sympathectomy: a neurocardiologic disorder

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 anesthesia)
Seizures
Guillain–Barre syndrome Alcohol

Chronic, primary

Pure 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

Acta Physiol Scand. 2000 Sep;170(1):33-8.

Middle cerebral artery blood velocity during exercise with beta-1 adrenergic and unilateral stellate ganglion blockade in humans.

Ide K1, Boushel R, Sørensen HM, Fernandes A, Cai Y, Pott F, Secher NH.

Author information

Abstract

A reduced ability to increase cardiac output (CO) during exercise limits blood flow by vasoconstriction even in active skeletal muscle. Such a flow limitation may also take place in the brain as an increase in the transcranial Doppler determined middle cerebral artery blood velocity (MCA V(mean)) is attenuated during cycling with beta-1 adrenergic blockade and in patients with heart insufficiency. We studied whether sympathetic blockade at the level of the neck (0.1% lidocaine; 8 mL; n=8) affects the attenuated exercise - MCA V(mean following cardio-selective beta-1 adrenergic blockade (0.15 mg kg(-1) metoprolol i.v.) during cycling. Cardiac output determined by indocyanine green dye dilution, heart rate (HR), mean arterial pressure (MAP) and MCA V(mean) were obtained during moderate intensity cycling before and after pharmacological intervention. During control cycling the right and left MCA V(mean) increased to the same extent (11.4 +/- 1.9 vs. 11.1 +/- 1.9 cm s(-1)). With the pharmacological intervention the exercise CO (10 +/- 1 vs. 12 +/- 1 L min(-1); n=5), HR (115 +/- 4 vs. 134 +/- 4 beats min(-1)) and delta MCA V(mean) (8.7 +/- 2.2 vs. 11.4 +/- 1.9 cm s(-1) were reduced, and MAP was increased (100 +/- 5 vs. 86 +/- 2 mmHg; P < 0.05). However, sympathetic blockade at the level of the neck eliminated the beta-1 blockade induced attenuation in delta MCA V(mean) (10.2 +/- 2.5 cm s(-1)). These results indicate that a reduced ability to increase CO during exercise limits blood flow to a vital organ like the brain and that this flow limitation is likely to be by way of the sympathetic nervous system.

Compensatory sweating following sympathectomy or sympathotomy is not compensatory

Compensatory sweating was originally thought to be a mechanism of excessive sweating (in an anatomical region with an intact sympathetic nervous system) to maintain a constant rate of total sweat secretion.90 However, this theory was not confirmed by other studies, demonstrating that compensatory sweating represented a reflex action by an altered feedback mechanism at the level of the hypothalamus which is dependent on the level at which sympathetic denervation occurs. Sympathectomy at the level of the T2 ganglion leads to decreased negative feedback to the hypothalamus. When performing a sympathectomy at a lower level, the negative feedback to the hypothalamus is less inhibited, leading to a decrease in compensatory sweating. Chou et al.91 have proposed the term ‘reflex sweating’ to replace compensatory sweating. Other side effects described in a review article by Dumont89 are gustatory sweating, cardiac effects, phantom sweating, lung function changes, dry hands and altered taste. Besides these side effects there are significant risks of complications during and after surgery (arterial or venous vascular injury, pneumothorax, infection, Horner syndrome etc.).

JEADV 2012, 26, 1–8 Journal of the European Academy of Dermatology and Venereology

sympathectomy and parasympathectomy lead to 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

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

The formation of the spinal nerve from the dorsal and ventral roots. (Photo credit: Wikipedia)

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

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)

sympathetic denervation disturbed the patterns of gut immune-associated cell distribution

The gut immune-associated cells were investigated by histology and immunohistochemistry method. This study found that from proximal to distal segments in small intestine of normal mice, the numbers of intraepithelial lymphocyte, IgA⁺ and mast cells decreased gradually, whereas CD4⁺ and CD8⁺ cell number increased gradually. When 6-hydroxydopamine (6-OHDA) was intraperitoneally injected into mice, IEL numbers were significantly decreased in whole small intestines. However, IgA⁺ and mast cell numbers decreased merely in the proximal segment while CD4⁺ and CD8⁺ cell numbers and their ratio reduced mainly in the distal segment. These findings indicated that sympathetic denervation disturbed the patterns of gut immune-associated cell distribution. It would substantiate the thesis of neuro-immune-endocrine and provide the new ideas for the intestinal disease prevention and drug developments.
http://scialert.net/fulltext/?doi=ajava.2011.935.943&org=10

Peripheral, autonomic regulation of locus coeruleus noradrenergic neurons in brain: putative implications for psychiatry and psychopharmacology

the new data seem to allow a better understanding of how autonomic vulnerability or visceral dysfunction may precipitate or aggravate mental symptoms and disorder.

T. H. Svensson¹

(1)	Department of Pharmacology, Karolinska Institute, Box 60 400, S-104 01 Stockholm, Sweden

Received: 20 June 1986 Revised: 25 November 1986
Psychopharmacology

"Locus coeruleus (LC) is located in the ventrallateral side of the fourth ventricle in the pontine, most of which are noradrenergic neurons projecting to the cortex, cingulate cortex, amygdala nucleus, thalamus, hypothalamus, olfactory tubercles, hippocampus, cerebellum, and spinal cord (Swanson and Hartman, 1975). Norepinephrine (NE) released from the nerve terminal of LC neurons contributes to about 70% of the total extracellular NE in primates brain (Svensson, 1987). It plays important roles not only in arousal, attention, emotion control, and stress (reviewed in Aston-Jones and Cohen, 2005; Berridge and Waterhouse, 2003; Bouret and Sara, 2005; Nieuwenhuis et al., 2005; Sara and Devauges, 1989; Valentino and Van Bockstaele, 2008), but also in sensory information processing (Svensson, 1987). LC directly modulates the somatosensory information from the peripheral system. Under the stress condition, LC could completely inhibit the input from painful stimuli through the descending projection to the spinal cord (Stahl and Briley, 2004). Dys-regulations of LC neurotransmission have been suggested to be involved in physical painful symptoms, attention deficit hyperactivity disorder (ADHD), sleep/arousal disorder, post-traumatic stress disorder, depression, schizophrenia, and Parkinson's disease (reviewed in Berridge and Waterhouse, 2003; Grimbergen et al., 2009; Mehler and Purpura, 2009)."
http://journal.frontiersin.org/Journal/10.3389/fnmol.2012.00029/full