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

Thursday, December 11, 2008

Sympathectomy can result in Dysautonomia

Dysautonomia is any disease or malfunction of the autonomic nervous system.
In some cases, dysautonomia results in a reduction in the ability of the heart and circulatory system to compensate for changes in posture, such as causing dizziness or fainting when standing or even sitting up. In other cases, inappropriate sinus tachycardia may cause the heart to race for no apparent reason. Other symptoms can include severe migraines, excessive urination.
Causes of dysautonomias are not fully understood, but they are thought to include viral illness, genetic factors, exposure to chemicals, pregnancy, autoimmune disorders, and a physical trauma or injury which damages the autonomic nervous system.[3]

There is no cure for dysautonomia, medications are used to stablize the condition on a long-term basis.
http://www.reference.com/browse/dysautonomia,+familial

galanin and VIP mRNA after sympathectomy

Large changes in neuronal gene expression occur in adult peripheral neurons after axonal transection. In the rat superior cervical ganglion, for example, neurons that do not normally express vasoactive intestinal peptide (VIP) or galanin do so after postganglionic nerve transection. These effects of axotomy could result from a number of aspects of the surgical procedure. To test the idea that the important variable might be the disconnection of axotomized neuronal cell bodies from their target tissues, we examined the effects of producing such a disconnection by means of the compound 6-hydroxydopamine (6-OHDA), a neurotoxin that causes degeneration of sympathetic varicosities and avoids many of the complications of surgery. Two days after 6-OHDA treatment, VIP and galanin immunoreactivities had increased two- and 40-fold, respectively. Nevertheless, these increases were substantially smaller than the 30- and 300-fold changes seen after surgical axotomy. When expression of VIP and galanin was examined at the mRNA level, however, comparable increases were found after either procedure. The results indicate that chemical destruction of sympathetic varicosities produces an equivalent signal for increasing VIP and galanin mRNA as does axonal transection.
Chemical sympathectomy and postganglionic nerve transection produce similar increases in galanin and VIP mRNA but differ in their effects on peptide content.
H. Hyatt-Sachs, M. Bachoo, R. Schreiber, S. A. Vaccariello, R. E. Zigmond *
Department of Neurosciences, Case Western Reserve University, School of Medicine, Cleveland, Ohio 44106-4975
Received: 9 January 1996; Accepted: 3 April 1996

Journal of Neurobiology

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