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PubMed1992

Reflex sympathetic dystrophy and causalgia.

Converging lines of research suggest that RSD is a form of reflex neurogenic inflammation. Early the sympathetic nervous system appears to have an initiating and sustaining role. In later states of the illness, structural changes at the DH level seem to correlate with centralization of the process. Neuropeptides and EAAs released from thin or unmyelinated nociceptive afferents may produce both the inflammation and the suspected central sensitization of DH neurons seen in later stages of the disease. Effective treatment will follow a clearer understanding of the physiology of each stage of the disease.

Causalgia↗
PubMed1996

[The sympathetic skin response--a useful method for the diagnosis of reflex sympathetic dystrophy?].

UNLABELLED: The aim of the present study was to examine the value of the sympathetic skin response (SSR) in the diagnosis of reflex sympathetic dystrophy (RSD). PATIENTS AND METHODS: SSR was recorded in 20 normal subjects and in 24 patients with predominantly chronic RSD. In 3 patients with RSD, additional recordings of the SSR were performed before and several times after administration of local anaesthetics via a plexus catheter on the diseased side. SSR was recorded with standard EMG apparatus. Disc electrodes were positioned on the middle of the volar and dorsal surfaces of the hands and feet. Electrical stimuli were applied to the middle of the forehead at irregular intervals longer than 60 s. RESULTS: In normal subjects inter- and intraindividually different monophasic, biphasic and triphasic potentials without difference in the waveform between sides were recorded. SSR abnormalities were found in 15 patients with RSD and correlated with the severity of the disease. In patients with slight dystrophy SSR was predominantly normal, while in most of those with intermediate dystrophy differences in the SSR waveform between sides were observed. In the presence of severe dystrophy SSR amplitude was predominantly decreased on the affected side. Following the administration of local anaesthetics via a plexus catheter, the differences in SSR waveform became smaller in patients with initial distinct side difference of the waveform. However, differences in SSR amplitudes or latencies between sides were not affected. CONCLUSIONS: Side differences in SSR waveform could be due to a mild, reversible unilateral sudomotor dysfunction, whereas differences in SSR amplitude or latency indicate more serious damage to sudomotor activity, possibly due to dysfunction of autonomic fibres. In patients with slight dystrophy sweat secretion is predominantly normal, while in severe dystrophy more serious damage to the sweat secretory system can be observed. SSR provides useful information on sudomotor dysfunction in patients with RSD. However, as there is no consensus on the clinical criteria for diagnosis of RSD, it is also not possible to determine the diagnostic value of SSR in the diagnosis of RSD.

English Abstract↗