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

Tuesday, October 13, 2009

Loss of coordinated autonomic responses to demands on heart rate and vascular tone

Autonomic dysreflexia - Spinal cord injuries (SCI) above T6 may be complicated by a phenomenon known as autonomic dysreflexia, a manifestation of the loss of coordinated autonomic responses to demands on heart rate and vascular tone [5,6]. Uninhibited or exaggerated sympathetic responses to noxious stimuli lead to diffuse vasoconstriction and hypertension. A compensatory parasympathetic response produces bradycardia and vasodilation above the level of the lesion, but this is not sufficient to reduce elevated blood pressure. SCI lesions lower than T6 do not produce this complication, because intact splanchnic innervation allows for compensatory dilatation of the splanchnic vascular bed.

The estimated frequency of this complication is quite variable, ranging from 20 to 70 percent of patients with SCI lesions above T6 [5,6]. Autonomic dysreflexia is unusual within the first month of SCI but usually appears within the first year [7,8].


Common clinical manifestations are headache, diaphoresis, and increased blood pressure [7]. Flushing, piloerection, blurred vision, nasal obstruction, anxiety, and nausea may also occur. Bradycardia is common; however, some patients have tachycardia instead. The severity of attacks ranges from asymptomatic hypertension to hypertensive crisis complicated by profound bradycardia and cardiac arrest or intracranial hemorrhage and seizures. The severity of the SCI influences both the frequency and severity of attacks.

CAD mortality also appears to be higher among SCI patients [4]. One contributing factor may be that SCI lesions above the T5 level may lead to atypical presentations for cardiac ischemia; manifestations may include autonomic dysreflexia or changes in spasticity rather than typical chest pain.

The autonomic nervous system dysfunction that results from SCI disrupts normal cardiovascular hemostasis. With SCI above the T6 level, baseline blood pressure is usually reduced, and baseline heart rate may be as low as 50 to 60 beats per minute [12,16]. This is generally not a clinical problem, but may contribute to hemodynamic instability and exercise intolerance.

Acute cervical SCI is associated with a risk of cardiac arrhythmia due to excess vagal tone, as well as complicating hypoxia, hypotension, and fluid and electrolyte imbalances.

http://www.uptodate.com/patients/content/topic.do?topicKey=~VwAwFq7EG6jGfV