Ji-Yeon Yoo

Influence of white matter hyperintensities on the cognition of patients with Parkinson disease.

BackgroundWhite matter hyperintensities (WMH) have been associated with cognitive impairment in elderly persons and in patients with Alzheimer disease. However, the role of WMH in Parkinson disease (PD) dementia remains to be elucidated. MethodsThe cohort for this study comprised 71 consecutive patients with PD, all of whom completed a clinical assessment, neuropsychologic investigation, and magnetic resonance imaging of brain. WMH were rated using the semiquantitative visual rating system proposed by Scheltens et al. ResultsThe PD dementia group had significantly more WMH than the PD without dementia group in the evaluated brain regions except for the infratentorial area. The WMH showed a significant correlation with age, Unified Parkinsons Disease Rating Scale, Mini-Mental State Examination, sum of the box of Clinical Dementia Rating, and many of the cognitive domains. The linear regression model showed that the WMH was independently associated with cognitive impairment in patients with PD, regardless of age, sex, duration or severity of PD symptoms, and vascular risk factors. ConclusionsThese findings confirm that WMH might be associated with cognitive decline in patients with PD, regardless of age, sex, education status, duration or severity of PD symptoms, and vascular risk factors. This result suggests that other nonvascular factors contribute to the progression of dementia in patients with PD.

Cognitive Impairment in Essential Tremor without Dementia

Background and purpose Several clinical studies have demonstrated that patients with essential tremor (ET) may have cognitive deficits; however, there are no published data regarding detailed neuropsychological assessments of ET without dementia. We therefore conducted a case-control study of cognitive function in patients with ET. Methods The cohort for this study comprised 34 consecutive patients with ET without dementia and 33 age-matched controls, all of who completed a dementia-screening questionnaire and underwent a detailed neuropsychological investigation. Results Severe impairments were observed in most domains for the ET group compared to the controls, including attention, part of language function, verbal memory, and frontal executive functions. Conclusions Our results support the finding that the subclinical cognitive deficits characterized by attention, verbal memory impairments, and executive dysfunction are a clinical feature of ET. In addition, our results also support the finding that age at examination and educational status are the most important risk factors associated with cognitive deficits in patients with ET.

Impact of tremor severity on cognition in elderly patients with essential tremor.

Several clinical studies have demonstrated that patients with essential tremor (ET) may have cognitive deficits; however, detailed neuropsychological assessments in comparison with motor tasks in patients with ET have not been reported. We conducted a prospective study to determine the correlation of cognition with age, disease duration, and motor task severity in patients with ET. Forty-seven patients with ET who underwent clinical assessment using the Fahn–Tolosa–Marin clinical rating scale and detailed neuropsychological investigation were included. Cognitive decline was significantly correlated with age at the time of examination, educational status, and tremor severity; cognitive decline however, was not related to disease duration or the presence of vascular risk factors. Multiple linear regression analysis revealed that the tremor severity was independently associated with cognitive impairment in patients with ET, regardless of age, gender, educational status, duration of ET symptoms, and vascular risk factors. Our results support the finding that the age at examination and educational status are risk factors associated with dementia in patients with ET, as with other types of dementia. In addition, the relationship between tremor severity and cognitive decline suggests there may be a pathophysiologic association between the two conditions, although the pathologic basis for dementia in the older onset ET cases requires further study.

Cardiac sympathetic denervation and its association with cognitive deficits in Parkinson's disease☆

BACKGROUND There is growing evidence to suggest that cognitive decline in patients with Parkinsons disease (PD) is associated with autonomic involvement, although the clinical and pathological correlations have not been firmly established. OBJECTIVE We prospectively investigated the pattern of myocardial sympathetic denervation deficits in PD and its correlation with cognitive decline. METHODS Twenty-eight patients with PD who underwent myocardial (123)I-metaiodobenzylguanidine (MIBG) scintigraphy, clinical assessment of stage and severity of PD and detailed neuropsychological investigation were included in the study. RESULTS There were significant differences in the MIBG uptake between the PD patients with cognitive deficits and those who did not have cognitive deficits. CONCLUSION These findings confirm that cognitive decline in patients with PD is associated with autonomic involvement and raises the possibility that the topographical spread of synuclein pathology involving the neocortical areas might be linked to the autonomic system in PD.

Cognitive Dysfunctions in Mild Parkinson’s Disease Dementia: Comparison with Patients Having Mild Alzheimer’s Disease and Normal Controls

Objective: Although the neuropsychological differences between Alzheimer’s disease (AD) and Parkinson’s disease dementia (PDD) have been scrutinized in several studies, no study to date has directly compared the cognitive impairment profiles of patients with mild PDD and those with mild AD. In this study, we investigated the cognitive changes of mild PDD patients as compared with age- and education-matched normal controls and matched mild AD patients. Methods: Thirty-one patients with PDD, 24 patients with probable AD (pAD), and 50 controls were recruited prospectively. All the subjects were evaluated with a battery of detailed neuropsychological tests for the assessment of attention, memory, language, and the visuospatial and frontal executive functions. Results: The PDD and pAD groups demonstrated significant impairments in all cognitive domains compared with the control group. These cognitive declines attributable to dementia were similar in the PDD and pAD patients, but they were not identical. In the subdomain analysis, the pAD group demonstrated more marked changes in delayed memory performance than did the PDD group. Conclusions: Our result showed that the cognitive changes in mild PDD patients did not differ from those in the mild pAD patients, except for delayed memory items. We concluded that it is difficult to sharply distinguish between mild PDD and mild AD.

Single-nucleotide polymorphisms (SNPs) and haplotype analysis in vascular endothelial growth factor (VEGF) gene in the patients with Parkinson disease and lung cancer

The epidemiologic data on smoking in association with Parkinson disease (PD) is puzzling. A lower incidence of smoking-related malignancies, especially lung cancer, has been reported by several studies in the patients with PD. In this study, we investigated polymorphic variations in the vascular endothelial growth factor (VEGF) gene, which has been proposed having a pivotal role in progressive damage of nigral dopaminergic neurons, between Korean patients with 188 PD and 321 lung cancer patients. There were no significant differences in the tested single-nucleotide polymorphisms (SNPs) between patients with PD and lung cancer; however, one haplotype was significantly different in comparisons between the two diseases. These results suggest that VEGF genetic polymorphisms might help understand the low incidence of lung cancer in the patients with PD.

Transient Global Amnesia Associated with Acute Intracerebral Hemorrhage at the Cingulate Gyrus

other neurological symptoms such as headache, dizziness or focal weakness. There was no history of hypertension, diabetes, transient ischemic attacks, stroke, epilepsy, migraine, psychiatric illness, head trauma or alcohol abuse. On examination, the patient was alert, with a blood pressure of 130/80 mm Hg, a regular heart beat of 75 beats/min and a temperature of 36.7 ° C. Physical examination demonstrated no pathologic findings. On cognitive function evaluation, comprehension was intact and the patient was fully conscious; however, he immediately forgot what was heard and continued repetitive questioning regarding what he was doing here. Except for memory deficits, the other cognitive profiles, which included attention, praxis, language and frontal function, were normal. The patient’s amnesia and repetitive questioning gradually resolved after 6 h. The next morning, the patient was oriented and had recovered anterograde and recent retrograde memory, but not memory during the attack. Laboratory studies including complete blood cell and platelet count, erythrocyte sedimentation rate, blood electrolytes, creatinine, liver enzymes, cholesterol, triglycerides, prothrombin and partial thromboplastin time, antithrombin III-protein C and protein S activity were all normal. In addition, autoantibody screens were also normal. Neither the electrocardiogram from a 24-hour Holter monitor nor transthoracic echocardiography revealed any cardiac abnormalities. The waking surface EEG during the episode was normal. Brain Dear Sir, Transient global amnesia (TGA) is a benign neurological syndrome characterized by temporary loss of anterograde and recent retrograde memory with preserved consciousness and self-awareness; it is usually accompanied by repetitive questioning and temporal disorientation for a limited period of time [1] . In the majority of TGA cases, no cause can be identified; structural imaging is invariably normal and CSF studies are generally not performed. EEGs that have been performed during an episode have been reported to demonstrate no epileptiform abnormalities [2] . Several different causes for this syndrome have been proposed, including ischemia, migraine, epileptic seizure, venous congestion and psychological disturbances; however, there remains no consensus on the etiology [3] . Moreover, TGA associated with intracerebral hemorrhage has rarely been reported. The patient described here presented with transient amnesia resulting from a left cingulate lesion. This is of particular interest because these findings suggest that activity in the cingulate gyrus and its outflow pathways may lead to TGA.

Comparative Genome Hybridization Array Analysis for Sporadic Parkinson’s Disease

Parkinson disease (PD) is a common neurodegenerative disorder, characterized by the loss of midbrain dopamine neurons and Lewy body inclusions. We investigated array CGH to analyze gain or loss of genetic material from 30 patients with PD. We identified the frequent copy number variations in PD; gains in 1p21.1, 4p15.31, 5p15.33, 6q24.1, 7q35, 8q24.3, 10q26.3, 11p15.5–15.4, 12q21.2, 16p13.3, 18q12.3 and 22q13.31, and losses in 1p36.33, and 5q13.2. These findings enable a better description of genetic variations in PD, and could provide a foundation for understanding the critical regions of the genome that may be involved in the development of PD.