Cell body reorganization in the spinal cord after surgery to trea sweaty palms and blushing

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

Monday, November 14, 2011

After peripheral nerve section the amount of GAL produced and present in sensory fibers proximal to the section is dramatically upregulated

Front Neuroendocrinol. 1992 Oct;13(4):319-43.

Galanin in sensory neurons in the spinal cord.

Department of Clinical Physiology, Karolinska Institute, Huddinge University Hospital, Sweden.

The distribution and physiological effects of the neuropeptide galanin (GAL) have been examined in the somatosensory system. GAL is normally present in a few sensory neurons that terminate in the dorsal horn of the spinal cord and it is colocalized with substance P and calcitonin gene-related peptide. After peripheral nerve section, but not dorsal root section, the amount of GAL produced and present in sensory fibers proximal to the section is dramatically upregulated. In parallel functional studies, we could demonstrate that exogenous GAL has a complex effect on the spinal cord reflex excitability, facilitatory at low doses and inhibitory at high doses. Furthermore, GAL inhibits the effect of excitatory neuropeptides physiologically released at the peripheral and central terminals of small diameter afferents that subserve a nociceptive function. After axotomy, the inhibitory effect of GAL is increased. We conclude that GAL may have an important role in the control of nervous impulses that underlie pain states that can occur after peripheral nerve injury.


Increased expression of galanin in the rat superior cervical ganglion after pre- and postganglionic nerve lesions


Galanin is a neuropeptide encoded by the GAL gene,[1] that is widely expressed in the brain, spinal cord, and gut of humans as well as other mammals. Galanin signaling occurs through three G protein-coupled receptors.[2]
The functional role of galanin remains largely unknown; however, galanin is predominately involved in the modulation and inhibition of action potentials in neurons. Galanin has been implicated in many biologically diverse functions, including: nociception, waking and sleep regulation, cognition, feeding, regulation of mood, regulation of blood pressure, it also has roles in development as well as acting as a trophic factor.[3] Galanin is linked to a number of diseases including Alzheimer’s disease, epilepsy as well as depression, eating disorders and cancer.[4][5] Galanin appears to have neuroprotective activity as its biosynthesis is increased 2-10 fold upon axotomy in the peripheral nervous system as well as when seizure activity occurs in the brain. It may also promote neurogenesis.[2]