Persons with restless legs syndrome (RLS) may have an increased risk of stroke or heart disease, compared to those without RLS, according to findings published in the January 1 Neurology. The study included more than 3,400 people (mean age, 68) who were enrolled in the Sleep Heart Health Study; about 7% of women and 3% of men had RLS. After the investigators adjusted for age, sex, race, BMI, diabetes, high blood pressure, and other factors, they found an odds ratio of 2.05 for coronary artery disease and 2.07 for cardiovascular disease among persons with RLS compared to those without RLS. In addition, the researchers noted that the association was strongest among patients who reported RLS symptoms at least 16 times per month and among those who reported more severe symptoms.

Stroke patients with mild to moderate impairment who underwent two weeks of constraint-induced movement therapy continued to show improved limb function, strength, and quality of life two years after treatment, according to findings in the January Lancet Neurology. Poststroke patients were randomized to receive constraint-induced movement treatment or usual and customary care. Intervention patients practiced functionally relevant repetitive tasks with the impaired limb, while the less severely affected arm was restricted. Follow-up at two years revealed that one-year improvements in weight lifting, grip strength, amount of use, and how well the limb was used did not decline significantly. The researchers also found continued improvements in strength, social participation, daily activities, and overall physical function. They noted that the largest changes were recorded in patients who were higher functioning.

A gene variant that has been shown to increase the risk of peripheral venous thrombosis may also be linked to cerebral venous thrombosis, according to the results of a study published in the January 8 Neurology. The researchers compared 78 patients with cerebral venous thrombosis to 201 control participants. Among those with cerebral venous thrombosis, 16.7% had the gene variant XII C46T, compared to 5.5% of those without the condition. The association remained after researchers controlled for age, gender, smoking, and the use of oral contraceptives. “These results need to be confirmed, but it appears that people with cerebral venous thrombosis should be tested for this gene and should be considered for use of blood thinning medication to prevent future blood clots,” concluded the researchers.

High blood pressure may be associated with an increased risk for mild cognitive impairment (MCI), according to a report in the December 2007 Archives of Neurology. A total of 918 Medicare recipients, 65 and older and without MCI at baseline, were followed for a mean of 4.7 years. During the follow-up, 334 participants developed MCI: 160 participants had amnestic MCI, and 174 participants had nonamnestic MCI. After adjusting for age and sex, the investigators found that hypertension was associated with an increased risk of all-cause MCI and nonamnestic MCI. The researchers noted that hypertension was not associated with amnestic MCI or a change in language and memory abilities over time. They reasoned that hypertension may cause cognitive impairment through cerebrovascular disease. Other possible explanations offered by the researchers included shared risk factors such as free radicals and the fact that hypertension may contribute to a blood-brain barrier dysfunction, which has been suggested to be associated with causing Alzheimer’s disease.

Telmisartan, used to help patients control blood pressure, may be an effective and potentially safe treatment for preventing stroke, reported researchers in the November 2007 Journal of the American Society of Hypertension. Twenty-five rats were fed a high-salt, stroke-inducing diet for eight weeks while receiving either no medication, telmisartan alone, ramipril alone, or a combination of the two drugs at either full- or half-doses. The researchers found that 83% of the rats given no medication showed signs of stroke, as did 56% of those receiving ramipril alone. However, rats given telmisartan only or telmisartan in combination with ramipril showed no signs of stroke. The researchers theorized that telmisartan’s ability to easily pass through the blood-brain barrier is likely associated with the neuroprotective effect found in the study.

Drinking green tea may protect brain cells against Parkinson’s disease, according to a recent study published in the December 15, 2007, Biological Psychiatry. The researchers found that green tea polyphenols dose-dependently protected dopaminergic neurons through inhibition of reactive oxygen species and nitric oxide in an animal model of Parkinson’s disease. They noted that the neuroprotective effects increased with the amount of green tea consumed. In addition, treatment with green tea polyphenols preserved the free radical scavenging capability of both the midbrain and the striatum. The investigators hope that “green tea polyphenols may be developed into a safe and easily administrable drug for Parkinson’s disease,” adding that “if green tea consumption can be shown to have meaningful neuroprotective actions in patients, this would be an extremely important advance."

Patients with venous thromboembolism have a substantially increased long-term risk of subsequent arterial cardiovascular events such as heart attack and stroke, according to a 20-year Danish cohort study in the November 24, 2007, Lancet. After excluding patients with known cardiovascular disease, the researchers assessed the risk of heart attack and stroke in 25,199 patients with deep venous thrombosis, 16,925 patients with pulmonary embolism, and 163,566 controls. The investigators found that in patients with deep venous thrombosis, the relative risk was 60% higher for heart attack and 119% higher for stroke, compared with controls. For patients with pulmonary embolism, the risk of heart attack was more than two and a half times higher than in controls and nearly three times higher for stroke. Moreover, results from the 20-year follow-up revealed a 20% to 40% combined increased risk for arterial cardiovascular events for those with either a provoked or an unprovoked venous thromboembolism.

Modulation of abnormal network activity underlies the clinical outcome following gene therapy for Parkinson’s disease, according to a study of 12 patients reported in the December 4, 2007, Proceedings of the National Academy of Sciences. The researchers observed elevated activity of metabolic networks associated with motor and cognitive functioning at baseline on fluorodeoxyglucose positron emission tomography scans. However, following unilateral subthalamic nucleus infusion of an adenoassociated virus vector expressing glutamic acid decarboxylase, thalamic metabolism on the operated side was significantly reduced, metabolism in the ipsilateral motor and premotor cortical regions increased, and activity in the cognition-related network did not change. “These network changes correlated with improved clinical disability ratings,” noted the authors. They concluded that network biomarkers may be used as assays in early-phase trials of experimental therapies for Parkinson’s disease and other neurodegenerative diseases.

Results of a study using a mouse model of Alzheimer’s disease suggest that an optimized hormone therapy with estrogen and progesterone may be useful in reducing the risk of Alzheimer’s disease in postmenopausal women. As reported in the November 28, 2007, Journal of Neuroscience, estrogen and progesterone were observed to independently and interactively regulate Alzheimer’s disease–like neuropathology. Sex hormones were depleted via ovariectomy in triple transgenic adult female mice, which led to increased b-amyloid accumulation and worsened memory performance. Treatment with estrogen, but not progesterone, prevented these effects; however, in combination, progesterone blocked estrogen’s beneficial effect on b-amyloid accumulation but not on behavioral performance. The authors added that progesterone alone or with estrogen also significantly reduced tau hyperphosphorylation.

A maternal history of Alzheimer’s disease was associated with reduced brain glucose metabolism in a study of 49 cognitively normal study participants ages 50 to 80, reported researchers in the November 14, 2007, Proceedings of the National Academy of Sciences. [18F]fluorodeoxyglucose positron emission tomography examinations showed that as compared with participants with paternal (n = 8) or no (n = 25) history of Alzheimer’s disease, participants with a maternal history (n = 16) had a “cerebral metabolic rate of glucose reductions in the same regions as clinically affected Alzheimer’s disease patients, involving the posterior cingulate cortex/precuneus, parietotemporal and frontal cortices, and medial temporal lobes,” said the researchers; the effects remained significant after age, gender, education, apolipoprotein E genotype, and subjective memory complaints were accounted for.

A cohort of 24 migraineurs—12 with aura and 12 without—were observed to have, on average, thicker somatosensory cortices than 12 control subjects, per a study reported in the November 20, 2007, Neurology. Investigators noted that the most significant thickness changes were observed in the caudal somatosensory cortex, where the trigeminal area is somatotopically represented. They also noted that the thickening “is in line with diffusional abnormalities observed in the subcortical trigeminal somatosensory pathway of the same migraine cohort in a previous study,” and they concluded that repetitive migraines may lead to or be the result of neuroplastic changes in cortical and subcortical structures of the trigeminal somatosensory system, as represented by the cortical thickening.

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