MRI for TIA – pro

TIA should be promptly evaluated to institute therapy as soon as possible to decrease risk of stroke. A standard algorithm for assessment of patients is not universally used, although guidelines have been developed; diagnostic evaluation is influenced by medical history and specific characteristics of the TIA. (See Figure.) The goals of imaging assessment are to identify candidates for specific surgical or medical therapeutic modalities, determine prognosis, and exclude rare nonvascular causes. Diagnostic imaging indications are based on yield of the test, management implications, risk to the patient, and cost. Hospitalization may be advised to keep the patient under medical observation soon after the TIA, perform cerebrovascular arteriography, and expedite the diagnostic assessment, which may include cardiac imaging.
Magnetic resonance imaging (MRI) of the head is used less often than CT for initial evaluation of patients with TIA because it is a more expensive, time-consuming diagnostic modality and is less available. However, MRI has certain advantages. Because of its higher contrast resolution and lack of bone-related artifacts, MRI is more capable of detecting acute and small infarcts, especially those involving the cerebral cortex. The prevalence of white matter hyperintense lesions seen on MRI is high in the general population (13%), increasing with age and the presence of risk factors for stroke. To be considered an infarction, a white matter hyperintense lesion in T2-weighted images should also be seen as hypointense in T1-weighted images. Freedom from distortions by bone artifact gives MRI the advantage of improved resolution of small infarcts in brain stem and cerebellar regions that escape detection by CT.

MRI can provide evidence of absence of the normal “flow voids” in the intracranial ICA, indicative of occlusive disorder at that level, or more proximally in the extracranial ICA, suggesting a cause of TIAs. MRI is better than CT for imaging vessels in the posterior fossa and can demonstrate decreased or absent flow voids of the basilar and vertebral arteries and their branches, suggesting compromised circulation. Findings of vascular ectasia, tortuosity, and stenosis suggest an atherosclerotic cause of TIA. Arterial dissections with subintimal hematoma replacing much of the arterial wall are well identified by MRI. Vascular wall dissection appears as a crescentlike or annular hyperintense profile on the cross-section of T1-weighted images of the vertebral or basilar arteries. The yield of MRI is also superior to that of CT for detection of incidental lesions such as AVM or subdural hematoma. Case reports suggest that MRI may detect isodense subdural hematomas that are unidentifiable on CT.

Despite the superior diagnostic yield of MRI over CT of the head, there is no indication for routine MRI of patients with TMB or TIA, because in general the presence of silent strokes does not change clinical treatment of patients. The panel recognizes that the presence of silent strokes has not been sufficiently evaluated and weighted in the treatment algorithm for symptomatic patients with appropriate carotid stenosis to modify recommendations at this time. Continued vigilance in this area is suggested. Superior identification and localization of symptomatic lesions in carotid or vertebrobasilar territories or vascular anomalies in the occasional patient with transient ischemia of nonatherosclerotic origin may facilitate diagnosis and influence management, but the indication remains subject to individual judgment based on clinical history and other medical circumstances. Diffusion-weighted and perfusion-weighted MRI, although not yet widely available, appear to have high sensitivity and specificity in the early detection of cerebral ischemia; these techniques may be able to differentiate TIA from acute stroke as well as reliably indicate areas at risk.

Albers GW: A review of published TIA treatment recommendations. Neurology 2004 Apr 27; 62(8 Suppl 6): S26-8
Antonio Culebras, MD, Chair; Carlos S. Kase, MD; Joseph C. Masdeu, MD; Allan J. Fox, MD; R. Nick Bryan, MD, PhD; C. Barrie Grossman, MD; Donald H. Lee, MD, Members; Harold P. Adams, MD; William Thies, PhD; Ex Officio Members Imaging in Transient Ischemic Attacks/Acute Stroke–Transient Monocular Blindness Stroke. 1997;28:1480-1497.

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