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E J Carregal

Publications and source records attributed to E J Carregal.

14 recordsLinked to original sources

Neurophysiology of pain-peripheral aspects. Speculation concerning the possibility of a unitary peripheral cutaneous input system for pressure, hot, cold and tissue damage.

The gate theory of pain is criticized at three levels: (1) at the dorsal horn "gate", where pre-synaptic inhibition in the primary afferent endings may go beyond mere reduction of synaptic power at the afferent endings and induce antidromic impulses (dorsal root reflexes) that may modulate peripherally by blocking; (2) central to the "gate", where postsynaptic neuronal repetitive (epileptiform) firing is believed to be an important underlying mechanism in clinical chronic pain syndromes; and, (3) in the periphery, where there is more to input coding than a balance between the ratio of large and smaller fiber inputs. Contrary to the belief of many sensory neurophysiologists, the present authors contend that pattern theory is viable; and that specificity, while important and not to be ignored, should be considered as only a partially evolved refinement superimposed on a basic underlying spatial and temporal patterning of input that probably requires central decoding, which begins in the dorsal horn.

Mechanoreceptors

The site of anoxic block in the spinal monosynaptic pathway.

Asphyxiation of the spinal cord for periods of 2-4 min leads to block of the monosynaptic pathway. At about the same time this blockage takes place, the afferent action potentials fail to invade the presynaptic terminals. Asphyxiation also interferes with the antidromic invasion of motoneurons, and the failure of the antidromic action potentials to invade the motoneuron dendrites coincides with the time of the disappearance of the orthodromic monosynaptic responses. During reoxygenation, both the presynaptic terminals and the dendrites recover their function, or rather their polarization, in a few seconds and yet synaptic transmission reappears only after several minutes. It is postulated that failure of synaptic transmission during asphyxia is due to depolarization of both the presynaptic terminals and the dendrites of the postsynaptic elements. However, repolarization of these elements during reoxygenation, is not sufficient to reestablish synaptic transmission, but recovery of some unidentified biochemical process is apparently necessary.

Animals