Although computed tomography (CT) remains the most frequently used imaging examination in acute cerebral infarction, its sensitivity for early detection of strokes remains limited. In middle cerebral artery (MCA) strokes less than 6 hours old, loss of definition of the gray-white interface in the lateral margins of the insula ("insular ribbon") was observed. The acute and subacute CT findings in 11 retrospective and 16 prospective patients are presented. Loss of the insular ribbon was detected in 12 of the prospective cases and in all 11 retrospective cases. The insular ribbon is supplied by the insular segment of the MCA and its claustral branches. With cessation of MCA flow, the insular ribbon becomes the region most distal from the anterior and posterior cerebral collateral circulations. Consequently, the insular ribbon effectively becomes a watershed arterial zone. Loss of the insular ribbon is thus a reflection of acute edema due to infarction. Loss of the insular ribbon appears to be another frequent and reliable finding in acute MCA stroke.
The authors investigated whether identification of corpus callosal (CC) involvement might increase the specificity of magnetic resonance (MR) imaging in differentiating multiple sclerosis (MS) from other periventricular white matter diseases (PWDs). They prospectively evaluated 42 patients with MS and 127 control patients with other PWDs. Ninety-three percent of the MS patients demonstrated confluent and/or focal lesions involving the callosal-septal interface (CSI). These lesions characteristically involved the inferior aspect of the callosum and radiated from the ventricular surface into the overlying callosum. CSI lesions were optimally demonstrated on sagittal long repetition time (TR)/short echo time (TE) images and frequently (45% of cases) went undetected on axial images. Only 2.4% of the control patients had lesions of the CC. The authors conclude that midsagittal long TR/short TE images are highly sensitive and specific for MS and that callosal involvement in MS is more common than previously reported.
Localized amyloidosis of the head and neck was found retrospectively in the nasopharynx (n = 3) and orbit (n = 1) of four female patients (mean age, 32 years), three of whom had a prior history of antigenic stimulation. In all patients, computed tomography revealed a slightly high absorption and a relatively homogeneous, partially calcified mass. In the one patient who underwent magnetic resonance (MR) imaging, a distinctive loss of signal intensity was seen on the long repetition time/echo time sequence. This enhanced T2 relaxation may be due to (a) static or slowly fluctuating internal magnetic fields arising from adjacent amyloid protons held in relatively fixed positions within the beta-pleated sheet, resulting in quick phase dispersion; (b) chemical exchange and spin-spin interaction with adjacent water protons; and (c) diffusion through differences in diamagnetic susceptibility. This unusual appearance at MR imaging may improve the ability of radiologists to distinguish focal amyloidosis from many other diseases that affect the head and neck.
Fifteen patients with biochemically documented phenylketonuria (PKU) were studied with use of magnetic resonance (MR) imaging with spin-echo T2-weighted pulse sequences. The resulting images demonstrated varying degrees of symmetric high signal intensity of the white matter within the posterior cerebral hemispheres. Involvement of the anterior hemispheres was seen only in cases with severe signal intensity changes. There was no involvement of the cerebral cortex, brain stem, or cerebellum. Moreover, no anatomic structural abnormalities were observed. Mild cortical atrophy was observed in eight of the 15 patients. There was no significant correlation between the patients' IQ scores and the level of MR signal intensity changes. Although MR imaging routinely shows relatively distinct abnormalities in patients with PKU, the clinical severity of the disease does not parallel its imaging severity.
A 27-year-old woman with a recent diagnosis of multiple sclerosis developed several episodes of noncardiogenic pulmonary edema over a 3-month period, each requiring intubation and ventilatory support. The development and subsequent resolution of an isolated lesion at the obex was correlated with the episodes. The literature regarding the anatomical basis of neurogenic pulmonary edema is reviewed.
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