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

Wednesday, July 30, 2014

QT dispersion was significantly reduced 1 month after surgery and the dispersion was further diminished 2 years later - significant change after sympathectomy

The HRV analysis showed a significant change of indices reflecting sympatho-vagal balance indicating significantly reduced sympathetic (LF) and increased vagal (HF, rMSSD) tone. These changes still persisted after 2 years. Global HRV increased over time with significant elevation of SDANN after 2 years. QT dispersion was significantly reduced 1 month after surgery and the dispersion was further diminished 2 years later.

The Change in Regional Cerebral Oxygen Saturation after Stellate Ganglion Block

The Change in Regional Cerebral Oxygen Saturation after Stellate Ganglion Block: "Korean J Pain. Jun 2010; 23(2): 142–146.
Published online May 31, 2010.


Stellate ganglion block (SGB) is known to increase blood flow to the innervations area of the stellate ganglion. Near infrared spectroscopy reflects an increased blood volume and allows continuous, non-invasive, and bedside monitoring of regional cerebral oxygen saturation (rSO2). We investigated the influence of SGB on bilateral cerebral oxygenation using a near infrared spectroscopy.


SGB was performed on 30 patients with 1% lidocaine 10 ml using a paratracheal technique at the C6 level and confirmed by the presence of Horner's syndrome. The blood pressure (BP), heart rate (HR) and rSO2 were measured before SGB and 5, 10, 15 and 20 minutes after SGB. Tympanic temperature of each ear was measured prior to SGB and 20 minutes after SGB.


The increments of the rSO2 on the block side from the baseline were statistically significant at 5, 10, 15 and 20 minutes. The rSO2 on the non-block side compared with the baseline, however, decreased at 15 and 20 minutes. The difference between the block and the non-block sides was significant at 15 and 20 minutes. The BP at 10, 15 and 20 minutes was increased and the HR was increased at 10 and 15 minutes. 


We observed an increment of the rSO2 on the block side from the baseline; however, the rSO2 on the non-block side decreased."

Sunday, July 27, 2014

Inflammation in dorsal root ganglia after peripheral nerve injury: Effects of the sympathetic innervation

Following a peripheral nerve injury, a sterile inflammation develops in sympathetic and dorsal root ganglia (DRGs) with axons that project in the damaged nerve trunk. Macrophages and T-lymphocytes invade these gan- glia where they are believed to release cytokines that lead to hyperexcitability and ectopic discharge, possibly contributing to neuropathic pain. Here, we examined the role of the sympathetic innervation in the inflammation of L5 DRGs of Wistar rats following transection of the sciatic nerve, comparing the effects of specific surgical in- terventions 10–14 days prior to the nerve lesion with those of chronic administration of adrenoceptor antago- nists. Immunohistochemistry was used to define the invading immune cell populations 7 days after sciatic transection. Removal of sympathetic activity in the hind limb by transecting the preganglionic input to the rele- vant lumbar sympathetic ganglia (ipsi- or bilateral decentralization) or by ipsilateral removal of these ganglia with degeneration of postganglionic axons (denervation), caused less DRG inflammation than occurred after a sham sympathectomy. By contrast, denervation of the lymph node draining the lesion site potentiated T-cell in- flux. Systemic treatment with antagonists of α1-adrenoceptors (prazosin) or β-adrenoceptors (propranolol) led to opposite but unexpected effects on infiltration of DRGs after sciatic transection. Prazosin potentiated the influx of macrophages and CD4T-lymphocytes whereas propranolol tended to reduce immune cell invasion. These data are hard to reconcile with many in vitro studies in which catecholamines acting mainly via β2-adrenoceptors have inhibited the activation and proliferation of immune cells following an inflamma- tory challenge. 

Autonomic Neuroscience: Basic and Clinical 182 (2014) 108117 

Neuroscience Research Australia, Randwick, NSW 2031, and the University of New South Wales, Sydney, NSW 2052, Australia