the cardiovascular and pulmonary effects that are observed after TS may be associated with the decrease in NA

Eur J Clin Invest. 1997 Mar;27(3):202-5.Links
Plasma catecholamine concentrations in essential hyperhidrosis and effects of thoracoscopic D2-D3 sympathicolysis.
Noppen M, Sevens C, Gerlo E, Vincken W.

Respiratory Division, Academic Hospital AZ-VUB, Free University of Brussels, Belgium.

Essential hyperhidrosis (EH) is caused by a poorly understood overactivity of the sympathetic fibres passing through the upper dorsal sympathetic ganglia D2 and D3. These ganglia are also in the pathway of the sympathetic innervation of the heart and lungs. Therefore, although the predominant sympathetic neurotransmitter at the eccrine sweat glands is acetylcholine, the plasma concentration of noradrenaline (NA) (which is the main sympathetic neurotransmitter at the end organs including the heart and the lungs) may be elevated. Furthermore, as there are some indications for generalized sympathetic overactivity in EH, the plasma concentration of adrenaline (A) may also be elevated. Plasma levels of NA and A were therefore determined in 13 EH patients before and after thoracoscopic D2-D3 sympathicolysis (TS). Preoperative NA and A plasma levels were all within the normal limits used in our laboratory. After TS, mean NA plasma levels are significantly decreased, whereas mean A are unchanged. We conclude that sympathetic overactivity in EH is limited to the upper dorsal sympathetic ganglia and that some of the cardiovascular and pulmonary effects that are observed after TS may be associated with the decrease in NA.

Endoscopic thoracic sympathectomy suppresses baroreflex control of heart rate in patients with essential hyperhidrosis

J Anesth. 2002;16(1):3.Click here to read Links

Comment on:
J Anesth. 2002;16(1):4-8.

The effect of thoracic sympathectomy on baroreflex control of circulation.
Hoka S

Anesth Analg. 2004 Jan;98(1):37-9, table of contents.Click here to read Links
Endoscopic thoracic sympathectomy suppresses baroreflex control of heart rate in patients with essential hyperhidrosis.
Kawamata YT, Kawamata T, Omote K, Homma E, Hanzawa T, Kaneko T, Namiki A.

Department of Anesthesiology, Nippon Telegraph and Telephone East Japan Sapporo Hospital, Sapporo, Japan.

Endoscopic thoracic (T2-3 or T3-4) sympathectomy (ETS) is a highly effective treatment for palmar hyperhidrosis. Because the T2-3 or T3-4 sympathetic ganglia are involved in direct sympathetic innervation of the heart, sympathectomy at this level may alter baroreflex control of heart rate. The purpose of our study was to examine the influence of ETS on baroreflex responses to pressor and depressor stimuli under small-dose sevoflurane anesthesia. We studied 40 patients with palmar or axillary hyperhidrosis who were scheduled to receive ETS. In the ETS procedure, the sympathetic trunk was identified by using thoracic endoscopy and was transected. Before and after ETS, the pressor or depressor test was performed by using an IV infusion of phenylephrine or nitroglycerin, respectively, under small-dose general anesthesia. Baroreflex sensitivity was calculated from R-R intervals and systolic blood pressure. ETS did not change heart rate and systemic blood pressure at rest, although ETS significantly altered baroreflex in both pressor and depressor tests in all patients. Baroreflex was completely suppressed in 1 of 19 patients in the pressor test and in 9 of 21 patients in the depressor test. We conclude that baroreflex responses are suppressed in patients who receive ETS. IMPLICATIONS: Endoscopic thoracic sympathectomy suppressed the baroreflex control of heart rate during pressor and depressor tests in patients with palmar or axillary hyperhidrosis.

Thoracoscopic D2-D3 sympathicolysis has a partial beta-blocker-like activity, which results in a decrease in heart rate at rest and during maximal exercise, and in the diastolic blood pressure response to the handgrip test. Further studies are needed to assess the long-term consequences of this procedure.
J Auton Nerv Syst. 1996 Sep 12;60(3):115-20.Click here to read Links
Changes in cardiocirculatory autonomic function after thoracoscopic upper dorsal sympathicolysis for essential hyperhidrosis.
Noppen M, Dendale P, Hagers Y, Herregodts P, Vincken W, D'Haens J.

Respiratory Department of the University Hospital AZ-VUB, Free University, Brussels, Belgium.

ARE WE PAYING A HIGH PRICE FOR SYMPATHECTOMY?

www.spinalinjection.com/pdf/newsletters/Summer2001.pdf


A Systematic Literature Review of Late Complications

Conclusions: Surgical sympathectomy irrespective of approach is accompanied by several potentially
disabling complications.


Andrea Furlan
MD, Angela Mailis
MD, MSc, FRCPC (PhysMed) and
Marios Papagapiou
MSc
Comprehensive Pain Program
and Toronto Western Hospital Research Institute
The Toronto Western Hospital, and Institute for Work & Health
, Toronto, Ontario,
Canada.

Regeneration after cervicothoracic sympathectomy producing gustatory responses.

Angiology. 1966 Mar;17(3):143-7.Links
Regeneration after cervicothoracic sympathectomy producing gustatory responses.
Bloor K.

http://www.ncbi.nlm.nih.gov/pubmed/5909808


Gustatory sweating demonstrated by infrared thermography]
[Article in German]

Plendl H, Paulus W, Witt TN.

Neurologische Klinik, Klinikum Grosshadern, Universität München.

The hypaesthesia improved, but the sympathetic nerve deficits remained. There were no other neurological signs. 9 months later, within one minute of eating a sour apple, the patient developed severe sweating over the left half of the face and the left chest. The reaction was confirmed by infra-red thermography which proved that the skin temperature in the sweating region had fallen to 3 degrees C. The likely cause of localized gustatory sweating is intra-operative damage of the stellate ganglion or its preganglionic nerve connections. Treatment is limited to avoidance of the precipitating gustatory stimulus.

Dtsch Med Wochenschr. 1992 Oct 9;117(41):1556-60.

Application of medical thermography to the diagnosis of Frey's syndrome.
Isogai N, Kamiishi H.

Department of Plastic and Reconstructive Surgery, Kinki University Hospital, Osaka, Japan.

BACKGROUND: In Frey's syndrome, the secretory parasympathetic fibers of the parotid gland are thought to communicate with the sympathetic nerve fibers of sweat glands and blood vessels of the skin following parotidectomy. Miscommunication results in subjective gustatory sweating and facial flushing, which appear early with postoperative mastication. In this study, we compared the efficacy of medical thermography to the Minor's starch-iodine test to determine the presence of gustatory sweating in Frey's syndrome. METHODS: Patients were considered to have Frey's syndrome if signs of gustatory sweating and localized skin flushing of the parotid region were present. In four patients who had undergone unilateral parotidectomy, gustatory sweating and facial flushing were present after gustatory stimulation, and the presence of Frey's syndrome was confirmed with Minor's starch test in all patients. Infrared thermography was then performed, and the same area measured. The contralateral side served as an internal control for each patient. RESULTS: Before gustatory stimulation, the isothermal pattern of the diseased side and the nonoperative side was similar. Stress thermography using a sialogogue (lemon, 3 mL) showed a cold spot at the operative site in all four patients with Frey's syndrome. The contralateral nonoperative side showed normal skin temperature distribution in all patients. Minor's test was positive in all patients. CONCLUSIONS: Thermography is a noninvasive, facile test that provides a qualitative visual analysis of the cutaneous capillary response in Frey's syndrome following parotid surgery.

Sympathetic ingrowth retards recovery processes.

Sympathetic sprouting and recovery of a spatial behavior.
Harrell LE, Barlow TS, Davis JN.

After lesions of the medial septum, peripheral sympathetic fibers from the superior cervical ganglion appear in the hippocampal formation. To assess the functional significance of this neuronal rearrangement, we analyzed behavior on a spatial/memory task sensitive to hippocampal dysfunction, the radial eight-arm maze. The procedure allowed evaluation of both working and reference memory. All rats were able to master the task. Half of the rats then underwent either medial septal lesions and ganglionectomy or sham neurosurgery and ganglionectomy, and the other half underwent medial septal lesions or sham neurosurgery followed by ganglionectomy after further behavioral testing. Medial septal lesions in both groups disrupted taks performance with recovery of performance occurring with time. However, the rate of recovery was significantly enhanced in rats which had septal lesions and ganglionectomies simultaneously. Removal of the ganglion after recovery produced no effects on maze performance. Our results suggest that sympathetic ingrowth retards recovery processes.

Exp Neurol. 1983 Nov;82(2):379-90

http://www.ncbi.nlm.nih.gov/pubmed/6628625

Leptin Affects Pancreatic Endocrine Functions through

AKIRA MIZUNO†, TAKASHI MURAKAMI†, SHIZUKA OTANI,
MASAMICHI KUWAJIMA, AND KENJI SHIMA
Department of Laboratory Medicine, School of Medicine, the University of Tokushima, Tokushima
770-8503, Japan
ABSTRACT
The effects of leptin on the secretion of insulin and glucagon were
examined. In an experiment involving insulin response to an iv glu-
cose load in vagotomized rats, the plasma concentrations of insulin
were significantly lower in the leptin (20 nmol/kg BW)-treated group
than in a control group. However, in intact rats and rats that had
undergone both vagotomy and chemical sympathectomy, this sup-
pressive effect of leptin on insulin secretion was not detected. In an
experiment involving a hypoglycemia-induced glucagon secretion test
in intact rats, an iv injection of leptin (20 nmol/kg BW) augmented the
plasma glucagon response to hypoglycemia. In the case of sympa-
thectomized rats, however, this stimulative effect of leptin on gluca-
gon secretion was not detected. In an experiment with perfused rat
pancreas, the addition of leptin (20 nM) to the perfusate slightly
suppressed insulin secretion, but had no effect on basal or glucopenia-
induced glucagon secretion. In intact rats infused with leptin (0.31

plasma concentration of glucose that signals the need by the central nervous system to mobilize energy reserves depends on a number of factors

Greenspan's Basic and Clinical Endocrinology, 8th Ed.


Pathophysiology of the Counterregulatory Response to Neuroglycopenia

Sections: Pathophysiology of the Counterregulatory Response to Neuroglycopenia, Counterregulatory Response to Hypoglycemia, Insulin, Catecholamines, Glucagon, Corticotropin and Hydrocortisone, Growth Hormone, Cholinergic Neurotransmitters, Maintenance of Euglycemia in the Postabsorptive State, Role of the Kidney, Role of PGC-1 in Regulation of Gluconeogenesis.

Topics Discussed: acetylcholine; catecholamines; corticotropin; glucagon; gluconeogenesis; hydrocortisone; hypoglycemia; insulin; kidney; liver; neuroglycopenia; somatotropin.

Excerpt: "The plasma concentration of glucose that signals the need by the central nervous system to mobilize energy reserves depends on a number of factors, such as the status of blood flow to the brain, the integrity of cerebral tissue, the prevailing arterial level of plasma glucose, the rapidity with which plasma glucose concentration falls, and the availability of alternative metabolic fuels.Endogenous insulin secretion is lowered both by reduced glucose stimulation to the pancreatic cell and by sympathetic nervous system inhibition from a combination of alpha-adrenergic neural effects and increased circulating catecholamine levels. This reactive insulinopenia appears to be essential for glucose recovery, because it facilitates the mobilization of energy from existing energy stores (glycogenolysis and lipolysis); increases hepatic enzymes involved in gluconeogenesis and ketogenesis; increases enzymes of the renal cortex, promoting gluconeogenesis; and at the same time prevents muscle tissue from consuming the blood glucose being released from the liver (Chapter 18)...."

Chemical sympathectomy resulted in a highly significant increase in acid and pepsin secretion.

The effect of chemical sympathectomy on insulin-stimulated gastric secretion in dogs.
Grabner P, Holian O, Kalahanis NG, Torma Grabner E, Bombeck CT, Nyhus LM.

Administration of 6 hydroxydopamine (6 OHDA) causes selective acute degeneration of the adrenergic nerve terminals, that is a reversible chemical sympathectomy. The effect of this drug was studied on the insulin stimulated gastric secretion. Insulin stimulated (0.15-0.4 IU/kg) gastric acid and pepsin output and serum gastrin was measured before and after 6 OHDA treatment (40 mg/kg) in gastric fistula dogs. Chemical sympathectomy resulted in a highly significant increase in acid and pepsin secretion. However, the hypoglycemic gastrin release was unaltered except the peak response, which showed a significant reduction. These data confirm earlier observations, that the sympathetic innervation of the stomach has an inhibitory effect on gastric secretion in the dog. Furthermore it seems that the adrenergic fibres in the vagus nerve might have some moduling effect on the insulin induced gastrin release.
Scand J Gastroenterol Suppl. 1984;89:95-8

http://www.ncbi.nlm.nih.gov/pubmed/6429840

hypoglycemia have also been found in patients following sympathectomy

Diseases of the Motor System - Google Books Result
by Pierre J. Vinken, G. W. Bruyn, Harold L. Klawans, J. M. B. V. de Jong - 1991 - Medical - 529 pages
Hypoglycemia induced by insulin is a potent stimulus for epinephrine secretion. ... hypoglycemia have also been found in patients following sympathectomy. ...
books.google.com.au/books?isbn=0444812784...

Adrenal tyrosine hydroxylase: compensatory increase in activity after chemical sympathectomy

Mueller RA, Thoenen H, Axelrod J.

Destruction of peripheral sympathetic nerve endings with 6-hydroxydopamine causes a disappearance of cardiac tyrosine hydroxylase, accompanied by a twofold increase in adrenal tyrosine hydroxylase and a small increase in phenyl-ethanolanine-N-methyl transferase. No change in adrenal catecholamine content occurs under these conditions.

Science. 1969 Jan 31;163(866):468-9

http://www.ncbi.nlm.nih.gov/pubmed/5762395

Sympathectomy for Inner-Ear Vascular Insufficiency

The Journal of Laryngology & Otology (1960), 74:951-970 Cambridge University Press
Copyright © JLO (1984) Limited 1960
doi:10.1017/S0022215100057388

Research Article
Observations on Sympathectomy in the Treatment of Ménière's Disease
Philip H. Golding-Wooda1
a1 “Oakleigh”, 19 The Landway, Bearsted, Maidstone, Kent

Rev Bras Otorinolaringol. 1952 Mar-Apr;20(2):31-40.Links
[Results of sympathectomy in 110 cases of Menière's disease.]
[Article in Undetermined Language]

PASSE EG.

Arch Otolaryngol. 1973 May;97(5):391-4.Links
Cervical sympathectomy in Meniere's disease.
Golding-Wood PH.

The Journal of Laryngology & Otology (1961), 75:259-267 Cambridge University Press
Copyright © JLO (1984) Limited 1961
doi:10.1017/S002221510005773X

Research Article
Sympathectomy for Inner-Ear Vascular Insufficiency
T. J. Wilmota1
a1 Tyrone County Hospital, Omagh, Co. Tyrone, Northern Ireland

Article author query
wilmot tj [PubMed] [Google Scholar]

Ultrastructural changes in the nerves innervating the cerebral artery after sympathectomy

The ultrastructure of the innervation of the anterior cerebral artery of the rat was studied in control animals and in animals after superior cervical ganglionectomy.
Fluorescence histochemistry shows a periarterial network of intensely fluorescent fibers which are divided into two groups, adventitial and periadventitial. The fluorescence begins to decrease 26 hours after, and completely disappears about 32 hours after, ganglionectomy.
Fine structural changes are first observed 18 hours after ganglionectomy, when the axoplasm of degenerating axons becomes electron dense. This density gradually increases up to about 32 hours. By 32 hours most axons with disintegrating axolemmas become inclusion bodies of the Schwann cells. At this stage, synaptic vesicles can still be distinguished as less dense areas, but the membrane structures of synaptic vesicles and mitochondria are difficult to recognize. The degenerating axons are gradually absorbed and by 38 hours dense, residual bodies are observed in the Schwann cells. Generally speaking, the degeneration occurs first in the adventitial fibers and then in the periadventitial fibers. The transient appearance of small, granular vesicles is noticed in axon terminals about 18 hours after denervation, although very few small, granular vesicles are seen in control tissue or at later stages of degeneration.

Takashi Iwayama1
(1) Department of Anatomy, Faculty of Medicine, Kyushu University, Fukuoka, Japan

Received: 22 June 1970

Ultrastructural changes in the nerves innervating the cerebral artery after sympathectomy
Journal Cell and Tissue Research

Issue Volume 109, Number 4 / December, 1970

Functional and organic vascular wall changes after sympathectomy and partial nerve damage

http://www.ncbi.nlm.nih.gov/pubmed/14443457

induces a selective dopaminergic sympathectomy that simulates ideopathic Parkinson's disease

MPTP

MPTP (1-methyl-4-phenyl-1,2,3,6- tetrahydropyridine) a chemical which induces a selective dopaminergic sympathectomy that simulates ideopathic Parkinson's disease is the product of an innacurate attempted synthesis of MPPP (1-methyl-4-phenyl-4-propionoxypiperidine) from MPHP (1-methyl-4-phenyl-4-hydroxypiperide) - these are meperidine (Demerol) analoges and not amphetamine derivatives.

In 1983 a group of heroin users attempted a demerol synthesis and obtained instead a compound called MPTP. The product had a similar appearance and melting point, and they injected it expecting a demerol high. In the brain, MPTP decomposes to MPP+ which selectively bonds to and destroys dopamine receptors. These individuals thus prematurely gave themselves Parkinson's disease. MPP+ closely resembles paraquat, a defoliant used by the US government, outside US borders, against marijuana (a bit heavy handed and reckless).

In order to understand the development and behavior of central dopaminergic neurons and molecular mechanisms involved in the degeneration of such neurons in PD and MPTP-induced PD, several investigators have developed an immortalized dopaminergic cell line. The cell line is called MES 23.5 and is derived by fusion of rat embryonic mesencephalon cells with murine N18TG2 neuroblastoma cells. The cell line expresses a complex range of neural properties found in the dopaminergic neurons of the substantia nigra (Crawford et al, 1992), including tyrosine hydroxylase, dopamine synthesis, and conotoxin receptors (control of calcium channels). Only dopamine, and no other catecholamine, is synthesized by the cells. Levels of tyrosine and dopamine are elevated by 3-7 fold with the treatment of dibutyrl-cAMP. This cell line offers several advantages over other cell lines including greater homogeneity (providing more obvious and consistent observations), and susceptibility to both free radical-mediated cytotoxicity and calcium-dependent cell death.

It has been recently proposed that cerebrospinal fluid (CSF) from PD patients may possess substances which are neurotoxic for dopaminergic cells (Klawans et al, 1993; Hao et al, 1995). To define the selectivity, specificity, and property of these cytotoxic factors, investigators have employed MES 23.5 cell cultures to examine cytotoxicity of CSF from PD and non-PD patients. Preliminary studies from 5 of 7 CSF samples from PD patients, but none of 5 CSF samples from control subjects, have shown significant cytotoxic effects on MES 23.5 cells as determined by cell viability assays. The damaged cells demonstrate a pattern of apoptotic morphology including nuclear chromatin condensation and nuclear fragmentation. An approach to identify the cytotoxic factors is underway. These results raise intriguing possibilities for the etiology and pathogenesis of PD.

http://www.namiscc.org/Research/2002/Psychosis.htm

gustatory sweating occurred in 32% of patients

Compensatory sweating is a frequent side effect after thoracoscopic sympathectomy for primary hyperhidrosis. Gustatory sweating is less commonly reported. It is defined as facial sweating when eating certain foods (particularly spicy food or acidic fruits) and has no generally accepted pathophysiologic explanation.
Overall, gustatory sweating occurred in 32% of patients, and the incidence was significantly associated with extent of sympathectomy (p = 0.04). However, because the extent of sympathectomy was always decided by the location of primary hyperhidrosis, the latter may also explain the risk of gustatory sweating. CONCLUSIONS: Gustatory sweating is a frequent side effect after thoracoscopic sympathectomy. This is the first study to report that its incidence is significantly related to the extent of sympathectomy or the location of primary hyperhidrosis. Although there is no pathophysiologic explanation of gustatory sweating, these findings should be considered before planning thoracoscopic sympathectomy and patients should be thoroughly informed.

Ann Thorac Surg. 2006 Mar;81(3):1047.

Compensatory sweating occurred in 89% of patients and was so severe in 35% that they often had to change their clothes during the day.

Department of Cardiothoracic Surgery, Skejby Sygehus, Aarhus University Hospital, Aarhus, Denmark.

BACKGROUND: Compensatory sweating is a well-known side effect after sympathectomy for hyperhidrosis. It is often claimed to correlate with the extent of sympathectomy, but results from the literature are conflicting, and few have actually considered differences in the intensity of compensatory sweating. METHODS: A total of 158 patients underwent thoracoscopic sympathectomy for primary hyperhidrosis or blushing, or both. Sympathectomy was performed bilaterally at Th2 for facial hyperhidrosis/blushing (n = 49), Th2-3 for palmar hyperhidrosis (n = 62), and Th2-4 for axillary hyperhidrosis (n = 47). RESULTS: Follow-up by questionnaire was possible in 94% of patients after a median of 26 months. Compensatory sweating occurred in 89% of patients and was so severe in 35% that they often had to change their clothes during the day. The frequency of compensatory sweating was not significantly different among the three groups, but severity was significantly higher after Th2-4 sympathectomy for axillary hyperhidrosis (p = 0.04). Gustatory sweating occurred in 38% of patients, and 16% of patients regretted the operation.

Ann Thorac Surg. 2004 Aug;78(2):427-31.

Sympathectomy induces adrenergic excitability of cutaneous C-fiber nociceptors

D. F. Bossut, V. K. Shea and E. R. Perl
Department of Physiology, University of North Carolina at Chapel Hill 27599-7545, USA.

1. The effects of ipsilateral removal of the superior cervical ganglion on the subsequent responsiveness of C-fiber polymodal nociceptors (CPMs) of the ear to close-arterial injections of norepinephrine (NE) were evaluated in adult, anesthetized rabbits. 2. In normal unanesthetized rabbits, the two ears were usually at the same temperature. Immediately after the ganglionectomy, the ipsilateral ear was warmer; however, at the time of electrophysiological recordings (4-23 days) the majority of animals had the ipsilateral ear cooler by > or = 1 degree C, suggestive of denervation supersensitivity. 3. NE (50 ng) did not activate any CPMs (n = 28) from intact animals. 4. Seven of 22 CPMs recorded from sympathectomized ears were activated by NE (50 ng). The responses varied considerably but typically consisted of 2-4 impulses in the 60 s after the NE injection. In some instances, repetitive activity continued for many minutes. Such prolonged discharge differs from the adrenergic responses seen after partial nerve damage. 5. The induction of adrenergic excitability in CPMs by sympathectomy is suggested to be a counterpart to postsympathectomy neuralgia in human beings and a possible part of the mechanism leading to sympathetically related pain states.
Journal of Neurophysiology, Vol 75, Issue 1 514-517,

blocking the sympathetic system - treatment for social phobia

The connection between psyche and sympathetic nervous system

Timo Telaranta M.D., Ph.D. and Paivi Pohjavaara M.D., Privatix Clinic, Tampere, Finland

In the central nervous system the arousal requires the brain stem, the thalamus and the cortex, attention is maintained in the right frontal lobe; the formation of memories happens in the medial temporal lobe, certain diencephalic nuclei and the basal forebrain. The amygdala rates the emotions of an experience. The limbic system is the centre of the human drives, their regulation requires an intact frontal cortex. The injury in the frontal lobe impairs the executive functions as motivation and attention. The sympathomedullary system and locus coerulaeus are activated in depression, mania, panic disorder and acute phases of schizophrenia. The autonomic nervous system is one of the most important mediators between the mind and the body. It has two roles in this function: the role in basic metabolic function as in energy storage and release, in the control of exocrine secretion and thus intake, in conservation, loss, and transformation of energy the role in behaviour, where the hypothalamus is involved in alert and defense reactions.

The sympathetic system is defined as an energy consumption system and the parasympathetic system is an energy conserving and balancing force. The sympathomedullary system is activated in various mental disorders. The biopsychosocial model is clearly seen in the social phobia. The "fight or flight " response of the sympathetic system can also be seen in the physical signs of the social phobia when the patient is in the centre of attention. With sympathetic overload the patient starts to fear the triggering situations and avoid them. The need-adaptive approach adjusts treatment plans of socially phobic patients who haven't had any help of medication and psychotherapy. It seems possible to treat their symptoms and cut the vicious circle of social phobia blocking the sympathetic system in the upper thoracic level with a surgical procedure. If a patient with the social phobia hasn't had any help of conventional treatment methods such as medication and psychotherapy, the sympathetic block could be a treatment of choice for them

Psychosurgery

In the early 20th century, a medical treatment for mental illness, first developed by Portuguese neurologist Egas Moniz, involved damaging the pathways connecting the frontal lobe to the limbic system. Frontal lobotomy (sometimes called frontal leucotomy) successfully reduced distress but at the cost of often blunting the subject's emotions, volition and personality. The indiscriminate use of this psychosurgical procedure, combined with the severe side effects and dangerous nature of the operation gained it a bad reputation and the frontal lobotomy has largely died out as a psychiatric treatment.

More precise psychosurgical procedures are still occasionally used, although are now very rare occurrences. They may include procedures such as the anterior capsulotomy (bilateral thermal lesions of the anterior limbs of the internal capsule) or the bilateral cingulotomy.

Poor regulation of dopamine pathways has been associated with schizophrenia

A report from the National Institute of Mental Health says a gene variant that reduces dopamine activity in the prefrontal cortex is related to poorer performance and inefficient functioning of that brain region during working memory tasks, and to slightly increased risk for schizophrenia.

Dopamine-sensitive neurons in the cerebral cortex are found primarily in the frontal lobes. The dopamine system is associated with pleasure, long-term memory, planning and drive. Dopamine tends to limit and select sensory information arriving from the thalamus to the fore-brain. Poor regulation of dopamine pathways has been associated with schizophrenia.

The so-called executive functions of the frontal lobes involve the ability to recognize future consequences resulting from current actions, to choose between good and bad actions (or better and best), override and suppress unacceptable social responses, and determine similarities and differences between things or events.

The frontal lobes also play an important part in retaining longer term memories which are not task-based. These are often memories with associated emotions, derived from input from the brain's limbic system, and modified by the higher frontal lobe centers to generally fit socially acceptable norms (see executive functions above). The frontal lobes have rich neuronal input from both the alert centers in the brain-stem, and from the limbic regions.

Orthostatic Intolerance

The normal response for a change in body position, results in a stabilization to the upright position in approximately sixty seconds. During this process, the normal change in heart rate would include an increase in heart rate of 10 to 15 beats per minute, and an increase in diastolic pressure of 10 mm Hg, with only a slight change in systolic pressure.

For those who are afflicted with Orthostatic Intolerance, there is an excessive increase in heart rate upon standing, resulting in the cardiovascular system working harder to maintain blood pressure and blood flow to the brain.

Upright posture also brings about a neurohumoral response, involving a change in the levels of vasopressin, renin, angiotensin and aldosterone levels - all of which are involved in the regulation of blood pressure.
Additionally, arterial baroreceptors, particularly those in the carotid sinus area, play an important role in the regulation of blood pressure and the response to positional changes. As the heart pumps blood to the body, the left atrium is passively filled with blood as a result of the force exerted by venous blood pressure. The baroreceptors in the left atrium respond, proportionately, to the pressure exerted by this venous blood pressure. Thus, a drop in venous blood pressure will trigger a compensatory response to increase blood pressure.

Any disruption in any of these processes, or their coordination, can result in an inappropriate response to an upright position, and can lead to a series of symptoms.


The symptoms for these conditions may include the following:

Excessive Fatigue
Exercise Intolerance
Recurrent Syncope or Near Syncope
Dizziness
Nausea
Tachycardia
Palpitations
Visual Disturbances
Tremulusness
Weakness - most noticeable in the legs
Chest Discomfort
Shortness of Breath
Mood Swings
Migraines and Other Headaches
Gastrointestinal Problems
National Dysautonomia Research Foundation
http://ndrf.org/orthostat.htm

dopamine receptors are widely expressed because they are involved in the control of locomotion, cognition, emotion

The D2 and D3 receptors vary in certain tissues and species as a result of alternative splicing, and the human D4 receptor gene exhibits extensive polymorphic variation. In the central nervous system, dopamine receptors are widely expressed because they are involved in the control of locomotion, cognition, emotion, and affect as well as neuroendocrine secretion. In the periphery, dopamine receptors are present more prominently in kidney, vasculature, and pituitary, where they affect mainly sodium homeostasis, vascular tone, and hormone secretion. Numerous genetic linkage analysis studies have failed so far to reveal unequivocal evidence for the involvement of one of these receptors in the etiology of various central nervous system disorders. However, targeted deletion of several of these dopamine receptor genes in mice should provide valuable information about their physiological functions.



PHYSIOLOGICAL REVIEWS Vol. 78 No. 1 January 1998, pp. 189-225
Copyright ©1998 The American Physiological Society
Dopamine Receptors: From Structure to Function

CRISTINA MISSALE, S. RUSSEL NASH, SUSAN W. ROBINSON, MOHAMED JABER, AND MARC G. CARON

Departments of Cell Biology and Medicine, Howard Hughes Medical Institute Laboratories, Duke University Medical Center, Durham, North Carolina

Changes in dopamine D2 receptors and 6-[18F]fluoro-L-3,4-dihydroxyphenylalanine uptake in the brain of 6-hydroxydopamine-lesioned rats

Ishida Y, Kawai K, Magata Y, Takeda R, Hashiguchi H, Abe H, Mukai T, Saji H.

Department of Psychiatry, Miyazaki Medical College, University of Miyazaki, Miyazaki, Japan.

We studied tracer distributions in positron emission tomography of ligands for dopamine D1 receptors ([11C]SCH23390) and D2 receptors ([11C]raclopride) and the dopamine precursor analog 6-[18F]fluoro-L-3,4-dihydroxyphenylalanine ([18F]FDOPA), as a measurement of presynaptic dopaminergic function, in the brain after 6-hydroxydopamine lesioning of the medial forebrain bundle in rats. The unilateral lesions were confirmed behaviorally by methamphetamine-induced rotation 2 weeks after lesioning, and the brains were analyzed by tissue dissection following an intravenous bolus of each tracer 3 weeks after lesioning. [11C]Raclopride, but not [11C]SCH23390, showed a higher accumulation in the striatum on the lesion side compared with that on the non-lesioned (intact) side. On the other hand, a lower accumulation of [18F]FDOPA was found in the striatum and cerebral cortex on the lesion side. Our studies demonstrate upregulation of dopamine D2 receptors in the striatum and a decrease in FDOPA uptake in both the striatum and cerebral cortex ipsilateral to the 6-hydroxydopamine lesions. Therefore, the combination of a D2 antagonist and FDOPA may provide a potentially useful method for assessing the effects of dopamine depletion in Parkinson's disease. Copyright 2004 S. Karger AG, Basel.

Neurodegener Dis. 2004;1(2-3):109-12.

S - increase in activity of the adrenal gland.

Depletion and recovery of catecholamines in several organs of rats treated with reserpine.

[My paper] Rubén Martínez-Olivares, Iván Villanueva, Radu Racotta, Manuel Piñón
Depto. de Fisiología, Escuela Nacional de Ciencias Biológicas, Instituto Politécnico Nacional, Carpio y Plan de Ayala s/n. Col. Santo Tomás, DF. CP. 11340, México.

Chemical sympathectomy with reserpine depletes catecholamines in every neuronal or nonneuronal cell producing a nonspecific temporal sympathectomy. After reserpine administration, most of the drug is distributed to tissues based on their blood flow and would then either be metabolized or be reversibly bound in lipid depots from where it might be released. Consequently, reserpine concentration and the catecholamine-depleting effect in the various tissues are expected to differ according to the route of administration. This study was designed to compare the effects of intraperitoneal (i.p.) and subcutaneous (s.c.) administration of reserpine on catecholamine depletion and recovery in the liver, portal vein, and adrenal gland on days 1, 4, and 10 after reserpine dosage. Catecholamine determinations were extended to 25 days after the treatment only in s.c. reserpine-treated rats and adding samples of heart and brown adipose tissue to the testing. I.p. and s.c. reserpine administration had the same norepinephrine-depleting effect in the portal vein and liver but full recovery was present in both tissues only in i.p. reserpine-treated rats. In the adrenal gland, both routes of administration produced the same depleting and recovery effect of norepinephrine and epinephrine concentrations. A significant temporary overshoot in epinephrine levels was observed several days after s.c. reserpine treatment. Except for the liver, reserpine injected s.c. depleted norepinephrine concentrations significantly in all other tissues up to the end of the experiment. Our results suggest that chemical sympathectomy caused by reserpine administered s.c. produces a generalized and prolonged decrease in peripheral sympathetic activity that could be compensated by an increase in activity of the adrenal gland.

Auton Neurosci. 2006 May 22; : 16723281 (P,S,E,B)

partial denervation by lesion of peripheral nerve or by tissue destruction induces a change in peripheral nociceptors, making them excitable

Edward R. Perl*

Department of Cell and Molecular Physiology, CB 7545, University of North Carolina, Chapel Hill, NC 27599

Control of expression of molecular receptors for chemical messengers and modulation of these receptors' activity are now established as ways to alter cellular reaction. This paper extends these mechanisms to the arena of pathological pain by presenting the hypothesis that increased expression of alpha -adrenergic receptors in primary afferent neurons is part of the etiology of pain in classical causalgia. It is argued that partial denervation by lesion of peripheral nerve or by tissue destruction induces a change in peripheral nociceptors, making them excitable by sympathetic activity and adrenergic substances. This excitation is mediated by alpha -adrenergic receptors and has a time course reminiscent of experimental denervation supersensitivity. The change in neuronal phenotype is demonstrable after lesions of mixed nerves or of the sympathetic postganglionic supply. Similar partial denervations also produce a substantial increase in the number of dorsal root ganglion neurons evidencing the presence of alpha -adrenergic receptors. The hypothesis proposes the increased presence of alpha -adrenergic receptors in primary afferent neurons to result from an altered gene expression triggered by cytokines/growth factors produced by disconnection of peripheral nerve fibers from their cell bodies. These additional adrenergic receptors are suggested to make nociceptors and other primary afferent neurons excitable by local or circulating norepinephrine and epinephrine. For central pathways, the adrenergic excitation would be equivalent to that produced by noxious events and would consequently evoke pain. In support, evidence is cited for a form of denervation supersensitivity in causalgia and for increased expression of human alpha -adrenergic receptors after loss of sympathetic activity.

Vol. 96, Issue 14, 7664-7667, July 6, 1999


PNAS

Bendroflumethiazide; Nadolol Tablets

What should my health care professional know before I receive Bendroflumethiazide; Nadolol?

They need to know if you have any of these conditions:

*

asthma, bronchitis or bronchospasm
*

autoimmune disease such as lupus
*

chest pain (angina)
*

circulation problems, or blood vessel disease (such as Raynaud's disease)
*

depression
*

diabetes
*

electrolyte imbalance (such as low or high levels of potassium in the blood)
*

emphysema, COPD, or other lung disease
*

gout
*

heart disease (such as heart failure or a history of heart attack)
*

kidney disease
*

liver disease
*

muscle weakness or myasthenia gravis
*

pancreatitis
*

pheochromocytoma
*

post-sympathectomy
*

psoriasis
*

thyroid disease
*

unusually slow heartbeat

Supersensitivity of effector cells (smooth muscle) occurs following long-term use, reminiscent of surgical sympathectomy.

Guanethidine and guanadrel

Adverse effects and toxicity: Postural hypotension and decreased blood flow to heart and brain. It causes delayed ejaculaiton in men, increased GI motility and diarrhea. Supersensitivity of effector cells (smooth muscle) occurs following long-term use, reminiscent of surgical sympathectomy.

The antihypertensive effects of thiazides may be enhanced in the post-sympathectomy patient.

PRODUCT MONOGRAPH

TENORETIC

Antihypertensive Agent

PRECAUTIONS:

The antihypertensive effects of thiazides may be enhanced in the post-sympathectomy patient.

Posterior Left Thoracic Cardiac Sympathectomy by Surgical Division of the Sympathetic Chain: An Alternative Approach to Treatment of the Long QT Syndr

Although high thoracic left Sympathectomy via art anterior surgical approach is a highly efficacious treatment for refractory ventricular arrhythmias in patients with the long QT syndrome, the degree of sympathetic denervation has been variable, success of the operation is influenced by anatomical differences between patients, and Horner's syndrome may result. We hypothesized that interruption of sympathetic input to the heart could be accomplished using a posterior thoracic approach to this variable and often complex anatomy by division of the sympathetic chain rather than by direct destruction of the stellate and superior thoracic ganglia with the more conventional anterior, supraclavicular approach. In addition, the posterior approach should decrease the risk of Horner's syndrome by avoiding the ocular sympathetic efferent nerves. This posterior approach is described in five patients with the long QT syndrome and recurrent ventricular arrhythmias. After a mean follow-up of 18 ± 12 months, all are alive without Homer's syndrome.

* ANDREW E. EPSTEIN11Division of Cardiovascular Disease, Department of Medicine, The University of Alabama at Birmingham, Birmingham, Alabama,
* MICHAEL J. ROSNER,**Division of Neurosurgery, Department of Surgery, The University of Alabama at Birmingham, Birmingham, Alabama
* GILBERT R. HAGEMAN,****Department of Physiology and Biophysics, The University of Alabama at Birmingham, Birmingham, Alabama
* JAMES H. BAKER, II11Division of Cardiovascular Disease, Department of Medicine, The University of Alabama at Birmingham, Birmingham, Alabama,
* VANCE J. PLUMB11Division of Cardiovascular Disease, Department of Medicine, The University of Alabama at Birmingham, Birmingham, Alabama, and
* G. NEAL KAY11Division of Cardiovascular Disease, Department of Medicine, The University of Alabama at Birmingham, Birmingham, Alabama

*
1Division of Cardiovascular Disease, Department of Medicine, The University of Alabama at Birmingham, Birmingham, Alabama *Division of Neurosurgery, Department of Surgery, The University of Alabama at Birmingham, Birmingham, Alabama **Department of Physiology and Biophysics, The University of Alabama at Birmingham, Birmingham, Alabama

Pindolol - inhibition of ejaculaiton

AccessPharmacy.com
... similar to those of surgical sympathectomy, including inhibition of ejaculation, ..... Daily doses of pindolol start at 10 mg; of acebutolol, at 400 mg; ...
www.accesspharmacy.com/Content.aspx?searchStr=acebutolol&aid=2500340 - 139k - Cached - Similar pages

Potentiation of the antihypertensive effect occurs with ganglionic or peripheral adrenergic blocking drugs and in the post sympathectomy patient

Name of the medicine: BARBLOC
The active ingredient of Barbloc is pindolol.

Chemical sympathectomy augments the severity of experimental allergic encephalomyelitis

神经肽Y及Th1/Th2细胞与多发性硬化Multiple sclerosis, neuropeptide Y ...

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Multiple sclerosis, neuropeptide Y and Th1/Th2 cell .... Chemical sympathectomy augments the severity of experimental allergic encephalomyelitis 《Journal ... scholar.ilib.cn/Abstract.aspx?A=xdkf200521094 - Similar pages - Note this

Maintenance of blood pressure is mostly dependent on sympathetic “tone”, and the sympathetic nerve innervates the entire vascular bed

Pharmacology and Physiology of Perivascular Nerves Regulating Vascular Function Role of Perivascular Sympathetic Nerves and Regional Differences in the Features of Sympathetic Innervation of the Vascular System

Hiromichi Tsuru1), Noriaki Tanimitsu2) and Tomohisa Hirai2)

1) Department of Pharmacology, Toho University School of Medicine 2) Department of Otorhinolaryngology, Hiroshima University School of Medicine

Maintenance of blood pressure is mostly dependent on sympathetic “tone”, and the sympathetic nerve innervates the entire vascular bed, excepting the capillaries. Although norepinephrine (NE) is the principal neurotransmitter released upon sympathetic nerve stimulation, neuropeptide Y and ATP are cotransmitters in various vascular tissues. In addition, dopamine and epinephrine, as well as acetylcholine, have been shown to be sympathetic neurotransmitters in specific vasculatures. Transmitter NE release is modified by a number of endogenous substances including the transmitter itself. Chronic denervation of the preganglionic fiber induces an increase in NE release per pulse, indicating postganglionic neuronal supersensitivity. So far, three main adrenoceptor types have been shown, α1, α2 and β, each of which is further divided into at least three subtypes, as well as the α1L-adrenoceptor, a phenotype of the cloned α1a-adrenoceptor, in the blood vessel. Thus, the response of vessels with different receptor types to a transmitter varies quantitatively and even qualitatively from one vessel to another. The remarkable diversity in the sympathetic innervation mechanism in the vascular system may play an important role in regional variations in the regulation of blood flow. The sympathetic nerve also exerts long-term trophic action on the blood vessel. In conclusion, the sympathetic nervous system plays an important role not only in the regulation of cardiovascular dynamics but in the maintenance of the vessel structure, as well.

The Japanese Journal of PharmacologyVol. 88 (2002) ,
No. 1 pp.9-13

The significant fall in left circumflex coronary flow was proportional to the decline in external heart work due to sympathectomy both at rest and und

E. Bassenge¹, J. Holtz¹, W. v. Restorff¹ and K. Oversohl¹

(1)	Physiologisches Institut der Ludwig-Maximilian-Universität München, Germany

Received: 18 April 1973

The exercise capacity and the increase of coronary and systemic hemodynamics under treadmill exercise were studied in 5 dogs, chemically sympathectomized with 6-hydroxy-dopamine.

Completeness of adrenergic denervation was verified by stimulation of the right stellate ganglion, by intravenous administration of tyramine, and by demonstration of supersensitivity to exogenous norepinephrine.

These dogs demonstrated a retarded adaptation of hemodynamics to a sudden start of exercise. A fall in mean arterial pressure below 45 mmHg within 10 to 15 sec lead to collapse. After a recovery period of 60–90 sec, moderate treadmill exercise could be continued; steady state attainment of hemodynamic parameters was considerably delayed.

A steady state of exercise with an O₂-consumption (vO₂) of 29.6±2.6 ml/min · kg and a cardiac outupt (CO) of 307±16 ml/min · kg was tolerated for at least 20 min.

An increase of vO₂ up to 42.0±1.7 ml/min · kg and of CO up to 357±13 ml/min · kg under exercise was tolerated for 5 min with steady state, maximal heart rate being 160±4 min^–1 at this level of exercise.

Mean arterial pressure and total peripheral resistance were significantly reduced at rest and during steady state of exercise as compared to controls prior to sympathectomy identical vO₂, whereas CO remained unchanged.

The significant fall in left circumflex coronary flow was proportional to the decline in external heart work due to sympathectomy both at rest and under exercise.

Differential Effects of Chemical Sympathectomy on Expression and Activity of Tyrosine Hydroxylase and Levels of Catecholamines and DOPA

Tyrosine hydroxylase (TH) mRNA and activity and concentrations of 3,4-dihydroxyphenylalanine (DOPA) and catecholamines were examined as markers of sympathetic innervation and catecholamine synthesis in peripheral tissues of sympathectomized and intact rats. Chemical sympathectomy with 6-hydroxydopamine (6-OHDA) markedly decreased norepinephrine and to a generally lesser extent TH activities and dopamine in most peripheral tissues (stomach, lung, testis, duodenum, pancreas, salivary gland, spleen, heart, kidney, thymus). Superior cervical ganglia, adrenals and descending aorta were unaffected and vas deferens showed a large 92% decrease in norepinephrine, but only a small 38% decrease in TH activity after 6-OHDA.

Minoru Kawamura^{1, 2}, Joan P. Schwartz¹, Takuo Nomura¹, Irwin J. Kopin¹, David S. Goldstein¹, Thanh-Truc Huynh¹, Douglas R. Hooper¹, Judith Harvey-White¹ and Graeme Eisenhofer¹

(1)	Clinical Neuroscience Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, 20892

(2)	Institute of Bio-Active Science, Nippon Zoki Pharmaceutical Co., Ltd. Hyogo, 673-14, Japan

Volume 24, Number 1 / January, 1999
JournalNeurochemical Research

the sympathetic nervous system regulates the clinical and pathological manifestations of experimental autoimmune encephalomyelitis (EAE)

Neuropeptide Y (NPY) suppresses experimental autoimmune encephalomyelitis: NPY1 receptor-specific inhibition of autoreactive Th1 responses in vivo.

[My paper] Sammy Bedoui, Sachiko Miyake, Youwei Lin, Katsuichi Miyamoto, Shinji Oki, Noriyuki Kawamura, Annette Beck-Sickinger, Stephan von Hörsten, Takashi Yamamura

Department of Immunology, National Institute of Neuroscience, NCNP, Ogawahigashi, Kodaira, Tokyo, Japan.

Prior studies have revealed that the sympathetic nervous system regulates the clinical and pathological manifestations of experimental autoimmune encephalomyelitis (EAE), an autoimmune disease model mediated by Th1 T cells. Although the regulatory role of catecholamines has been indicated in the previous works, it remained possible that other sympathetic neurotransmitters like neuropeptide Y (NPY) may also be involved in the regulation of EAE. Here we examined the effect of NPY and NPY receptor subtype-specific compounds on EAE, actively induced with myelin oligodendrocyte glycoprotein 35-55 in C57BL/6 mice. Our results revealed that exogenous NPY as well as NPY Y(1) receptor agonists significantly inhibited the induction of EAE, whereas a Y(5) receptor agonist or a combined treatment of NPY with a Y(1) receptor antagonist did not inhibit signs of EAE. These results indicate that the suppression of EAE by NPY is mediated via Y(1) receptors. Furthermore, treatment with the Y(1) receptor antagonist induced a significantly earlier onset of EAE, indicating a protective role of endogenous NPY in the induction phase of EAE. We also revealed a significant inhibition of myelin oligodendrocyte glycoprotein 35-55-specific Th1 response as well as a Th2 bias of the autoimmune T cells in mice treated with the Y(1) receptor agonist. Ex vivo analysis further demonstrated that autoimmune T cells are directly affected by NPY via Y(1) receptors. Taken together, we conclude that NPY is a potent immunomodulator involved in the regulation of the Th1-mediated autoimmune disease EAE.

J. Immunol. 2003 Oct 1;171 (7):3451-8 14500640 (P,S,E,B) Cited:3

Autonomic innervation of immune organs and neuroimmune modulation.

Autonomic & Autacoid Pharmacology. 23(1):1-25, February 2003.
Mignini, F.; Streccioni, V.; Amenta, F.

Abstract:
Summary: 1 Increasing evidence indicates the occurrence of functional interconnections between immune and nervous systems, although data available on the mechanisms of this bi-directional cross-talking are frequently incomplete and not always focussed on their relevance for neuroimmune modulation.

2 Primary (bone marrow and thymus) and secondary (spleen and lymph nodes) lymphoid organs are supplied with an autonomic (mainly sympathetic) efferent innervation and with an afferent sensory innervation. Anatomical studies have revealed origin, pattern of distribution and targets of nerve fibre populations supplying lymphoid organs.

3 Classic (catecholamines and acetylcholine) and peptide transmitters of neural and non-neural origin are released in the lymphoid microenvironment and contribute to neuroimmune modulation. Neuropeptide Y, substance P, calcitonin gene-related peptide, and vasoactive intestinal peptide represent the neuropeptides most involved in neuroimmune modulation.

4 Immune cells and immune organs express specific receptors for (neuro)transmitters. These receptors have been shown to respond in vivo and/or in vitro to the neural substances and their manipulation can alter immune responses. Changes in immune function can also influence the distribution of nerves and the expression of neural receptors in lymphoid organs.

5 Data on different populations of nerve fibres supplying immune organs and their role in providing a link between nervous and immune systems are reviewed. Anatomical connections between nervous and immune systems represent the structural support of the complex network of immune responses. A detailed knowledge of interactions between nervous and immune systems may represent an important basis for the development of strategies for treating pathologies in which altered neuroimmune cross-talking may be involved.

NPY in the regulation of autoimmune Th1 cells

Substantial evidence indicates a dysfunctional communication between the sympathetic nervous system and the immune system in Th1-mediated autoimmune diseases, such as rheumatoid arthritis and multiple sclerosis. In this Opinion, we propose that the sympathetic regulation of immunity is not only mediated by catecholamines but also involves neuropeptide Y (NPY), an additional postganglionic SNS transmitter that is shown to modulate various immunological functions in vitro and in vivo. Based on recent experimental findings, we believe that a more precise understanding of the role of NPY in the regulation of autoimmune Th1 cells will provide novel insights into the neuroimmunological basis of autoimmunity.

Sammy Bedoui^a, Sachiko Miyake^c, Rainer H. Straub^b, Stephan von Hörsten^a and Takashi Yamamura^c,

^aDepartment of Functional and Applied Anatomy, Medical School of Hannover, 30625 Hannover, Germany

^bDepartment of Internal Medicine I, University Hospital Regensburg, 93042 Regensburg, Germany

^cDepartment of Immunology, National Institute of Neuroscience, 4-1-1 Ogawahigashi, Kodaira, Tokyo 187-8502, Japan

Available online 20 August 2004.

Sympathetic Neurotransmitters in Joint Inflammation

Rainer H. Straub MD^, and Peter Härle MD

Laboratory of Neuroendocrinoimmunology, Department of Internal Medicine I, University Hospital Regensburg, FJS-Allee 11, 93042 Regensburg, Germany

Available online 5 January 2005.

This article is not included in your organization's subscription. However, you may be able to access this article under your organization's agreement with Elsevier.

This article demonstrates the dual pro- and anti-inflammatory role of the sympathetic nervous system (SNS) in inflammatory joint disease (IJD) by way of distinct adrenoceptors. The dual role of the SNS depends on involved compartments, timing of distinct effector mechanisms during the inflammatory process, availability of respective adrenoceptors on target cells, and an intricate shift from β-to- adrenergic signaling in the progressing course of the inflammatory disease (β-to- adrenergic shift). Additional critical points for the dual role of the SNS in inflammation are the underlying change of immune effector mechanisms during the process of disease progression and the behavior of sympathetic nerve fibers in inflamed tissue (nerve fiber loss). This is accompanied by a relative lack of anti-inflammatory glucocorticoids in relation to inflammation. In quintessence, in early stages of IJD, the SNS plays a predominantly proinflammatory role, whereas in late stages of the disease the SNS most probably exerts anti-inflammatory effects.

Does bilateral thoracic sympathectomy predispose to reflex bronchospasm following tracheal intubation?

A 31 year old old non-smoking woman, 60 kg, withouth a history of allergy or asthma was scheduled for left knee arthroscopy. Two months previously she had an uneventful general anesthetic for bilateral thorascopic sympathectomy to treat essential hyperhidrosis.

Immediately following intubation, ventilation became difficult. Chest auscultation revealed bilateral expiratory wheezing associated with decreased air entry and increased airway pressure up to 60 cm H2O. Oxygen saturation, as monitored by pulse oximetry, decreased from 100% to 80%.

The severe bronchospams occured immediately following tracheal intubation, suggesting that it may have been a reflex response which was triggered by instrumentation of the airway under light level of anesthesia.

Sympathectomy results in a decrease of plasma norepinephrine, and parasympathetic predominance which may increase airway resistance.

Thus, patients with essential hyperhidrosis who have undergone bilateral thoracic sympathectomy, may be more liable to develop reflex bronchospams under light levels of anesthesia.

Ahed Zeidan MD
Nazih Nahle MD
Anis Baraka MD FRCA
Sahel General Hospital, American Universisty of Beirut Medical Center

Hypoxaemia is of a major concern during thorascopic sympathectomy

Hypoxaemia is of a major concern during thorascopic sympathectomy. However, the pathophysiology of hypoxaemia and consequent decrease in SpO2 differs between the two anaesthetic techniques. The normal physiological response to massive atelectasis is an increase in pulmonary vascular resistance (hypoxic pulmonary vasoconstriction) with re-routing of blood to well ventilated lung zones and consequent improvement in PaO2. HOWEVER, DURING ENDOBRONCHIAL ANAESTHESIA FOR THORACIC SYMPATHECTOMY THERE IS AN APPARENT FAILURE OF THIS COMPENSATORY MECHANISM. When more then 70% of the lung is atelectatic, compensation by hypoxic pulmonary vasoconstriction appears ineffective. During carbon dioxide insufflation using endobronchial intubation, Hartrey and colleagues reported a decrease in systolic arterial pressure of >20mm Hg in 21% of patients. Similarly we have reported sudden hypotension and bradycardia after injudicious carbon dioxide insufflation. Although extremely rare, sudden cardiac arrest has been reported after left T2-3 sympathetic nerve transection. While the exact pathophysiology of this occurence is unclear, it is postulated that before complete transection of the sympathetic trunk, continuous sympathetic stimulation to the stellate ganglions results in a reduction in the ventricular finrillation threshold, arrhythmia and cosequent cardiac arrest. In an iteresting study of the delayed cardiac effects of T2-$ symtpathectomy, Drott and colleagues demonstrated significantly reduced heart rate at rest, and during both exercise and the recovery phase of exercise. Changes is the electrical axis and shortening of the QT interval have also been reported. Irrespective of the technique used the reported incidence of postoperative pneumpthorax is variable, occuring in 2-15% of cases. In a study by Gothberg, Drott and Claes, postoperative chest x-ray after 1274 procedures, in 602 patients demonstrated that a small apical pneumothroax was a usual occurence. Conclusion: Because of the anaesthetic implications and possible surgical complications, many surgeons are reluctant to perform transthoracic sympathectomy. British Journal of Anaesthesia 1997; 79: 113-119 B. Fredman, D. Olsfanger and R. Jedeikin

Left, but not right, one-lung ventilation causes hypoxemia during endoscopic transthoracic sympathectomy

Anesth Analg 2000;90:28
© 2000 International Anesthesia Research Society

---

CARDIOVASCULAR ANESTHESIA

Sequential Changes of Arterial Oxygen Tension in the Supine Position During One-Lung Ventilation

Seiji Watanabe, MD, Eiko Noguchi, MD, Shinichi Yamada, MD, Nobuya Hamada, MD, and Tatsuhiko Kano, MD

Department of Anesthesiology, Kurume University School of Medicine, Fukuoka, Japan

Implications: Close observation and prompt counteractions including termination of one-lung ventilation (OLV) are crucial for patients under OLV in the supine position, because life-threatening hypoxemia frequently occurs approximately 10 min after starting OLV, even under 100% oxygen inhalation. The left semilateral decubitus position was as effective as the left lateral decubitus position in avoiding life-threatening hypoxemia during OLV.

Incidence of chest wall paresthesia after needlescopic video-assisted thoracic surgery for palmar hyperhidrosis

Alan D.L. Sihoe, Clement S.K. Cheung, Ho-Kei Lai, Tak-Wai Lee, Kin-Hoi Thung, Anthony P.C. Yim^*

Department of Surgery, Division of Cardiothoracic Surgery, The Chinese University of Hong Kong, Prince of Wales Hospital, Shatin, Hong Kong SAR, China

Received 5 September 2004; received in revised form 28 September 2004; accepted 22 October 2004.

^* Corresponding author. Tel.: +86 852 2632 2629; fax: +86 852 2647 8273. (E-mail: yimap@cuhk.edu.hk).

Objective: Chest wall paresthesia is a reported sequela of thoracotomy and Video-Assisted Thoracic Surgery (VATS) which is distinct from wound pain. Although needlescopic VATS confers less post-operative pain and better cosmesis, the incidence of paresthesia after needlescopic VATS has not been quantified. Methods: For homogeneity of the patient cohort, we studied 50 patients who received bilateral needlescopic VATS sympathectomy (T2-T4 excision) for palmar hyperhidrosis using 2 or 3mm instruments during a 36-month period at a single institute. A standard questionnaire was administered by telephone interview, with 34 patents responding (68.0%). The median post-operative observation time was 16.5 months (range: 10–40 months). Collected data were compared with a historical group who received conventional VATS using 10mm ports. Results: Paresthetic discomfort distinguishable from wound pain was described by 17 patients (50.0%). The most common descriptions were of ‘bloating’ (41.2%), ‘pins and needles’ (35.3%), or ‘numbness’ (23.5%) in the chest wall. The paresthesia resolved in less than two months in 12 patients (70.6%), but was still felt for over 12 months in three patients (17.6%). Post-operative paresthesia and pain did not impact on patient satisfaction with the surgery, whereas compensatory hyperhidrosis in 24 patients (70.6%) did (P=0.001). The rates and characteristics of the paresthesia following needlescopic VATS are similar to those observed after conventional VATS. Conclusions: Chest wall paresthesia affects a significant but previously overlooked proportion of patients following needlescopic VATS

The effects of hypoxemia, G-6-PD deficiency and sympathectomy might all add to the development of acute pulmonary edema

Transaxillary endoscopic sympathectomy of thoracic ganglia (T₂-T₃) has recently gained wider acceptance as the treatment of choice for palmar hyperhidrosis. It requires one-lung ventilation to facilitate the surgery. One-lung ventilation, however, is not without complications, among which acute pulmonary edema has been reported. In this case report, we present a patient with palmar hyperhidrosis complicated by glucose-6-phosphate dehydrogenase (G-6-PD) deficiency, who received bilateral endoscopic sympathectomy under alternate one-lung anesthesia, and developed acute pulmonary edema immediately after recruitment of the successive collapsed lung. The effects of hypoxemia, G-6-PD deficiency and sympathectomy might all add to the development of acute pulmonary edema secondary to reexpansion of each individual lung after alternate one-lung ventilation. The possibilities of the inferred causes are herein discussed.

Source: Acta Anaesthesiologica Scandinavica, Volume 45, Number 1, January 2001

Haemodynamic changes during thoracoscopic surgery

Haemodynamic changes during thoracoscopic surgery: The effects of one-lung ventilation compared with carbon dioxide insufflation.

Main Articles

Anaesthesia. 55(1):10-16, January 2000.
Brock, H. 1; Rieger, R. 2; Gabriel, C. 3; Polz, W. 4; Moosbauer, W. 1; Necek, S. 5

Abstract:
Summary: We investigated the haemodynamic and respiratory effects of one-lung ventilation and carbon dioxide insufflation in 13 adult patients undergoing video-assisted thoracoscopy. Cardiorespiratory variables were determined during carbon dioxide insufflation at intrahemithoracic pressures of 5, 10 and 15 mmHg, and after 5 and 15 min of one-lung ventilation. Carbon dioxide insufflation was associated with a clear deterioration in circulatory function. The cardiac index decreased subsequent to increasing intrathoracic pressures. The mean cardiac index (SD) at pressures of 10 and 15 mmHg was 1.86 (0.39) and 1.52 (0.46), respectively, and may be compared with the reduced venous return consistent with tension pneumothorax. One-lung ventilation did not affect haemodynamic variables but reduced arterial oxygenation indices (PaO2/FIO2) from 424.29 (160.79) after induction of anaesthesia, to 207.72 (125.50) after 5 min and 172.04 (72.03) after 15 min of one-lung ventilation, respectively. The oxygenation index was not influenced by intrahemithoracic carbon dioxide insufflation. One-lung ventilation via a double-lumen endobronchial tube is safe and convenient for video-assisted thoracoscopic surgery. It has no further consequences on haemodynamic variables, whereas the compression of the lung by carbon dioxide insufflation may cause circulatory dysfunction.

one-lung ventilation causes hypoxemia during endoscopic transthoracic sympathectomy

Hypoxemia is an abnormal deficiency in the concentration of oxygen in arterial blood (Mosby's Medical Dictionary). A frequent error is made when the term is used to describe poor tissue diffusion as in hypoxia. It is possible to have a low oxygen content (e.g., due to anaemia) but a high PO₂ in arterial blood so incorrect use can lead to confusion.

Journal of Vascular Surgery : Reply - Published by Elsevier

2 Y Katz, E Zisman, S Isserles and B Rosenberg,
Left, but not right, one-lung ventilation causes hypoxemia during endoscopic transthoracic sympathectomy.

ETS sympathetically maintained pain, and vasospastic or ischemic vascular disease

Sympathectomy for Pain and Hyperhidrosis: Based on the Breakfast Seminar of April 24, 2001, at the 69th Annual Meeting of the American Association of Neurological Surgeons, Toronto, Ontario, Canada.

Article

Neurosurgery Quarterly. 12(2):89-99, June 2002.
Wilkinson, Harold A.

Abstract:
Summary: Surgical resections of sympathetic ganglia from the thoracic, splanchnic, and lumbar area have been carried out for more than 100 years. In the past decade, neurosurgeons have become more interested in surgery on the sympathetic nervous system as less invasive techniques have been developed. Percutaneous radiofrequency and video-assisted endoscopic techniques have largely replaced open surgical thoracic sympathectomy. Lumbar and splanchnic sympathetic ablation is commonly done by percutaneous chemical techniques or, occasionally, by radiofrequency ablation, but the open techniques are still widely used. Sympathectomy is most widely employed for pathologic hyperhidrosis (especially the palmar component), sympathetically maintained pain, and vasospastic or ischemic vascular disease. The less invasive techniques are especially attractive for treating the sympathetically mediated cardiac diseases, including Prinzmetal angina, "syndrome X," and congenital long Q-T interval syndrome.

Surgical complications are usually manageable, but deaths have occurred (even with endoscopic techniques).

Endoscopic sympathetic block in the treatment

In this study, endoscopic sympathetic block was useful in reducing the symptoms of
severe social phobia. Although the method is surgical and the effect hence mainly biolog-
ical, the psychological symptoms of social phobia were also significantly reduced. The
results are best if the main symptoms are blushing or palpitation, but even a smaller
reduction in the other symptoms is important if it helps the patient to break his isolation.
Knowledge of the elimination of embarrassing physical symptoms in social situations
helps the patient to expose himself to formerly impossible situations, and success in them
also causes psychological symptoms to subside. But the relief of psychological symp-
toms may also be due to direct a biological effect of the operation on the anxiety-mediat-
ing areas in the nervous system. The only meaningful side effect is compensatory sweat-
ing of the trunk, but not even that is significant when modern surgical method are used.
Clamping is as good as bilateral cauterisation, and the results may be equally good with
unilateral and bilateral clamping, but because there were only eight patients who had
undergone a unilateral clamping procedure, the material is not sufficient to allow definite
conclusions concerning that. The results remain unchanged over time, which shows that
they were not due to a placebo effect. In the future, it is important to compare this treat-
ment to traditional treatment in order to find out its place among the other, officially
approved methods of treating social phobia.

PÄIVI
POHJAVAARA
Faculty of Medicine,
Department of Psychiatry,
University of Oulu
OULU 2004

A qualitative study of the development of social phobia

PÄIVI POHJAVAARA
SOCIAL PHOBIA: AETIOLOGY, COURSE
AND TREATMENT WITH ENDOSCOPIC
SYMPATHETIC BLOCK (ESB)
A qualitative study of the development of social phobia
and its meaning in people's lives and a quantitative study
of ESB as its treatment
Academic Dissertation to be presented with the assent of
the Faculty of Medicine, University of Oulu, for public
discussion in the Väinö Pääkkönen Hall of the Department
of Psychiatry, on December 3rd, 2004, at 12 noon.

Thanks to modern research techniques, we know a lot of the location of attention, emo-
tion and arousal modulation in the brain. Arousal requires involvement of the brain stem,
the thalamus and the cortex, while attention is maintained by the function of the right
frontal lobe (Kaplan & Sadock 1998, Nagahama et al. 2001). The amygdala rates the
emotional importance of an experience, and the limbic system is the centre of human
drives, whose regulation appears to require an intact frontal cortex. Crude emotions are
produced and handled in the midbrain structures and the olfactory cortex, while distinct-
ly human emotions are generated in the cortex (Kaplan & Sadock 1998).

Homeostatic responses mediated by the autonomic
nervous system are achieved by altering the balance between the sympathetic, parasympa-
thetic and different hormonal systems (Mosqueda-Garcia 1996). The most apparent link
between the autonomic and endocrine systems is manifested by the interactions between
the adrenal cortex and the adrenal medulla.

The neuroanatomical circuits, which support fear and anxiety behaviour, are modulated
by a variety of chemical neurotransmitter systems (Charney 2003). These include the
peptidergic neurotransmitters, corticotrophin-releasing hormone (CRH), neuropeptide
Yand substance P, the monoaminergic transmitters, norepinephrine, serotonin and dopam-
ine, and the amino acid transmitters, gamma-aminobutyric acid and glutamate.
The connection between the sympathetic nervous system and the psyche is best seen in
anxiety and especially in social phobia. The observed usefulness of beta-adrenergic antag-
onists in performance phobia supports this hypothesis (Sutherland & Davidson 1995).

There are studies indicating possible supersensitivity of the central serotonin systems in
social phobia and schizophrenia patients (Tancer et al. 1995, Malhotra et al. 1998). It has
been shown using SPECT (Pirker et al. 2000) that, in a solitary case study, the decreased
5-HTT activity of a social phobic patient was normalized by a sympathetic block (Kuikka
et al. 2000). Among the many neurotransmitters implicated in social anxiety disorder, the
complex interactions between the noradrenergic and serotonergic systems and the HPA
axis overlap those found seen in fear and anxiety (Marcin & Nemeroff 2003).

The physical symptoms of social phobia might be treated by blocking the sympathetic
system at the upper thoracic level with a surgical procedure (Crozier 2001, Telaranta
1998). Sympathectomy was first used to treat the exophthalmos of Basedow disease
(Jonnesco 1896) and angina pectoris (Le Riche 1913, Jonnesco 1921) in the late 19th and
early 20th centuries. Its beneficial effect on the treatment of facial sweating was noticed
as early as the 1930s, and its impact on palmar sweating was reported in the 1950s, when
the procedure was already carried out endoscopically (Kux 1954).

Endoscopic sympathicotomy and endoscopic sympathetic block strongly influence typical symptoms of patients with social phobia

Social phobia is an anxiety disorder which causes fear and anxiety in social interaction or performance situations and can in its worst forms be very debilitating. The patients tend to isolate themselves and suffer from comorbid disorders such as depression, other anxiety disorders and drug and alcohol abuse. Traditional treatment methods such as medication and psychotherapy cause improvement in only 50–70% of patients. METHODS: 164 patients who had been suffering from social phobia for at least 5 years and who were resistant to conservative treatment (medication and/or psychotherapy) were enrolled in this open, uncontrolled, prospective follow-up study. 71 patients underwent endoscopic sympathicotomy (cauterisation); 93 underwent endoscopic sympathetic block (clamping) of the T2–T3 ganglia. Severity of psychic and physical symptoms was assessed by a modified version of Davidson’s brief social phobia scale and patients’ satisfaction was evaluated 1, 6, and 12 months postoperatively. RESULTS: Fear of observation, performance anxiety and embarrassment were alleviated and alertness increased. Likewise, palpitations, trembling of hands and heads, blushing and hyperhidrosis were relieved. All changes were statistically significant. Patients’ satisfaction was high and remained stable over time. Gender, age, and education did not influence satisfaction rates. CONCLUSIONS: Endoscopic sympathicotomy and endoscopic sympathetic block strongly influence typical symptoms of patients with social phobia.

JournalEuropean Surgery
Volume 37, Number 3 / June, 2005

http://www.springerlink.com/content/w986882515290647/

During Thoracoscopic sympathectomy hypotension occurs frequently.

Background : During Thoracoscopic sympathectomy hypotension occurs frequently. In this study we compared propofol with etomidate as a main anesthetic agent for thoracoscopic sympathectomy by observing intraoperative vital signs, postoperative
recovery
and side effects.
Methods : Thirty adult patients scheduled for both thoracoscopic sympathectomy were allocated to groups P (propofol) or E (etomidate). P-deletion test (PDT) was dome and plasma cortisol level was measured. In group P (n = 16), anesthesia was
induced
with fentanyl 100 μg, propofol target controlled infusion (TCI) and vecuronium. Anesthesia was maintained with N2O (60%)-propofol. MAP, HR and bispectral index were measure before induction, right after positioning, at the beginning of
right
and left sympathectomy. In group E(n = 14), anesthesia was induced and maintained with etomidate instead of propofol. Postoperative recovery was assessed on the basis of modified Aldrete scoring system at 5, 15, 30, 60 minutes postoperatively. PDT
was
performed at 1, 2 hours postoperatively. Plasma cortisol level was measured 2 h and 3 days after operation. Occurrence of myoclonic movement and nausea was recorded.
Results : MAP was lover in group P (P < 0.05). There was no difference between groups in HR, plasma cortisol concentration. The values of BIS, PDT, recovery score of group P were higher than those of group E (P< 0.05). The incidence of nausea was significantly higher in group E (P < 0.05). Conclusions : Etomidate anesthesia provided more stable vital signs during thoracoscopic sympathectomy compared to propofol anesthesia. However, in terms of recovery and nausea, better outcome was suggested in propofol anesthesia.

http://kmbase.medric.or.kr/Main.aspx?d=KMBASE&m=VIEW&i=0858220000040040262

Sympathetic regulation of Autoimmune Disease

In animal models of human autoimmune disease, alterations in sympathetic innervation, NE concentration and lymphocyte AR expression have been demonstrated. ....reduced splenic noradrenergic innervation and decreased splenic NE concentration were apparent before the onset os disease symptoms. In myelin basic protein-induced EAE and MS-like disease, a reduction in splenic NE concentration was reported at the time of maximal antigen-induced lymphocyte proliferation and was accompanied by an increase in the density of of splenic lymphocyte beta-AR. In chronic/relapsing EAE (CREAE) induced in rats, splenocyte beta-AR density correlated positively with the severity of CREAE. Removal of noradrenergic innervation by chemical sympathectomy with 6-OHDA enhanced the severity of symptoms in EAE...

Neuropsychiatry

By Randolph B. Schiffer, Stephen M. Rao, Barry S. Fogel
Published 2003
Lippincott Williams
& Wilkins

Alterations in autonomic activity have been reported in RA and MS

Neuropsychiatry

By Randolph B. Schiffer, Stephen M. Rao, Barry S. Fogel

The SNS may elicit different, and often opposing functions at different anatomic sites. Localized denervation of draining lymph nodes, with sparing of the nerves innervating the joint, exacerbated joint pathology, but sympathetic removal of sympathetic input, either by beta-AR blockade or chemical sympathectomy with 6-OHDA or guanethidine reduced arthritic symptoms. These results suggest that noradrenergic innervation of draining lymph nodes inhibits the generation of antigen-specific T cells but promotes inflammation of the joints. A similar complexity was demonstrated after beta-agonist administration. Administration of a high dose of EPI reduced the severity of experimental arthritis by an alpha2-AR-mediated mechanism, but a low dose of EPI exacerbated joint injury. These results indicate that care must be used in manipulating the SNS therapeutically in complex diseases.
The SNS may also influence autoimmune processes in humans. Alterations in autonomic activity have been reported in RA and MS, but it is not known whether these changes are induced in response to disease or whether alterations in the SNS play a role in initiating the disease. In children with juvenile RA, increased sympathetic activity and autonomic hyporesponsiveness were associated with disease exacerbation.

Published 2003
Lippincott Williams
& Wilkins

a possible mechanism for sympathectomy-induced adrenal hypertrophy

Journal of Hypertension. 17(7):933-940, July 1999.
Qiua, Jingxin 1; Nelsona, Sharon H. 1; Spethb, Robert C. 2; Wanga, Donna H. 1,3

Abstract:
Objective: Previous studies indicate that the adrenal gland plays a compensatory role in the maintenance of blood pressure in chemically sympathectomized rats. However, the mechanisms responsible for compensatory adrenal responses are poorly understood. This study examined the regulation of adrenal growth and type 1A, 1B, and type 2 angiotensin II (Ang II) receptor (AT1A, AT1B and AT2) expression in the adrenal gland induced by sympathectomy.

Methods: Five-week-old male Sprague-Dawley rats were treated with either guanethidine (50 mg/kg per day, intraperitoneally) or vehicle for 5 weeks. Norepinephrine and epinephrine levels in the atrium of the heart were measured by high-pressure liquid chromatography. Plasma renin activity was determined by radioimmunoassay. Adrenal AT1 and AT2 receptor density was determined by radioligand binding assay. Adrenal AT1A, AT1B and AT2 mRNA levels were determined by Northern blot analysis.

Results: Norepinephrine and epinephrine levels in the atrium of the heart were decreased 86% (P <>0.05), were increased in guanethidine-treated rats compared with vehicle (P < r =" 0.9," r =" 0.6," r =" 20.01,"> 0.05) expression.

Conclusions: Impairment of the sympathetic nervous system with guanethidine withdraws the normal stimulation of this system on the circulating renin-angiotensin system, but upregulates the expression of adrenal Ang II receptors. Increased expression of adrenal AT2 and AT1A receptors may play an important role in adaptive adrenal hypertrophy and hormonal responses to sympathectomy.

Associations between neuropeptide Y nerve terminals and intraparenchymal microvessels in rat and human cerebral cortex

Neuropeptide Y (NPY) can influence local brain perfusion, possibly via direct relationships with the microvascular bed. To evaluate this possibility, the authors quantitatively analyzed by light and electron microscopy the morphological associations between immunostained NPY neuronal elements and intraparenchymal microvessels in the rat and human cerebral cortex. At the light microscopic level in the rat frontoparietal cortex, about 16% of NPY neurons and large proximal processes as well as a subset of nerve terminals not affected by double sympathectomy were associated with penetrating arterioles and local microvessels. In human temporal cortex, a dense network of NPY nerve fibers was observed, many of which approached and/or contacted intracortical vessels. At the ultrastructural level, 14% of NPY axonal varicosities in the rat cerebral cortex were considered perivascular and associated with capillaries (70%) or microarterioles (30%). They were particularly enriched in the immediate vicinity (<0.25 src="http://www3.interscience.wiley.com/giflibrary/12/mgr.gif" align="absbottom" border="0">m) of the microvessels, where the perivascular astrocytic leaflets represented a frequent target. In human cerebral cortex, NPY varicosities were observed in proximity to microvessels corresponding primarily to capillaries. Perivascular NPY varicosities never established synaptic junctions with vascular or astroglial elements. The results show that central NPY nerve terminals associate with microvessels and perivascular astroglial cells in the rat and human cerebral cortex. Thus, NPY released from these nerves could possibly influence (via a parasynaptic mode of action) vascular and/or astrocytic functions depending on the distribution of NPY receptors in these cellular compartments. These results provide morphological support for the effects of NPY on brain perfusion and homeostasis. J. Comp. Neurol. 388:444-453, 1997. © 1997 Wiley-Liss, Inc.
Roger Abounader, Edith Hamel ^*Laboratory of Cerebrovascular Research, Montreal Neurological Institute, Montréal, Québec H3A 2B4, Canada

clear association between the head pain and the release of the neuropeptide calcitonin gene-related peptide (CGRP)

In support, there is a clear association between the head pain and the release of the neuropeptide calcitonin gene-related peptide (CGRP) from the trigeminovascular system. In cluster headache there is, in addition, release of the parasympathetic neuropeptide vasoactive intestinal peptide (VIP) that is coupled to facial vasomotor symptoms. Triptan administration, activating the 5-HT_1B/1D receptors, causes the headache to subside and the levels of neuropeptides to normalise, in part through presynaptic inhibition of the cranial sensory nerves. These data suggest a central role for sensory and parasympathetic mechanisms in the pathophysiology of primary headaches. The positive clinical trial with a CGRP receptor antagonist offers a new promising way of treatment.

Lars Edvinsson^{a, ,} and Rolf Uddman^b

^aDepartment of Internal Medicine, University Hospital, S-221 85 Lund, Sweden

^bDepartment of Otorhinolaryngology, Malmö University Hospital, Malmö, Sweden

Accepted 8 September 2004.

Available online 18 November 2004.