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

Sunday, July 13, 2008

The severity and manifestations of the autonomic hyperreflexia are affected by the level of the sympathectomy

Autonomic Hyperreflexia is caused by noxious stimulation below the level of the lesion in a patient with a sympathectomy at or above T6.

...The efferent sympathetic fibers recover from the initial injury but remain unaffected by central inhibitory input from the brain stem and hypothalamus.
The severity and manifestations of autonomic hyperreflexia are affected by the level of the sympathectomy. With mid-thoracic lesions below the level of cardiac accelerator fibers, hypertension is accompanied by reflex bradycardia transmitted via cardiac accelerator fibers and the vagus. In patients whose sympathectomy is above the level of the thoracic cardiac accelerator fibers, tachycardia may occur because cardiac accelerator fibers become part of the efferent sympathetic activity rather than part of the central inhibitory input from the brain stem and hypothalamus. Arrythmias and occasional heart block may accompany changes in heart rate.
Clinical manifestations of autonomic hyperreflexia include vasodilation, decresed sympathetic activity, and increased vagal activity above the level of the lesion such as nasal congestion, flushing, headache, dyspnea, nausea, and visceral muscle contraction. Vasoconstriction and increased sympathetic activity below the level of the lesion cause vasoconstrictive pallor, sweating, piloerection, and somatic muscle fasciculation. Patients also develop hypertension with headache, blurred vision, myocardial infarction, andretinal, subarachnoid and cerebral hemorrhages that may lead to syncope, convulsion and death.
Handbook of Neuroanesthesia
page 343
By Philippa Newfield, James E. Cottrell
Contributor Philippa Newfield, Stephen Onesti, James E. Cottrell
Published 2006, Lippincott Williams & Wilkins