Neurochemical studies in animal models of epilepsy have demonstrated the importance of multiple neurotransmitters and their receptors in mediating seizures. The role of opiate receptors and endogenous opioid peptides in seizure mechanisms is well developed and is the basis for measuring opiate receptors in patients with epilepsy. Patients with complex partial seizures due to unilateral temporal seizure foci were studied by positron emission tomography using 11C-carfentanil to measure mu-opiate receptors and 18F-fluoro-deoxy-D-glucose to measure glucose utilization. Opiate receptor binding is greater in the temporal neocortex on the side of the electrical focus than on the opposite side. Modeling studies indicate that the increase in binding is due to an increase in affinity or the number of unoccupied receptors. No significant asymmetry of 11C-carfentanil binding was detected in the amygdala or hippocampus. Glucose utilization correlated inversely with 11C-carfentanil binding in the temporal neocortex. Increased opiate receptors in the temporal neocortex may represent a tonic anticonvulsant system that limits the spread of electrical activity from other temporal lobe structures.

D2 dopamine and S2 serotonin receptors were imaged and measured in healthy human subjects by positron emission tomography after intravenous injection of 11C-labeled 3-N-methylspiperone. Levels of receptor in the caudate nucleus, putamen, and frontal cerebral cortex declined over the age span studied (19 to 73 years). The decline in D2 receptor in males was different from that in females.

Although the lumbar intervertebral discs with posterior combined anular tears are likely to produce pain, the validity of these signs for predicting discogenic lumbar pain is limited.

We report on a new familial neurodegenerative disease with associated dementia that has presented clinically in the fifth decade, in both genders, and in each of several generations of a large family from New York State-a pattern of inheritance consistent with an autosomal dominant mode of transmission. A key pathological finding is the presence of neuronal inclusion bodies distributed throughout the gray matter of the cerebral cortex and in certain subcortical nuclei. These inclusions are distinct from any described previously and henceforth are identified as Collins bodies. The Collins bodies can be isolated by simple biochemical procedures and have a surprisingly simple composition; neuroserpin (a serine protease inhibitor) is their predominant component. An affinity-purified antibody against neuroserpin specifically labels the Collins bodies, confirming their chemical composition. Therefore, we propose a new disease entity-familial encephalopathy with neuroserpin inclusion bodies (FENIB). The conclusion that FENIB is a previously unrecognized neurodegenerative disease is supported by finding Collins bodies in a small kindred from Oregon with familial dementia who are unrelated to the New York family. The autosomal dominant inheritance strongly suggests that FENIB is caused by mutations in the neuroserpin gene, resulting in intracellular accumulation of the mutant protein.

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This study evaluated the effect of age on susceptibility to muscular weakness and damage caused by eccentric (ECC) exercise and determined whether this susceptibility was altered by resistance training. Young and older women performed concentric (CON) and ECC one repetition maximum (1 RM) strength tests of the quadriceps femoris. Older women also performed knee extension training for 12 weeks. An unaccustomed bout of ECC knee extension exercise was performed before and after training, and CON and ECC 1 RM were reassessed for 11 days after the ECC bout. Magnetic resonance imaging was used to evaluate changes in muscle water content associated with muscle damage. Before training, older subjects showed a larger decline in CON (p =.008) and ECC (p =.03) strength induced by the unaccustomed ECC bout, compared with the young subjects. One day following the ECC bout, the older women showed a 24% reduction in CON and a 27% reduction in ECC 1 RM, compared with only 6% (CON) and 10% (ECC) in the younger women. A magnetic resonance imaging evaluation indicated that edema or damage was significantly greater in the older untrained women than it was in young women (p <.05), but the resistance-trained older women showed no greater muscle injury than the young women (p >.05). Resistance-trained older women showed no greater decline than sedentary young women in either CON (p >.05) or ECC (p >.05) strength. In conclusion, sedentary older women are more susceptible to ECC-induced muscle dysfunction, but resistance training reduces this susceptibility.

Clinical, neuroimaging (cerebral CT), and angiographic observation suggest that a subset of anti-Ro(SS-A) antibody-positive, in contrast with -negative, CNS-SS patients have more serious and extensive CNS disease, some with frank cerebral angiopathy. Anti-Ro(SS-A) antibodies are postulated to play a role in mediating or potentiating vascular injury in CNS-SS.

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