Isolated ventral and dorsal rat spinal roots incubated in normal (2.5 mM) or high glucose (25 mM) concentrations or in high concentrations of other hexoses were exposed transiently to hypoxia (30 min) in a solution of low buffering power. Compound nerve action potentials, extracellular direct current potentials, and interstitial pH were continuously recorded before, during, and after hypoxia. Ventral roots incubated in 25 mM D-glucose showed resistance to hypoxia. Dorsal roots, on the other hand, revealed electrophysiological damage by hyperglycemic hypoxia as indicated by a lack of posthypoxic recovery. In both types of spinal roots, interstitial acidification was most pronounced during hyperglycemic hypoxia. The changes in the sensitivity to hypoxia induced by high concentrations of D-glucose were imitated by high concentrations of D-mannose. In contrast, D-galactose, L-glucose, D-fructose, and L-fucose did not have such effects. Resistance to hypoxia, hypoxia-generated interstitial acidification, and hypoxia-induced electrophysiological damage were absent after pharmacological inhibition of nerve glycolysis with iodoacetate. These observations indicate 1) that enhanced anaerobic glycolysis produces resistance to hypoxia in hyperglycemic peripheral nerves and 2) that acidification may impair the function of peripheral axons when anaerobic glycolysis proceeds in a tissue with reduced buffering power.

TEE and c-TCD are not concurrent diagnostic tools to detect PFO. Both supplement each other. If both methods are used in all PFO-suspected patients, PFO detection rate is higher than when using either method alone.

These data (incidence, relative risk) can, by taking into consideration various aspects of specialist and hospital hygienic practices, contribute to a continuing optimization of the prevention and treatment of disease.

A compilation of 6 distinctive 18 F-fluorodeoxyglucose positron emission tomography (PET) combined with computed tomography (CT) findings in the acute setting of neurohospital care is presented. In case 1, PET/CT allowed the final diagnosis of circumscribed ischemic infarction by demonstrating a clear pattern of luxury perfusion. In case 2, diagnosis of thalamic abscess was made, whereby PET/CT demonstrated an empty zone. Hypermetabolic enlarged hilar lymph nodes and hypermetabolic spinal lumbar roots in PET/CT led to the diagnosis of neurosarcoidosis in case 3. In case 4, a hypermetabolic brain focus in PET/CT identified the seizure focus in epilepsia partialis continua. A cerebral hemispheric hypometabolism in PET/CT in case 5 supported the diagnosis of Creutzfeldt-Jakob disease, which initially mimicked acute stroke. In case 6, PET/CT detected infective endocarditis as a source of multiple cerebral ischemic lesions. In conclusion, PET/CT can contribute importantly to find the correct diagnosis in acute neurohospital patients.