Background: An elevated plasma homocysteine (Hcy) level has been prospectively associated with an increased risk of vascular and degenerative dementias. An Hcy elevation is prevalent in patients with Parkinson disease (PD) in part because levodopa metabolism produces Hcy. The clinical relevance of an elevated Hcy level in patients with PD is unknown.Objective: To determine if hyperhomocysteinemia in patients with PD is associated with depression or with cognitive or physical impairments.Design: Ninety-seven people with a mean (SD) PD duration of 3.6 (1.6) years completed the Beck Depression Inventory, a battery of 11 cognitive tests, and the motor and function components of the Unified Parkinson's Disease Rating Scale. Normalized scores for the affective, cognitive, and physical measures were compared between those with a normal Hcy level (n=66) and those with hy-perhomocysteinemia (n = 31) (Hcy level, Ͼ1.89 mg/L [Ͼ14 µmol/L]), controlling for age, sex, disease duration, and treatment.Results: Subjects with an elevated Hcy level were slightly older (68 vs 62 years), but had similar plasma concentrations of vitamin B 12 and folate. Hyperhomocysteinemic patients were more depressed (P=.02) and had worse cognition (PϽ.01), but the physical measure did not differ.Conclusions: Patients with PD and hyperhomocysteinemia are more likely to be depressed and to perform worse on neuropsychometric tasks compared with normohomocysteinemic patients. Further research is warranted to see if hyperhomocysteinemia is a reversible risk factor for neuropsychiatric burden in patients with PD.

We wanted to determine the neurocognitive profile of adult patients with moyamoya disease prior to neurosurgical intervention. The experience of three United States medical centers, Columbia University, University of Illinois at Chicago, and the University of Texas Southwestern Medical Center at Dallas, were combined. Clinical data from adult patients (N = 29) referred for neuropsychological evaluation from 1996 to 2008 were reviewed. Neurocognitive functioning was assessed using standardized neuropsychological tests and all data were converted to z-scores. Memory, attention, processing speed, verbal memory, visuo-spatial, language, and executive functions were examined. Cognitive dysfunction was defined as performance in two or more cognitive domains 1.5 standard deviations below age-corrected normative means OR one or more cognitive domains two standard deviations below age-corrected normative means. Manual strength and dexterity, as well as depressive symptoms, were also assessed. Two-thirds of patients demonstrated neurocognitive dysfunction. A large proportion of patients were found to have pronounced cognitive dysfunction (>2 SD below the mean) on tests of processing speed (29%), verbal memory (31%), verbal fluency (26%) and executive function (25%). Manual strength and dexterity were also affected in many patients, with impairment found in 36-58% of patients. Twenty-eight percent of patients reported moderate to severe depression, but depressive symptoms did not correlate with neurocognitive findings. A large proportion of adults with moyamoya disease demonstrate disruption of neurocognition in a broad range of functions, particularly those mediated by subcortical and frontal regions. The pattern of deficits suggests a mechanism of diffuse small vessel disease possibly caused by chronic hypoperfusion.

This study explored the utility of the Montreal Cognitive Assessment (MoCA) in the detection of cognitive change over time in a community sample (age ranging from 58 to 77 years). The MoCA was administered twice approximately 3.5 years apart ( n = 139). Participants were classified as mild cognitive impairment (MCI) or cognitively intact at follow-up based on multidisciplinary consensus. We excluded 33 participants who endorsed cognitive complaints at baseline. The MCI group ( n = 53) showed a significant decrease in MoCA scores ( M = -1.83, p < .001, d = 0.64). When accounting for age and education, the MCI group showed a decline of 1.7 points, while cognitively intact participants remained stable. Using Reliable Change Indices established by cognitively intact group, 42% of MCI participants demonstrated a decline in MoCA scores. Results suggest that the MoCA can detect cognitive change in MCI over a 3.5-year period and preliminarily supports the utility of the MoCA as a repeatable brief cognitive screening measure.

History of TBI with reported LOC appears to be a risk factor for earlier AD onset. This is the first study to use autopsy-confirmed cases, supporting previous investigations that used clinical criteria for the diagnosis of AD. Further investigation as to possible underlying mechanisms of association is needed. (PsycINFO Database Record

No abstract