Brain, Vol. 117, No. 1, 185-197, 1994
© 1994 Oxford University Press
research-article |
The triple cold syndrome
Cold hyperalgesia, cold hypoaesthesia and cold skin in peripheral nerve disease
1Department of Neurology and Department of Neurosurgery, Good Samaritan Hospital Medical Center, and Oregon Health Sciences University Portland Oregon, USA 2Department of Neurology, Rambam Medical Center and Technion Medical School Haifa, Israel
Correspondence to:
Correspondence to: Professor J. L. Ochoa, Department of Neurology, 1040 NW 22nd Avenue 460, Portland, OR 97210, USA
A syndrome of cold hyperalgesia associated with cold hypoaesthesia is described in 28 patients with peripheral polyneuropathy or mononeuropathy of various aetiologies. A mechanism of sensory disinhibition, where diminished cold-specific A delta input releases cold pain input carried by C nociceptors, is proposed to explain the hyperalgesia. In most patients, the symptomatic skin is abnormally cold. This is a likely consequence of vasospasm, due to sympathetic denervation supersensitivity, caused by dropout of sympathetic efferents as part of the small caliber nerve fibre insult. The term ‘triple cold syndrome’is coined to describe this specific pathophysiological condition. Descriptively it is a mirror image of erythralgia, as described by Sir Thomas Lewis (1936) and updated by one of the present authors, a human condition also centred around anomalous primary nociceptor input, in which there is heat hyperalgesia and hot symptomatic skin due to C nociceptor sensitization and vasodilatation from antidromic discharge. Thus, like the latter condition, the triple cold syndrome emerges as an independent clinical entity with definable abnormal mechanisms which should be retrieved out of the all-embracing, descriptive, diagnostic category ‘reflex sympathetic dystrophy—causalgia’.
Received August 19, 1992. Revised January 11, 1993. Accepted October 30, 1993.
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