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Objective To analyze the texture of T2-weighted magnetic resonance imaging (MRI) of postmortem multiple sclerosis (MS) brain, and to determine whether and how MRI texture correlates with tissue pathology. Methods Ten brain samples from 3 subjects with MS were examined. Areas of complete, partial, or no loss of Luxol fast blue (myelin) and Bielschowsky (axons) staining were marked on histological images, and matched on corresponding MRI as lesions, diffusely abnormal white matter (DAWM), and normal-appearing white matter (NAWM). The number of CD45+ cells (inflammation) was also counted. MRI texture was computed using polar Stockwell transform and compared to histology. Results Thirty-four lesions, 17 DAWM regions, and 36 NAWM regions were identified. After mixed effects modeling, MRI texture heterogeneity was greater in lesions than in DAWM (p

Magnetic resonance imaging (MRI) provides an objective method of evaluating multiple sclerosis clinical trials and is at least five times more sensitive to disease activity. In a recent clinical trial, MRI was also approximately twice as sensitive as clinical measurements to the treatment effect of a drug.

The extent of disease as detected by magnetic resonance imaging was compared between 32 patients with benign multiple sclerosis (MS) and 32 patients with the chronic progressive form matched for age, sex, and disease duration. Computer-assisted quantitation of magnetic resonance images revealed a higher mean lesion load in chronic progressive multiple sclerosis (CPMS); however, in approximately 20% of benign MS patients the lesion load was higher than that in the CPMS patients. CPMS patients had a higher number of infratentorial lesions, yet similar numbers of supratentorial lesions, when compared with benign MS patients. The degree of confluency of lesions and the clinical expression of infratentorial lesions were typically higher in the CPMS patients. Benign MS was characterized by a lower degree of confluency and a higher number of asymptomatic infratentorial lesions. Thus, magnetic resonance imaging shows characteristic differences in magnetic resonance-detected changes between MS patients with different clinical courses.

We employed 6-fluorodopa to study the integrity of the nigrostriatal dopaminergic projection by positron emission tomography in 4 subjects with clinical features of mild parkinsonism caused by exposure to manganese. The 6-fluorodopa scans were normal. This finding suggests that in early manganism sufficient to cause parkinsonian deficits, damage may occur in pathways postsynaptic to the nigrostriatal system, probably involving striatal or pallidal neurons. Fluorodeoxyglucose scans showed decreased cortical glucose metabolism, the significance of which is discussed.

Variations in the size of the human corpus callosum were examined as a possible morphological substrate of functional asymmetries of the cerebral hemispheres, such as cerebral speech dominance. The midsagittal surface area of the corpus callosum, obtained by magnetic resonance imaging, was measured in 50 patients with epilepsy and 50 neurologically normal control subjects. The mean callosal area did not differ significantly between patients and control subjects, between left-handed and right-handed subjects, or between men and women. When measurements were compared among 44 patients, whose cerebral speech dominance had been determined by the intracarotid injection of sodium amytal, the area of the corpus callosum was significantly greater in patients with right-hemisphere cerebral speech dominance. The mean callosal area was greater by 109 to 159 square millimeters (18-28%) when compared to that of patients with either left-hemisphere speech dominance or bilateral speech representation. This difference in midsagittal surface area could represent as many as 37 to 54 million additional callosal axons in subjects with right-hemisphere cerebral speech dominance.

Eight patients in the chronic progressive stage of multiple sclerosis were studied prospectively with magnetic resonance imaging of the head and neurological examination every 2 weeks for 6 months. There were no clinical relapses and disability ratings did not change between the start and completion of the study. Despite the clinical inactivity, a total of 86 active events (new, reappearing, or enlarging lesions) were identified by magnetic resonance imaging over the 6 months, with 50 (51%) of 98 follow-up scans showing evidence of one or more active lesions. New and changing lesions were indistinguishable in appearance, distribution, and temporal pattern from those previously seen in patients who had relapsing and remitting multiple sclerosis. However, as noted previously, the patients in the chronic progressive stage had many more confluent lesions than did the group in relapse. These results strongly suggest that the frequently observed clinical evolution of multiple sclerosis into a chronic progressive course is not accompanied by a fundamental change in the disease process. In fact the chronic progressive stage seems associated with more active changes demonstrated by scans than does relapsing and remitting multiple sclerosis. This study also confirms our previous experience that serial magnetic resonance imaging is much more sensitive than clinical examination in detecting disease activity in multiple sclerosis.