Sympathetic vasodilatation in human limbs

During the 1950s and early 1960s a variety of experiments were conducted, expanding on these original observations. Many of these studies were conducted by
Professor Barcroft's protégés (Roddie, 1977; Roddie & Shepherd, 1998). In these studies (Fig. 3), conducted before rigorous human studies review boards, severe
mental or emotional stress evoked physiological changes similar to the 'defence reaction' and caused forearm blood flow to rise by up to 10-fold (for a discussion
of the mental stress used see Roddie, 1977). The forearm vasodilatation was absent after surgical sympathectomy, and in most subjects a portion of the
vasodilatation could be blunted by atropine (Fig. 3).

Along these lines, recent observations in animals indicate that chronic sympathectomy eliminates endothelial NO synthase expression
in sympathectomised blood vessels (Aliev et al. 1996). This suggests that normal NO-mediated responses to local and circulating factors would be present
following acute sympathectomy with local anaesthetics or drugs injected into the brachial artery, but that these responses would be absent in the months and
years following surgical sympathectomy.

Individual records from two subjects during periods of severe mental stress. A, in a patient with a unilateral cervical sympathectomy, mental stress
(hatched bar) evoked profound increases in forearm blood flow in the normal arm. These increases in forearm blood flow were absent in the sympathectomised forearm. B, a second subject was studied with normal innervation to both upper extremities. Atropine given selectively to one
forearm blunted but did not eliminate the vasodilator responses to severe mental stress. Adapted from Blair et al. (1959).



http://jp.physoc.org/cgi/content/full/526/3/471

Alterations of the Three-Phase Bone Scan After Sympathectomy

Alterations of the Three-Phase Bone Scan After Sympathectomy

The data demonstrated that alterations in TPBS after sympathectomy are identical to those reported in early RSD and these alterations bear no relationship to the success of sympathectomy regarding pain relief. The mechanisms underlying alterations of TPBS as well as the potential mechanisms of sympathectomy failures are discussed.

Clinical Journal of Pain. 10(2):146-155, June 1994

sympathectomy is based on poor quality evidence, uncontrolled studies and personal experience

The practice of surgical and chemical sympathectomy is based on poor quality evidence, uncontrolled studies and personal experience. Furthermore, complications of the procedure may be significant, in terms of both worsening the pain or producing a new pain syndrome; and abnormal forms of sweating (compensatory hyperhidrosis and pathological gustatory sweating). Therefore, more clinical trials of sympathectomy are required to establish the overall effectiveness and potential risks of this procedure.
Cochrane Database Syst Rev. 2003;(2):CD002918.

Painful sweating after nerve sprouting

The authors propose that after destruction of cutaneous nerves, aberrant regenerant sprouting innervates sweat glands, producing gustatory sweating as in auriculotemporal syndrome (Frey syndrome), and innervates nociceptors, producing pain.

http://www.neurology.org/cgi/content/abstract/63/8/1471

Sexual function after bilateral lumbar sympathectomy

In patients who had only bilateral sympathectomy, these complications occurred in 24% and mainly consisted of ejaculation disturbances. Only three patients became impotent, each having had aortic surgery.

http://www.ncbi.nlm.nih.gov/pubmed/7364866

Sympathectomy as a cure for psychiatric mischief...

Of those I have
met, however, some have been supposed to be subject to deep psychiatric
mischief, none has benefited from psychiatric treatment, and all have been
cured by sympathectomy. Furthermore it must be noted as a matter of
special interest that the cure is permanent, and the trouble does not recur
even in patients who show evidence of some return of sympathetic function.

SOME UNSOLVED PROBLEMS IN THE SURGERY OF THE
SYMPATHETIC NERVOUS SYSTEM
Bradshaw Lecture delivered at the Royal College of Surgeons of England
on 11th June, 1953
by
Professor Sir James Paterson Ross, K.C.V.O., F.R.C.S.
Vice-President, Royal College of Surgeons of England

The haemodynamic effect of thoracoscopic cardiac sympathectomy

The sympathetic denervated heart showed little chronotropic response to anaesthetic and surgical stimulation. On the contrary, the parasympathetic response was predominant. An episode of severe bradycardia occurred during endotracheal suctioning prior to extubation. The haemodynamic response to cardiac sympathetic denervation corresponded to the efferent effect of beta-receptor blockade.

Copyright © 1998 Taylor and Francis Ltd.

http://www3.interscience.wiley.com/journal/106568649/abstract