The spinal component to skin blood flow abnormalities in reflex sympathetic dystrophy
H. A. Kurvers, M. J. Jacobs, R. J. Beuk, F. A. van den Wildenberg, P. J. Kitslaar, D. W. Slaaf and R. S. Reneman
Department of Surgery, University Hospital Maastricht, The Netherlands.
OBJECTIVE: To determine whether the mechanisms of reflex sympathetic
dystrophy, a neuropathic pain syndrome characterized by skin blood flow
abnormalities associated with sympathetic vasoconstrictor and antidromic
vasodilator mechanisms, are solely of peripheral origin or have an
additional spinal component and act exclusively through neural or also
involve humoral pathways. PATIENTS: The 54 patients with unilateral reflex
sympathetic dystrophy were divided into the following three stages
according to their perception of skin temperature in the clinically
affected hand: stage I, stationary warmth sensation; stage II, intermittent
warmth and cold sensation; and stage III, stationary cold sensation.
METHODS: Investigation of basal skin blood flow and vasoconstrictive
response to dependency of skin microvessels in the clinically unaffected
hand and the clinically affected hand of patients with reflex sympathetic
dystrophy and the left hand of 16 control subjects. Microcirculation was
investigated at the predominantly neurally controlled thermoregulatory
level (Doppler laser flowmetry) and at the predominantly humorally
controlled nutritive level (capillary microscopy). RESULTS: In the
clinically unaffected hand, at the thermoregulatory level of the
microcirculation: (1) basal skin blood flow was increased at stage I
compared with the control subjects, whereas no differences could be
observed at this stage compared with the clinically affected hand; (2) the
vasoconstrictive response to dependency (defined as skin blood flow at
heart level divided by skin blood flow in the dependent position) was
attenuated at stage I compared with the control subjects, whereas no
differences could be observed at this stage compared with the clinically
affected hand; and (3) basal skin blood flow and the vasoconstrictive
response to dependency did not differ from the control subjects at stages
II and III. In the clinically unaffected hand, at the nutritive level, no
differences could be observed at any stage of the syndrome compared with
the control subjects. CONCLUSIONS: This study indicates that there is a
spinal component to microcirculatory abnormalities at stage I of the reflex
sympathetic dystrophy syndrome that most likely acts through neural
(antidromic vasodilator) mechanisms and that may be initiated by traumatic
excitation of a peripheral nerve on the clinically affected side.
