Dr. Giudiceandrea Alberto, general and vascular surgeon
http://sympathectomy.info/
Possible side effects, ranging from trivial to devastating, are of even greater importance with these more permanent procedures.
G D Schott Consultant neurologist
Interrupting the sympathetic outflow in causalgia and reflex sympathetic dystrophy – A futile procedure for many patients
The National Hospital for Neurology and Neurosurgery, London
1998;316;789-790 BMJ
Sympathectomy reduces DOPAMINE – Latent inhibition and creative drive
Dopamine in the mesolimbic pathway increases general arousal and goal directed behaviors and decreases latent inhibition; all three effects increase the creative drive of idea generation. This has led to a three-factor model of creativity involving the frontal lobes, the temporal lobes, and mesolimbic dopamine.[34]
This calcification was observed in both feet of 93% of patients, who had
undergone bilateral operation. After unilateral sympathectomy the incidence of calcified arteries on the side of operation was significantly higher than that on the contralateral side (88% versus 18%, p less than 0.01). Although diabetic patients showed longer stretches of calcification than non-diabetic subjects, the difference was not significant in terms of incidence and length. Of 20 patients who had no evidence of calcinosis pre-operatively, 11 developed medial calcification after unilateral operation exclusively on the side of sympathectomy. In seven patients calcinosis was detected in both feet after
bilateral operation. In conclusion, sympathetic denervation is one of the causes of Monckeberg’s sclerosis regardless of diabetes mellitus.
Diabetologia. 1983 May;24(5):347-50, PMID: 6873514 [PubMed – indexed for MEDLINE]
Goebel FD, Fuessl HS.
Some of these side-effects, as listed on the Swedish support group website:
- Side effects of the elective surgery:
- Severe compensatory sweating = disabling sweating
- Decreased physical capacity
- Reduced blood circulation
- Stomach problems (constipation or diarrhea)
- Impotence
- Oversensitivity to stress
- Oversensitivity to sounds
- Oversensitivity to light
- Muscle weakness (“lactic acid in the arms”)
- Cold hands and feet – denervation supersensitivity
- Horners syndrome
- Reduced pulse reaction – delay in heart rate and BP responses, dizziness
- Shortness of breath
- Pain in arms and back – due to nerve sprouting
- Chronic fatigue, lack of energy – S affects adrenaline levels
- Raynauds disease – denervation supersensitivity
and from research:
- Autonomic dysfunction
- Vascular disturbances
- Calcification of arteries
- Permanently disabled thermoregulation
- blocked nose or watery discharge/dripping from nose
- dry, inflamed eyes
- Reduced physical capacity, even when going up a flight of stairs – HR and BP responses delayed
- depression – ETS reduces NE and catecholamines, increases serotonin
- mood-swings
- Altered sympathetic tone, feeling sedated/detached – beta-blocker effect
- Inability to experience/respond to strong emotions – S disrupts signals from the viscera
- Reduces/eliminates fear
- difficulty concentrating, foggyness, memory affected
- lack of motivation/drive/cognitive function – reduction of small vessels in the anterior cingulate cortex, altered catecholamines
- overheating due to disabled thermoregulation, even when extreme sweating present – fever in hot weather or with physical activity/brain overheating
- difficulty falling asleep/getting up – S eliminates circadian rhythm
- Destabilized heart rate, arrythmia, dropped beats, morphofunctional changes in the myocardium
- Reduced heart rate = reduced alertness, reduced emotional responses, (‘not feeling alive’), all affecting long term memory (encoding).
- Suppressed or eliminated Baroreflex = MAP instability
- Mean Arterial Pressure instability, reduced short-term haemodynamic variability (‘not feeling alive’)
- Hair loss, loss of eyebrows, eyelashes – altered blood flow in the skin
- Dehydrated skin on upper body, face, scalp, – dandruff, skin infections, reduced immune responses
- Reduced antibody responses – altered immune system
Several publications/books interchange ‘Sympathectomy’ and ‘Spinal Cord Injury’ due to the similarity in presentation/ symptoms.
Sweating after sympathetic surgery is a reflex cycle between the sympathetic system and the anterior portion of the hypothalamus according to our investigations. Reflex sweating will not happen if hand sweating can be stopped without interrupting sympathetic tone to the human brain. (sic!)
Chien-Chih Lin, M.D., *Timo Telaranta, M. D.
Presentation at the 4th International Symposium on Sympathetic Surgery
ETS is a relatively safe and simple procedure. However the side effects are possibly devastating All physicians providing this service and all peoples preparing to undergo this treatment should know this well.
Min-Huei Hsu (10 January 2005)
http://www.cmaj.ca/cgi/eletters/172/1/69#1908
Cervical sympathectomy inhibits axonal transport of gonadotropin-releasing hormone during continuous exposure to light
GNRH secretion is pulsatile in all vertebrates, and is necessary for correct reproductive function. Thus, a single hormone, GNRH1, controls a complex process of follicular growth, ovulation, and corpus luteum maintenance in the female, and spermatogenesis in the male.
http://en.wikipedia.org/wiki/Gonadotropin-releasing_hormone
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