Brain, Vol. 112, No. 3, 621-647, 1989
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CHRONIC HYPERALGESIA AND SKIN WARMING CAUSED BY SENSITIZED C NOCICEPTORS
Departments of Neurology, Good Samaritan Hospital Portland, OR, USA Oregon Health Sciences University Portland, OR, USA Department of Clinical Neurophysiology, Academic Hospital Uppsala, Sweden
Correspondence to:
Correspondence to: Dr J. Ochoa, Department of Neurology, Suite 460, 1040 NW 22nd Avenue, Portland, OR 97210, USA
SUMMARY
A patient suffering from an acquired painful syndrome, due to injury to primary somatic afferent units, was studied. Clinical features included chronic spontaneous burning pain in one hand, abnormal painful response to nonnoxious cutaneous stimuli, and deviation of temperature and dystrophic changes in symptomatic skin Diagnostic stellate ganglion blocks did not improve spontaneous or stimulus-induced pains, and observation of sympathetic efferent neural actIIIity and vasomotor effector responses revealed no abnormality, failing to support an autonomic contribution to the pathogenesis of the pains.
A quantitative psychophysical assessment documented exaggerated magnitude of pain in response to noxious stimuli in symptomatic skin, together with abnormal painful quality and prolongation of sensation induced by nonnoxious tactile or warm stimuli. Such mechanical and thermal hyperalgesia persisted during A fibre blocks, suggesting transmission by primary afferents with unmyelinated C fibres and implying sensitization of C polymodal nociceptors. Direct microneurographic recordings of single, identified C polymodal nociceptors from symptomatic skin confirmed the presence of units with pathologically enhanced receptor responses: lowered threshold and very prolonged afterdischarges While bypassing skin receptor, strongly intraneural microstimulation in fascicles supplying symptomatic or control skin evoked equivalent magnitudes and temporal profiles of pain from both sides. Thus secondary CNS dysfunction need not be postulated to explain the painful syndrome.
Skin grafted onto the affected region partially recovered tactile and thermal sensation (but not pain) without expressing the painful syndrome. This supports the overall conclusion that in this patient A fibres are not involved as primary carriers of input decoded as pain.
Sensitization of C polymodal nociceptors is consistent with the features of hyperalgesia in this patient pain evoked by nonnoxious stimuli, exaggerated pain magnitude, and abnormally prolonged aftersensation of pain. This is the first documentation of chronic sensitization of human C polymodal nociceptors as a symptom of disease. In the context of sensitized C nociceptors and in the absence of sympathetic vasoconstrictor deficit, the abnormally elevated temperature in symptomatic skin is interpreted as due to antidromic vasodilatation triggered by neurosecretion from hyperactive nociceptors.
This study calls for reexamination of concepts relating to hyperalgesia as a sequel of injury to the peripheral nervous system, and to reflex sympathetic dystrophy, and presents pathophysiological data on a particular variety of neuropathic painful syndrome featuring signs of vasomotor dysfunction.
Received January 5, 1988. Revised May 23, 1988. Accepted July 8, 1988.
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