sleep problems might be a side effect of sympathectomy for hyperhidrosis

Finally, if the patients with an abolished melatonin rhythm do not regain their melatonin rhythm, they might encounter sleep problems. The daily rhythm of melatonin secretion is important for a normal sleep–wake cycle (Scheer and Czeisler, 2005). Therefore, sleep problems might be a side effect of sympathectomy for hyperhidrosis. 

Mol Cell Endocrinol. 2006 Jun 27;252(1-2):40-5. Epub 2006 May 2.
Influence of sympathectomy in humans on the rhythmicity of 6- sulphatoxymelatonin urinary excretion. 

Our results show that [3H]substance P binding in the intermediolateral cell column is dependent on the integrity of sympathetic postganglionic neurons

Guanethidine-induced destruction of sympathetic postganglionic neurons in neonatal rats leads to transneuronal degeneration of the sympathetic preganglionic neurons. Using this model, we have been able to show a approximately 35% decrease in [3H]substance P ([3H]SP) binding in the intermediolateral cell column--suggesting that sympathetic preganglionic neurons possess substance P receptors. Our results show that [3H]substance P binding in the intermediolateral cell column is dependent on the integrity of sympathetic postganglionic neurons.

Brain Res. 1985 Apr 29;193-6. pii:0006-8993(85)90146-5.
Reduction of [3H]substance P binding in the intermediolateral cell column after sympathectomy. Takano Y,Loewy AD
https://www.gcbi.com.cn/gclib/html/pubmed/detail/2581658

https://archive.is/bfPLv

Substance P is an important element in pain perception. The sensory function of substance P is thought to be related to the transmission of pain information into the central nervous system. Substance P coexists with the excitatory neurotransmitter glutamate in primary afferents that respond to painful stimulation.[16] Substance P has been associated with the regulation of mood disorders, anxiety, stress,[17] reinforcement,[18] neurogenesis,[19] respiratory rhythm,[20] neurotoxicity, nausea and emesis,[21] pain, and nociception.[22] Substance P and other sensory neuropeptides can be released from the peripheral terminals of sensory nerve fibers in the skin, muscle, and joints. It is proposed that this release is involved in neurogenic inflammation, which is a local inflammatory response to certain types of infection or injury.[23] The regulatory function of SP also involves the regulation of its high-affinity receptor, NK-1. Substance P receptor antagonists may have important therapeutic applications in the treatment of a variety of stress-related illnesses, in addition to their potential as analgesics.

https://en.wikipedia.org/wiki/Substance_P

Snipping the nerve may stop 'flight-or-fight' stress response

What do sweaty palms and abnormal heart rhythms have in common? Both can be initiated by the nervous system during an adrenaline-driven "flight-or-fight" stress reaction, when the body senses danger.

Hyperhidrosis, an abnormal flight-or-fight response of the sympathetic nervous system that causes excessively sweaty palms may also contribute to problems like dangerous irregular rhythms from the lower chambers of the heart, known as ventricular arrhythmias.

UCLA cardiologists have now found that surgery to snip nerves associated with the sympathetic nervous system on both the left and right sides of the chest may be helpful in stopping dangerous, incessant ventricular arrhythmias — known as an "electrical storm" — when other treatment methods have failed. This same type of surgery has been used for years to alleviate hyperhidrosis.

The UCLA team's findings are reported in the Dec. 27–Jan. 3 issue of the Journal of the American College of Cardiology. The study is one of the first to assess the impact of bilateral cardiac sympathetic denervation (BCSD), surgery on both sides of the heart, to control arrhythmias. The research builds on previous work at UCLA in which a similar procedure was performed only on the left side. But for some patients to obtain relief, the researchers said, it must be done bilaterally. 

http://newsroom.ucla.edu/releases/snipping-key-nerves-may-help-life-220281 

5 (11%) thermoregulation difficulties, 4 (9%) a sensation of left arm paresthesia, and 3 (7%) sympathetic flight/fright response loss

Patients with LQTS (N=40) and catecholaminergic polymorphic ventricular tachycardia (N=7) underwent video-assisted thoracoscopic left cardiac sympathetic denervation, with a median follow-up of 29 months (range, 1-67 months). Clinical records were reviewed; 44 patients completed a telephone survey. Of 47 patients (53%), 25 were preoperatively symptomatic (15 syncope, 7 near-drowning, and 3 resuscitated sudden death). Indications for left cardiac sympathetic denervation included β-blocker intolerance (15; 32%) or nonadherence (10; 21%) and disease factors (18; 38%; catecholaminergic polymorphic ventricular tachycardia [6], near-drowning [2], exertional syncope [1], symptoms on therapy [2], LQT3 [1], QTc>520 ms [6]). Other indications were competitive sports participation (2), family history of sudden death (1), and other (1). Median QTc did not change among patients with LQTS (461±60 to 476±54 ms; P=0.49). Side effects were reported by 42 of 44 (95%). Twenty-nine patients (66%) reported dryness on left side, 26 (59%) a Harlequin-type (unilateral) facial flush, 24 (55%) contralateral hyperhidrosis, 17 (39%) differential hand temperatures, 5 (11%) permanent and 4 (9%) transient ptosis, 5 (11%) thermoregulation difficulties, 4 (9%) a sensation of left arm paresthesia, and 3 (7%) sympathetic flight/fright response loss.

Circ Arrhythm Electrophysiol. 2015 Oct;8(5):1151-8. doi: 10.1161/CIRCEP.115.003159. Epub 2015 Jul 29.

Physical and Psychological Consequences of Left Cardiac Sympathetic Denervation in Long-QT Syndrome and Catecholaminergic Polymorphic Ventricular Tachycardia.

http://www.ncbi.nlm.nih.gov/pubmed/26224781

Endoscopic view of the right hemithorax:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2749196/figure/F0003/

Sympathectomy: a neurocardiologic disorder - a variety of expected and unexpected consequences can result

Bilateral thoracic sympathectomies or sympathotomies are done for refractory palmar hyperhidrosis [85–87]. Iontophoresis, botulinum toxin injection, and glycopyrrolate cream are alternatives. Because sweating is mediated mainly by sympathetic cholinergic fibers, autonomic neurosurgery is usually effective; however, a variety of expected and unexpected consequences can result, including ectopic (e.g., plantar) hyperhidrosis, gustatory sweating, Horner syndrome, and decreased heart rate responses to exercise. The latter seems to be related to partial cardiac denervation [88].

Anecdotally, fatigue, altered mood, blunted emotion, and decreased ability to concentrate can develop after bilateral thoracic sympathectomies.
β-Adrenoceptor blockers are a mainstay of treatment for CPVT. An automated defibrillator may have to be implanted. Treatment for CPVT also includes left sympathectomy. Such treatment leaves open the theoretical possibilities of denervation supersensitivity of cardiac adrenoceptors and compensatory activation of the adrenomedullary hormonal system; however, plasma levels of catecholamines have not been assessed in CPVT with or without therapeutic cardiac denervation.Table 1.
Neurocardiologic disorders that feature abnormal catecholaminergic function
Disorders where abnormal catecholaminergic function is etiologic
Hypofunctional states without central neurodegeneration
Acute, primary Neurocardiogenic syncope
Spinal cord transection
Acute pandysautonomia
Sympathectomy
Acute,
secondary Drug-related (e.g., alcohol, tricyclic antidepressant, chemotherapy, opiate, barbiturates, benzodiazepines, sympatholytics, general anaesthesia)Seizures
Guillain–Barre syndrome
Alcohol
Chronic,
primaryPure autonomic failure
Horner's syndrome
Familial dysautonomia
Carotid sinus syncope
Adie's syndrome
Dopamine-β-hydroxylase deficiency

Sympathectomy 

http://onlinelibrary.wiley.com/doi/10.1111/j.1755-5922.2010.00244.x/full

https://archive.is/UMW1w

the clinical results of both surgical and neurolityc sympathectomy are uncertain

Blood diverted from muscle to skin after sympathectomy

However, the clinical results of both surgical and neurolityc sympathectomy are uncertain. Indeed these procedures lead to a redistribution of the blood flow in the lower limbs from the muscle to the skin, with a concomitant fall of the regional resistance, mainly in undamaged vessels. The blood flow will be diverted into this part of the vascular tree, so that a "stealing" of the blood flow may occur. 
Vito A. Peduto, Giancarlo Boero, Antonio Marchi, Riccardo Tani Bilateral extensive skin necrosis of the lower limbs following prolonged epidural blockade 
Anaesthesia 1976; 31: 1068-75.

sympathectomy created imbalance of autonomic activity and functional changes of the intrathoracic organs

Surgical thoracic sympathectomy such as ESD (endoscopic thoracic sympathectic denervation) or heart transplantation can result in an imbalance between the sympathetic and parasympathetic activities and result in functional changes in the intrathoracic organs.

Therefore, the procedures affecting sympathetic nerve functions, such as epidural anesthesia, ESD, and heart transplantation, may cause an imbalance between sympathetic and parasympathetic activities (1, 6, 16, 17). Recently, it has been reported that ESD results in functional changes of the intrathoracic organs.


In conclusion, our study demonstrated that ESD adversely affected lung function early after surgery and the BHR was affected by an imbalance of autonomic activity created by bilateral ESD in patients with primary focal hyperhidrosis.
Journal of Asthma, 46:276–279, 2009
http://informahealthcare.com/doi/abs/10.1080/02770900802660949

Post-sympathectomy neuralgia is proposed here to be a complex neuropathic and central deafferentation/reafferentation syndrome

Pain. 1996 Jan;64(1):1-9.

Post-sympathectomy neuralgia: hypotheses on peripheral and central neuronal mechanisms.

Kramis RC1, Roberts WJ, Gillette RG.

Author information

Abstract Post-sympathectomy neuralgia is proposed here to be a complex neuropathic and central deafferentation/reafferentation syndrome dependent on: (a) the transection, during sympathectomy, of paraspinal somatic and visceral afferent axons within the sympathetic trunk; (b) the subsequent cell death of many of the axotomized afferent neurons, resulting in central deafferentation; and (c) the persistent sensitization of spinal nociceptive neurons by painful conditions present prior to sympathectomy. Viscerosomatic convergence, collateral sprouting of afferents, and mechanisms associated with sympathetically maintained pain are all proposed to be important to the development of the syndrome. 

http://www.ncbi.nlm.nih.gov/pubmed/8867242

Sympathectomy and parasympathectomy leads to the hyperfunction of the serotoninergic system and pathology

We studied the balance of activity of sympathetic, parasympathetic, and serotoninergic divisions of the autonomic nervous system in the regulation of the heart function in rabbits. High activities of the sympathetic and parasympathetic system are associated with antagonistic interactions between them. Moderation of activity of these systems could be accompanied by activation of the serotoninergic system. Physiological sympathectomy and parasympathectomy lead to hyperfunction of the serotoninergic system and pathology.

Bulletin of Experimental Biology and Medicine, Vol. 140, No. 5, 2005 PHYSIOLOGY

Disturbances in brain serotonergic systems result in a range of phenotypes such as depression, suicide and anxiety disorders.

http://www.biomedcentral.com/1471-2202/10/50

Thoracic sympathectomy for peripheral vascular disease can lead to severe bronchospasm and excessive bronchial secretions

Thoracic sympathectomy for peripheral vascular disease can lead to severe bronchospasm and excessive bronchial secretions. A 57-year-old male patient suffering from Buerger's disease presented with pre-gangrenous changes in right foot and ischemic symptoms in right hand. Computed tomographic angiography revealed diffuse distal disease not suitable for vascular bypass and angioplasty. Right lumbar sympathectomy was done using a retroperitoneal approach followed 1 year later by right thoracic sympathectomy using a transaxillary approach. Postoperatively, the patient had severe bronchospasm and excessive secretions in the respiratory tract resistant to theophylline and sympathomimetic group of drugs and without any clinical, laboratory and radiological evidence of infection. The patient was started on anticholinergics in anticipation that sympathectomy might have lead to unopposed cholinergic activity and the symptoms improved rapidly. The patient recovered well and was discharged on 10(th) post-operative day. http://www.ncbi.nlm.nih.gov/pubmed/25624604

http://www.ncbi.nlm.nih.gov/pubmed/25624604

peripheral sympathectomy causes a dramatic increase in NGF levels in the denervated organs

Increased Nerve Growth Factor Messenger RNA and Protein

Peripheral NGF mRNA and protein levels following
sympathectomy
It has been shown previously that peripheral sympathectomy
causes a dramatic increase in NGF levels in the denervated
organs (Yap et al., 1984; Kanakis et al., 1985; Korsching and
Thoenen, 1985).
Increased ,&Nerve Growth Factor Messenger RNA and Protein
Levels in Neonatal Rat Hippocampus Following Specific Cholinergic
Lesions
Scott R. Whittemore,” Lena Liirkfors,’ Ted Ebendal,’ Vicky R. Holets, 2,a Anders Ericsson, and HBkan Persson
Departments of Medical Genetics and’ Zoology, Uppsala University, S-751 23 Uppsala, Sweden, and *Department of
Histology, Karolinska Institute, S-104 01 Stockholm, Sweden

Sympathectomy reduces emotional, stress-induced sweating indicating that it affects the stress-response

"...for reasons that are not obvious, many patients with facial hyperhidrosis and hyperhidrosis of the feet will benefit from upper thoracic sympathectomy. " 

(The Journal of Pain, Vol 1, No 4 (Winter), 2000: pp 261-264)

"Bilateral upper thoracic sympathicolysis is followed by redistribution of body perspiration, with a clear decrease in the zones regulated by mental or emotional stimuli, and an increase in the areas regulated by environmental stimuli, though we are unable to establish the etiology of this redistribution." 

(Surg Endosc. 2007 Nov;21(11):2030-3. Epub 2007 Mar 13.) 


"Palmar hyperhidrosis of clinical severity is a hallmark physical sign of many anxiety disorders, including generalized anxiety disorder, panic disorder, posttraumatic stress disorder, and especially social phobia.4 These are increasingly well understood and highly treatable neurobiological conditions. They are mod- erately heritable hard-wired fear responses,5 and are linked to amygdalar and locus coeruleus hyper-reactivity during psycho- social stress.6,7 Anxiety disorders are known to be much more common among women. This is consistent with the finding of Krogstad et al. that among controls sweating was reported more often by men, while among the hyperhidrosis group sweating was reported more often among women."

"A surgical treatment for anxiety-triggered palmar hyperhidrosis is not unlike treating tearfulness in major depression by severing the nerves to the lacrimal glands. We have recently made a similar argument advocating a psychopharmacological, rather then a surgi- cal, first-line treatment for blushing.9" 
(Journal Compilation - 2006 British Association of Dermatologists - British Journal of Dermatology 2006, DOI: 10.1111/j.1365-2133.2006.07547.x)

cervical sympathectomy induces mast cell hyperplasia and increases histamine and serotonin content in the rat dura mater,

Long-term superior cervical sympathectomy induces mast cell hyperplasia and increases histamine and serotonin content in the rat dura mater, 

Neuroscience 96 (2000) 205–213. 


Mast cells are critical players in allergic reactions, but they have also been shown to be important in immunity and recently also in inflammatory diseases, especially asthma. Migraines are episodic, typically unilateral, throbbing headaches that occur more frequently in patients with allergy and asthma implying involvement of meningeal and/or brain mast cells. These mast cells are located perivascularly, in close association with neurons especially in the dura, where they can be activated following trigeminal nerve, as well as cervical or sphenopalatine ganglion stimulation. Neuropeptides such as calcitonin gene-related peptide (CGRP), hemokinin A, neurotensin (NT), pituitary adenylate cyclase activating peptide (PACAP), and substance P (SP) activate mast cells leading to secretion of vasoactive, proinflammatory, and neurosensitizing mediators, thereby contributing to migraine pathogenesis. Brain mast cells can also secrete proinflammatory and vasodilatory molecules such as interleukin-6 (IL-6) and vascular endothelial growth factor (VEGF), selectively in response
to corticotropin-releasing hormone (CRH), a mediator of stress which is known to precipitate or exacerbate migraines. A better understanding of brain mast cell activation in migraines would be useful and could lead to several points of prophylactic intervention.

D 2005 Elsevier B.V. All rights reserved.

Brain Research Reviews 49 (2005) 65 – 76
The role of mast cells in migraine pathophysiology