International journal of stroke : official journal of the International Stroke Society
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Intima-media thickness (IMT) has been measured for over 20 years, and is widely regarded as a surrogate for atherosclerosis. However, in the carotid arteries atherosclerosis is focal, manifesting as plaques. IMT is often measured deliberately where no plaque exists, or multiple measurements may be averaged, including only one or two that intersect plaque. ⋯ While 3-D ultrasound requires special equipment, total plaque area can be measured using the same equipment as IMT. Because plaque and IMT are biologically and genetically distinct entities, representing different phenotypes of atherosclerosis, both should be measured in any situation where IMT is measured, with the exception of studies in children too young for the occurrence of plaque. IMT should not be called 'atherosclerosis': the phenotype being assessed should be specified.
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Black dots in the brain parenchyma diagnosed in T2(*)-weighted magnetic resonance imaging should be interpreted in light of the patient's history as well as the location, number and distribution of the lesions and associated imaging findings. These dots will correspond to haemoglobin degradation products in most of the cases referred to as cerebral microbleeds in patients with small vessel disease. Cerebral microbleeds have a prevalence of 5.7% (range 3.7-7.7%) and are observed more frequently with increasing age. cerebral microbleeds have been observed in 47-80% of the primary intracerebral haemorrhage patients and in 0-78% of the patients with ischaemic cerebrovascular disease and appear to be a general marker of various types of bleeding-prone, small vessel disease and a predictor of recurrent vascular events. ⋯ Current data does not support the hypothesis that cerebral microbleeds are associated with a higher risk for a clinically relevant intracerebral haemorrhage, after anticoagulation/antiaggregation therapy, or after thrombolytic therapy in stroke patients. Therefore, the current data do not support the general exclusion of patients from therapy based on the presence of cerebral microbleeds. In the future, cerebral microbleeds may be incorporated into the design of clinical trials of anticoagulation/antiaggregation drugs in stroke patients for potential individual stratification for both the risk of recurrent ischaemic stroke and for the risk of intracerebral haemorrhage.
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Hypothermia is the most potent neuroprotective therapy available. Clinical use of hypothermia is limited by technology and homeostatic mechanisms that maintain core body temperature. ⋯ We reviewed the preclinical and early clinical trials of hypothermia for a variety of indications, the putative mechanisms for neuroprotection with hypothermia, and offer several hypotheses that remain to be tested in clinical trials. Therapeutic hypothermia is promising, but further Phase 1 and Phase 2 development efforts are needed to ensure that cooling of stroke patients is safe, before definitive efficacy trials.