Dementia is a common complication of Parkinson's disease (PD), but the cause is incompletely understood. In previous studies, dementia has been associated with an increase in hyperintense lesions in the cerebral white matter. The aim of this study was to explore whether white matter hyperintensities (WMH) on cerebral magnetic resonance imaging (MRI) are associated with dementia in PD. For this study, 35 patients with PD, 16 with dementia (PDD) and 19 without (PDND), and 20 control subjects were recruited. MRI scans of patients and controls were rated for WMH, blind to diagnosis, using the Scheltens visual rating scale. Both bivariate and multivariate statistical analyses were carried out. Cerebrovascular risk factors, education, gender, or age were similar across groups. Compared with the PDND group, the PDD group had significantly higher level of WMH in the deep white matter and in the periventricular areas. WMH in the deep white matter was the only variable that was associated significantly with Mini-Mental State Examination score and explained 38% of the variance in the multivariate linear regression analysis. Our findings suggest that WMH in the deep white matter may contribute to dementia in PD.

Headache, cognitive dysfunction and mood disorders are common in both diseases, but otherwise there are distinct differences in NP involvement, with cerebrovascular diseases more prevalent in SLE and neuropathies more common in PSS. This indicates that some NP disease mechanisms are shared while others differ between the two diseases.

Microvascular obstruction is an important determinant of infarct healing. The effect of MO on infarct size translated into distinct patterns of LV remodelling during long-term follow-up.

Background Circulating cardiac troponin levels increase following prolonged intense physical exercise. The aim of this study was to identify participants with highly elevated cardiac troponins after prolonged, high intensity exercise, and to evaluate these for subclinical coronary artery disease. Methods and results Ninety-seven recreational cyclists without known cardiovascular disease or diabetes, participating in a 91 km mountain bike race were included, 74 (76%) were males, age: 43 ± 10 years, race duration: 4.2 (3.6-4.7) h. Blood samples, rest electrocardiogram and physical examination were obtained 24 h prior to, and at 0, 3 and 24 h following the race. Median cardiac troponin I level at baseline: 3.4 (2.1-4.9) ng/l (upper limit of normal: 30.0 ng/l). There was a highly significant ( p < 0.0001) increase in circulating cardiac troponin I in all participants: immediately following the race; 50.5 (28.5-71.9) ng/l, peaking at 3 h 69.3 (42.3-97.7) ng/l and declining at 24 h: 14.2 (8.5-27.9) ng/l. No cyclist had symptoms or rest electrocardiogram changes compatible with coronary artery disease during or following the race. Coronary artery disease was detected by coronary angiography in the three cyclists with the three of the four highest cardiac troponin values (>370 ng/l) at 3 and 24 h following the race. Computed tomographic coronary angiography was performed in an additional 10 riders with the subsequently highest cardiac troponin I values, without identifying underlying coronary artery disease. Conclusions This study suggests that there is a pathologic cardiac troponin I response following exercise in individuals with subclinical coronary artery disease. This response may be associated with an excessive cardiac troponin I increase at 3 and 24 h following prolonged high-intensity exercise.

Objective. Cognitive dysfunction is common in both systemic lupus erythematosus (SLE) and primary Sjögren's syndrome (SS). Antibodies against the NR2 subtype of the N-methyl-D-aspartate receptor (anti-NR2 antibodies) cause hippocampal atrophy and cognitive impairment in mice and have been associated with memory impairment in both patients with SLE and patients with primary SS. In addition, a reduced volume of hippocampal gray matter has been demonstrated in both SLE and primary SS. This study was undertaken to investigate whether there is a connection between the presence of anti-NR2 antibodies and hippocampal atrophy in human diseases.Methods. Fifty patients with SLE and 50 patients with primary SS underwent clinical examination and cerebral magnetic resonance imaging. Anti-NR2 antibodies in cerebrospinal fluid (CSF) were measured, and hippocampal gray matter volumes were compared between patients who were positive for and those who were negative for anti-NR2 antibodies.Results. Patients with anti-NR2 antibodies in CSF had less hippocampal gray matter than patients without these antibodies. No other differences regarding gray matter volumes in other parts of the brain were identified.Conclusion. The present findings indicate that anti-NR2 antibodies in patients with SLE and primary SS cause neuronal death manifested as reduced hippocampal gray matter, as has been previously demonstrated in mice with autoimmune disease.