkinson's disease.

The authors describe neuropsychological outcomes in people with Parkinson's disease (PD) after their participation in an NIH-sponsored, randomized, controlled trial of cognitive-behavioral treatment for depression. Improvements in mood were associated with modest gains in verbal memory and executive functioning over the 10-week treatment period and accounted for greater variance in neuropsychological outcomes at the end of treatment than other known correlates of cognitive functioning in PD, such as disease severity, age, and education. Baseline working memory and executive skills were also associated with depression improvement over time.

Validation of the Italian version of Parkinson’s Disease-Cognitive Rating Scale (PD-CRS)

Cognitive impairment (CI) is a frequent feature associated with both early and advanced stages of Parkinson's disease (PD). An evaluation of cognitive functions is relevant to identify those parkinsonians at risk of developing dementia. In the present study, the Italian version of Parkinson's Disease-Cognitive Rating Scale (PD-CRS) assessing fronto-subcortical and cortical cognitive functions in PD was validated in 387 parkinsonians and was used to test the empirical validity of the item 1.1 (cognitive impairment) of the Italian version of MDS-UPDRS as screening tool for CI in PD. PD-CRS was free from floor and ceiling effect. The mean PD-CRS score was 76.1 (mean cortical score, 24.5±4.6; mean subcortical score, 51.5±17.5). The internal consistency was satisfactory (α=0.89); corrected item-total correlation was 0.570 (naming) to 0.696 (working memory). The correlation between PD-CRS and part I-IV of MDS-UPDRS was weak. The low agreement between classification of PD sample into patients with mild cognitive impairment (PD-MCI), dementia (PD-D) and normal cognition (PD-NC) according to scores of item 1.1 and classification according to cutoff scores of PD-CRS for PD-MCI, PD-D and PD-NC indicated a poor empirical validity of item 1.1 of MDS-UPDRS as cognitive screening tool for CI in PD (Κ=0.114; weighted Κ=0.17; SE of Κ=0.038; 95% confidence interval from 0.040 to 0.1895). The Italian version of PD-CRS is an easy, consistent and valid tool for assessment of the cognitive cortical and subcortical impairments in PD.

Neuropsychiatric Symptoms as a Putative Crescendo Warning of a Striatocapsular Infarct?

Neuropsychiatric Symptoms as a Putative Crescendo Warning of a Striatocapsular Infarct?

Neuropsychiatry of Parkinson's Disease

Parkinson's disease (PD) is traditionally regarded as a motor or a movement disorder. In recent years, however, an increased interest has been directed to its nonmotor symptoms as they seem to determine significant disability at all stages of the disease. Some PD patients consider their nonmotor symptoms even more disabling than motor signs. Among these nonmotor symptoms, neuropsychiatric syndromes (or behavioral and psychological symptoms) are of paramount importance. They include a wide array of syndromes such as anxiety, depression, psychosis, impulse control disorders, apathy, and cognitive dysfunction. Their pathogenesis in PD is rather complex, involving neurodegenerative, drug-related, and psychological mechanisms. Their recognition and management represent a great challenge. The paper by R. de la Fuente-Fernandez presents a staging model named PD-related frontostriatal cognitive dysfunction (PDFCD) that provides a clinical and hypothesis-testing framework for neuropsychiatric syndromes in PD. De La Fuente-Fernandez's PDFCD model proposes three stages based on the sequential process of dopamine depletion occurring in different regions of the striatum (stages I and II) and the frontal cortex (stage III). Therefore, PD patients would present executive dysfunction and mental fatigue (stage I), depression/anxiety (stage IIa), apathy/pain (stage IIb), and dementia (stage III). The paper by J. Calleo et al. summarizes the current literature on the cognitive rehabilitation programs in PD patients. Despite limited available data and heterogeneity of motor and nonmotor symptoms in PD, cognitive rehabilitation seems to be promising in this context. The paper by Y. Bogdanova and A. Cronin-Golomb1 presents an original study that assessed cognitive correlates of anxiety and apathy in PD patients. In comparison with matched controls, PD patients exhibited higher levels of anxiety and apathy which were correlated with disease duration. Interestingly, anxiety and apathy correlated differently with cognitive functions. The question remains open whether the treatment of both conditions impacts on cognitive functioning in PD. Until recently, most studies have focused on the impact of motor disability and depressive symptoms on the quality of life of PD patients, neglecting the role of anxiety. The paper by K. K. Hanna and A. Cronin-Golomb addressed this issue, reporting that anxiety, more than depressive, cognitive, and motor symptoms, significantly affected quality of life in PD. Dopaminergic strategies remain the mainstay of PD treatment. However, they are frequently associated with neuropsychiatric syndromes, notably psychosis. Alternative therapeutic options have been searched in the last years, and adenosine A2A receptor antagonists seem to be very promising. The paper by C. J. Bleickardt et al. demonstrates that, in comparison with dopamine receptor agonists, adenosine A2A antagonists exhibit better neuropsychiatric profiles as they do not interfere with prepulse inhibition in rodents (a model of psychosis). The paper by E. C. Lauterbach et al. presents a comprehensive review of the neuroprotective effects of the psychotropic drugs used in PD. Antonio L. Teixeira Leonardo F. Fontenelle Edward C. Lauterbach Sergio Starkstein

Neuropsychological correlates of mild to severe hallucinations in Parkinson's disease

The development of visual hallucinations (VH) is a frequent complication of Parkinson's disease (PD). Presence of hallucinations is one of the main risk factors associated with dementia, and severity progression of VH mainly contributes to impaired quality of life in PD. The neuropsychological features associated with severity progression of VH are unknown and might help to detect patients at risk of a more severe outcome. We aimed to explore the neuropsychological deficits associated with the different types of VH observed in PD, from minor hallucinations to well-formed VH with loss of insight. Prospective study of 57 PD patients with (n = 29) and without VH (n = 28) matched for age, education, antiparkinsonian medications, and disease duration. Description of VH was assessed by the Hallucinations and Psychosis item of the MDS-UPDRS. Cognition was assessed with the Parkinson's Disease-Cognitive Rating Scale (PD-CRS) and the Mattis Dementia Rating Scale (MDRS). Patients with minor VH did not differ from patients without VH in any cognitive domain. PD patients with major VH and insight retained performed worse on the action verbal fluency task (P < 0.04), and patients with VH and loss of insight showed a greater impairment on the PD-CRS posterior cortical score (P = 0.021) and the clock copying item (P = 0.01). A double dissociation was found in the neuropsychological profile of patients with VH with and without loss of insight. While the presence of major VH with insight retained appeared related to a predominant frontal-striatal impairment, loss of insight was characterized by further impairment of cognitive functions related to posterior cortical areas. A comprehensible continuum pattern of clinical relationships emerged among VH and cognitive functioning in PD.

The relationship between depression and regional cerebral blood flow in Parkinson’s disease and the effect of selegiline treatment

We examined the relationship between severity of depression in Parkinson's disease (PD) and regional cerebral blood flow (rCBF) using single photon emission computed tomography (SPECT) and the reaction to levodopa-selegiline combination therapy. We evaluated 52 patients with PD and nine age-matched controls with SPECT and the Unified Parkinson's Disease Rating Scale (UPDRS) part III, Mini-Mental State Examination (MMSE), and Beck Depression Inventory (BDI) to evaluate depression severity and its connection with rCBF. Furthermore, we examined rCBF in patients with PD treated with levodopa with or without selegiline. A significant fall in rCBF was observed in the bilateral posterior cingulate, hippocampus, and cuneus and the superior parietal and primary visual areas in PD patients with minor depression and in all regions in those with major depression. Elevations in UPDRS part III and BDI scores and falls in MMSE scores were of significantly lower magnitude in the levodopa-selegiline group than in the levodopa group. Whole brain rCBF fell significantly less in the levodopa-selegiline group than in the levodopa group. These results indicate that selegiline controlled not only worsening of motor function and cognitive function in PD but also aggravation of minor depression, and restrained a fall in whole brain rCBF.

Relationship between changes of body mass index and cognitive decline in Parkinson's disease

Although the relation between body mass index (BMI) changes and risk of dementia is not always associated linearly, decreased BMI has been reported that it may be associated with increased risk of cognitive decline in the elderly. Weight loss is very common in patients with Parkinson's disease (PD) because of changes in appetite due to medication or chewing and swallowing difficulty related with muscular rigidity or higher energy expenditure due to involuntary movement. However, studies comparing BMI changes with cognitive function in PD have not been done yet. We performed this study to evaluate association between BMI changes and rate of cognitive decline and to know whether co-morbid conditions occur more frequently in BMI reduction group of PD. PD patients who measured their height and weight to calculate BMI and evaluated cognitive function regularly at the movement clinic of CNUH were recruited retrospectively. The patients (n = 78) were divided into two groups according to BMI changes during initial 6 months: decreased vs. stable BMI groups. Cognitive functions were evaluated by the Korean versions of Mini-Mental State Examination (MMSE) and the modified Mini-Mental State (3MS) test. Clinical examination, MMSE and 3MS were done at 6-, 12-, 24- and 36-month of follow-up. The rate of cognitive decline (MMSE and 3MS score changes/months) was compared in both groups from the baseline to each follow up. The co-morbid conditions such as pneumonia or bone fracture were evaluated through detailed chart review. The decreased BMI group showed more rapid decline of cognitive function than that of stable BMI group in PD. The rate of cognitive decline measured by both MMSE and 3MS tests was significantly faster especially at the 24- and 36- month of the follow-ups compared with the initial 1-year period of the follow-up in the decreased BMI group. No significant difference in the frequency of co-morbid diseases was found between the two groups. This study suggests that decreased BMI might be a useful indicator for future risk of dementia and let clinicians predict faster rate of cognitive decline in patients with PD.

Acute Bouts of Passive Leg Cycling Can Improve Cognitive Function in Parkinson's Patients

Parkinson's disease (PD) often leads to a deficit in cognitive function. Pharmacological therapies are effective in treating motor symptoms in PD, but do not slow the progression of cognitive decline. A number of studies have reported that intensive exercise can improve cognitive function. However, individuals with PD often have difficulties participating in high-intensity exercise. PURPOSE: The purpose of this study is to determine if acute bouts of passive leg cycling can improve cognitive function in PD, and if different rates of pedaling have variable effects on cognitive function. METHODS: Nineteen, mild to moderate idiopathic PD patients (12 men, 7 women, age- 63.2 ± 8.6), reported to the exercise science laboratory on four separate occasions, separated by one week. On the first visit, PD patients completed a YMCA cycling test (Excalibur 1300 W cycle ergometer) to estimate maximal oxygen consumption and a computer based psychomotor tests consisting of Trail Making Test (TMT) A and B while 'on' anti-Parkinson's medication. For the next three visits PD patients participated in passive leg cycling (MOTOmed viva2) at 60, 70 and 80 revolutions per minute (rpm) while 'off' anti-Parkinson's medications. Cycling rates were randomly administered. The TMT A and B were administered prior to and immediately after each cycling session. RESULTS: Data were analyzed using a 3 (trial) by 2 (time) analysis of variance (ANOVA) with repeated measures on both variables. TMT A scores did not differ between trials (p=0.569) or across time (p=0.207). In addition, no trial by time interaction was observed for TMT A Scores (p=0.555). TMT B scores improved across time (70.3 ± 3.7 vs. 62.4 ± 2.6 sec, p=0.003) with no difference between trials (p=0.919) or trial by time interactions observed (p=0.841). The difference in scores between TMT B and A showed a main effect of time (pre: 37.6 ± 2.6, post: 31.0 ± 1.9 sec, p=0.006). CONCLUSION: These data suggest that passive leg cycling can improve executive function in PD patients, as measured by the TMT B. Lack of improvement in the TMT A suggests that TMT B improvement is due to changes in visual search and motor speed alone. However, there is no association between cognitive improvement and passive cycling rate. Future studies will compare these results with active-assisted cycling at variable rates.

Cerebrospinal tau, phospho‐tau, and beta‐amyloid and neuropsychological functions in Parkinson's disease

Alzheimer's disease (AD)-pathology may play a role in Parkinson's disease (PD)-related dementia (PDD). The aim of this study was to assess cerebrospinal fluid (CSF) levels of tau, phospho-tau, and beta-amyloid, proposed AD biomarkers, and their relationship with cognitive function in PD. Forty PD patients [20 nondemented (PDND); 20 PDD] and 30 controls underwent CSF tau, phospho-tau, and beta-amyloid analysis using specific ELISA techniques. All PD patients and 15 controls underwent neuropsychological testing of fronto-subcortical (attention, fluency) and neocortical (memory, naming, visuoperceptive) functions. CSF markers levels were compared between groups, and compared and correlated with neuropsychological measures in PDND and PDD separately and as a continuum (PD). CSF tau and phospho-tau were higher in PDD than in PDND and controls (P < 0.05). CSF beta-amyloid ranged from high (controls) to intermediate (PDND) and low (PDD) levels (P < 0.001). In all PD and PDD patients, high CSF tau and phospho-tau were associated with impaired memory and naming. In PDND, CSF beta-amyloid was related with phonetic fluency. These findings suggest underlying AD-pathology in PDD in association with cortical cognitive dysfunction, and that low CSF beta-amyloid in PDND patients with impaired phonetic fluency can constitute an early marker of cognitive dysfunction.

Deep brain stimulation does not affect cognitive functions in Parkinson disease

Deep brain stimulation does not affect cognitive functions in Parkinson disease

Pre- and post-synaptic dopamine imaging and its relation with frontostriatal cognitive function in Parkinson disease: PET studies with [ 11C]NNC 112 and [ 18F]FDOPA

Frontostriatal cognitive dysfunction is common in Parkinson disease (PD), but the explanation for its heterogeneous expressions remains unclear. This study examined the dopamine system within the frontostriatal circuitry with positron emission tomography (PET) to investigate pre- and post-synaptic dopamine function in relation to the executive processes in PD. Fifteen non-demented PD patients and 14 healthy controls underwent [ 18F]FDOPA (for dopamine synthesis) and [ 11C]NNC 112 (for D 1 receptors) PET scans and cognitive testing. Parametric images of [ 18F]FDOPA uptake ( K i) and [ 11C]NNC 112 binding potential (BP ND) were calculated using reference tissue models. Group differences in K i and BP ND were assessed with both volume of interest and statistical parametric mapping, and were correlated with cognitive tests. Measurement of [ 18F]FDOPA uptake in cerebral cortex was questionable because of higher K i values in white than adjacent gray matter. These paradoxical results were likely to be caused by violations of the reference tissue model assumption rendering interpretation of cortical [ 18F]FDOPA uptake in PD difficult. We found no regional differences in D 1 receptor density between controls and PD, and no overall differences in frontostriatal performance. Although D 1 receptor density did not relate to frontostriatal cognition, K i decreases in the putamen predicted performance on the Wisconsin Card Sorting Test in PD only. These results suggest that striatal dopamine denervation may contribute to some frontostriatal cognitive impairment in moderate stage PD.

Smoking and cognitive function in Parkinson's disease

The risk of dementia among Parkinson's disease (PD) patients is greatly elevated compared to controls, yet little is known about determinants of cognitive function among PD patients. We assessed the relation between cigarette smoking prior to disease onset and later cognitive function among PD patients (n = 286) and age- and sex-matched controls (n = 1144) participating in the Nurses' Health Study and Health Professionals Follow-up Study. Both groups completed telephone-administered assessments of cognitive function. We used linear regression to calculate mean differences in cognitive test scores across smoking categories, adjusted for age, education, sex, age at onset of PD, and years since diagnosis. PD patients scored significantly worse on all tests than their matched controls. In analyses only among PD cases, but not among controls, current smokers at PD onset scored worse than never smokers on the Telephone Interview for Cognitive Status (difference = -0.82, 95% CI: -1.33, -0.30, P = 0.002) as well as on a global score combining results of all tests (difference = -0.36, 95% CI: -0.72, 0.01, P = 0.06). This difference was equivalent to the difference in global score observed among controls approximately 10 years apart in age. Analyses of pack-years of smoking prior to disease onset gave similar results. These findings, nested in prospective cohort studies, suggest that cigarette smoking prior to disease onset is associated with worse cognitive function in PD.

Metabolic brain networks associated with cognitive function in Parkinson's disease

The motor manifestations of Parkinson's disease (PD) have been linked to an abnormal spatial covariance pattern involving basal ganglia thalamocortical pathways. By contrast, little is known about the functional networks that underlie cognitive dysfunction in this disorder. To identify such patterns, we studied 15 non-demented PD patients using FDG PET and a voxel-based network modeling approach. We detected a significant covariance pattern that correlated ( p < 0.01) with performance on tests of memory and executive functioning. This PD-related cognitive pattern (PDCP) was characterized by metabolic reductions in frontal and parietal association areas and relative increases in the cerebellar vermis and dentate nuclei. To validate this pattern, we analyzed data from 32 subsequent PD patients of similar age, disease duration and severity. Prospective measurements of PDCP activity predicted memory performance ( p < 0.005), visuospatial function ( p < 0.01), and perceptual motor speed ( p < 0.005) in this validation sample. PDCP scores additionally exhibited an excellent degree of test–retest reliability (intraclass correlation coefficient, ICC = 0.89) in patients undergoing repeat FDG PET at an 8-week interval. Unlike the PD-related motor pattern, PDCP expression was not significantly altered by antiparkinsonian treatment with either intravenous levodopa or deep brain stimulation (DBS). These findings substantiate the PDCP as a reproducible imaging marker of cognitive function in PD. Because PDCP expression is not altered by routine antiparkinsonian treatment, this measure of network activity may prove useful in clinical trials targeting the progression of non-motor manifestations of this disorder.

Plasma testosterone levels in Alzheimer and Parkinson diseases

Testosterone deficiency, a treatable condition commonly seen in aging men, has been linked to Parkinson disease (PD) and Alzheimer disease (AD). In normal subjects, low testosterone levels are associated with cognitive and neuropsychiatric symptoms, yet the relationship between testosterone levels and cognitive function in PD and AD remains unclear. To examine the relationship of testosterone levels to age and cognitive function in PD and AD. Plasma testosterone levels were determined in men enrolled in a clinical registry of subjects with PD and AD, and neuropsychological testing was performed on subjects who consented. Testosterone levels in men with PD were compared with those in men with AD. In both groups, the relationship between testosterone levels and neuropsychological test scores was analyzed, adjusting for age and education. Linear regression analysis revealed that testosterone levels decreased with age in male PD patients (p < 0.03) and male AD patients (p < 0.07). The rate of decline was similar for the two groups. In PD patients, lower testosterone levels were associated with poorer performance on Trails B Seconds (p < 0.02). There is a similar age-related decline in plasma testosterone levels in men with either PD or AD. Previously described associations between low testosterone levels and frontal lobe dysfunction in normal aged men, together with these results, suggest that the hormonal deficiency may act as a "second hit" to impair cognitive function in neurodegenerative disease.

Effects of bilateral subthalamic stimulation on cognitive function in Parkinson disease.

Chronic bilateral subthalamic deep brain stimulation (STN-DBS) is known to improve motor function in patients with Parkinson disease (PD). However, the possible effects of STN-DBS on neuropsychological functions have been studied less. To investigate the effects of STN-DBS on neuropsychological functions in PD. Before-after trial. Fifteen consecutive patients were assessed before and 3 months after implantation of stimulators for STN-DBS (postsurgical assessment with the stimulators switched on). Both assessments were performed with patients in a drug-free condition. The neuropsychological battery consisted of tests measuring memory and visuospatial and frontal functions. The comparison between presurgical and postsurgical performance showed a moderate deterioration in verbal memory and prefrontal and visuospatial functions, and a moderate improvement in a prefrontal task and obsessive-compulsive traits. The motor state improved in all patients. Therapy with STN-DBS improves motor symptoms in PD without any clinically relevant neuropsychological deterioration.

Validity of the Dementia Rating Scale in assessing cognitive function in Parkinson's disease.

Two studies examined the validity of the Dementia Rating Scale (DRS) as a measure of cognitive functioning among patients with Parkinson's disease (PD). The DRS accounted for more variation in the level of cognitive functioning of PD patients than either the Mini-Mental Status Examination or a battery of tests selected to assess specific cognitive deficits associated with PD. Further, DRS subtests displayed strong convergent and discriminant validity with a comprehensive Criterion Neuropsychology Battery. The DRS subtests appear to be valid measures of attention, perseveration, conceptualization, and memory among PD patients. However, the DRS-Construction subtest should be supplemented with additional visuoconstructional items to provide a thorough screen of cognitive functioning in PD. Although about three-quarters of nondemented PD patients did not appear to have any specific cognitive deficits on the DRS, the remaining patients were impaired on the Construction or Initiation/Perseveration subtests of the DRS. In summary, the DRS is a valid mental status screening test of cognitive functioning for individuals with PD.

Parkinson's disease, cognition and aging Clinical, neuropsychological, electrophysiological and cranial computerized tomographic assessment

Forty-three patients with Parkinson's disease (PD) and thirty-seven normal volunteers were subjected to clinical, neuropsychological, neurophysiological (P300 component of the event-related potentials ERP) and radiological (cranial computerized tomographic scanning CCT) evaluation. Intentional memory was more impaired in PD than in normal controls, more so in the demented group of patients, and was related to enlargement of third ventricular size in CCT. While intentional memory was age related in PD patients, perception was age-related in normal controls. Neither global nor specific cognitive functions were related to duration, severity of parkinsonian motor disability, or depression. However, depression in PD was significantly related to parkinsonian motor disability. P300 latency was more prolonged in PD patients than normal controls. P300 parameters of PD patients were not influenced by age, cognitive functions, duration or severity of motor disability, or depression. The reaction time was the only P300 parameter that was age-related in normal controls. Subcortical atrophy as indicated by CCT was more marked in PD and correlated with age in both patients and controls. Subcortical atrophy was significantly related to cognitive functions in PD but not in normal controls. It was concluded that cognitive impairment in PD could be attributed to complex cognitive changes rather than age. It is a disease process, though not directly related to parkinsonian motor disability or depression. PD differed from normal aging as regards the effect of age on the specific cognitive functions, where in PD patients, age was related to intentional memory, yet in normal controls, it was related to perception. Intentional memory deterioration was found to be specific of PD, being related to subcortical atrophy as well as being more pronounced in the demented group of patients.

Evaluation of Influential Factors of Cognitive Impairments in Idiopathic Parkinson’s Disease

Using multivariate analysis, we investigated the influence on cognitive functions of aging, brain atrophy, incidental cerebral hyperintensities (CHs), medication, and severity, duration and the initial symptoms of the disease in 53 patients with idiopathic Parkinson's disease (PD). We semiquantitatively assessed the degree of brain atrophy and CHs based on previously established methods. Cognitive functions were significantly and diffusely impaired in PD when compared with controls who were matched for age as well as for the degree and location of CHs. Patients with PD, however, had larger ventricles. Prefrontal dysfunctions were associated with a variety of predictors such as CHs, brain atrophy, severity of PD and medication whereas dorsolateral frontal functions were related simply to age and CHs in the periventricular region. Posterior brain functions had association with severity of illness, ventricular dilatation and total CH score. Clinically observed cognitive impairments in PD may consist of cognitive defects intrinsic to the disease which are variously modified by these factors. It is essential to consider all these predictors simultaneously in any discussion of cognitive functions in PD.