Our findings suggest that a loss of bundle coherence is present in prefrontal white matter. This loss of coherence may contribute to prefrontal cortical pathology in patients with bipolar disorder.
It is unclear whether sporadic reports of concurrent multiple sclerosis (MS) and chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) represent coincidence or whether these two demyelinating disorders are pathogenically related. We utilized the sensitivity of magnetic resonance imaging (MRI) in detecting central nervous system (CNS) lesions to investigate 16 patients with CIDP. Six of the 16 had periventricular, subcortical, and brainstem white matter lesions indistinguishable from those seen in MS. Three of these patients had definite clinical and laboratory evidence of MS; three others with abnormal MRIs had no findings indicative of CNS disease. Previous reports have indicated that a significant number of MS patients have peripheral nerve demyelination. Our study suggests that many CIDP patients have concurrent CNS demyelination. Taken together, these observations support the existence of a central-peripheral inflammatory demyelinating syndrome. Whether this combined demyelinating syndrome lies on a spectrum between MS and CIDP or is a separate pathogenic entity will require further investigation.
Although neurosarcoidosis seems to occur in only 5% to 10% of patients who have sarcoidosis, it may lead to significant complications. The diagnosis of neurosarcoidosis usually relies on indirect information from imaging and spinal fluid examination. Although MR imaging remains the most sensitive technique for detecting neurologic disease, other tests, including positron emission tomography scanning and cerebral spinal fluid examination, can provide important information. The role of immunosuppressive agents such as methotrexate, cyclophosphamide, and azathioprine has been expanded, and these agents should be considered for the treatment of some manifestations of neurosarcoidosis. Reports of the antitumor necrosis factor agent infliximab suggest that this drug can be helpful for patients who have neurosarcoidosis.
Institutional review board approval, with waived consent, was obtained to develop a spine-labeling algorithm with retrospectively obtained deidentified HIPAA-compliant data. An automated magnetic resonance (MR) imaging technique to rapidly survey the entire spine and provide definitive numbering of disks and vertebrae was compared with neuroradiologist assignments in 50 cases. Contiguous two-station sagittal fast gradient-recalled-echo sequences with 35-cm fields of view (FOVs) were preprogrammed for full cervical, thoracic, and lumbar spine coverage (combined 70-cm FOV, seven sections, 15 mm left of to 15 mm right of midline, 4-mm section thickness, 1-mm intersection gap, 512 x 352 matrix, 58/2.0 [repetition time msec/echo time msec], 30 degrees flip angle, 15.6-kHz bandwidth, 42-second acquisition time). In all cases, the neuroradiologist could visualize and definitively number all cervical, thoracic, and lumbar levels on automated spine survey iterative scan technique localizer studies. Automated disk-vertebra detection and numbering were concordant with neuroradiologist assignments in all cases. The entire spine can be surveyed with subminute, submillimeter in-plane resolution MR imaging. Cervical, thoracic, and lumbar vertebrae and disks can be readily identified and definitively numbered by means of visual inspection or semiautomated computer algorithm.
Chronic administration of vigabatrin (gamma-vinyl GABA) in dogs produces reversible microvacuolation (intramyelinic edema) in discrete brain regions. Histologic changes are most notable in the columns of the fornix and regions of the hypothalamus, thalamus, optic tract, and hippocampus. In an attempt to image these changes in vivo, we performed high-field MRI on seven treated and four control dogs at baseline and after 15 weeks of dosing with vigabatrin (300 mg/kg/d). All dogs underwent parallel electrophysiologic assessment to determine the effects of vigabatrin on afferent conduction. At 15 weeks, all treated dogs showed increased T2- and decreased T1-weighted signals, with changes from baseline most prominent in the columns of the fornix and to a lesser degree in the surrounding hypothalamus and thalamus. MRIs performed on control dogs were unremarkable. We then perfused a random selection of four treated and two control dogs and imaged their brains ex vivo prior to sectioning. Ex vivo imaging confirmed the in vivo findings and strongly correlated with both electrophysiologic and subsequent histopathologic findings. Imaging was repeated in the surviving dogs 5 and 12 weeks after discontinuation of dosing. Signal abnormalities in the treated dogs progressively diminished during recovery, paralleling the electrophysiologic and histopathologic results. These findings demonstrate that MRI can detect signal changes anatomically congruent with vigabatrin-induced intramyelinic edema and suggest that MRI may provide a useful noninvasive tool for monitoring patients during clinical trials.
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