Narrow Results

The interaction of large populations of neurons gives rise to electrical events in the brain, which can be observed at several spatial scales. We show that mutually consistent explanations and simulation of experimental data can be achieved for cortical gamma activity, synchronous oscillation, and the main features of the EEG power spectrum including the cerebral rhythms, and evoked potentials. These simulations include consideration of dendritic and synaptic dynamics, AMPA, NMDA and GABA receptors, and intracortical and cortical/subcortical interactions.

The dynamic properties exhibited in the simulations, Hebbian synaptic modification regulated by a limited set of innate "reward" mechanisms, and infomax principles, can be combined to yield an explanation of elementary adaptive learning.

Background: Although different types of neural mobilization (NM) exercises induce different amounts of longitudinal nerve excursion and strain, the question whether the increased longitudinal stress and nerve excursion from sliding or tensioning intervention may subtly affect the neural functions has not been answered yet.

Objective: To compare the effects of tensioning NM versus sliding NM of the median nerve on peripheral and autonomic nervous system function.

Methods: In this randomized controlled trial, 90 participants were randomly assigned to tensioning NM, sliding NM, or sham NM. The neurophysiological outcome measures included peak-to-peak amplitude of the dermatomal somatosensory evoked potential (DSSEP) for dermatomes C6, C7, C8, and T1. Secondary outcome measures included amplitude and latency of skin sympathetic response. All outcome measures were assessed pretreatment, immediately after the two weeks of treatment and one week after the last session of the treatment.

Results: A 2-way repeated measures ANOVA revealed significant differences between the three groups. The post hoc analysis indicated that tensioning NM significantly decreased the dermatomal amplitude for C6, C7, C8, and T1 ($p<0.005$). Sympathetic skin responses in the gliding NM group showed lower amplitudes and prolonged latencies post-treatment when compared to tensioning NM group ($p<0.05$). In contrast, no significant changes were observed in the DSSEPs and skin sympathetic responses for participants in the sham treatment group ($p>0.05$).

Conclusions: A tensioning NM on the median nerve had a possible adverse effect on the neurophysiology variables of the nerves involved in the neural mobilization. Thus, tensioning NM with the current parameters that place increased stress and strain on the peripheral nervous system should be avoided.

Despite extensive experimental investigations of human amnesia, the basic nature of this vivid syndrome remains surrounded by controversy. The dynamics of amnesia, the rapid, selective and long-lasting plasticity of hippocampal synapses, and the connections between the hippocampal formation and association neocortex. all suggest that amnesia may result from damage to the medial temporal site where the recent declarative memory trace is temporarily laid down. Alternatively, amnesics' preserved capacity for procedural learning on indirect memory tests suggests that their deficit may rather be in intentional, sustained and directed (i.e., active) encoding/retrieval processes. It has been difficult to distinguish between these possibilities because amnesics are most impaired on direct memory tasks that involve both a new integrative trace and active processes. It is possible that different amnesics may have a relatively greater defect either in the memory trace, or in active memory processes, or both, and these differences could correspond to differences in their anatomical lesions. Specifically, hippocampal formation lesions may disrupt all recent declarative memory traces, whereas brainstem lesions could produce amnesia by impairing modulatory processes essential for encoding/retrieval or for storage. In this model, the different areas of association neocortex with bidirectional hippocampal connections would contribute specificity to encoding/retrieval, with posterior areas encoding the sensory/semantic aspects of events, and prefrontal cortex the ongoing context. Active modulatory processes arising in the brainstem would then function to integrate this extensive declarative memory system. The cognitive correlates and neural substrates of the evoked potentials recorded during declarative memory tasks suggest that they may embody such modulatory processes. Finally, since the prefrontal cortex and the medial temporal lobe appear to control the onset, intensity and duration of the ascending neuromodulation, lesions of these structures may impair aspects of both the trace and of the processes supporting declarative memory. In summary, a model is proposed in which the association neocortex (encoding/retrieval) and hippocampus (trace) are integrated by the brainstem (modulation) to produce the psychological properties of declarative memory.