Magnetic resonance imaging (MRI) has proven to be an effective noninvasive technique for identifying lesions in patients with temporal lobe epilepsy. It has also been suggested that MRI may be sensitive to transient functional or metabolic changes in brain tissue. Increased brain electrical activity as monitored by electroencephalography causes changes in cerebral metabolism that may be responsible for focal or regional alterations in signal in the MRI of some patients. To test this hypotheses, experimental interictal cortical foci were produced in rats by topical application of penicillin to one hemisphere of the brain. In vivo MRI and phosphorous-31 (31P) spectroscopy of the focal and contralateral hemifield were performed in a 30-cm bore 1.89-T Bruker MSL system. 31P spectroscopy revealed no quantifiable differences in pH or in phosphocreatinine and ATP levels between the focal area and the contralateral hemisphere or between experimental and saline-treated control animals. There were also no differences in proton MRI. Similar areas of prolonged T2 were found near the cortex and in the deeper parenchyma in 55% of the experimental animals and 50% of the controls. These results suggest that the electrical activity from an interictal cortical spike focus is not severe enough to perturb cerebral metabolism sufficiently to be detectable by 31P spectroscopy or proton imaging techniques.
The effects of the non-glucocortioid 21-aminosteroid, tirilazad mesylate (U-74006F), on MRI and clinical findings in guinea pigs with experimental allergic encephalomyelitis were compared to treatment with methylprednisolone sodium succinate (MPSS). A dose response experiment for U-74006F was performed 1, 3 and 10 mg/kg/day IP on day 0–12 after immunization. Additionally, the 3 mg/kg/day IP dose was extended to 24 and 35 days. MPSS was given in three different protocols at doses ranging from 0.8 to 3.2 mg/kg/day. Abnormalities in T2-weighted images were assessed as measures of edema and inflammation and gadolinium-DTPA enhanced TI-weighted images were used to determine blood-brain barrier integrity. U-74006F improved the clinical status at doses of 3 and 10 mg/kg. For example, maximum clinical score was halved at 10 mg/kg/day (P < 0.01). The presence of gadolinium-DTPA in the parenchyma was also decreased at 3 and 10 mg/kg/day U-74006F although maximum MRI scores were decreased only in the 10 mg/kg U-74006F group. Clinical disease suppression seen with 3 mg/kg treatment on days 0–12 reverted to control at > 24 days of dosing. MPSS treatment considerably worsened the clinical outcome of EAE Mean clinical scores for vehicle and the highest MPSS dose were 0.94 ± 0.66 versus 2.64 ± 1.49 (P < 0.05). The combination of decreased T2-weighted abnormalities, clinical signs and gadolinium-DTPA permeation in the U-74006F treated animals suggested protection of the blood–brain barrier without the severe glucocorticoid effects associated with steroid therapy.
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