The amount of compensatory sweating depends on the patient, the damage that the white rami communicans incurs, and the amount of cell body reorganization in the spinal cord after surgery.
Other potential complications include inadequate resection of the ganglia, gustatory sweating, pneumothorax, cardiac dysfunction, post-operative pain, and finally Horner’s syndrome secondary to resection of the stellate ganglion.
www.ubcmj.com/pdf/ubcmj_2_1_2010_24-29.pdf

After severing the cervical sympathetic trunk, the cells of the cervical sympathetic ganglion undergo transneuronic degeneration
After severing the sympathetic trunk, the cells of its origin undergo complete disintegration within a year.

http://onlinelibrary.wiley.com/doi/10.1111/j.1439-0442.1967.tb00255.x/abstract

Saturday, December 6, 2008

Neuroma following Sympathectomy

The authors conclude recomemnding the application of clips and if the syndrome nevertheless appears novocaine infiltration of the upper end of the sympathetic chain. The authors are convinced that the theory of Hermann and Cooley about neuroma formation at the ends of the sympathetic chain after resection of a segment is true.
http://www.revangiol.com/sec/resumen.php?or=web&i=e&id=227082.

Traumatic neuroma follows different forms of nerve injury (often as a result of surgery). They occur at the end of injured nerve fibres as a form of ineffective, unregulated nerve regeneration; it occurs most commonly near a scar, either superficially (skin, subcutaneous fat) or deep (e.g., after a cholecystectomy). They are often very painful. It is also known as "pseudoneuroma".

postsympathectomy syndrome

In both groups two cases of postsympathectomy syndrome were seen, with one leg being colder and dryer than the other.

Clinical Orthopaedics & Related Research. 360:122-126, March 1999.

neuropathic and central deafferentation/reafferentation syndrome

Post-sympathectomy neuralgia is proposed here to be a complex neuropathic and central deafferentation/reafferentation syndrome dependent on: (a) the transection, during sympathectomy, of paraspinal somatic and visceral afferent axons within the sympathetic trunk; (b) the subsequent cell death of many of the axotomized afferent neurons, resulting in central deafferentation; and (c) the persistent sensitization of spinal nociceptive neurons by painful conditions present prior to sympathectomy. Viscerosomatic convergence, collateral sprouting of afferents, and mechanisms associated with sympathetically maintained pain are all proposed to be important to the development of the syndrome.

Pain.
1996 Jan;64(1):1-9

http://www.ncbi.nlm.nih.gov/pubmed/8867242?ordinalpos=2&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum

Postsympathectomy pain and changes in sensory neuropeptides

Postsympathectomy limb pain, postsympathectomy parotid pain, and Raeder's paratrigeminal syndrome are pain states associated with the loss of sympathetic fibres and in particular with postganglionic sympathetic lesions. There is a characteristic interval of about 10 days between surgical sympathectomy and onset of pain. It is proposed that this pain in man is correlated with the delayed rise in sensory neuropeptides seen in rodents after sympathectomy. These chemical changes probably reflect the sprouting of sensory fibres and may result from the greater availability of nerve growth factor after sympathectomy. The balance between the sensory and sympathetic innervations of a peripheral organ may be determined by competition for a limited supply of nerve growth factor.
Lancet. 1985 Nov 23;2(8465):1158-60
http://www.ncbi.nlm.nih.gov/pubmed/2414615?dopt=Abstract

sensory abnormalities, abnormal body sweating, and pathologic gustatory sweating

The aim of this study is to describe the incidence and characteristics of pain, sensory abnormalities, abnormal body sweating, and pathologic gustatory sweating in pain patients with persistent post-sympathectomy pain.
Results: Seventeen adults (13 females and 4 males) with a mean age of 37 years (range 25-52) at the time of sympathectomy met the inclusion criteria. Five of the 17 patients experienced temporary pain relief for an average of 4 months (range 2-12 months), 3/17 retained the same pain as before the surgery, 1 patient was cured of her original pain but experienced a new debilitating pain, and 8/17 patients continued to have the same or worse pain in addition to a new or expanded pain. Pathologic gustatory sweating was present in 7/11 patients asked, and abnormal sweating (known as compensatory hyperhidrosis) in 11/13 patients asked. Discussion: The present study does not allow for conclusions about the effectiveness of surgical sympathectomy for neuropathic pain. However, our findings indicate that if the pain persists after the procedure, the complications may be quite serious and at times worse than the problem for which the surgery was originally performed.
The Clinical journal of pain
2003, vol. 19, no3, pp. 192-199
http://cat.inist.fr/?aModele=afficheN&cpsidt=14775091

Recurrent sweating occurred in 17.6% of patients

J Neurosurg Spine. 2005 Feb;2(2):151-4.
http://www.ncbi.nlm.nih.gov/pubmed/15739526

Post-sympathectomy the peripheral vascular failure or the reduced cardiac chronotropic response can impair the body’s capacity to compensate for shock

First, the abolition of sweating from the upper body as well as the axillae and both upper limbs may have significantly reduced the capacity of the patient to lose heat through sweating during exercise. Anhidrosis in the head and neck after sympathectomy affects a proportion of patients, but is often neglected in most reports of post-sympathectomy complications [3]. The loss of head and neck sweating in this patient may have further impaired overall heat loss. However we would also note that the degree of heat loss impairment after sympathectomy has never been quantified, and its effect on body temperature during exercise remains to be established.

Second, thoracic sympathectomy has been demonstrated to abolish or alter sympathetic vasoconstrictive responses in the skin, and this may contribute to abnormal peripheral vascular responses to temperature [4]. Paradoxically it has been suggested that in some cases there may be abnormal vasoconstriction rather than the expected vasodilatation after sympathectomy [5]. It is not impossible that such atypical peripheral vascular responses to rising body temperature may have contributed to impaired heat loss during exercise or to an inappropriate response to shock on the development of the heat stroke.
In the post-sympathectomy patient, the abnormal sympathetic skin response may lead to peripheral vascular failure or the reduced cardiac chronotropic response may impair the body’s capacity to compensate for shock. These may have contributed to the rapid development of shock and severe multiple organ dysfunction syndrome in this patient.

Third, it has been shown that thoracic sympathectomy can impair the autonomic nervous system’s increase of the heart rate in response to exercise [6]. Although absolute tachycardia is not eliminated, given the endocrine and paracrine stimuli during exercise, the maximum heart rate reached during exercise has been shown to be significantly reduced after sympathectomy. Thus for a given workload during exercise, there will be a relative bradycardia. This may possibly affect the circulatory system’s ability to convey heat from the body core to the extremities for heat loss.

Is Previous Thoracic Sympathectomy a Risk Factor for Exertional Heat Stroke?

Alan D.L. Sihoe, FRCSEd(CTh)a,*, Raymond W.T. Liu, MRCPb, Alex K.L. Lee, MRCPb, Chak-Wah Lam, FHKAMb, Lik-Cheung Cheng, FRCSa
http://ats.ctsnetjournals.org/cgi/content/full/84/3/1025

Atrial Fibrillation chemically induced

Pituitary adenylate cyclase-activating polypeptide-27 causes a biphasic chronotropic effect and atrial fibrillation in autonomically decentralized, anesthetized dogs.
Author: Hirose, M : Furukawa, Y : Nagashima, Y : Lakhe, M : Chiba, S

J-Pharmacol-Exp-Ther. 1997 Nov; 283(2): 478-87

Effect of local autonomic denervation on in vitro responsiveness of lymphocytes

The results further indicate that an appropriate sympathetic and parasympathetic local environment may be needed for immunomodulation, as well as for cyclosporine activity in lymphoid tissue.
Journal of the Autonomic Nervous System
Volume 62, Issue 3, 17 February 1997, Pages 155-162
http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6T05-3PKTG6C-6&_user=10&_rdoc=1&_fmt=&_orig=search&_sort=d&view=c&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=da81efda6c250763623b89537aed8109

Origins of the sympathetic projections to rat thyroid and parathyroid glands

These results indicate that postganglionic sympathetic perikarya innervating the thyroid-parathyroid territory are located in the middle and/or inferior cervical ganglia and send their axons through the SCG and the external carotid nerve to these glands.
http://lib.bioinfo.pl/pmid:3772028
J Auton Nerv Syst. 1986 Sep ;17 (1):63-70 3772028

stress responses and adrenal sensitivity to ACTH.

Walker CD.
Chemical sympathectomy and maternal separation affect neonatal stress responses and adrenal sensitivity to ACTH.
Am J Physiol Regul Integr Comp Physiol 268: R1281–R1288, 1995.

Decrease in neuronal uptake of noradrenaline

Shibata K, Takei S, Kawai T, Imaizumi Y, and Watanabe M.
Decrease in neuronal uptake of noradrenaline simply explains the supersensitivity
after sympathectomy in the rat iris dilator.
Jpn J Pharmacol 50: 19 –29, 1989.D

Sympathetic nervous system activity in rat thyroid: potential role in goitrogenesis

Unilateral superior cervical ganglion decentralization led to a reduction in thyroid weight, in 125I uptake by thyroid tissue, and in TSH-induced stimulation of 125I uptake in decentralized hemithyroids. These results suggest that sympathetic activity in thyroid contributes to gland enlargement and may modulate tissue responsiveness to TSH.
Am J Physiol Endocrinol Metab 288: E861-E867, 2005. First published December 7, 2004
http://ajpendo.physiology.org/cgi/content/full/288/5/E861

lack of free noradrenaline after sympathectomy

The similarity of the ultrastructural changes in the light pinealocytes occurring after sympathectomy and after continuous illumination was striking. It is supposed that these changes have a common cause,viz. the lack of free noradrenaline, the pinealotropic neurotransmitter.
Journal of Neural Transmission Volume 36, Numbers 3-4 / September, 1975
http://www.springerlink.com/content/j121443576128248/

SYMPATHETIC REINNERVATION DOES NOT RESTORE NORMAL FUNCTION

SYMPATHETIC REINNERVATION OF THE PINEAL GLAND AFTER
POSTGANGLIONIC NERVE LESION DOES NOT RESTORE NORMAL
PINEAL FUNCTION’
C. W. BOWERS,’ C. BALDWIN, AND R. E. ZIGMOND3
Department of Pharmacology, Harvard Medical School, Boston, Massachusetts 02115
Received October 6, 1983; Revised January 5, 1984; Accepted February 17, 1984

www.jneurosci.org/cgi/reprint/4/8/2010.pdf

Degeneration activity of the pineal gland after sympathetic denervation

The present findings confirm that, in endocrine glands and similarly to other autonomically innervated organs, acute denervation induces degeneration acitivity.
http://www.springerlink.com/content/u573421xk753rk83/