Skin denervation in vasculitic neuropathy

Epidermal nerve fiber densities were significantly reduced in the skin of all patients, consistent with concomitant small-fiber neuropathies.
http://www.ncbi.nlm.nih.gov/pubmed/16216940

90% can experience gustatory sweating after sympathectomy

Some individuals (up to 90%) may experience another type of sweating that is increased while eating or smelling certain foods (gustatory sweating) (Hornberger).

Source: Medical Disability Advisor

http://www.mdguidelines.com/sympathectomy

sympathectomy can cause postsympathectomy pain called sympathalgia in up to 44% of patients

The sympathalgia secondary to sympathectomy usually starts around the first 2 weeks of the surgical procedure. It is a dull and cramping pain and occasionally can be a sharp pain. Although it is temporary in some patients, in others it can persist for several months or years.

H. Hooshmand, M.D.
Chronic Pain, page 156

83% of patients who underwent T2 sympathectomy reported severe compensatory sweating

one year after surgery and the majority of those reported they regretted the decision to have the surgery.
Heather Ennis. Medical Post. Toronto: Feb 15, 2005. Vol. 41, Iss. 7; pg. 17, 2 pgs

Serious complications reported after sympathectomy

Surgery involving the clamping of sympathetic nerve trunks to prevent excessive perspiration and blushing appears to be of questionable value.

Complications have been reported, ranging from phantom perspiration to blood clots in the brain.

The Finnish Office for Health Care Technology Assessment (FinOHTA), which is part of the National Research and Development Centre for Welfare and Health (STAKES) recently conducted a survey on the various effects of hyperhidrosis surgery at the request of the Finnish Medical Association.

Finnish surgeon Timo Telaranta has performed about 2,000 such operations at private clinics in Helsinki and Oulu in the past ten years.
The National Authority for Medicolegal Affairs has issued three warnings to Telaranta and the Provincial Government of Southern Finland has issued one.
There are currently no complaints pending against Telaranta, and the authority has not considered restricting his rights to practice medicine.

The Finnish Patient Insurance Centre has processed 20 complaints concerning Telarantas Privatex clinic. The complaints resulted in 14 decisions to pay compensation. All except two of the surgeries were conducted by Telaranta himself.
Telaranta says that he treats patients suffering from difficult social anxiety with endoscopic surgery in which an incision is made into the upper part of the chest cavity, and the sympathetic nerve trunk is severed or clamped.
Most patients are satisfied with the treatment. However, FinOHTA found that there were many negative side-effects, some of which were very serious.
With most patients, heavy perspiration of the palms has moved to other parts of the body, below the breasts. As many as 15% of those who have undergone the surgery said that the surge in body perspiration forces them to change underwear several times a day.
Other side-effects have included drying of the skin on the face and hands, as well as perspiration triggered by eating spicy food. There are also reports of phantom perspiration - the feeling of perspiration when none takes place - as well as a weakened tolerance for cold.

More serious effects include collapsing of a lung, breathing difficulties, and blood clots in the brain. Some patients got a hanging eyelid, while others reported a sudden raspiness of their voice.
One of Dr. Telarantas patients who had made a complaint began to experience strong reactions of anxiety which did not go away even after corrective surgery. Later the patient committed suicide.

Dr. Telaranta himself says that the side-effects are regrettable. However, he says that he has developed a procedure which does not cause any such side effects.
He also says that it is important to examine patients carefully, and to perform surgery only on those who are suited for the procedure.
Many doctors have serious reservations about the idea of treating complaints such as excessive perspiration, blushing, and performance anxiety by severing peoples nerves.
Helsingin Sanomat
http://www.hs.fi/english/article/1101979734791

decreased conditioning-related activity in insula and amygdala in patients with autonomic denervation

The degree to which perceptual awareness of threat stimuli and bodily states of arousal modulates neural activity associated with fear conditioning is unknown. We used functional magnetic neuroimaging (fMRI) to study healthy subjects and patients with peripheral autonomic denervation to examine how the expression of conditioning-related activity is modulated by stimulus awareness and autonomic arousal. In controls, enhanced amygdala activity was evident during conditioning to both "seen" (unmasked) and "unseen" (backward masked) stimuli, whereas insula activity was modulated by perceptual awareness of a threat stimulus. Absent peripheral autonomic arousal, in patients with autonomic denervation, was associated with decreased conditioning-related activity in insula and amygdala. The findings indicate that the expression of conditioning-related neural activity is modulated by both awareness and representations of bodily states of autonomic arousal.

http://www.ncbi.nlm.nih.gov/pubmed/11856537

Effect of sympathectomy on mechanical properties of common carotid and femoral arteries

Compared with the intact animals, sympathectomized rats showed a marked increase in arterial distensibility over the entire systolic-diastolic pressure range. When quantified by the area under the distensibility-pressure curve, the increase was 59% and 62% for the common carotid and femoral arteries, respectively (P<.01 for both). In the femoral but not in the common carotid artery, sympathectomy was accompanied also by an increase in arterial diameter (+18%, P<.05 versus intact). Therefore, in the anesthetized normotensive rat, sympathetic activity exerts a tonic restraint on large-artery distensibility. This restraint is pronounced in elastic vessels and even more pronounced in muscle-type vessels.

http://www.ncbi.nlm.nih.gov/pubmed/9369260

endoscopic sympathicotomy in carotid and vertebral arteries in the surgical treatment of primary hyperhidrosis

Analyze, in patients with primary hyperhidrosis (PH) who was undergone to videothoracoscopic sympathicotomy, the degree of vascular denervation after surgical transection of the thoracic sympathetic chain by measuring ultrasonografic parameters in carotid and vertebral arteries.

METHODS:

Twenty-four patients with PH underwent forty-eight endoscopic thoracic sympathicotomy and were evaluated by duplex eco-Doppler measuring systolic peak velocity (SPV), diastolic peak velocity (DPV), pulsatility index (PI) and resistivity index (RI) in bilateral common, internal and external carotids, besides bilateral vertebral arteries. The exams were performed before operations and a month later. Wilcoxon test was used to analyse the differences between the variables before and after the sympatholisis.

RESULTS:

T3 sympathicotomy segment was the most frequent transection done (95.83%), as only ablation (25%) or in association with T4 (62.50%) or with T2 (8.33%). It was observed increase in RI and PI of the common carotid artery (p < 0.05). The DPV of internal carotid artery decreased in both sides (p < 0.05). The SPV and the DPV of the right and left vertebral arteries also increased (p < 0.05). Asymmetric findings were observed so that, arteries of the right side were the most frequently affected.

CONCLUSIONS:

Hemodynamic changes in vertebral and carotid arteries were observed after sympathicotomy for PH. SPV was the most often altered parameter, mostly in the right side arteries, meaning significant asymmetric changes in carotid and vertebral vessels. Therefore, the research findings deserve further investigations to observe if they have clinical inferences.

http://www.ncbi.nlm.nih.gov/pubmed/16186983

most experts do not recommend ETS for the treatment of hyperhidrosis

http://www.sweathelp.org/English/PFF_Treatment_Surgery.asp

sweating from these areas could be under cortical control, separate from the hypothalamic centers involved in thermoregulation

Compensatory hyperhidrosis is excessive sweating of the abdomen, chest, back, thighs, and face,[6,72] usually in response to increased temperature.[46] This is the most common complication following ETS, reported to occur at an average rate of about 60%, with a range of 3% to 98%.[46] Higher rates have been reported from countries with warmer climates, such as in Asia and the Middle East.[46,82] The sweating can be severe for 10% to 40% of patients.[10] Although it has been written that compensatory sweating diminishes with time, several series have documented continued symptoms with longer-term follow-up.[46] In one series of 270 patients followed for a mean of 15 years postsympathectomy, 67% still complained of compensatory sweating, and overall satisfaction fell from an initial level of 96% to 67%.[55] It is possible that patients begin to notice compensatory sweating some time after ETS, as they are initially more aware of the marked reduction of their primary hyperhidrosis.[46] The mechanism for compensatory sweating is unclear; the most likely explanation is that sweating in the trunk increases to compensate for the lack of sweating from the denervated areas in order to maintain thermoregulation.[82] The occurrence of decreased sweating in other areas not innervated by the ganglia treated by ETS suggests that the response to ETS is more complex. The soles are the most common area with decreased sweating post-ETS, and, along with the axillae and palms, sweating from these areas could be under cortical control, separate from the hypothalamic centers involved in thermoregulation.[72] It has also been proposed that ganglion destruction affects axons of neurons in the interomediolateral spinal cord, which could lead to cell death or re-organization, changing the control of the sympathetic system by the spinal cord and higher, leading to increased sympathetic tone in the other body areas not treated by ETS.[10]  http://www.sweathelp.org/English/HCP_Treatment_ETS_Surgery_Complications.asp?printfriendly=true

the decrease in CBF induced by chronic sympathectomy cannot be attributed to the development of hypersensitivity

Thus the decrease in CBF induced by chronic sympathectomy cannot be attributed to the development of hypersensitivity to catecholamines. This decrease remained stable whatever the value of resting flow and was maintained under anesthesia. It is concluded that, as in the peripheral circulation, chronic sympathectomy affects the equilibrium of the vascular smooth muscle fibers, but that circulating amines play no compensatory role in the cerebral circulation because of the blood-brain barrier.

http://www.sciencedirect.com/science/article/pii/0006899385902434

Sympathectomy - a surgically induced neuropathy

"Vascular and neural diseases are closely related and intertwined. Blood vessels depend on normal nerve function, and nerves depend on adequate blood flow. The first pathological change in the microvasculature is vasoconstriction. As the disease progresses, neuronal dysfunction correlates closely with the development of vascular abnormalities, such as capillary basement membrane thickening and endothelial hyperplasia, which contribute to diminished oxygen tension and hypoxia."

http://en.wikipedia.org/wiki/Diabetic_neuropathy

Sympathectomy results in vascular abnormalities, loss of vasoconstriction, capillary basement thickening and endothelial hyperplasia...

oedema associated with the interruption of preganglionic sympathetic tract

Swelling and oedema is often observed in patients with Raynaud's disease or causalgia after acute interruption of post-ganglionic sympathetic fibres such as a wide-spread sympathectomy. Complete sympathetic 

block dilates vein and capillary and increases peripheral pooling, which raises hydrostatic the shins and feet (fig 2), constipation and 

abdominal distention, and dysuria were observed. Oedema was not noted in the 

hands or face. 

 There were no signs or abnormal laboratory data suggesting heart failure, renal failure, liver dysfunction, thyroid dysfunction or local inflammation. Venography of the left leg did not show obstruction in the deep veins. 

 We showed that the preganglionic sympathetic tract in the spinal cord was often 

disturbed in patients with multiple sclerosis with myelopathy.' Most patients with com- 

plete transection of the spinal cord due to injury showed swelling of the lower limbs or 

oedema, but they gradually subsided within several months even without restoration of 

somatic function. Probably some compensatory mechanism improves the hydrostatic 

condition in the chronic stage and explains why oedema is not noted in patients with 

chronic autonomic failure syndrome.

http://www.ncbi.nlm.nih.g...f/jnnpsyc00488-0062b.pdf

The indications for neurolytic or surgical sympathectomy are uncertain

The indications for neurolytic or surgical sympathectomy are uncertain. There is no clear correlation between the degree or duration of pain relief and the actual period of sympathetic blockade and the same patient may show variable responses on different occasionsv (Loh et al 1980). Some patients demonstrate unexpected responses such as contralateral or delayed blocks and some are made worse (Purcell-Jones &Justins 1988, Evans et al 1980, Kleiman 1954)

http://www.springerlink.com/content/7013w45630522h6k/

Sympathectomy causes depigmentation of the skin

In this article, 2 patients were submitted to video-assisted thoracoscopic sympathectomy, and after approximately 8 months they noticed depigmentation of the region corresponding to the blockage of sympathetic stimulus. This fact could be explained by the possible effect of the nervous system on the melanocytes of human skin. 

Sympathectomy? 

Skin Depigmentation: Could it Be a Complication Caused by Thoracic 

 2009;88:42-43 Ann Thorac Surg 

http://ats.ctsnetjournals.org/cgi/reprint/88/4/e42.pdf 

platelet aggregation significantly lower after sympathectomy

It was shown that platelet aggregation in partially (with stellate ganglia containing 25% neurons of normal amount) and completely (0,5% neurons) sympathectomized rats was significantly lower than in intact animals. Concurrently the blood coagulation system of sympathectomized rats was hyperactive. The reasons for sympathectomy-induced changes seems likely to be elevated adrenalin blood concentration in such rats.

http://www.ncbi.nlm.nih.gov/pubmed/7388153

Cardiac Autonomic Function in Patients Suffering from Primary Focal Hyperhidrosis

At the high-frequency band (0.15-0.5 Hz), which represents parasympathetic cardiac innervation, an interaction of type and position influencing spectral power was detected. Our highly interesting findings indicate that primary focal hyperhidrosis is based on a much more complex autonomic dysfunction than generalised sympathetic overactivity and seems to involve the parasympathetic nervous system as well.
Eur Neurol 2000;44:112-116 (DOI: 10.1159/000008207)

the sympathetic block, regularly extends six or more spinal segments above the level of sensory block

Chamberlain et al, using a very sensible technique with thermographic imaging, showed that the sympathetic block, at least partial, regularly extends six or more spinal segments above the level of sensory block [8].

Therefore, it seems that a partial sympathetic blockage exists on substantial area over and under of the level of somatic block. In fact, preganglionic sympathetic fibers, once they quit the dura, enter the paravertebral sympathetic chain. From there, these fibers can ascend or descend, synapsing with up to 18 postganglionic fibers, which may project to dermatomes well above and below the spinal segment from which they originated [9].

Bradycardia associated with spinal block is usually light, and contributes modestly to the drop of blood pressure. Rarely, bradycardia is associated with cardiac collapse. Traditional explanation of this bradycardia originating from a spinal anesthesia is the blockage of cardiac accelerator sympathetic nerves (T1-4). Many studies showed than the incidence and the severity of bradycardia is not related to the height of the sensory block.

Onset time of the bradycardia has poor relation with the timing of the spinal block [10]. Carpenter, in a prospective study on 1000 patients under spinal block., showed that bradycardia occured in 13% (heart rate < 50/min) with an onset time of 47 min (range from1 to 204).

There is a pulse rate paradoxical response to movement of the operation table. Under a spinal or epidural anesthesia, when one lift patient head, blood pressure decreases caused by pooling of the venous blood. But in place of a reflex tachycardia mediated by baroreceptors, there is a paradoxical bradycardia. Interestingly, in situation associated with severe reduction of venous return, paradoxical bradycardia can be seen even in the absence of sympathetic block.

There is similarities between hypotension related to bradycardia of the spinal anesthesia and vasovagal reaction. Vasovagal shock is characterized by hypotension and bradycardia, and can progress to syncope. It has a central or a peripheral etiology.

Because of their rare occurrence, almost all studies on cardiac arrest during spinal anesthesia are retrospective, therefore limited in their ability to identify variables and incidents of such events.

Caplan [14] in 1988 has identified 14 cases of sudden cardiac arrest on patients in good health and undergoing minor surgical procedures. None of these patients had unusually high block, nor received badly inadequate resuscitative care. Despite all this, only 8 of 14 patients survived, and only one survivors had acceptable neurological functions Retrospectively, respiratory insufficiency was suspected, secondary to a strong sedation, as the main etiology of the cardiac arrest. Even a complete sympathectomy leaves a good arterial vascular tone, but in presence of hypoxia and acidosis can lead to a fall in arterial tone, to an exaggerated decrease in blood pressure and cardiac collapse. Early sympathetic responses to hypoxia, which are tachycardia and vasoconstriction, are almost severely blunt by spinal anesthesia [15].

Mackey reported 3 cases of severe bradycardia during spinal anesthesia in the absence of hypoxia and strong sedation [16]. He concludes that severe bradycardya was caused by a drop in venous return triggering Bezold-Jarisch reflex which in presence of sympathetic block led to exaggerated bradycardia, hypotension and arrest.

http://www.esra-learning.com/site/generalites/pathology/b_haemodynamic.htm