This preliminary study provides support for the existence of neuronal loss, neuronal metabolic dysfunction, or interneuronal neuropil reduction in the hippocampal region in male patients with familial bipolar I disorder. The finding of normal hippocampal choline levels in these patients does not provide support for ongoing myelin breakdown or glial cell proliferation in this brain region in familial bipolar I disorder. The significant association between illness duration and N-acetylaspartate concentration in the right hippocampus supports the idea that neuronal pathology may increase with disease progression and that this effect may be lateralized, involving the right but not the left hippocampus.

Many variables appear to impact the mortality rate within the neurosurgical population. The authors' observations have illuminated some of the reasons why: the data are elusive, documentation is variable, and the modes of statistical analysis are questionable. The first step in addressing this issue is to identify that there is a problem. The authors believe that this study has done so. Presently there is no definitive or reliable source for rating the quality of overall neurosurgical care, nor is there a good and complete source for understanding the quality of neurosurgical care in the US. It is important to view these results as the initial steps to a better understanding of patient outcomes, their measures, and their impact on neurosurgical practice.

A 13-year-old girl presented acutely with an episode of headache and signs of elevated intracranial pressure from a pineal gland tumor causing obstructive hydrocephalus. After an endoscopic third ventriculostomy and pineal gland biopsy, she was diagnosed with pineoblastoma. She was treated with surgical resection, craniospinal radiotherapy, and subsequent chemotherapy. Brain MRIs were performed every 3 months after surgery and remained stable with no new lesions or signs of residual tumor. However, a follow-up brain MRI performed 6 months after chemotherapy showed some small white matter nonenhancing lesions in supratentorial subcortical areas and within the cord at C7. She had no neurologic symptoms at that time and the white matter lesions improved over the next 3 months.However, 10 months later, she developed acute weakness of her left arm and leg and blurry vision. Her neurologic examination confirmed left optic neuritis and moderate left hemiparesis. Routine laboratories did not show any abnormalities. A new brain MRI showed new and enhancing lesions in the brain and spinal cord, including cerebellar hemispheres, left cerebellar peduncle, subcortical white matter, left optic nerve, and multilevel (thoracic and lumbar) intramedullary spinal cord lesions ( figure, A and B). Some of them were round and had a complete ring-enhancing pattern. Additional MRI sequences such as diffusionweighted imaging and perfusion-weighted imaging did not clarify the nature of the lesions (normal apparent diffusion coefficient [ADC] values and slightly increased perfusion in enhancing areas). Spectroscopy was normal. Magnetic resonance angiography demonstrated no flow-limiting stenosis. The patient and her family declined a lumbar puncture. She was empirically treated with high-dose IV steroids and her examination results returned to normal after 6-8 weeks.Question for consideration:1. What is your differential diagnosis regarding her second neurologic presentation?GO TO SECTION 2