Faculty Bibliography

We report a patient with a third nerve palsy and contralateral eyelid retraction from a thalamic-midbrain infarction. Magnetic resonance imaging confirms that this unusual clinical combination, previously termed 'the plus-minus lid syndrome,' results from a lesion in the region of the nucleus of the posterior commissure with extension to the third nerve fascicle

The authors report a 32-year-old woman who had undergone repair of an occipital encephalocele in infancy and who experienced a 20-year history of progressive hearing loss and intermittent vertigo. After parturition, she developed a rapidly progressive quadriparesis and brain-stem dysfunction associated with persistent intraventricular and subarachnoid hemorrhage. Serial magnetic resonance (MR) images showed progressive deposition of hemosiderin along the surface of the brain, brain stem, and spinal cord, and enhanced thickened membranes at the site of the original encephalocele repair. Posterior fossa exploration disclosed hemorrhagic membranes, which were resected; despite removal of this tissue, the patient deteriorated and died. Postmortem examination confirmed iron-containing pigment along the meninges, cerebral hemispheres, brain stem, spinal cord, and cranial nerves accompanied by atrophy of the superficial cerebellar cortex. It is concluded that superficial siderosis may accompany encephalocele repair. This is believed to be the first report in the literature of superficial siderosis of the central nervous system to correlate in vivo MR images with autopsy results

PURPOSE: Recent papers have hypothesized that diamagnetic effects of clotting and conformational changes in aging red blood cells immobilize the hemoglobin protein and thus are responsible for the marked hypointensity of acute hematomas on T2-weighted spin-echo MR images. To test that hypothesis, the authors evaluated 24 hemorrhagic components of intracranial hemorrhagic lesions using accepted criteria based on spin-echo images as the definitions of the stage of the hemorrhage. METHODS: As a measure of the effects of macromolecular (hemoglobin protein) immobility, magnetization transfer contrast was elicited using a pulsed saturation magnetization transfer experiment. The apparent magnetization transfer contrast (AMTC) was determined by comparing the signal intensities of saturated with unsaturated images and quantified for acute isolated hemorrhages, acute nonisolated hemorrhagic lesions, and subacute-to-chronic hemorrhages. RESULTS: The AMTC of isolated acute hemorrhage was significantly less than that of normal, white matter and gray matter, indicating the lack of significant magnetization transfer and therefore the lack of effects of restriction of hemoglobin mobility on the signal intensity of acute hemorrhage. Acutely hemorrhagic tissue (nonisolated acute hemorrhage) has significantly more AMTC than isolated acute hemorrhage, but still not exceeding that of brain parenchyma. CONCLUSION: This in vivo data concurs with in vitro data and reinforces the concept that the marked hypointensity of acute hematomas is mainly a magnetic susceptibility effect

PURPOSE: To assess, in an in vitro model of acute hematoma, whether hemoglobin immobilization by clot and red cell membrane aging can account for the T2 shortening usually attributed to deoxyhemoglobin. METHODS: Clotted and heparinized blood samples were packed (100% hematocrit). The apparent magnetization transfer rate (AMTR), T1 and T2 relaxation rates of the samples, and images with a volunteer's head were obtained at 1.5 T. RESULTS: The AMTR and T1 and T2 relaxation rates were unaffected by the presence of clot. The AMTR was unaffected by red cell aging. The diamagnetic packed blood samples, which are much denser than brain, were isointense to gray matter on T2-weighted images and had about one-fifth the AMTR of white matter. CONCLUSIONS: Hemoglobin immobilization by clot structure or red cell contraction with aging is insignificant and does not contribute to the T2 shortening of acute hematoma. The low AMTR and T2 relaxation rates of diamagnetic blood appear to be caused by the mobility of hemoglobin and by the red cell's lack of immobile macromolecular structures such as those associated with nucleated brain cells

Because administration for 1 week of the GnRH antagonist Nal-Glu GnRH had been shown to decrease FSH secretion from supranormal to normal in men with gonadotroph adenomas, we investigated the effect of prolonged administration of Nal-Glu on the size of gonadotroph adenomas. To quantitate the effect of Nal-Glu GnRH on gonadotroph adenoma size, we first developed a technique for calculating adenoma volume. The technique involved collecting magnetic resonance (MR) imaging data from each adenoma at 1-mm slice intervals in the coronal, axial, and sagittal views and using the Softvu computer program to calculate adenoma volume from the MR data. The precision of this technique, as judged by the coefficients of variation of the calculations of the same view of the same study three times, was 1.7%, 1.0%, and 1.0% for each of three studies. When Nal-Glu GnRH (5 mg, sc, every 12 h) was self-administered for 3-12 months to five men with gonadotroph adenomas and supra-normal serum FSH concentrations, the serum FSH concentrations decreased to normal or below normal for the entire treatment period. Adenoma size, however, did not change during treatment in any of the five men. We conclude that calculating pituitary adenoma volume from MR data using the Softvu computer program is a highly reproducible technique, but that Nal-Glu GnRH is not an effective treatment for reducing gonadotroph adenoma size. The failure of Nal-Glu to reduce adenoma size despite its success in reducing FSH secretion suggests that FSH secretion from gonadotroph adenomas is dependent on endogenous GnRH, but growth of gonadotroph adenomas is not

The purpose of this study was to characterize the proton magnetic resonance (MR) spectroscopic findings in the brains of patients infected with human immunodeficiency virus (HIV). Peak areas were used to calculate metabolite ratios. Spectra were analyzed by blinded readers who calculated areas under metabolite peaks. MR images were evaluated by blinded readers, with both white and gray matter being rated as normal or abnormal. An aggregate index that combined N-acetylaspartate/creatine (Cr), choline/Cr, and marker peak/Cr ratios resulted in mean scores for patients and control subjects of 4.4 +/- 1.5 (standard deviation [SD]) and 2.5 +/- 0.4, respectively (P = .001). Eight of 11 patients (73%) had abnormal MR images versus four of 11 control subjects. Thirteen of 15 patient spectra (87%) were abnormal (> 2 SDs from the mean of the control subjects), while only one of 10 control spectra was abnormal. These initial results indicate that proton MR spectroscopy is a potentially useful modality for detecting HIV involvement in the central nervous system

We report a patient with biopsy proven chronic inflammatory demyelinating polyneuropathy whose magnetic resonance imaging demonstrated abnormal enhancement of the cauda equina after administration of gadolinium. Enhancement may reflect alteration of the blood-nerve barrier secondary to inflammation. Magnetic resonance imaging of the cauda equina could be a useful adjunct in the early diagnosis of chronic inflammatory demyelinating polyneuropathy