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.

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.

Spinal cord infarction occurring during thoraco-lumbar sympathectomy
J Neurol Neurosurg Psychiatry 1963;26:418-421 doi:10.1136/jnnp.26.5.418

Saturday, November 19, 2011

Post sympathectomy syndrome is a poorly understood condition

Post sympathectomy syndrome is a poorly understood condition, which occurs in up to 50% of patients undergoing sympathectomy. This is proposed to be a complex neuropathic and central deafferentation and reafferentation sydnrome. This can occur anywhere from few days to weeks following chemical or surgical sympathectomy. This is characterized by deep, aching pain with superficial burning and hyperesthesia, which may or may not respond to narcotic analgesics. Tricyclic antidepressants may help to reduce the incidence of postsympathoctomy neuralgia. Phenytoin, Carbamazepine or Gabapentin may be useful to reduce spontaneous pain and allodynia. Mexiletine and I.V. lignocaine may help some patients. Occasionally invasive therapies like sympatheic block or more complete sympathectomy can also help.

Stellate ganglion block is one of the most frequently performed procedures in he practice of chronic pain. It can provide good diagnostic, therapeutic and prognostic value.
It can produce complete sympathectomy to the head and neck structures but only a partial sympathetic block of the upper extremity in some patients with variation in anatomy.

Interventional Pain Management

DK. Baheti, Bombay Hospital

Jaypee Brothers Publishers, 2009

Friday, November 18, 2011

There is a fairly extensive literature on pain after lumbar sympathectomy

Sympathectomy useless, even detrimental

A number of surgical procedures have been developed, which, although well-intentioned, are found unfortunately by further study to prove useless, or even detrimental. It is believed at present that lumbar sympathetic ganglionectomy in the treatment of the post-thrombotic type of ulceration of the lower extremity should be placed in this category.

Monday, November 14, 2011

Spinal Ischemic Stroke from complications of abdominal surgery, esp. sympathectomy

B. Arterial feeders (e.g. thoracic, intercostal, or cervical branch from subclavian or vertebral artery)
1) thromboembolic disease!
2) complications of abdominal surgery (esp. sympathectomy)
3) dural AV fistulas (between radicular arteries and veins outside dura mater) – cause venous
hypertension → characteristic dilated veins that course on spinal cord surface.

Viktor’s Notes℠ for the Neurosurgery Resident
Please visit website at
Updated: April 17, 2010

"Sympathectomy frequently interferes with ejaculation"

Kaplan & Sadock's synopsis of psychiatry:

behavioral sciences/clinical psychiatry
Front Cover
Lippincott Williams & Wilkins, 2007 - 1470 pages

Sunday, November 13, 2011

After peripheral nerve section the amount of GAL produced and present in sensory fibers proximal to the section is dramatically upregulated

Front Neuroendocrinol. 1992 Oct;13(4):319-43.

Galanin in sensory neurons in the spinal cord.

Department of Clinical Physiology, Karolinska Institute, Huddinge University Hospital, Sweden.

The distribution and physiological effects of the neuropeptide galanin (GAL) have been examined in the somatosensory system. GAL is normally present in a few sensory neurons that terminate in the dorsal horn of the spinal cord and it is colocalized with substance P and calcitonin gene-related peptide. After peripheral nerve section, but not dorsal root section, the amount of GAL produced and present in sensory fibers proximal to the section is dramatically upregulated. In parallel functional studies, we could demonstrate that exogenous GAL has a complex effect on the spinal cord reflex excitability, facilitatory at low doses and inhibitory at high doses. Furthermore, GAL inhibits the effect of excitatory neuropeptides physiologically released at the peripheral and central terminals of small diameter afferents that subserve a nociceptive function. After axotomy, the inhibitory effect of GAL is increased. We conclude that GAL may have an important role in the control of nervous impulses that underlie pain states that can occur after peripheral nerve injury.

Increased expression of galanin in the rat superior cervical ganglion after pre- and postganglionic nerve lesions

Galanin is a neuropeptide encoded by the GAL gene,[1] that is widely expressed in the brain, spinal cord, and gut of humans as well as other mammals. Galanin signaling occurs through three G protein-coupled receptors.[2]
The functional role of galanin remains largely unknown; however, galanin is predominately involved in the modulation and inhibition of action potentials in neurons. Galanin has been implicated in many biologically diverse functions, including: nociception, waking and sleep regulation, cognition, feeding, regulation of mood, regulation of blood pressure, it also has roles in development as well as acting as a trophic factor.[3] Galanin is linked to a number of diseases including Alzheimer’s disease, epilepsy as well as depression, eating disorders and cancer.[4][5] Galanin appears to have neuroprotective activity as its biosynthesis is increased 2-10 fold upon axotomy in the peripheral nervous system as well as when seizure activity occurs in the brain. It may also promote neurogenesis.[2]

Compensatory changes in contralateral sympathetic neurons of the superior cervical ganglion and in their terminals in the pineal gland following unilateral ganglionectomy

The sympathetic noradrenergic neurons of the rat superior cervical ganglia (SCGs) provide the major source of innervation to the pineal gland. The present study sought to determine if this sympathetic innervation can undergo collateral sprouting following partial denervation of the pineal by unilateral removal of the SCG (ganglionectomy), and whether such growth of axon terminals is associated with biochemical changes in the contralateral SCG. In the pineal gland following partial denervation, residual noradrenergic terminals underwent compensatory changes indicative of collateral sprouting, as evidenced by: a rapid reduction in tyrosine hydroxylase (TH) activity and in [3H]norepinephrine (NE) uptake, to about 50% of control by 2 days, which was followed by a gradual but sustained increase to levels of approximately 80% of control by 10 days and a reduction in the intensity and density but not in the distribution of fibers containing NE-induced fluorescence by 2 days, which was followed by a sustained increase. In the contralateral SCG, choline acetyltransferase (CAT) activity, a marker of cholinergic preganglionic terminals, was transiently increased to about 115% of control by 4 days and returned to control levels by 14 days after unilateral ganglionectomy; later, TH activity in noradrenergic cell bodies was gradually increased to about 140% of control by 10 days where it remained for up to 52 days. Unilteral ganglionectomy combined with decentralization of the contralateral SCG by preganglionic nerve cut prevented the compensatory changes in noradrenergic nerve terminals within the pineal.

Hypertrophy and neuron loss: structural changes in sheep SCG induced by unilateral sympathectomy

Interaction effects between time and ganglionectomy-induced changes were significant for SCG volume and mean perikaryal volume. These findings show that unilateral superior cervical ganglionectomy has profound effects on the contralateral ganglion. For future investigations, it would be interesting to examine the interaction between SCGs and their innervation targets after ganglionectomy. Is the ganglionectomy-induced imbalance between the sizes of innervation territories the milieu in which morphoquantitative changes, particularly changes in perikaryal volume and neuron number, occur? Mechanistically, how would those changes arise? Are there any grounds for believing in a ganglionectomy-triggered SCG cross-innervation and neuroplasticity?


The effect of unilateral extirpation of the stellate and the superior cervical ganglia on the amount of the pericardial fat and the effect of unilateral extirpation of the lumbar and sacral ganglia on the abdominal and subcutaneous fat on the denervated side make it likely that the effects of the splanchnic nerves on the perirenal fat may be extended to describe the relation between fat storage in and sympathetic innervation of connective tissue in general.