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.
www.ubcmj.com/pdf/ubcmj_2_1_2010_24-29.pdf

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.

http://onlinelibrary.wiley.com/doi/10.1111/j.1439-0442.1967.tb00255.x/abstract

Spinal cord infarction occurring during thoraco-lumbar sympathectomy
J Neurol Neurosurg Psychiatry 1963;26:418-421 doi:10.1136/jnnp.26.5.418

Thursday, December 8, 2011

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.

http://www.ncbi.nlm.nih.gov/pubmed/1281124

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

http://www.ncbi.nlm.nih.gov/pubmed/7515354

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]
http://en.wikipedia.org/wiki/Galanin

Sunday, October 30, 2011

Patients with sympathectomy are not suitable controls for sleep study. Why?

Exclusions:
Patients with permanent pacemaker, non-sinus cardiac arrhythmias, peripheral vasculopathy or neuropathy, severe lung disease, status postbilateral cervical or thoracic sympathectomy, finger deformity that precludes adequate sensor application, using a-adrenergic receptor blockers, or alcohol or drug abuse during the last 3 years.

Evaluation of a Portable Device Based on Peripheral Arterial Tone for Unattended Home Sleep Studies

 The clinic sleep laboratory of the Technion Sleep Medicine Centre, Israel
http://chestjournal.chestpubs.org/content/123/3/695.long
CHEST March 2003 vol. 123 no. 3 695-703

MSAC Application no 1130, Assessment Report

Friday, October 21, 2011

The amount of compensatory sweating depends the amount of cell body reorganization in the spinal cord after surgery

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.
www.ubcmj.com/pdf/ubcmj_2_1_2010_24-29.pdf

ETS considered psychiatric surgery - says Dr Nagy

"ETS (sympathectomy)  can alter many bodily functions, including sweating , heart rate , heart stroke volume , blood pressure , thyroid , baroreflex , lung volume , pupil dilation, skin temperature, goose bumps and other aspects of the autonomic nervous system . It can diminish the body's physical reaction to exercise and/or strong emotion, and thus is considered psychiatric surgery. In rare cases sexual function or digestion may be modified as well. "
http://www.lvhyperhidrosis.com/treatment.html

Monday, October 17, 2011

Individual cardiovascular response to different levels of sympathetic blockade varies widely, depending on the degree of sympathetic tone before the block

The cardiovascular responses to epidural anaesthesia are almost entirely due to the fact that the local anaesthetic injected into the epidural space not only blocks somatic, sensory and motor fibres, but also produces preganglionic sympathetic denervation.

Postganglionic sympathetic nerves play an important role in controlling cardiac function and vascular tone. The most important of the cardiovascular effects are related to blockade of vasoconstrictor fibres (below T4) with resulting dilatation of resistance and capacitance vessels and/or cardiac sympathetic fibres with loss of chronotropic and inotropic drive to the myocardium (T1-5) (Figure 1).

The cardiac sympathetic outflow emerges from C5 to T5 levels, with the main supply to the ventricles from T1 to T43. A significant part of the chronotropic and inotropic control of the heart is mediated through the upper four thoracic spinal segments.
Denervation of preganglionic cardiac accelerator fibres leaving the cord at T1-T5 results in minimal vasodilatory consequences. Changes however in heart rate, left ventricular function and myocardial oxygen demand may occur due to high thoracic epidural blockade and are discussed below.

The major determinant of heart rate is the balance between sympathetic and parasympathetic systems with the latter predominating. A high thoracic epidural anaesthesia (TEA) covering the cardiac segments (T1-T4) produces small but significant reductions in heart rate4-8. During cardiac sympathetic denervation, parasympathetic cardiovascular responses, including those involved in baroreflexes, may dominate.


It was suggested that the sympathetic control of heart rate modified the dominating parasympathetic tone, rather than functioning as an active cardiac accelerator. In this study there was no compensation for changes in preload;
therefore cardiopulmonary baroreceptors affected by changes in central volume secondary to peripheral vasodilatation or vasoconstriction might have altered arterial baroreceptor heart rate reflex as well.



High TEA added to general anaesthesia significantly decreased the cardiac acceleration in response to decreasing blood pressure, suggesting that baroreflex-mediated heart rate response to a decrease in arterial blood pressure depends on the integrity of the sympathetic nervous system. However general anaesthesia, in addition to high levels of epidural anaesthesia, may have modified the balance between sympathetic and parasympathetic tone as well.
By applying power spectral analysis, i.e., frequency analysis of electrocardiographic R-R interval, the individual components of the autonomic nervous system can be discerned and can be used as a sensitive indicator of sympathovagal interaction.


Individual cardiovascular response to different levels of sympathetic blockade varies widely, depending on the degree of sympathetic tone before the block.
Anaesth Intensive Care 2000; 28: 620-635
B. T. VEERING*, M. J. COUSINS†
Department of Anesthesiology, Leiden University Medical Center, Leiden, The Netherlands and Department of Anaesthesia and
Pain Management, University of Sydney, Royal North Shore Hospital, Sydney, New South Wales

diabetic autonomic neuropathy has already sympathectomized the patient

Although not specific, the symptoms suffered by diabetics from sweating disturbances are fairly typical [5]. Initially there is heat intolerance accompanied by hyperhidrosis of the upper half of the body, particularly affecting the face, neck, axillae and hands. It is of interest that these patients rarely perspire excessively below the umbilicus. This diabetic syndrome has been attributed to a lesion of the sympathetic nerve fibres which control sweat secretion [11] and follow the course of the peripheral nerves [12]. This affects the efferent branch of the reflex arch and is identical to that occurring distal to a surgical sympathectomy [13].

There was no difference found between the histological changes in the nerves of the spontaneous anhidrotic patients
(Fig. 1) and those of the two previously sympathectomized patients.

A number of papers have been published which stressed [22-24] the high failure rate of sympathectomy operations in diabetics. We believe that the failure of the operation is due to the fact that diabetic autonomic neuropathy has already sympathectomized the patient. The results of the present study are compatible with this idea.
http://www.springerlink.com/content/v21h52461037653k/

Monday, October 10, 2011

sympathectomy will block the chronotropic response

Around 50% of patients have bradycardia in the following minutes of a bilateral surgery with mean and diastolic blood pressure significant reduction. Since the sympathectomy will block the chronotropic response, a significant increase of the ejection volume is observed when the patient moves in the erect position from dorsal decubitus [6]. Two cardiovascular complications were reported in the literature. First, an asystolic cardiac arrest in an 18-year-old woman during the second side (left) of bilateral sympathectomy for severe hyperhidrosis, requiring resuscitation maneuvers, with no chronic sequelae [7]. The second case was reported in a 23-year-old woman in whom a bilateral T2 sympathectomy was performed for facial hyperhidrosis. Two years later, following electrophysiologic studies confirming unopposed vagotonic stimulation, she underwent permanent pacemaker insertion for symptomatic bradycardia [8].
http://icvts.ctsnetjournals.org/cgi/content/full/8/2/238

HAZARDS ASSOCIATED WITH CERVICO-THORACIC SYMPATHECTOMY

The need for a realistic appraisal of the potentialities for harm in Cervico-Thoracic sympathectomy is apparent on anatomic grounds alone (Orkin et al. ] 950). Fatalities occur from time to time, but only a few reports of such fatalities find their way into the literature (Adriani et al. 1952). Reported complications associated with Ccrvico-Thoracic sympathectomy, which is, in effect a permanent Stellate
Ganglion block (Moore 1954), include pneumothorax, Horner's syndrome, phrenic and recurrent laryngeal nerve damage, infection from oesophageal puncture, cardiac arrhythmias (Tochinai 1974), and very infrequently cardiac arrest (Moore 1954).
The following is a case report of a healthy 18-year-old woman who had bilateral Cervico-Thoracic sympathectomy done in two stages for severe hyperhidrosis in the palms of her hands.
Two episodes of asystolic arrest occurred during the 2nd stage left Cervico-Thoracic sympathectomy.
The cause of hyperhidrosis apparently originates from some poorly understood stimulation of the sympathetic nervous system (Cloward 1969), and in sensitive patients this may possibly lead to excessive vagal stimulation to counteract it,
as illustrated by the bradycardia and asystolic reaction to the sudden removal of the sympathetic control, and by the high doses of sympathomimetic drugs necessary to recommence cardiac activity. Anatomically the heart is innervated by the cardiac plexus which consists of the cardiac nerves derived from the cervical and upper thoracic ganglia of the
sympathetic trunk and branches of the vagus. The pacemaker of the heart, the sino-atrial node, is innervated by both the parasympathetic and sympathetic nerves (King and Coakley 1958). The ventricular muscle of the heart is
supplied solely by the sympathetic nerves, and the larger branches of the coronary arteries are also predominantly innervated by sympathetics (Woollard 1926). These factors may also have a bearing on the hazard of a bilateral cervico-thoracic sympathectomy, which leaves the heart solely under vagal control. Usually, following
denervation, the heart will initiate its own impulse, without recourse to external agencies, but there may be a place for transvenous electrode cardiac pacing, if spontaneous initiation of impulse is delayed, or bradycardia is severe.
Anaesthesia and Intensive Care, Vol. V, No. 1, February, 1977

R. F. Y. ZEE
Royal Perth Hospital, Perth

Wednesday, October 5, 2011

abnormalities of the autonomic nervous system are correlated with death risk

Michael Lauer: It's been known for a long time that abnormalities of the autonomic nervous system are correlated with death risk, but the problem is that the way in which these abnormalities are measured are very difficult. They require sophisticated equipment and they require the kind of tests which simply have not entered the realm of normal clinical practice. What we find is that these very, very simple measures that are obtained as part of regular routine exercise testing deflect what happens to the autonomic nervous system and provides us with just as powerful predictors of risk of death.
(Dr Michael Lauer, cardiologist, Cleveland Clinic in Cleveland, Ohio)
http://www.abc.net.au/rn/talks/8.30/helthrpt/stories/s63595.htm

Sunday, September 25, 2011

So numerous are the possible variations that the outcome of a sympathectomy is unpredictable

The sympathetic pathways to the heart are extremely variable in their topography, and the diversity of arrangements encountered accounts for the morphological contradictions in the literature. So numerous are the possible variations that the outcome of a sympathectomy is unpredictable. Where denervation is incomplete, collateral sprouting and regeneration of nerves could even lead to hyperstimulation via the sympathetic pathways.
http://onlinelibrary.wiley.com/doi/10.1002/aja.1001240203/abstract

After severing the cervical sympathetic trunk, the cells of the cervical sympathetic ganglion undergo transneuronic degeneration

In consequence of right-sided smpathectomy at the level of C5 it was found that in the sheep the cervical sympathetic trunk contains nerve fibres which proceed from cells situated in the first four segments of the thoracic part of the spinal cord and in the stellate ganglion. These fibres are about 85 per cent of all fibres of the sympathetic trunk. The remaining 15 per cent proceed from nerve cells situated nasally of the anterior cervical ganglion.

The spinal cord. Changes found in the segment Th1 – Th4 in sheep III and IV closely resembled those
seen in the stellate ganglion (Figures 6, 7).

2. After severing the sympathetic trunk, the cells of its origin undergo complete disintegration within
a year.

3. After severing the cervical sympathetic trunk, the cells of the cervical sympathetic ganglion
undergo transneuronic degeneration.
http://onlinelibrary.wiley.com/doi/10.1111/j.1439-0442.1967.tb00255.x/abstract

Wednesday, September 14, 2011

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

Monday, September 12, 2011

important relationship among cognitive performance, HRV, and prefrontal neural function

These findings in total suggest an important relationship among cognitive performance, HRV, and prefrontal neural function that has important implications for both physical and mental health. Future studies are needed to determine exactly which executive functions are associated with individual differences in HRV in a wider range of situations and populations.
http://www.ncbi.nlm.nih.gov/pubmed/19424767

Low HRV is a risk factor for pathophysiology and psychopathology

The intimate connection between the brain and the heart was enunciated by Claude Bernard over 150 years ago. In our neurovisceral integration model we have tried to build on this pioneering work. In the present paper we further elaborate our model. Specifically we review recent neuroanatomical studies that implicate inhibitory GABAergic pathways from the prefrontal cortex to the amygdala and additional inhibitory pathways between the amygdala and the sympathetic and parasympathetic medullary output neurons that modulate heart rate and thus heart rate variability. We propose that the default response to uncertainty is the threat response and may be related to the well known negativity bias. We next review the evidence on the role of vagally mediated heart rate variability (HRV) in the regulation of physiological, affective, and cognitive processes. Low HRV is a risk factor for pathophysiology and psychopathology. Finally we review recent work on the genetics of HRV and suggest that low HRV may be an endophenotype for a broad range of dysfunctions.
http://www.ncbi.nlm.nih.gov/pubmed/18771686

Friday, September 9, 2011

ELECTRICAL STIMULATION OF THE SYMPATHETIC NERVE CHAIN

The present invention provides a method of affecting physiological disorders by stimulating a specific location along the sympathetic nerve chain. Preferably, the present invention provides a method of affecting a variety of physiological disorders or pathological conditions by placing an electrode adjacent to or in communication with at least one ganglion along the sympathetic nerve chain and stimulating the at least one ganglion until the physiological disorder or pathological condition has been affected.

[0009] A number of treatment regiments utilizing electrical stimulation can be employed for a vast array of physiological disorders or pathological conditions associated with the sympathetic and parasympathetic nervous system. Physiological disorders that may be treated include, but are not limited to, hyperhydrosis, complex regional pain syndrome and other pain syndromes such as headaches, cluster headaches, abnormal cardiac sympathetic output, cardiac contractility, excessive blushing condition, hypertension, renal disease, heart failure, angina, hypertension, and intestinal motility disorders, dry eye or mouth disorders, sexual dysfunction, asthma, liver disorders, pancreas disorders, and heart disorders, pulmonary disorders, gastrointestinal disorders, and biliary disorders. The number of disorders to be treated is limited only by the number, variety, and placement of electrodes (or combinations of multiple electrodes) along the sympathetic nervous system.
http://www.faqs.org/patents/app/20110098762

Surgical left cardiac sympathetic denervation for long QT syndrome: effects on QT interval and heart rate

The maximum heart rate during the exercise tests decreased from 162+/-4 beats/min before surgery to 129+/-10 beats/min (P<0.01). The exercise-induced increase in QTc remained unchanged after the surgery (P>0.05).
http://www.ncbi.nlm.nih.gov/pubmed/16025361

Left cardiac sympathetic denervation in the therapy of congenital long QT syndrome. A worldwide report.

http://www.ncbi.nlm.nih.gov/pubmed/1860195

PRODUCTION OF NEUROGENIC ELECTROCARDIOGRAPHS CHANGES BY UNILATERAL ALTERATION OF SYMPATHETIC TONE

Changes of the electrocardiogram and of ventricular refractory period were measured following either unilateral stellate ganglion stimulation or ablation in the open chest dog preparation.
Right stellate ganglionectomy or left stellate stimulation produces prolonged Q-T intervals and increased T-wave amplitude. Left stellate ganglionectomy or right stellate stimulation produces increased T-wave negativity without measurable change in the Q-T interval.
The differing patterns of electrocardiographic wave form resulting from changes in sympathetic tone mediated by right and left stellate innervation could be correlated with changes in ventricular refractory period. Following right stellate ganglionectomy, refractory period prolongations were most marked over the anterior ventricular surface; left stellate ganglionectomy produced the greatest prolongation on the posterior surface.
Although the right and left stellate innervations of the ventricles overlap, the left stellate influence is predominant over the posterior wall of the ventricles, while right stellate influence dominates the anterior ventricular walls.
The electrocardiographic form changes observed following unilateral alteration of sympathetic tone paralleled those electrocardiographic abnormalities seen in patients with lesions of the central nervous system, suggesting a possible functional explanation for these clinical findings.
http://circres.ahajournals.org/content/18/4/416.short

Monday, September 5, 2011

ganglion block for unbalanced sympathetic nervous system disorders

Stellate ganglion blocks (SGB) are widely used for pain relief in outpatient clinics due to its many therapeutic indications and easy maneuvering. It is used locally over stellate ganglion territory disorders in the craniocervical (head and neck) or upper limbs and systemically for angina pectoris, psychosomatic disorders, hormonal disorders, or unbalanced sympathetic nervous system disorders [1].
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2872892/

Saturday, September 3, 2011

sympathectomy can result in spinal cord infarction

Uncommon causes include decompression sickness, which has a predilection for spinal ischemic damage; complications of abdominal surgery, particularly sympathectomy;...

http://www.neurology-asia.com/Spinal_Cord_Infarction.php

Friday, September 2, 2011

For blood pressure control in certain acute hypotensive states (e.g., pheochromocytomectomy, sympathectomy...

Norepinephrine (Levophed ®) -
For blood pressure control in certain acute hypotensive states (e.g., pheochromocytomectomy, sympathectomy, poliomyelitis, spinal anesthesia, myocardial infarction, septicemia, blood transfusion, and drug reactions).
http://www.globalrph.com/norepinephrine_dilution.htm

Tuesday, August 23, 2011

To date, sufficient importance has not been placed on the long term effects that could cause dorsal sympathectomy

A scientific society has been created for surgery of the sympathetic nervous system, the International Society of Sympathetic Surgery (ISSS); and in the most recent thoracic surgery and related specialities congresses it fills up a considerable percentage of the programme.
On the other hand, this surgery, especially for hyperhidrosis and facial reddening, is the one that on a percentage basis generates more demands and complaints from the patients, even with medico-legal connotations.7 Despite that the majority of the patients show a very high degree of satisfaction, the presence of a patient operated for hyperhidrosis with important compensatory sweating that repeatedly manifest their dissatisfaction to the surgeon is a very annoying situation with an intractable solution. There are even forums on the Internet that constantly manifest their discomfort with this type of surgery in a violent and insulting tone, for example, the World Against Sympathectomy Website.

In summary, we are faced with a new disorder that is being attended massively in our hospitals and needs a moment of contemplation. What are we doing? Are we doing it properly? What are the future implications in these patients of dorsal sympathetic denervation? For the first 2 questions, we could find the answer in the new clinical guidelines and scientific society norms and with the publication of linger series, randomised systematic studies, reviews and meta-analyses. However, it is perhaps the latter of these that implies greater consideration. To date, sufficient importance has not been placed on the long term effects that could cause dorsal sympathectomy, and the effects on lung function, heart function, skin colouring and psychological state are being studies, among others;10 the most important being the first 2. secondary consequences of the operation.

The consequences of sympathetic denervation after a dorsal sympathectomy on lung function have been studied on several occasions11 and reductions in forced vital capacity, forced expiratory flow in the first second and maximum mesoexpiratory flow have been found, but with no clinical significance. It therefore seems that, despite sympathetic innervation being scarce, it directly influences motor tone, especially of the fine respiratory tracts, which cause a light obstructive pattern after the operation and favours bronchial hyperreactivity.12 It is of great interest to know the results of the research being carried out to recognise the long term effects.
Something similar occurs with heart function, the sympathectomy in the short term causes bradycardia due to a lack of sympathetic stimulation to the heart. Several cases of myocardial infarction13 and
chronotropic heart failure requiring the insertion of a pacemaker14 have been reported. In the long term, dorsal sympathetic interruption causes an effect similar to beta blockers on the heart, and produced a decrease in average heart rate, but with no significant changes in the electrocardiogram (normal Q-T).15 It may be good to know through long term prospective studies which effects it truly has on heart function and what it could mean for the daily lives of the operated patients. For the time being, those individuals who practice aerobic sports (for example, long distance runners and cyclists)
should be informed that with sympathectomy their heart rate may be reduced in situations of maximum effort and lower their performance.16


M. Congregado / Arch Bronconeumol. 2010;46(1):1-2

Monday, August 8, 2011

significant change after sympathectomy: reduced sympathetic and increased vagal tone

The HRV analysis showed a significant change of indices reflecting sympatho-vagal balance indicating significantly reduced sympathetic (LF) and increased vagal (HF, rMSSD) tone. These changes still persisted after 2 years. Global HRV increased over time with significant elevation of SDANN after 2 years. QT dispersion was significantly reduced 1 month after surgery and the dispersion was further diminished 2 years later.
http://www.sciencedirect.com/science/article/pii/S0167527399001011

Wednesday, August 3, 2011

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

Tuesday, August 2, 2011

Sympathecomy - a treatment for chronic refractory angina

Despite all the therapeutic measures discussed above many patients will remain severely incapacitated by their chest pain. In such cases, other therapeutic options, such as transcutaneous electric nerve stimulation (TENS), spinal cord stimulation (SCS), left stellate ganglion blockade (LSGB), endoscopic thoraco- scopic sympathectomy (ETS), transmyocardial laser revascularization (TMR) and angiogenesis have to be considered.

Endoscopic transthoracic sympathicotomy was developed by Go¨ ran Claes in the mid 1980s[114].
Initially it was used to treat palmar hyperhidrosis. In the late 1980s, Claes, Wettervik et al. started to use high transthoracic endoscopic sympathicotomy to treat refractory angina pectoris. 

The procedure is performed under general anaesthesia. The pleural cavity is entered through the second or third intercostal space anteriorally. Carbon dioxide is then insufflated and the lung collapsed. Sympathetic ganglia are electrocoagulated using an electroresectoscope. Transsection of the thoracic ganglia T1–T5 is usually performed. The procedure is normally performed on the left side. If the effect is unsatisfactory the operation is done bilaterally. Note that the procedure should not be performed on the right side only as this carries a risk of inducing ventricular arrhythmia. (Mannheimer et al.)
European Heart Journal (2002) 23, 355–370

Sunday, July 31, 2011

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

Saturday, July 30, 2011

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

Saturday, July 23, 2011

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

Sunday, July 10, 2011

In a person who had a sympathectomy, the sympathetic component of the baroreceptor mechanism is absent

The baroreceptor reflex is only a short-term regulator of blood pressure because the receptors adapt by raising the threshold and lowering discharge rate.
8. Describe the reflex compensations when someone suddenly stands up from a supine position. What would happen in a patient who just had a sympathectomy?

Sudden standing causes pooling of blood in the leg veins. This results in decreased venous return to the heart, which leads to decreased cardiac output (Frank-Starling mechanism), which leads to decreased MAP. This decrease in MAP is detected by the carotid sinus baroreceptors, which relay a message to the medullary cardiovascular control center, which increases sympathetic outflow and decreases parasympathetic outflow, this causes:

* An increase in HR and myocardial contractility, tending to restore cardiac output.
* Vasoconstriction in skeletal musculature, skin, kidneys and gut, reducing blood flow to these organs and increasing TPR.
* Venoconstriction decreasing capacitance and increasing venous return

A patient with a sympathectomy would experience what's referred to as orthostatic hypotension (which might lead to syncope). Orthostatic hypotension is a decrease in arterial pressure when going from supine to a standing position. A person with a normal baroreceptor mechanism will try to restore MAP. In a person who had a sympathectomy, the sympathetic component of the baroreceptor mechanism is absent.

Heart Physiology II

M.A.S.T.E.R. Learning Program, UC Davis School of Medicine
Date Revised: Jan 16, 2002
Revised by: Gordon Li and Carolyn Nguyen

Saturday, July 9, 2011

blunted hypoxic pulmonary vasoconstriction due to partial interruption of the sympathetic nerve supply to the lung by bilateral thoracic sympathectomy

Anaesth Intensive Care. 2003 Oct;31(5):581-3.

Orthodeoxia--an uncommon presentation following bilateral thoracic sympathectomy.

Source

Departments of Intensive Care and Vascular Surgery, Sir Charles Gairdner Hospital, Pharmacology Unit, School of Medicine and Pharmacology, University of Western Australia, Perth, Western Australia.

Abstract

We present a case of orthodeoxia (postural hypoxaemia) which resulted from a combination of lung collapse/consolidation and blunted hypoxic pulmonary vasoconstriction due to partial interruption of the sympathetic nerve supply to the lung by bilateral thoracic sympathectomy.
http://www.ncbi.nlm.nih.gov/pubmed/14601286

Bezold-Jarisch Reflex and Sympathectomy

Much attention has been focused on the Bezold-Jarisch Reflex as the cause of sudden acute bradycardia during spinal or epidural anesthesia. The basis of this reflex is a decrease in stretch tension on mechanoreceptors located in the left ventricle. A sudden empty left ventricle triggers this paradoxical reflex which resulst in increased parasympathetic activity. Sympathetic output is also inhabited. Anything that decreases left ventricular end-diastolic volume suddenly, such as spinal anesthesia may rigger his reflex.
   By contrast, bradycardia that is slow on onset, developing after administration of spinal anesthesia, has been recognized and attributed to decreased activity of the cardioaccelerator nerves to the heart. This is a different phenomenon than the sudden bradycardia or asystole in the patient presented above. Complete sympathectomy of the heart itself reduces heart rate by about 20%.

Complications of regional anesthesia

Front Cover
Springer, 2007 - 506 pages










An unopposed vagal tone secondary to sympathectomy

1.) An unopposed vagal tone secondary to sympathectomy. This sympathectomy occurs 2-6 dermatomes higher than sensory block, so that a sensory block of T6 can conceivably inhibit all of the sympathetic innervation to the heart.

2.) The Bezold-Jarisch reflex – which may be widely under appreciated phenomenon. You’ll be surprised how many clinicians are not well versed in this essential physiology.

Sympathectomy → reductions in venous tone → profound decreased venous return. This activates mechanoreceptors embedded within the walls of the myocardium → stimulating vagal afferents → vasomotor center of medulla → increased vagal tone to the heart, thus slowing or stopping the heart entirely to allow enough filling time to generate an effective stroke volume. 
http://allnurses.com/certified-registered-nurse/sympathectomies-and-atropine-124910.html

Wednesday, July 6, 2011

A depression in the heart rate and decrease in response to stress is expected to some degree in all patients after sympathectomy

A depression in the heart rate with resultant drop in the heart rate product and decrease in response to stress is expected to some degree in all patients. Some series have described this finding in most patients, whereas others report at least a 10% drop in heart rate in all patients. This is a possible major cause for postoperative dysfunction and should be cautiously sought after. Patients with resting heart rate that is below 50 to 60 beats/min should undergo electrocardiography. It is recommended that if the heart rate is low on a subsequent electrocardiogram as well, that a tilt test should be performed to exclude patients in whom there is an inordinately high risk of postoperative bradycardia.

In conclusion, thoracoscopic sympathectomy can be done as an outpatient procedure safely and efficiently. Debate continues about the correct transection levels, but at this time there is a consensus that division or clipping is equal to resection. Although the procedure has several severe side effects, they are rare. The predominant complication remains compensatory sweating, which may occur regardless of the level transected or the indication. Future clinical trials should compare some of the different techniques to achieve a global consensus of the surgical approach.
http://ats.ctsnetjournals.org/cgi/content/full/85/2/S764

Tuesday, June 28, 2011

dennervation sensitization increases the arrhythmia susceptibility

The NA content in the heart was not measured but it is likely to be small at least at the 10-day period. It is known that three days after chemical sympathectomy NA content is only 7% of normal value [6]. Second, the development of adrenoceptor supersensitivity in the transplanted heart was demonstrated clearly with enhanced heart rate responses to NA or propranolol (at Day 10) [1]. As dennervation sensitization increases the arrhythmia susceptibility [6], it is thus possible that, in the presence of receptor supersensitivity, adrenergic activation occurs by either increase in circulating catecholamines and possibly local release of residual NA, which might still have been sufficient to contribute to arrhythmia development.
Role of sympathoadrenergic mechanisms in arrhythmogenesis
Xiao-Jun Du* and Anthony M. Dart
Baker Medical Research Institute, Melbourne, Victoria, Australia 
Cardiovascular Research 1999 43(4):832-834;

Monday, June 27, 2011

Sympathectomy altered electroactivity on the heart

The influences on the cardiac autonomic nerve system of the ETS of upper thoracic sympathetic nerve were seen to be of a lesser degree at rest. However, the response to sympathetic stimulation was suppressed after the surgery.
Eur J Cardiothorac Surg 1999;15:194-198
http://ejcts.ctsnetjournals.org/cgi/content/full/15/2/194

Sunday, June 26, 2011

reduced high-frequency power after sympathetic blockade

Alternatively, reduced high-frequency power after sympathetic blockade may also be explained by diminished “accentuated antagonism,” a phenomenon described more than three decades ago (4). Heart rate response to vagal nerve stimulation is accentuated when sympathetic tone is elevated, and vice versa. Thus, cardiac sympathetic withdrawal by high spinal or epidural blockade may have resulted in diminished beat-to-beat fluctuations of R-R intervals without alteration of actual vagal nerve activity. To draw a definitive conclusion regarding the mechanism, determinations of central vagal/sympathetic outflow would be mandatory by an animal experiment.
http://www.anesthesia-analgesia.org/content/100/4/1216.2.full

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