Episodic memory bias and the symptoms of schizophrenia.

Much of the research on episodic memory in schizophrenia spectrum disorders has focused on memory deficits and how they relate to clinical measures such as outcome. Memory bias refers to the modulatory influence that state or trait psychopathology may exert on memory performance for specific categories of stimuli, often emotional in nature. For example, subjects suffering from depression frequently have better memory for negative stimuli than for neutral or positive ones. This dimension of memory function has received only scant attention in schizophrenia research but could provide fresh new insights into the relation between symptoms and neurocognition. This paper reviews the studies that have explored memory biases in individuals with schizophrenia. With respect to positive symptoms, we examine studies that have explored the link between persecutory delusions and memory bias for threatening information and between psychosis and a memory bias toward external source memory. Although relatively few studies have examined negative symptoms, we also review preliminary evidence indicating that flat affect and anhedonia may lead to some specific emotional memory biases. Finally, we present recent findings from our group delineating the relation between emotional valence for faces and memory bias toward novelty and familiarity, both in schizophrenia patients and in healthy control subjects. A better understanding of the biasing effects of psychopathology on memory in schizophrenia (but also on other cognitive functions, such as attention, attribution, and so forth) may provide a stronger association between positive and negative symptoms and memory function. Memory measures sensitive to such biases may turn out to be stronger predictors of clinical and functional outcome.     

Generalization of Frequency Discrimination Learning Across Frequencies and Ears: Implications for Underlying Neural Mechanisms in Humans

Frequency discrimination thresholds (FDTs) at 750, 1500, 3000, and 6000 Hz were measured in 32 normal-hearing listeners before and after each listener practiced the task for 12 h at one of the above frequencies using a single ear. Marked improvements in thresholds taking place over several hours were observed during the frequency- and ear-specific training period. Comparisons between pre- and posttraining thresholds showed large improvements at the trained frequency, but also at other frequencies. The improvements were initially slightly—but significantly—larger at the trained frequency than at untrained frequencies. However, this trained-frequency advantage disappeared rapidly during the course of the two-hour multifrequency posttraining session, suggesting rapid relearning or learning generalization across frequencies. In contrast, no significant ear specificity was found, not even at early stages of the posttraining session. These findings add to earlier results suggesting that, in humans, frequency discrimination learning is only weakly frequency-specific, and they reveal that a complete generalization across frequencies can occur rapidly with little retraining at the initially untrained frequencies. Implications regarding underlying mechanisms are discussed.     

Le traitement du signal en électromyographie: mise au point

Automatic analysis of electromyography (EMG) signals, first operated in 1950 with analogic machines, steeply expanded from 1980 when fast computers and worthwhile programs became available. On-line measurement of response area and latency, averaging of low amplitude waves, fast sorting of motor unit potential shape parameters, computation of the “jitter” between two muscle fibers, turns/amplitude and spectral analysis of interferential pattern records, are some examples of programs currently offered in modern EMG machines. Other techniques are still reserved for research purposes: scanning EMG, decomposition of nerve and muscle compound potentials, measurement of the threshold and firing rate of motor units, trace analysis using tracking models. Finally, the credit for artificial intelligence systems (knowledge based systems, fuzzy logic, neuronal networks) is still not clearly stated.     

Fas receptor expression on B-lineage cells

Mice homozygous for the lpr mutation have B and T cell defects and develop autoantibodies, suggesting that lpr plays a role in their genesis. The lpr defect has been identified as a mutation in the apoptosis-associated Fas receptor (FasR) gene. To begin to define the role of FasR in B cells, we have surveyed FasR expression on B-lineage cells from early progenitors in the bone marrow through their maturation in the periphery. Contrary to some reports, we found that FasR is expressed on B cells at all stages of their development and is highest on germinal center B cells. FasR is not expressed on lpr/lpr-derived cells. These data are consistent with the idea that lpr/lpr mice have an intrinsic B cell defect that may be manifested in developing as well as peripheral B cells. An unexpected finding is that B-1 (CD5) B cells do not constitutively express FasR: FasR becomes detectable on B-1 B cells only after activation.