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M R Crain

Publications and source records attributed to M R Crain.

23 records · Page 2Linked to original sources

Postcontrast CT in the diagnosis and assessment of response to thrombolysis in massive pulmonary embolism.

We present a case of massive acute pulmonary embolism where contrast enhanced helical CT was compared with standard angiography for diagnosis and for monitoring subsequent response to thrombolytic therapy. There was very close concordance of the findings on these modalities suggesting that contrast enhanced helical CT may be an easy and reliable alternative to standard angiography.

Aged↗

Renal transplant evaluation with MR angiography and MR imaging.

Magnetic resonance (MR) angiography is a widely used, noninvasive tool for evaluating the aorta and its branches. It is particularly useful in renal transplant recipients because it provides anatomic detail of the transplant artery without nephrotoxic effects. Volume rendering is underutilized in MR angiography, but this technique affords high-quality three-dimensional MR angiograms, especially in cases of tortuous or complex vascular anatomy. An imaging protocol was developed that includes gadolinium-enhanced MR angiography of the transplant renal artery with volume rendering and multiplanar reformation postprocessing techniques. Axial T2-weighted and contrast material-enhanced T1-weighted MR images are also obtained to examine the renal parenchyma itself and to evaluate for hydronephrosis or peritransplant fluid collections. This imaging protocol allows rapid global assessment of the renal transplant arterial system, renal parenchyma, and peritransplant region. It can also help detect or exclude many of the various causes of renal transplant dysfunction (eg, stenosis or occlusion of a transplant vessel, peritransplant fluid collections, ureteral obstruction). Conventional angiography can thus be avoided in patients with normal findings and reserved for those with MR angiographic evidence of stenosis.

Adult↗

MR imaging of cerebral ischemia: findings in the first 24 hours.

MR changes of cerebral ischemia have been shown to occur as early as 1-2 hr after vessel occlusion in experimental models of stroke. However, the MR findings in the early stages of ischemic stroke in the clinical population have not been well established. We studied 41 lesions in 39 patients in whom MR was performed within the first 24 hr after onset of ischemic symptoms. Twenty-five lesions were studied with gadopentetate dimeglumine. Vascular flow-related abnormalities, including absence of normal flow void and presence of arterial enhancement, were the earliest MR findings, detected within minutes of onset. Morphologic changes (brain swelling) on T1-weighted images without signal changes on T2-weighted images could be detected within the first few hours. Signal changes were not usually found before 8 hr on T2-weighted images or before 16 hr on T1-weighted images. In contrast to the absence of parenchymal enhancement typically found in cortical infarctions in the first 24 hr, a few lesions (including transient occlusions, partial occlusions, and isolated watershed infarctions) exhibited early, exaggerated parenchymal enhancement. We conclude that signal changes may not be reliable in detecting ischemic stroke within the first 8 hr after onset. Vascular abnormalities, when present, are the most reliable and earliest findings. Other MR findings of early ischemic stroke, including morphologic changes and early, exaggerated parenchymal enhancement, may also precede signal changes. Paramagnetic contrast administration often provides valuable information in the detection and evaluation of acute ischemia.

Adult↗

Cerebral ischemia: evaluation with contrast-enhanced MR imaging.

Eighty patients with a total of 82 ischemic lesions were examined with contrast-enhanced MR imaging 1 hr to 1 month after onset of symptoms. The studies were reviewed retrospectively to determine the presence of arterial enhancement and the patterns of parenchymal enhancement. Arterial enhancement was often detected on the initial MR examination (45%), was frequently demonstrated in cortical infarction (86%), in some cases preceded the development of signal changes on T2-weighted images, and resolved by 11 days. The presence of arterial enhancement appeared to be a better indicator of clinical severity than was the presence of proximal vessel occlusion on MR or angiographic studies. Two patterns of parenchymal enhancement were seen: progressive enhancement and early and/or intense enhancement. In patients with the progressive pattern, parenchymal enhancement on postcontrast T1-weighted images was rarely seen before 7 days, while signal abnormalities on T2-weighted images were intense during the first few days. The early and/or intense enhancement pattern was usually present within the first 3 days, approximated or exceeded the area and intensity of signal changes on T2-weighted images, and was usually associated with minimal or reversible neurologic sequelae (except when located in or near a watershed zone), suggesting a lesser degree of ischemic insult than was associated with the progressive pattern.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

Arterial enhancement in acute cerebral ischemia: clinical and angiographic correlation.

PURPOSE: To investigate the cause and clinical significance of arterial enhancement (AE) in contrast-enhanced T1-weighted MR examinations after acute cerebral ischemia. METHODS: Contrast MR examinations and conventional angiograms of 17 patients studied following an acute ischemic event or an internal carotid occlusion were retrospectively reviewed. MR and angiographic studies were performed within 1 day of each other. The presence of AE was correlated with both angiographic findings and patient clinical status. RESULTS: AE was not confined to patients with angiographic evidence of complete arterial occlusion. Only 64% of patients demonstrating AE had complete occlusion angiographically. Complete arterial occlusion did not always correlate with AE. In two of nine patients with complete occlusion, no AE was identified. In five of 10 patients with AE, angiographic slow flow was identified. In patients without AE, no angiographic slow flow was identified. In the 64% of patients with AE, significant symptoms were identified. Patients without AE were either asymptomatic or had mild symptoms at the time of the MR study. CONCLUSIONS: Our data support the hypothesis that arterial slowing is the cause of AE, which appears to be an indicator of decreased brain perfusion. Such MR findings may add important supplemental information to those provided by conventional angiography.

Acute Disease↗