Hyperglycemia-induced unilateral basal ganglion lesions occur mostly in Asian patients. A signal abnormality in the basal ganglion region is evident on these patients' neuroimaging. Despite characteristic imaging findings and clinical manifestations, the underlying mechanism is still unclear. To clarify the underlying pathophysiology of unilateral basal ganglion lesions, we examined the [18F]-fluorodeoxyglucose (FDG) positron emission tomography (PET) findings in 3 patients with hyperglycemia. The PET studies were performed at 3 weeks, 5 weeks, and 7 months after clinical onset. The markedly reduced rates of cerebral glucose metabolism in the corresponding lesions on T1-weighted magnetic resonance images provided direct evidence of regional metabolic failure. We suggest that the metabolic derangements associated with hyperglycemia and vascular insufficiency contribute to regional metabolic failure in patients with poorly controlled diabetes mellitus.

Colchicine and 3-hydroxy-3-methy-glutaryl coenzyme A (HMG-CoA) reductase inhibitors are well known to cause myopathy. Myotoxicity is dose-dependent in both drugs; therefore, the onset of symptoms usually takes months or years. We report the case of a patient with chronic renal failure who had been taking simvastatin for 2 years and developed acute weakness 2 weeks after the start of treatment with colchicines for recurrent gout. The electromyography and elevated muscle enzymes indicated that his symptoms were caused by myopathy. When this patient stopped taking both drugs, his weakness resolved rapidly. Acute myopathy induced by combination therapy with colchicines and simvastatin is rare. In patients with chronic renal failure, co-administration of colchicine with simvastatin may accelerate the onset of myopathy because CYP3A4 (part of cytochrome P450) is crucial in the breakdown of both drugs. When adding colchicine to a medication regimen that includes a HMG-CoA reductase inhibitor for patients with renal insufficiency, drugs that are metabolized outside the CYP3A4 system (e.g., fluvastatin and pravastatin) should be selected instead.

ABSTRACT. A 12-year-old female miniature poodle showed a 3-month history of neurological signs. Magnetic resonance imaging disclosed a high intensity tumor mass in the right cerebral hemisphere with compression of the lateral ventricle. At necropsy, a 2 × 3 cm white, friable mass was found in the right ventral pyriform lobe. Microscopically, the tumor cells were large, polygonal to round cells supported by a sparse fibrovascular stroma. The tumor cells typically possesed finely granular, pale eosinophilic cytoplasm with strongly positive periodic acid-Schiff (PAS) reaction. The tumor cells were immunopositive for vimentin, NSE and S-100. Ultrastructurally, the tumor cells showed large amounts of granules in the cytoplasm, and absence of basement membrane. Based on the above-mentioned findings, the intracranial granular cell tumor was diagnosed.

Background and purpose: To investigate the relationships of diabetic neuropathy to all-cause and diabetes-related mortality in patients with type 2 diabetes after controlling for significant correlates. Methods: We examined 326 patients diagnosed as diabetic polyneuropathy by nerve conduction study in Keelung city, Taiwan, in 2002 and followed them up to ascertain the cause and date of death until the end of 2006. The cause and date of death were recorded for the deceased patients. Information on significant correlates in association with diabetic polyneuropathy and all-cause and diabetes-related mortality was also collected. Results: With median follow-up time of 62.28 months, 44 patients with type 2 diabetes died. The cause of death related to diabetes accounted for 59% (n = 26) of the deceased. Univariate analysis shows that the presence of diabetic neuropathy confers higher risk for all-cause mortality (hazard ratio [HR] = 4.88) and mortality from diabetes (HR = 6.58). The significant finding still persisted after adjustment for age, gender, blood pressure, smoking, history of cardiovascular/cerebrovascular disease, duration of diabetes, waist circumference, fasting plasma glucose, total cholesterol, hemoglobin, and creatinine (adjusted HR = 4.44 for all-cause death and adjusted HR = 11.82 for diabetes-related mortality, respectively). Conclusions: Diabetic polyneuropathy was an independent predictor for all-cause and diabetes-related mortality. The presence of neuropathy together with other significant prognostic factors is informative to predict all-cause death and death from diabetes-related disease for patients diagnosed as type 2 diabetes.