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

Friday, August 7, 2009

Skin denervation

Epidermal nerve fiber densities were significantly reduced in the skin of all patients, consistent with concomitant small-fiber neuropathies. Perivascular infiltration by T cells and macrophages was demonstrated by immunohistochemistry. All patients experienced neurologic improvement in muscle strength and alleviation of sensory symptoms after immunotherapy with corticosteroids, plasma exchange, or cyclophosphamide. Conclusions: Small-diameter sensory nerves are affected in vasculitis in addition to the well-known effect of vasculitis on large-diameter nerves. Significant inflammatory vasculopathy is present in the skin despite the absence of clinically active vasculitic lesions.
Archives of neurology ISSN 0003-9942 CODEN ARNEAS
2005, vol. 62, no10, pp. 1570-1573 [4 page(s) (article)] (24 ref.)


sympathetic vascular innervation in sympathectomized patients

We measured arterial and venous plasma catecholamines and used laser-Doppler flowmetry to measure cutaneous microcirculatory flow in the sympathectomized and in the intact limbs of 3 patients who had undergone regional sympathectomies. Venous concentrations of norepinephrine, the sympathetic neurotransmitter, exceeded arterial concentrations in the intact limbs--a normal finding--but invariably were less than arterial in the sympathectomized limbs of the same patients, both during baseline conditions and during sympathetic stimulation using tilt, standing and the cold pressor test (mean arteriovenous decrement about 40%). Arterial epinephrine levels exceeded venous levels with or without sympathectomy. Skin microvascular flow rapidly decreased during the cold pressor test and the Valsalva maneuver in the intact but not in the sympathectomized limbs, and spontaneous flow oscillations occurred in the sympathectomized limbs. The results suggest that an arteriovenous increment in plasma norepinephrine reflects local release of norepinephrine from sympathetic nerve endings, whereas removal of circulating catecholamines can occur with or without sympathetic neural impulses. Laser-Doppler flowmetry can measure reflexive sympathetically mediated responses of skin microvascular flow and so can detect sympathetic denervation.
PMID: 3517118 [PubMed - indexed for MEDLINE

Impaired skin vasomotor reflexes

Not surprisingly, diminished vasoconstrictor responses, similar to the current findings, have been found
in patients with sympathetic dystrophies [26], dysautomias [27], post-regional sympathectomy [28] and
diabetic neuropathies [11].


Additionally, there have been a few reports of EM patients benefitting from sympathectomy or neurolitic
irreversible blocks of the lumbar sympathetic ganglia [22,23], while others have found the symptoms of EM to
be aggravated by such treatment [24,25], possibly as a result of denervation supersensitivity.
Clinical Science (1999) 96, 507ñ512 (Printed in Great Britain)
Roberta C. LITTLEFORD, Faisel KHAN and Jill J. F. BELCH
University Department of Medicine, Section of Vascular Medicine and Biology, Ninewells Hospital and Medical School,
Dundee DD1 9SY, Scotland, U.K.

Peripheral Nervous System Disease

Combined with loss of active vasodilation, anhidrosis places tetraplegic patients at risk for hyperthermia.

Peripheral Nervous System Disease

With normal aging, thermoregulatory sweat output declines due to peripheral neural and eccrine glandular factors, which vary in degree depending on genetic predisposition and level of physical conditioning.[75] Extensive anhidrosis may also accompany disease of the peripheral nervous system. When exposed to an elevated ambient temperature or physical exercise, these individuals may present with symptoms of heat intolerance, dizziness, weakness, flushing, dyspnea, or palpitations and may be at risk for heat exhaustion and hyperthermia.

Peripheral Neuropathy

Distal anhidrosis, although often subclinical, is detectable by clinical sudomotor testing in many patients with peripheral neuropathy.[76,77] Diabetes mellitus, the most common cause of autonomic neuropathy in the developed world, typically impairs thermoregulatory sweating in a stocking and glove distribution.[78] As the neuropathy progresses, asymmetric truncal anhidrosis or global anhidrosis may develop.[76]

Some immune-mediated neuropathies selectively target the autonomic neuron. Autoimmune autonomic neuropathy typically presents with sicca complex, anhidrosis, gastrointestinal hypomotility, orthostatic hypotension, abnormal pupillary light reflexes, and neurogenic bladder that may be subacute or insidious in onset. Autoantibodies to the ganglionic acetylcholine receptor have been demonstrated in these patients.[29,79,80] Subacute autonomic neuropathy may signal an occult malignancy, most commonly small cell lung carcinoma. The dysautonomia in paraneoplastic autonomic neuropathy can be manifested mainly by cholinergic failure presenting as gastrointestinal dysfunction and anhidrosis.

Hypohidrosis commonly occurs in the autonomic neuropathy associated with Sjögren's syndrome.[83,84] Hypohidrosis also accompanies neuropathies due to amyloidosis, alcoholism, Tangier disease, vasculitis, and Fabry's disease.[85] Focal areas of hypohidrosis may be found in patients with leprosy.[86]

Anhidrosis is a prominent feature of hereditary sensory and autonomic neuropathies type IV and V (congenital insensitivity to pain with anhidrosis), in which absent skin innervation is associated with mutations of the NTRK1 gene encoding the neurotrophic tyrosine kinase receptor type 1.[30]

http://www.medscape.com/viewarticle/473206_3