Abnormal skin temperature and abnormal sympathetic vasomotor innervation in an experimental painful peripheral neuropathy

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Abstract
A chronic constriction injury to the sciatic nerve of the rat produces a neuropathic pain syndrome that has many of the symptoms that are seen in humans with painful peripheral neuropathy. In particular, both the clinical and experimental conditions are accompanied by an abnormality of cutaneous temperature regulation in the painful area. A time course study was made of this phenomenon in the experimental model. In normal rats, there is little or no difference between the temperature of the two hind paws (plantar skin). After nerve injury, however, approximately 75% of the rats (N = 30) had abnormally large (greater than ± 0.9°C) temperature differences (ΔT) between the affected and sham-operated sides. The abnormal ΔTs could be either positive or negative i.e., the affected side could be hotter or colder than normal. For individual cases, the temperature abnormality was highly variable over time periods of hours to days; abnormally hot skin could switch to being abnormally cold, and vice versa, and small ΔTs in the normal range could switch between abnormal extremes. Despite this individual variability, the average ΔT of the group as a whole displayed a clear evolution over the course of the 30-day observation period: abnormally hot initially and progressing to abnormally cold. A parallel time course study was made of the status of the sympathetic vasoconstrictor innervation to the affected hind paw (plantar artery and vein). As demonstrated with a histofluorescence method that visualizes cate-cholamines, there was a gradual loss of norepinephrine (NE)-containing sympathetic efferents on the nerve-injured side. The decrease was first noted on postoperative day 5 (PO5), was very marked by PO10–PO14, and progressed to a complete or nearly complete loss by PO30. There was a concommitant decrease in staining for two other substances found in vasoconstrictor efferents, dopamine-β-hydroxylase (DBH) and neuropeptide Y (NPY). The NE-containing innervation of the contralateral (sham-operated) plantar vessels appeared to be normal at all times. Lastly, in order to determine whether there was any relation between the temperature abnormality and the status of the sympathetic perivascular plexus, additional rats were sacrificed immediately after skin temperature measurement and the hind paw vessels were stained for NE. The vasculature of some abnormally cold paws had no detectable NE. Some rats that did not appear to have a temperature abnormality also had no detectable NE on the affected hind paw's vasculature. The vasculature of some abnormally hot paws had normal NE. Although it is a common clinical assumption that the temperature abnormality that accompanies painful neuropathies is a reflection of the level of sympathetic vasomotor activity, the present results suggest that this is not necessarily true.

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