PURPOSE The hippocampus is central to the pathophysiology of schizophrenia. Histology shows abnormalities in the dentate granule cell layer (DGCL), but its small size (~100 micron thickness) has precluded in vivo human studies. We used ultra high field magnetic resonance imaging (MRI) to compare DGCL morphology of schizophrenic patients to matched controls’. METHOD Bilateral hippocampi of 16 schizophrenia patients (10 male) 40.7±10.6 years old (mean ±standard deviation) were imaged at 7 Tesla MRI with heavily T2*-weighted gradient-echo sequence at 232 micron in-plane resolution (0.08 μL image voxels). Fifteen matched controls (8 male, 35.6±9.4 years old) and one ex vivo post mortem hippocampus (that also underwent histopathology) were scanned with same protocol. Three blinded neuroradiologists rated each DGCL on a qualitative scale of 1 to 6 (from “not discernible” to “easily visible, appearing dark gray or black”) and mean left and right DGCL scores were compared using a non-parametric Mann-Whitney test. RESULTS MRI identification of the DGCL was validated with histopathology. Mean right and left DGCL ratings in patients (3.2±1.0 and 3.5±1.2) were not statistically different from controls’ (3.9±1.1 and 3.8±0.8), but patients’ had a trend for lower right DGCL score (p=0.07), which was significantly associated with patient diagnosis (p=0.05). The optimal 48% sensitivity and 80% specificity for schizophrenia was achieved with a DGCL rating of ≤2. CONCLUSION Decreased contrast in the right DGCL in schizophrenia was predictive of schizophrenia diagnosis. Better utility of this metric as a schizophrenia biomarker may be achieved in future studies of patients with homogeneous disease subtypes and progression rates.

A healthy 25-year-old man presented with a mass in the right submandibular triangle that had been present for several months. At physical examination, a firm 3-cm mass was noted along the posterior aspect of the right mandibular condyle. Trigeminal and facial nerve functions were intact, and no mucosal lesions were identified. Panoramic radiography and contrast material-enhanced computed tomography (CT) of the facial bones were performed. The patient underwent marginal mandibulectomy and biopsy of the mass, which confirmed the diagnosis of ameloblastoma and dentigerous cyst. Next, segmental mandibulectomy, from the right condyle to the mid portion of the right mandibular body, was performed with curative intent, and the mandible was reconstructed with an osteocutaneous fibular free flap and a reconstruction plate. Subsequent complex closure of the incision with multiple end-to-end vascular anastomoses was required.

Functional MR imaging is being performed with increasing frequency in the typical neuroradiology practice; however, many readers of these studies have only a limited knowledge of the functional anatomy of the brain. This text will delineate the locations, anatomic boundaries, and functions of the cortical regions of the brain most commonly encountered in clinical practice---specifically, the regions involved in movement and language.

Purpose. Metronidazole-induced encephalopathy (MIE) has been rarely reported. We report a case in a patient with end-stage liver disease (ESLD). Summary. A 63-year-old male with ESLD secondary to hepatitis C virus presented with progressively worsening fatigue, slurred speech, aphasia, vomiting, and left-sided facial droop after completing a 2-week course of metronidazole for recurrent Clostridium difficile-associated diarrhea. He completed a previous course of metronidazole 3 weeks prior to presentation. He is on the liver transplant waiting list and has known hepatic encephalopathy. MRI revealed hyperintense T2 signals involving the bilateral dentate nuclei, inferior colliculi and splenium of the corpus callosum, and increased diffusion restriction at the splenium of the corpus callosum. His neurological function improved over the next several days. He underwent liver transplantation 6 days after admission. A follow-up MRI 6 weeks after presentation revealed resolution of abnormalities; however, paresthesias persisted 6 months after MIE diagnosis. Conclusion. An ESLD patient with hepatic encephalopathy developed MIE after a relatively short course of metronidazole. Metronidazole has been shown to accumulate in patients with ESLD. Increased awareness for neurotoxicity when using metronidazole in ESLD patients is warranted, especially in those with potentially confounding hepatic encephalopathy.

No abstract