Clinical Evaluation and Therapeutic Options in Stroke (Continued)

CT is readily available in most hospitals and reliably demonstrates the presence or absence of intracerebral hemorrhage. Immediately after the onset of bleeding, intracerebral hematomas (ICHs) are seen on CT as well-circumscribed areas of high density with smooth borders. Edema develops within the first days and is seen as a dark rim around the white hematoma. Subarachnoid bleeding is demonstrated by a high-density signal within the cerebrospinal fluid and brain cisterns. Early signs of brain infarction include obscuring of the basal ganglia density, blurring of the distinction between the grey matter of the cerebral cortex and the underlying white matter, and loss of definition of the insular cortex. Later, infarction appears as a low-density lesion. Specific vascular abnormalities include hyperdense arteries, indicating thrombosis or slow flow and calcific emboli within arteries. The signs of infarction on CT scans are often subtle when images are taken within several hours of the onset of symptoms. Viewing images on a computer with the ability to vary the contrast helps identify subtle abnormalities and asymmetries.

Diffusion-weighted MRI images (DWI) and fluidattenuated inversion recovery (FLAIR) images are particularly useful and sensitive for detection of acute brain infarcts. Infarcted areas appear bright on DWI and dark on apparent diffusion coefficient (ADC) images. The location, pattern, and multiplicity of DWI ischemic lesions help to suggest the most likely causative stroke mechanism. DWI positivity wanes during the first 7 to 10 days after stroke onset. Lesions seen on DWI images (and confirmed by ADC) usually, but not always, correspond to areas of infarction. T2-weighted scans show established infarcts as bright. MRI can also accurately show ICH, especially when echo-planar gradient-echo susceptibility-weighted images (T2*) are performed. These T2*-weighted (susceptibility) images can also show thrombi within intracranial arteries and dural sinuses and veins.

Vascular imaging can be performed using CT (CT angiography [CTA]) or MR (MR angiography [MRA]), or by using ultrasound. CTA and MRA images can be obtained concurrently with the respective primary brain imaging. CTA requires intravenous dye infusion. The neck and intracranial arteries and veins can be shown well by either technique. Duplex ultrasound, which includes a B-mode image combined with a pulsed Doppler spectrum analysis, can accurately show occlusive lesions within neck arteries. Transcranial Doppler ultrasound (TCD) involves insonation of intracranial arteries by measuring blood flow velocities using a probe placed on the orbit, temporal bone, and foramen magnum. Areas of narrowing or occlusion can be detected; these probes also provide a means to monitor for embolic materials passing under them. Dye contrast digital angiography shows neck and intracranial arteries in more detail than CTA and MRA and is now used to clarify vascular lesions not shown well by these screening techniques; it is also pursued at the time of intravascular interventions, such as coiling of aneurysms, stenting, and intra-arterial thrombolysis or mechanical clot extraction. In patients in whom strokes cause seizures, electroencephalography (EEG) can be helpful.

Treatment of acute stroke patients depends heavily on the type and cause of the stroke. In subarachnoid hemorrhage patients, aneurysms and vascular malformations can be controlled by cranial surgical clipping or coiling through an intravenous interventional approach. The vasoconstriction that follows bleeding and surgery also is a target for therapy. In patients who have had an intracerebral hemorrhage, blood pressure control, reversal of bleeding diatheses, and drainage of space-taking hematomas, especially those that are lobar and near the surface, are the major therapeutic strategies.

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