Background and Purpose Some prior studies have linked ambient temperature with risk of cerebrovascular events. If causal, the pathophysiologic mechanisms underlying this putative association remain ...unknown. Temperature-related changes in cerebral vascular function may play a role, but this hypothesis has not been previously evaluated. Methods We evaluated the association between ambient temperature and cerebral vascular function among 432 participants greater than or equal to 65 years old from the MOBILIZE Boston Study with data on cerebrovascular blood flow, cerebrovascular resistance, and cerebrovascular reactivity in the middle cerebral artery. We used linear regression models to assess the association of mean ambient temperature in the previous 1 to 28 days with cerebrovascular hemodynamics adjusting for potential confounding factors. Results A 10 degree C increase in the 21-day moving average of ambient temperature was associated with a 10.1% (95% confidence interval CI, 2.2%, 17.3%) lower blood flow velocity, a 9.0% (95% CI, 0.7%, 18.0%) higher cerebrovascular resistance, and a 15.3% (95%CI, 2.7%, 26.4%) lower cerebral vasoreactivity. Further adjustment for ozone and fine particulate matter (PM2.5) did not materially alter the results. However, we found statistically significant interactions between ambient temperature and PM2.5 such that the association between temperature and blood flow velocity was attenuated at higher levels of PM2.5. Conclusions In this elderly population, we found that ambient temperature was negatively associated with cerebral blood flow velocity and cerebrovascular vasoreactivity and positively associated with cerebrovascular resistance. Changes in vascular function may partly underlie the observed associations between ambient temperature and risk of cerebrovascular events.
Central nervous system symptoms occur in a substantial portion of patients with systemic lupus erythematosus. However, coma is a rare presentation and is usually secondary to complications such as ...subarachnoid hemorrhage, seizure, or ischemia. Here, we present a 49-year-old woman with lupus erythematosus and a history of recurrent aseptic meningitis and mild subarachnoid hemorrhage who presented with altered mental status and lethargy that progressed rapidly over hours to the herniation syndrome of coma, extensor posturing, and unilateral pupillary dilation. Spinal fluid showed massive protein elevation (>1600), and head computed tomography revealed global cerebral edema. The clinical and radiologic findings rapidly reversed with intravenous corticosteroids and mannitol within 24 hours, and her mental status improved to baseline. Her course was complicated by 2 episodes of recurrent encephalopathy when corticosteroids were tapered; these resolved after resuming high dosing. Because of ongoing pancytopenia, chemotherapy immunosuppression was delayed, and instead she received intravenous immunoglobulin with improvement in the pancytopenia. She remained cognitively intact during subsequent corticosteroid tapering. Rapid development of coma in lupus patients may be due to a primary process of the disease impacting blood brain barrier integrity. Although rare, this potentially fatal complication may be reversible with acute corticosteroid administration.
Iron is the most abundant transition metal in the brain, where it functions as an important cofactor in a host of vital metabolic processes and plays an absolutely essential role in cell viability. ...Free iron is also very toxic when present in high concentrations, thus placing this essential metal at the core of neurotoxic injury in a number of neurological disorders. The pivotal role of iron in cellular homeostasis, including its latent toxicity, necessitates a tight regulation of iron metabolism. Oxygen and iron appear to play an important role in iron homeostasis. They appear to exert their homeostatic role by modulating the proteins involved in a complex interplay between iron sensing, transport, and storage. These key regulatory proteins include ferritin (intracellular storage), transferrin (extracellular transport), transferrin receptor, and iron regulatory protein (sensor of intracellular iron concentration). The interplay of iron and oxygen is most intriguing in the setting of stroke, where hypoxia and free iron appear to interact in causing the subsequent neuronal death.
To report the very early magnetic resonance imaging features of eclampsia.
Case report.
Inpatient neurology service.
A 35-year-old woman who developed late postpartum eclampsia with cerebral edema, ...caudate hemorrhage, and ischemic strokes. Main Outcome Measure Very early magnetic resonance imaging features.
Magnetic resonance imaging with gadolinium showed posterior sulcal hyperintensity and leptomeningeal enhancement preceding the development of posterior reversible encephalopathy syndrome, hemorrhage, and ischemic strokes by days.
Magnetic resonance imaging with gadolinium shows early characteristic findings that precede the more classic clinical presentation of eclampsia.
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