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Showing papers by "Patrick D. Wall published in 1983"


Journal ArticleDOI
01 Dec 1983-Pain
TL;DR: The dorsal root ganglion with its ongoing activity and mechanical sensitivity could be a source of pain producing impulses and could particularly contribute to pain in those conditions of peripheral nerve damage where pain persists after peripheral anaesthesia or where vertebral manipulation is painful.
Abstract: Single units were recorded in dorsal roots or in the sciatic nerve of anaesthetised rats. It was shown by making sections, by stimulation and by collision that some ongoing nerve impulses were originating from the dorsal root ganglia and not from the central or peripheral ends of the axons. In a sample of 2731 intact or acutely sectioned myelinated sensory fibres, 4.75% +/- 3.7% contained impulses generated within the dorsal root ganglia. In 2555 axons sectioned in the periphery 2-109 days before, this percentage rose to 8.6% +/- 4.8%. There was a considerable variation between animals; 0-14% in intact and acutely sectioned nerves and 1-21% in chronically sectioned nerves. The conduction velocity of the active fibres did not differ significantly from the conduction velocity of unselected fibres. The common pattern of ongoing activity from the ganglion was irregular and with a low frequency (about 4 Hz) in contrast to the pattern of impulses originating in a neuroma which usually have a higher frequency with regular intervals. Slight mechanical pressure on the dorsal root ganglion increased the frequency of impulses. Unmyelinated fibres were also found to contain impulses originating in the dorsal root ganglion. In intact or acutely sectioned unmyelinated axons, the percentage of active fibres 4.4% +/- 3.5% was approximately the same as in myelinated fibres but there were no signs of an increase following chronic section. Fine filament dissection of dorsal roots and of peripheral nerves and collision experiments showed that impulses originating in dorsal root ganglia were propagated both orthodromically into the root and antidromically into the peripheral nerve. It was also shown that the same axon could contain two different alternating sites of origin of nerve impulses: one in the neuroma or sensory ending and one in the ganglion. These observations suggest that the dorsal root ganglion with its ongoing activity and mechanical sensitivity could be a source of pain producing impulses and could particularly contribute to pain in those conditions of peripheral nerve damage where pain persists after peripheral anaesthesia or where vertebral manipulation is painful.

640 citations


Journal ArticleDOI
TL;DR: The aim of these experiments was to sample the properties of lamina I neurones with long ascending projections and, in contrast to cells of deeper laminae, the majority of units were excited following activation of descending pathways in the dorsolateral funiculus.
Abstract: The aim of these experiments was to sample the properties of lamina I neurones with long ascending projections. Recordings have been made from 136 units at the LA/5 level, with ascending axons reaching C2. More than 80% of the units projected via the contralateral dorsolateral white matter and only 10% via the contralateral ventral quadrant. None projected via the dorsal columns. Receptive fields were typically 1–2 cm2 and although a substantial number of units responded to a limited range of intense stim-uli, a greater number of units were fired by both low- and high-threshold stimulation. In contrast to cells of deeper laminae, the majority of units were excited following activation of descending pathways in the dorsolateral funiculus. The functional role of these units is not obvious, but the location of the ascending projection and the influence of descending pathways does not support the notion that the output of lamina 1 constitutes a simple “pain pathway”.

96 citations


Journal ArticleDOI
TL;DR: The results are consistent with the hypothesis that primary afferent C fibers which innervate the spinal cord but not the DCN, play a role in the formation and stability of RFs formed by A fibers in adult animals.

49 citations




Journal ArticleDOI
01 Jun 1983-Pain
TL;DR: It is concluded that primary afferent depolarization is sensitive to peripheral nerve lesions and that it may be particularly dependent on the integrity of the unmyelinated afferents in spite of the fact that p.a.d. is measured as a phenomenon of myelinated Afferents acting on myelination central terminals.
Abstract: 1. In anaesthetized adult rats with intact peripheral nerves, a conditioning orthodromic volley in myelinated afferents produces a prolonged increase in the excitability of the terminals of the afferents which have carried the orthodromic volley and in the terminals of their passive neighbours. This phenomenon, primary afferent depolarization, p.a.d., is shown by the antidromic stimulation of afferents with a micro-electrode in the dorsal horn and by recording the antidromic volley on a cut peripheral nerve.2. If a peripheral nerve is cut and ligated, the size of the myelinated afferent volley generated by stimulation proximal to the cut and measured on dorsal roots is not affected for 14 days after the cut (Wall & Devor, 1981). Similarly the size of the volleys ascending the cord in axons from cord cells remains unaffected.3. If a peripheral nerve is cut and tested after 7-14 days, it produces a markedly decreased p.a.d. on itself and on its neighbours.4. If a nerve is crushed rather than cut, it produces a normal p.a.d. on itself and its neighbours after 7-14 days.5. In animals treated neonatally with capsaicin, there is a severe loss of unmyelinated afferents. Testing the effect of an orthodromic volley in myelinated afferents on the excitability of myelinated afferent central terminals shows that there is a strongly decreased p.a.d. in these animals.6. It is concluded that primary afferent depolarization is sensitive to peripheral nerve lesions and that it may be particularly dependent on the integrity of the unmyelinated afferents in spite of the fact that p.a.d. is measured as a phenomenon of myelinated afferents acting on myelinated afferents.

3 citations