Showing papers by "Patrick D. Wall published in 1981"

The distribution of nine peptides in rat spinal cord with special emphasis on the substantia gelatinosa and on the area around the central canal (laminaX)

Abstract: The comparative distribution of nine peptides was examined in the L4 segment of the rat cord using the peroxidase antiperoxidase technique. The peptides examined were substance P, neurotensin, cholecystokinin, methionine-enkephalin, oxytocin, neurophysin, adrenocorticotrophin, thyrotropin releasing hormone, and vasoactive intestinal polypeptide. No transport blocking agents were used and in spite of this cell bodies containing substance P, neurotensin, cholecystokinin, and methionine-enkephalin were observed. All peptides except for thyrotropin releasing hormone were observed in fibers in laminae I and II. All peptides were present in the area around the central canal, lamina X. Each peptide had its own characteristic distribution within fibers in the gray and white matter.

Plasticity in the spinal cord sensory map following peripheral nerve injury in rats.

Abstract: The medial part of the L4 and 5 dorsal horn in adult rats is dominated by afferents from the toes and foot. After transection of the sciatic and saphenous nerves, virtually all cells in this region are left without any peripheral receptive field. Beginning 4 to 5 days after nerve section, however, many peripherally deafferented cells take on a novel receptive field on the thigh, lower back, or perineum. The new receptive fields are served by intact nerves ending in proximal skin rather than by misdirected sprouts of cut toe-foot nerves. Thus, peripheral axotomy results in synaptic reorganization in the spinal cord proper. Receptive field reorganization occurs after nerve transection, ligation, or ligation with distal transection but does not occur if the nerve is crushed. If a cut nerve is sutured and regeneration is permitted, spinal reorganization is reversed and the toe-foot afferents regain exclusive dominance of the medial dorsal horn.

Effect of peripheral nerve injury on receptive fields of cells in the cat spinal cord

Abstract: When the sciatic and saphenous nerves are cut and ligated in adult cats, the immediate effect is the production of a completely anesthetic foot and a region in medial lumbar dorsal horn where almost all cells have lost their natural receptive fields (RFs). Beginning at about 1 week and maturing by 4 weeks, some 40% of cells in the medial dorsal horn gain a novel RF on proximal skin, that is, upper and lower leg, thigh, lower back, or perineum. This new RF is supplied by intact proximal nerves and not by sciatic and saphenous nerve fibers that sprouted in the periphery. During the period of switching of RFs from distal to proximal skin there was no gross atrophy of dorsal horn grey matter and no Fink-Heimer stainable degeneration of central arbors and terminals of peripherally axotomized afferents. In intact animals medial dorsal horn cells showed no sign of response to mechanical stimulation of proximal skin. RFs of some of the cells had spontaneous variations in size and sensitivity, but these were not nearly sufficient to explain the large shifts observed after chronic nerve section. Tetanic electrical stimulation of skin or peripheral nerves often caused RFs to shrink, but never to expand. Although natural stimuli of proximal skin would not excite medial dorsal horn cells in intact or acutely deafferented animals, it was found that electrical stimulation of proximal nerves did excite many of these cells, often at short latencies. In the discussion we justify our working hypothesis that the appearance of novel RFs is due to the strengthening or unmasking of normally present but ineffective afferent terminals, rather than to long-distance sprouting of new afferent arbors within the spinal cord.

Effects of capsaicin applied locally to adult peripheral nerve. II. Anatomy and enzyme and peptide chemistry of peripheral nerve and spinal cord

Abstract: (1) Capsaicin solution was applied for 15 min around a 1 cm length of sciatic nerve in the mid upper leg of adult rats. (2) Electron microscopic examinations of the nerve in the treated region after 14 days shows no signs of degeneration of either myelinated or unmyelinated fibres attributable to the capsaicin. (3) Fluoride resistant acid phosphatase FRAP disappears from the central terminals of the treated nerve by 7 days. (4) 1.5 mM capsaicin is sufficient to product a complete reduction of FRAP in the spinal cord. (5) The peptides substance P and cholecystokinin (CCK) are markedly depleted in the region of spinal cord terminations of the treated nerve at 14 days. (6) Substance P and CCk are not affected in spinal cord regions other than in the unmyelinated afferent terminal zone. Similarly neurotensin and neurophysin which are not present in afferent fibres are not influenced by capsaicin treatment of the sciatic. (7) It is concluded that there are chemical changes in the spinal cord terminals of fine afferents after local peripheral capsaicin.

Implications of the failure of nerve resection and graft to cure chronic pain produced by nerve lesions.

Abstract: Seven patients had developed pain and abnormal sensitivity in the area supplied by a single nerve which had been injured. They were treated unsuccessfully for periods ranging from 3 to 108 months by conservative methods including neurolysis, local anaesthesia, sympathetic blocks, guanethidine, transcutaneous stimulation and analgesics. All then had the damaged nerve resected and in five cases a sural nerve graft was inserted to bridge the resected gap. The patients were then examined 20 to 72 months after the operation. In all seven cases pain and abnormal sensitivity of some intensity recurred in the same area and with the same qualitative characteristic as experienced before the operation. This operation should not be done in patients with this condition. Reasons are given to suggest that peripheral nerve damage induces changes in the central nervous system which are not reversed by treatment directed at the area of the original injury.

Effects of capsaicin applied locally to adult peripheral nerve. I. Physiology of peripheral nerve and spinal cord

Abstract: (1) Systemic capsaicin treatment of neonatal and adult rats is known to affect unmyelinated afferents. However, the systemic route of administration presents several disadvantages and in order to overcome these a method was explored where a single nerve in adult rats was locally treated. (2) Sciatic nerves were exposed and a 10 mm length was soaked for 15 min in 1.5% capsaicin in vehicle or in the vehicle alone (10% Tween 80, 10% ethyl alcohol in saline). (3) Both the capsaicin solution and the vehicle caused acute block of the C compound action potential while in contact with the nerve. Removal of the solutions, however, resulted in substantial recovery of C fibre conduction. The A fibre volley was totally unaffected. (4) 13-21 days after treatment, the size of the myelinated and unmyelinated volleys evoked by maximal stimulation of the capsaicin treated nerve were unchanged but there was a 20% decrease of conduction velocity in the C fibres. (5) The ability of the maximal C volley from the treated nerve to excite cells in the spinal cord was substantially decreased (by 50%) 13-21 days after local capsaicin.

Have the authors addressed themselves to the topic “pain mechanisms in the spinal cord”?

Abstract: Publisher Summary This chapter discusses the details of pain mechanisms that provide a possible probe into the functional conditions under which the brain varies the thresholds and intensities of reaction to an injury. Pain is that sensory experience evoked by stimuli that injures or threatens to destroy tissue. Pain is composed of, first, a separate and distinct sensation and, second, the individual's reaction to pain. The adequate stimulus for pain is the rate of destruction of a tissue innervated by pain fibres. Biologists recognize that those stimuli that cause pain are liable to damage tissue. The unmyelinated afferent sensory fibres contain a large population of fibres responding only to injury or to intense pressure, temperature, or chemical stimuli. For this reason and many others, there has been a general acceptance that the unmyelinated afferent sensory fibres play a major role in triggering pain. There is no doubt that all of the spinal cord cells that are candidates for transmitting information about injury are affected both by convergent impulses from non-noxious stimuli in the periphery and by descending systems from the brain.