Thus sympathectomy enhances sensory neuron CGRP and SP expression that contributes to the BP reduction.
S. C. Supowit,1 R. T. Ethridge,2 H. Zhao,3 K. A. Katki,1 and D. J. DiPette
Am J Physiol Heart Circ Physiol 289
Submitted 21 September 2004 ; accepted in final form 4 May 2005
"Sympathectomy is a technique about which we have limited knowledge, applied to disorders about which we have little understanding." Associate Professor Robert Boas, Faculty of Pain Medicine of the Australasian College of Anaesthetists and the Royal College of Anaesthetists, The Journal of Pain, Vol 1, No 4 (Winter), 2000: pp 258-260
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
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
Saturday, May 24, 2008
Saturday, May 17, 2008
Sympathetic regulation of the cerebral circulation by the carotid chemoreceptor reflex
S. F. Vatner, L. L. Priano, J. D. Rutherford and W. T. Manders
The effects of carotid chemoreceptor reflex stimulation (intracarotid injection of nicotine 0.2 microgram/kg) were examined in conscious dogs on the cerebral circulation, using the radioactive microsphere technique to measure cerebral blood flow. In intact dogs (n = 18) with ventilation controlled, carotid chemoreceptor reflex stimulation increased (P less than 0.01) mean arterial pressure by 36 +/- 5% (SE) and calculated cerebral vascular resistance by 58 +/- 13%, whereas cerebral blood flow fell by 7 +/- 6% (NS). After bilateral cervical sympathectomy (n = 9), carotid chemoreceptor reflex stimulation induced significantly different (P less than 0.01) effects on cerebral blood flow, which rose by 42 +/- 8%, and cerebral vascular resistance, which did not change. To determine whether the difference in effect was due to the sympathectomy or merely to the repetition of the stimulus, another group of dogs (sham; n = 6) that had intact sympathetic nerves were studied a second time. In "sham" dogs, the repeat response to carotid chemoreceptor stimulation also induced significantly different effects from those in dogs with sympathectomy. Thus, in the conscious dog, stimulation of the carotid chemoreceptor reflex elicits significant sympathetically mediated vasoconstriction in cerebral vessels.
Am J Physiol Heart Circ Physiol 238: H594-H598, 1980;
The effects of carotid chemoreceptor reflex stimulation (intracarotid injection of nicotine 0.2 microgram/kg) were examined in conscious dogs on the cerebral circulation, using the radioactive microsphere technique to measure cerebral blood flow. In intact dogs (n = 18) with ventilation controlled, carotid chemoreceptor reflex stimulation increased (P less than 0.01) mean arterial pressure by 36 +/- 5% (SE) and calculated cerebral vascular resistance by 58 +/- 13%, whereas cerebral blood flow fell by 7 +/- 6% (NS). After bilateral cervical sympathectomy (n = 9), carotid chemoreceptor reflex stimulation induced significantly different (P less than 0.01) effects on cerebral blood flow, which rose by 42 +/- 8%, and cerebral vascular resistance, which did not change. To determine whether the difference in effect was due to the sympathectomy or merely to the repetition of the stimulus, another group of dogs (sham; n = 6) that had intact sympathetic nerves were studied a second time. In "sham" dogs, the repeat response to carotid chemoreceptor stimulation also induced significantly different effects from those in dogs with sympathectomy. Thus, in the conscious dog, stimulation of the carotid chemoreceptor reflex elicits significant sympathetically mediated vasoconstriction in cerebral vessels.
Am J Physiol Heart Circ Physiol 238: H594-H598, 1980;
study demonstrates that cerebral autoregulation is influenced by the autonomic innervation of cerebral vessels
Alpha adrenergic blockade improves impaired autoregulation when cerebral perfusion pressure (CPP) is lowered but worsens it when CPP is raised, indicating that PBZ impairs the ability of cerebral vessels to constrict during induced hypertension and improves their ability to dilate during induced hypotension.
JOHN STIRLING MEYER M.D.1; KUNIO SHIMAZU M.D.1; SHIGEMICHI OKAMOTO M.D.1; ATSUO KOTO M.D.1; TADAO OHUCHI M.D.1; ATSUO SARI M.D.1; ARTHUR DALE ERICSSON M.D.1
1 Department of Neurology, Baylor College of Medicine, and the Baylor-Methodist Center for Cerebrovascular Research, Houston, Texas 77025
© 1973 American Heart Association, Inc.
JOHN STIRLING MEYER M.D.1; KUNIO SHIMAZU M.D.1; SHIGEMICHI OKAMOTO M.D.1; ATSUO KOTO M.D.1; TADAO OHUCHI M.D.1; ATSUO SARI M.D.1; ARTHUR DALE ERICSSON M.D.1
1 Department of Neurology, Baylor College of Medicine, and the Baylor-Methodist Center for Cerebrovascular Research, Houston, Texas 77025
© 1973 American Heart Association, Inc.
Changes of Catecholamines
1. The contents of norepinephrine, epinephrine, dopamine, and dopa of the heart were determined fluorimetrically in 24 dogs from 1 to 50 days following bilateral cervical sympathectomy. The results were compared with those obtained from intact dogs in the previous studies. 2. After bilateral cervical sympathectomy, the norepinephrine content show a rapid decrease from 4 days to 7 days and a slow decrease within the following 14 days. No tendency of recovery was apparent in the heart for 50 days following the operation, the norepinephrine content remaining almost at an equal level. The same operative procedure, however, had no significant effect on the concentrations of dopamine and dopa 3. It was postulated that norepinephrine could not be synthesized and/or accumulated in the heart following bilateral cervical sympathectomy, but that cardiac muscle might synthesize dopamine for itself.
Japanese circulation journal
Vol.29, No.1(19650120) pp. 11-15
KIMATA SHIN-ICHI 1
1The Third Department of Internal Medicine, Faculty of Medicine, University of Tokyo
Japanese circulation journal
Vol.29, No.1(19650120) pp. 11-15
KIMATA SHIN-ICHI 1
1The Third Department of Internal Medicine, Faculty of Medicine, University of Tokyo
sympathectomy – its effect in the treatment of refractory angina pectoris
To document an improvement in the quality of life in a group of patients with refractory angina and videothoracoscopic sympathectomy (VTSY) during the early postoperative period and a six-month follow-up. Methods: Ten patients with angina CCS IV refractory to a conventional therapy underwent VTSY between the years 1998 and 2002 at our institution. All patients underwent a complex preoperative evaluation, including pain assessment using a visual analog scale (VAS). Proximal thoracic sympathetic blockage was performed in all patients as a diagnostic test. The resection of bilateral Th2-Th4 ganglions was performed under general anesthesia and selective lung ventilation. All patients were monitored 6 months after the VTSY. Results: No deaths occurred in our group of patients, with an average hospital stay of 4.1 days. Nine of the ten operated patients referred an important subjective relief of pain. There was a drop from 10 to 4 according to VAS (P<0.05), and from 4 to 2.4 according to CCS (P<0.05). Decreases in basal heart rate, norepinephrine level, and an occurrence of ventricular premature beats reached the level of statistical significance. Conclusions: The increasing number of patients with refractory angina prompted a search for an effective and safe therapy to improve the quality of their life. New evidence in the pathophysiology of an ischemic myocardium and investigation of the impact of thoracic sympathectomy suggests sympathetic denervation seems to be a possible alternative method for the treatment of refractory angina pectoris.
Martin Striteskya, Milos Dobiasa, Rudolf Demesb, Michal Semradc,*, Eva Poliachovaa, Tomas Cermaka, Jiri Charvatd and Ivan Maleke
Interact CardioVasc Thorac Surg 2006;5:464-468. doi:10.1510/icvts.2005.118976
© 2006 European Association of Cardio-Thoracic Surgery
Martin Striteskya, Milos Dobiasa, Rudolf Demesb, Michal Semradc,*, Eva Poliachovaa, Tomas Cermaka, Jiri Charvatd and Ivan Maleke
Interact CardioVasc Thorac Surg 2006;5:464-468. doi:10.1510/icvts.2005.118976
© 2006 European Association of Cardio-Thoracic Surgery
Dopamine
Adrenalectomy, adrenal demedullation, denervation and chemical sympathectomy have been reported to decrease plasma dopamine levels.
Autonomic Pharmacology
By Kenneth J. Broadley
Published 1996
CRC PRESS
Autonomic Pharmacology
By Kenneth J. Broadley
Published 1996
CRC PRESS
Sympathectomy alters acetylcholinesterase expression
Acetylcholinesterase was analysed after destruction of adrenergic nerves by 6-hydroxy-dopamine or bilateral stellate sympathectomy. Effectiveness of treatment was verified by determining noradrenaline concentrations in right ventricle. Acetylcholinesterase activity was assayed in homogenates of atria and portions of left ventricular free wall.
Sympathectomy caused a small decrease in acetylcholinesterase activity, due to a decrease in the activity of the tetrameric globular form of the enzyme. Choline acetylcholinesterase activity was not altered by sympathectomy, which is an indication that cholinergic nerves were not affected.
Conclusions – The contribution of adrenergic neurones to the cardiac pool of acetylcholinesterase is measurable and consists primarily of the tetrameric globular form of the enzyme.
Copyright © 1990, European Society of Cardiology
Cynthia Nyquist Battie and Nancy Moran
Sympathectomy caused a small decrease in acetylcholinesterase activity, due to a decrease in the activity of the tetrameric globular form of the enzyme. Choline acetylcholinesterase activity was not altered by sympathectomy, which is an indication that cholinergic nerves were not affected.
Conclusions – The contribution of adrenergic neurones to the cardiac pool of acetylcholinesterase is measurable and consists primarily of the tetrameric globular form of the enzyme.
Copyright © 1990, European Society of Cardiology
Cynthia Nyquist Battie and Nancy Moran
Serum Dopamine-beta-Hydroxylase: Decrease after Chemical Sympathectomy
Dopamine-{beta}-hydroxylase, the enzyme which converts dopamine to norepinephrine, is released into the perfusate upon stimulation of the isolated perfused adrenal gland and after stimulation of the nerves to the isolated perfused spleen. This study was undertaken to determine whether dopamine-{beta}-hydroxylase activity could be detected circulating in blood. By using a sensitive new enzymatic assay, a dopamine-{beta}-hydroxylase activity was found in the blood of both man and the rat. It is located in the serum and is not associated with the formed elements of blood. The serum activity is similar to that of purified bovine adrenal dopamine-{beta}-hydroxylase in that it requires the presence of ascorbic acid, catalase, fumarate and oxygen for full activity. Furthermore, as is also the case with the adrenal enzyme, serum activity is increased in the presence of cupric ions. The Km values for substrate in human and rat sera are similar, and both are close to values determined in rat adrenal glands and stellate ganglia. The mean activity ±SE in the serum of six rats was 2.27±.04 nmoles/ml serum/20 min, and that of four normal humans ranged from 96.2 to 284 nmoles/ml/20 min.
1 Laboratory of Clinical Science, National Institute of Mental Health, Bethesda, Maryland 20014
RICHARD WEINSHILBOUM 1 JULIUS AXELROD
(Circulation Research. 1971;28:307.)
© 1971 American Heart Association, Inc.
1 Laboratory of Clinical Science, National Institute of Mental Health, Bethesda, Maryland 20014
RICHARD WEINSHILBOUM 1 JULIUS AXELROD
(Circulation Research. 1971;28:307.)
© 1971 American Heart Association, Inc.
NE synthesis was abolished by chronic sympathectomy
This study presents evidence that dopaminergic neurons innervate the cat carotid body. Immunocytochemical studies revealed many tyrosine hydroxylase (TH)-positive nerve fibers in the carotid body which establish extensive contacts with type I cells. All TH-positive intralobular profiles disappeared with chronic carotid sinus nerve (CSN) section, but survived sympathectomy following removal of the superior cervical ganglion. The level of endogenous dopamine (DA) in the CSN was higher than that for norepinephrine (NE). While both catecholamines were synthesized by the nerve at similar rates, NE synthesis was abolished by chronic sympathectomy, but DA synthesis remained largely unchanged following this procedure. Our data indicate that DA is not present in the CSN as a mere precursor of NE. Following a 3-hour incubation of carotid bodies with their attached nerves in media containing 20 µM3H-tyrosine, electrical stimulation of CSN C-fibers in chronically sympathectomized preparations provoked the release of 3H-DA, but not 3H-NE.
Copyright © 1993 S. Karger AG, Basel
Neurosignals 1993;2:16-26 (DOI: 10.1159/000109474)
L. Almaraz, Z.-Z. Wang, L.J. Stensaas, S.J. Fidone
Copyright © 1993 S. Karger AG, Basel
Neurosignals 1993;2:16-26 (DOI: 10.1159/000109474)
L. Almaraz, Z.-Z. Wang, L.J. Stensaas, S.J. Fidone
sympathectomy on dopamine, noradrenaline and adrenaline content in some peripheral tissues
Dopamine, noradrenaline (NA) and adrenaline (Ad) depletion by 6-hydroxydopamine (6-OHDA) and pargyline plus 6-OHDA was investigated in the cat left ventricle, mesenteric and renal arteries, renal cortex, renal medulla and adrenal medulla. Catecholamine concentrations in plasma were also analyzed in these two experimental conditions. 6-OHDA alone or in combination with pargyline induced parallel decreases of NA and dopamine contents in the left ventricle. In the main trunk and proximal branches of the mesenteric artery and renal artery 6-OHDA selectively reduced NA without a parallel decrease in dopamine content. Previous treatment with pargyline abolished this selectivity. In the kidney of control animals, dopamine content was greater than could be attributed to its presence only in noradrenergic neurones. In the renal cortex 6-OHDA reduced significantly dopamine and NA contents, and in the renal medulla only NA levels were decreased by this drug. Pargyline plus 6-OHDA did not deplete the NA content either in the renal cortex or in the renal medulla, and only reduced significantly the dopamine content in the renal cortex. NA concentrations in plasma were increased by pargyline plus 6-OHDA whilst Ad remained unaffected. In the adrenal medulla only NA content was reduced either by 6-OHDA or pargyline plus 6-OHDA.
Br J Pharmacol. 1985 October; 86(2): 351–356.
M. M. Caramona and P. Soares-da-Silva
Br J Pharmacol. 1985 October; 86(2): 351–356.
M. M. Caramona and P. Soares-da-Silva
Sympathectomy also reduced the percent of DA (Dopamine)
The catecholamines (CAs), dopamine (DA) and norepinephrine (NE), are synthesized and stored in carotid body chemosensory type I cells. Previous studies in our laboratory demonstrated that low concentrations of nicotine preferentially evoke the release of NE from rabbit type I cells, whereas hypoxia mobilizes DA and NE in proportion to their stores in the tissue. The primary objective of the present study was to examine whether hypoxia, nicotine and elevated concentrations (30 mM) of K+ evoke the preferential release of DA vs. NE from cat carotid bodies superfused in vitro. In this species, where tissue stores of DA and NE are nearly equal, hypoxia evoked the preferential release of DA from normal carotid bodies. This pattern of release evoked by low O2 was also present following chronic removal of the superior cervical ganglion, which eliminated NE contained in the sympathetic innervation to the carotid body. In contrast, nicotine and high-K + preferentially mobilized NE in these sympathectomized animals. Sympathectomy also reduced the percent of DA (but not NE) content released from type I cells in response to any of the three stimuli. Our findings suggest that chemosensory type I cells possess stimulus-specific mechanisms for CA mobilization and that the sympathetic innervation modulates the metabolism and release of CAs in the cat carotid bodv.
CHEN J. (1) ; GOMEZ-NINO A. (2) ; GONZALEZ C. (2) ; DINGER B. (1) ; FIDONE S. (1) ;
Journal of the autonomic nervous system ISSN 0165-1838 CODEN JASYDS
Source / Source
1997, vol. 67, no1-2, pp. 109-113 (17 ref.)
CHEN J. (1) ; GOMEZ-NINO A. (2) ; GONZALEZ C. (2) ; DINGER B. (1) ; FIDONE S. (1) ;
Journal of the autonomic nervous system ISSN 0165-1838 CODEN JASYDS
Source / Source
1997, vol. 67, no1-2, pp. 109-113 (17 ref.)
Dopamine-beta-Hydroxylase: Decrease after Chemical Sympathectomy
Serum Dopamine-beta-Hydroxylase: Decrease after Chemical Sympathectomy
Richard Weinshilboum 1 and Julius Axelrod 2
1 Pharmacology-Toxicology Program, National Institute of General Medical Sciences, Bethesda, Maryland 20014
2 Laboratory of Clinical Science, National Institute of Mental Health, Bethesda, Maryland 20014
Dopamine-beta- hydroxylase is an enzyme that is localized to catecholamine-containing vesicles in sympathetic nerves and the adrenal medulla, and is also found in the serum. Treatment of rats with 6-hydroxydopamine, a drug which destroys sympathetic nerve terminals, leads to a decrease in serum dopamine-beta-hydroxylase activity. The decrease is not due to an effect on the adrenal medulla or to an increase in circulating inhibitor or inhibitors of enzyme. These data represent evidence that at least a portion of the circulating dopamine-beta-hydroxylase activity arises from sympathetic nerve terminals.
Richard Weinshilboum 1 and Julius Axelrod 2
1 Pharmacology-Toxicology Program, National Institute of General Medical Sciences, Bethesda, Maryland 20014
2 Laboratory of Clinical Science, National Institute of Mental Health, Bethesda, Maryland 20014
Dopamine-beta- hydroxylase is an enzyme that is localized to catecholamine-containing vesicles in sympathetic nerves and the adrenal medulla, and is also found in the serum. Treatment of rats with 6-hydroxydopamine, a drug which destroys sympathetic nerve terminals, leads to a decrease in serum dopamine-beta-hydroxylase activity. The decrease is not due to an effect on the adrenal medulla or to an increase in circulating inhibitor or inhibitors of enzyme. These data represent evidence that at least a portion of the circulating dopamine-beta-hydroxylase activity arises from sympathetic nerve terminals.
structural damage to the peripheral arteries
Longterm sympathetic denervation has been shown to
cause structural damage to the peripheral arteries.
The effects of long-term sympathectomy include
smooth muscle atrophy in the vessels, leading to
ultimate structural changes in the arterial tree. This in-
crease in blood flow has been implicated as an impor-
tant factor in the development of Charcot joint and
pedal ulceration. Ward et al.16 postulated that, flow in
the small distal vessels is inadequate as a result of
faster flow from ateriovenous shunting. Abnormally
high blood flow, vasodilation, and arteriovenous
shunting that result from sympathetic denervation
lead to abnormal venous pooling.
Richard M. Stess
Marilyn J. Waller
cause structural damage to the peripheral arteries.
The effects of long-term sympathectomy include
smooth muscle atrophy in the vessels, leading to
ultimate structural changes in the arterial tree. This in-
crease in blood flow has been implicated as an impor-
tant factor in the development of Charcot joint and
pedal ulceration. Ward et al.16 postulated that, flow in
the small distal vessels is inadequate as a result of
faster flow from ateriovenous shunting. Abnormally
high blood flow, vasodilation, and arteriovenous
shunting that result from sympathetic denervation
lead to abnormal venous pooling.
Richard M. Stess
Marilyn J. Waller
Hemodynamic responses were abolished after bilateral sympathectomy
Hemodynamic responses were diminished after bilateral vagotomy and abolished after bilateral
sympathectomy.
Conclusion Since activation of cardiac afferent nerves and reflex responses remained intact after
TMLR, but changed after vagotomy or sympathectomy, TMLR does not denervate the heart sufficiently
to be the cause of improved angina after TMLR (Transmyocardial laser revascularization)
Chemoreflexes
An Experimental Study
Benjamin B. Y. Chiang, MD; Andrew M. Roberts, PhD; Abul M. Kashem, MD, PhD;
William P. Santamore, PhD; Sufan Chien, MD; Laman Gray, Jr, MD;
Robert Dowling, MD
Vol. 135 No. 5, May 2000 Archives
Arch Surg.
sympathectomy.
Conclusion Since activation of cardiac afferent nerves and reflex responses remained intact after
TMLR, but changed after vagotomy or sympathectomy, TMLR does not denervate the heart sufficiently
to be the cause of improved angina after TMLR (Transmyocardial laser revascularization)
Chemoreflexes
An Experimental Study
Benjamin B. Y. Chiang, MD; Andrew M. Roberts, PhD; Abul M. Kashem, MD, PhD;
William P. Santamore, PhD; Sufan Chien, MD; Laman Gray, Jr, MD;
Robert Dowling, MD
Vol. 135 No. 5, May 2000 Archives
Arch Surg.
ipsilateral ptosis, miosis, facial anhydrosis, vasomotor rhinitis
In contrast, cosmetic complications from ETS include Horner syndrome (ipsilateral ptosis, miosis, facial anhydrosis, vasomotor rhinitis) and, most importantly from a patient-satisfaction perspective, an increase in sweating elsewhere on the body (CH). To minimize these complications, much attention has been focused on how, and how much, sympathetic nerve innervation should be interrupted.
With traditional sympathectomies or ganglionectomies (Figure 3), severe CH may occur in 10% to 40% of postoperative patients.37 It is interesting that the sites affected with CH are generally the thermoregulatory, nonglabrous skin regions of the trunk/back, buttocks, groin, and thighs that sweat normally before ETS.
This may lead ultimately to long-term debilitating CH with few treatment options, and at least 5% of patients may regret undergoing the operation.
Mayo Clin Proc. 2005;80:824-828
Hyperhidrosis: Evolving Therapies for a Well-Established Phenomenon
JOHN H. EISENACH, MD; JOHN L. D. ATKINSON, MD; ROBERT D. FEALEY, MD
With traditional sympathectomies or ganglionectomies (Figure 3), severe CH may occur in 10% to 40% of postoperative patients.37 It is interesting that the sites affected with CH are generally the thermoregulatory, nonglabrous skin regions of the trunk/back, buttocks, groin, and thighs that sweat normally before ETS.
This may lead ultimately to long-term debilitating CH with few treatment options, and at least 5% of patients may regret undergoing the operation.
Mayo Clin Proc. 2005;80:824-828
Hyperhidrosis: Evolving Therapies for a Well-Established Phenomenon
JOHN H. EISENACH, MD; JOHN L. D. ATKINSON, MD; ROBERT D. FEALEY, MD
Friday, May 16, 2008
Sympathectomy in the treatment of Tinnitus
Sympathectomy is an effective treatment of certain forms of of tinnitus, such as that which occurs in Meniere's disease and it has therefore been suggested that the sympathetic nervous system may modulate (increase) the sensitivity of cochlear hair cells.
Aage R. Moller:
Hearing: Anatomy, Physiology, and Disorders of the Auditory System
Academic Press, 2006
ISBN: 0123725194
Aage R. Moller:
Hearing: Anatomy, Physiology, and Disorders of the Auditory System
Academic Press, 2006
ISBN: 0123725194
Thursday, May 15, 2008
Sympathectomy for moyamoya disease
The history of neurosurgical procedures for moyamoya disease
Other options such as cervical carotid sympathectomy and superior cervical ganglionectomy have also been proposed. In this paper the authors describe the history of the development of surgical techniques for treating moyamoya disease.
Keywords: moyamoya disease; superficial temporal artery–middle cerebral artery bypass; encephaloduroarteriosynangiosis; bur hole.
Cassius V. C. Reis, M.D., Sam Safavi-Abbasi, M.D., Ph.D., Joseph M. Zabramski, M.D., Sebastião N. S. Gusmão, M.D., Ph.D., Robert F. Spetzler, M.D., and Mark C. Preul, M.D.
Other options such as cervical carotid sympathectomy and superior cervical ganglionectomy have also been proposed. In this paper the authors describe the history of the development of surgical techniques for treating moyamoya disease.
Keywords: moyamoya disease; superficial temporal artery–middle cerebral artery bypass; encephaloduroarteriosynangiosis; bur hole.
Cassius V. C. Reis, M.D., Sam Safavi-Abbasi, M.D., Ph.D., Joseph M. Zabramski, M.D., Sebastião N. S. Gusmão, M.D., Ph.D., Robert F. Spetzler, M.D., and Mark C. Preul, M.D.
Wednesday, May 14, 2008
Alteration of antioxidant status following sympathectomy
Toleikis, P.M., and Godin, D.V., Alteration of antioxidant status following sympathectomy: differential effects of modified plasma levels of adrenaline and noradrenaline, Molecular and Cellular Biology (1995) 152:39-49.
PROTECTION OF CEREBRAL VESSELS BY SYMPATHETIC NERVES
PROTECTION OF CEREBRAL VESSELS BY SYMPATHETIC NERVES*
Donald D. Heistad
Cardiovascular Division
Dept. Internal Medicine and Cardiovascular Ctr.
University of Iowa Coil. Med. and
Veterans Administration Hosp., Iowa City
Donald D. Heistad
Cardiovascular Division
Dept. Internal Medicine and Cardiovascular Ctr.
University of Iowa Coil. Med. and
Veterans Administration Hosp., Iowa City
Intracerebral gas partial pressure changes under vasoactive drugs
Pflügers Archiv European Journal of Physiology
Publisher Springer Berlin / Heidelberg
0031-6768 (Print) 1432-2013 (Online)
Volume 375, Number 1 / June, 1978
Publisher Springer Berlin / Heidelberg
0031-6768 (Print) 1432-2013 (Online)
Volume 375, Number 1 / June, 1978
Sunday, May 11, 2008
Prejunctional Supersensitivity to Norepinephrine after Sympathectomy
Sympathetic Innervatlon of Cerebral Arteries: Prejunctional Super-
sensitivity to Norepinephrine After Sympathectomy or Cocaine
Treatment
L. Edvinsson, P Aubineau, C. Owman, R. Sercombe, and J. Seylaz
sensitivity to Norepinephrine After Sympathectomy or Cocaine
Treatment
L. Edvinsson, P Aubineau, C. Owman, R. Sercombe, and J. Seylaz
Sympathectomy in the treatment of chronic pelvic pain
Presacral neurectomy and ovarian sympathectomy in treatment of chronic pelvic pain in young women - JR Fliegner
Melbourne Research Office
Research Data Collection & Performance Statistics
University of Melbourne
Melbourne Research Office
Research Data Collection & Performance Statistics
University of Melbourne
Saturday, May 10, 2008
Sympathectomy in the treatment of pancreatic cancer pain
Krishna S, Chang VT, Shoukas JA, Donahoo J. Video assisted thora-
scopic sympathectomy-splanchnicectomy for pancreatic cancer pain.
J Pain Symptom Manage 2001;22:610–6.
scopic sympathectomy-splanchnicectomy for pancreatic cancer pain.
J Pain Symptom Manage 2001;22:610–6.
Sympathectomy in the treatment of Tako-tsubo cardiomyopathy
Lastly, there is some evidence that TTC may be neurally mediated. Similar transient wall motion abnormalities are seen frequently in patients with subarachnoid haemorrhage, in whom the wall motion abnormality is thought to be due to neurally mediated localised microvascular ischaemia. Histopathological features of the myocardium are very similar, with contraction band necrosis,27 and can be prevented by cardiac sympathectomy.
eMJA The Medical Journal of Australia
Tako-tsubo cardiomyopathy: how stress can mimic acute coronary occlusion
Irfan Abdulla and Michael R Ward
eMJA The Medical Journal of Australia
Tako-tsubo cardiomyopathy: how stress can mimic acute coronary occlusion
Irfan Abdulla and Michael R Ward
many people have a decreased quality of life after this procedure.
Sympathectomy for hyperhidrosis is not considered as a reliable treatment and recent research has shown that many people have a decreased quality of life after this procedure.
http://www.skinrevision.net.au/hyperhidrosis
http://www.skinrevision.net.au/hyperhidrosis
porcine femoral arteries following sympathectomy
Lamawansa, M.D., Wysocki, S.J., House, A.K. and Norman, P.E. The changes seen in balloon-injured porcine femoral arteries following sympathectomy, Cardiovascular Surgery, 7:5, pp 526 - 531 (1999)
Sympathectomy abolishes trigger points activity.
http://www.pain-education.com/100125.php
Medical Pain Education
Liason Officer Marilyn Strauss
Medical Pain Education
Liason Officer Marilyn Strauss
Sympathectomy in the treatment on Long QT syndrome
A Charles Sturt University (CSU) biomedical science lecturer has returned home after performing life-saving surgery in China.
Dr Lexin Wang, who was attending the first international conference on Long QT syndromes in Beijing, worked side-by-side with thoracic surgeons from Taiwan and Peking universities to perform a sympathectomy on four patients with life-threatening Long QT syndrome – the first operation of its kind in the world.
Dr Wang said the heart condition can often go unnoticed and is more prevalent in children, with frequent blackouts a symptom. The operations were broadcast live to the conference and featured in two major national Chinese newspapers.
“One of the patients was only six years old with frequent blackouts weeks before the surgery – none have been reported four weeks after the operation,” Dr Wang said.
“We have seen an immediate reversal of electrocardiogram (ECG) abnormalities. It’s a huge progression in the overall treatment and management of this condition.”
Dr Lexin Wang, who was attending the first international conference on Long QT syndromes in Beijing, worked side-by-side with thoracic surgeons from Taiwan and Peking universities to perform a sympathectomy on four patients with life-threatening Long QT syndrome – the first operation of its kind in the world.
Dr Wang said the heart condition can often go unnoticed and is more prevalent in children, with frequent blackouts a symptom. The operations were broadcast live to the conference and featured in two major national Chinese newspapers.
“One of the patients was only six years old with frequent blackouts weeks before the surgery – none have been reported four weeks after the operation,” Dr Wang said.
“We have seen an immediate reversal of electrocardiogram (ECG) abnormalities. It’s a huge progression in the overall treatment and management of this condition.”
Thursday, May 8, 2008
Sympathectomy in the treatment of vulvodynia -
Third, four subjects having successful blocks had laparoscopic presacral neurectomy, yielding one durable success, two transient remissions, and one nonresponse. We investigated open dissection instead. Six patients with disabling pain (including two who failed laparoscopic procedures) underwent complete pelvic sympathectomy (superior hypogastric plexus and lateral chains). Five have no vulvar pain and one has a bizarre but generally transient pain (sympathalgia).58 Fourth, since the peripheral sympathetic nerve fibers are primarily an efferent system, it has been postulated that the afferent limb of this reflex arc is provided by "sensitization" of otherwise silent somatic C fibers that travel in the adventitia of musculocutaneous blood vessels .58, 71 Sensitization means that the polymodal nociceptors (pain receptors) on these C fibers can be fired by noradrenalin, rather than acetylcholine, hence producing a pain loop maintained by activity within the adjacent sympathetic efferents. Preliminary experience with a quantitative thermal testing machine in vulvodynia patients has shown microneurographic patterns of chronic C fiber inflammation.
http://www.vulvodynia.com.au/articles/002.htmlhttp://www.vulvodynia.com.au/index.html
http://www.vulvodynia.com.au/articles/002.htmlhttp://www.vulvodynia.com.au/index.html
Sympathectomy for chronic inflammation of the pancreas - Brisbane, AU
The operation, a thoroscopic
sympathectomy, is not a particu-
larly common procedure, but for
patients suffering from chronic
inflammation of the pancreas it
provides significant pain relief.
Thoroscopic sympathectomy
surgery is performed at the Royal
Brisbane and Women’s Hospital
about 15 to 20 times a year.
An official publication of Queensland Health Vol 9 No 1 February 2004
sympathectomy, is not a particu-
larly common procedure, but for
patients suffering from chronic
inflammation of the pancreas it
provides significant pain relief.
Thoroscopic sympathectomy
surgery is performed at the Royal
Brisbane and Women’s Hospital
about 15 to 20 times a year.
An official publication of Queensland Health Vol 9 No 1 February 2004
The hypothalmus also regulates body temperature
Question:
The hypothalamus controls hunger, thirst, [1] fatigue, anger, and circadian cycles.It also regulates body temperature. Can the subsequent Compensatory Sweating that follows after Symoathectomy be a symptom of the dysregulated hypotalamus. Can the severity of the CS be a reflection of the extent of the damage?
The hypothalamus controls hunger, thirst, [1] fatigue, anger, and circadian cycles.It also regulates body temperature. Can the subsequent Compensatory Sweating that follows after Symoathectomy be a symptom of the dysregulated hypotalamus. Can the severity of the CS be a reflection of the extent of the damage?
The acute effect of superior cervical ganglionectomy
The acute effect of superior cervical ganglionectomy (SCGx) on the pituitary-thyroid axis was examined in rats subjected to surgery 3-24 h earlier. SCGx caused an abrupt decline in thyroid norepinephrine content (an index of degeneration of sympathetic nerve terminals) to 5-10% of controls between 8 and 16 h. Rats subjected to SCGx 14 h earlier exhibited a significant depression of thyroid 131I uptake, total and free serum T4 levels and serum TSH levels.
Efferent Neuroendocrine Pathways of Sympathetic Superior Cervical Ganglia
Early Depression of the Pituitary-Thyroid Axis after Ganglionectomy
D.P. Cardinali, M.A. Pisarev, M. Barontini, G.J. Juvenal, R.J. Boado, M.I. Vacas
Neuroendocrinology 1982;35:248-254
Efferent Neuroendocrine Pathways of Sympathetic Superior Cervical Ganglia
Early Depression of the Pituitary-Thyroid Axis after Ganglionectomy
D.P. Cardinali, M.A. Pisarev, M. Barontini, G.J. Juvenal, R.J. Boado, M.I. Vacas
Neuroendocrinology 1982;35:248-254
The results further support that a regional sympathectomy causes qualitative alterations in bone modeling and remodeling, leading to bone resorption.
To assess the effect of a local sympathectomy on bone metabolism, the effect of a unilateral superior cervical ganglionectomy (Gx) on growth and bone mineral content and density of the ipsi- and contralateral mandibles was examined in female rats. A significant increase in the hemi-mandibular bone ipsilateral to Gx was found as compared to the contralateral, sham-operated side 30 days, but not 15 days, after surgery. Bone mineral content of the hemi-mandibular bones was significantly lower in the side ipsilateral to Gx in the group of rats killed on the 30th day after surgery. Since no difference in areas between innervated and denervated hemi-mandibles was found, bone mineral density was also significantly lower in the hemi-mandible ipsilateral to Gx. The results further support that a regional sympathectomy causes qualitative alterations in bone modeling and remodeling, leading to bone resorption.
Marta G. Ladizeskya, Rodolfo A. Cutrerab, Verónica Boggiob, Carlos Mautalena and Daniel P. Cardinalib, *
a Sección Osteopatías Médicas, Hospital de Clínicas “José de San Martín”, Argentina
b Departamento de Fisiología, Facultad de Medicina, Universidad de Buenos Aires, Paraguay 2155, 7o. Piso, 1121 Buenos Aires, Argentina
Received 27 May 1999;
revised 12 August 1999;
accepted 23 August 1999.
Available online 21 January 2000.
Marta G. Ladizeskya, Rodolfo A. Cutrerab, Verónica Boggiob, Carlos Mautalena and Daniel P. Cardinalib, *
a Sección Osteopatías Médicas, Hospital de Clínicas “José de San Martín”, Argentina
b Departamento de Fisiología, Facultad de Medicina, Universidad de Buenos Aires, Paraguay 2155, 7o. Piso, 1121 Buenos Aires, Argentina
Received 27 May 1999;
revised 12 August 1999;
accepted 23 August 1999.
Available online 21 January 2000.
Cervical sympathectomy affects gonadotropin-releasing hormone, luteinizing hormone and testosterone
Therefore, long-term and repeated stellate ganglion block may inhibit the increases of GnRH, LH, and TS secretions induced by continuous light.
Hiroshi Iwama1 Contact Information, Choichiro Tase1, Yoshikazu Tonosaki2 and Yasuo Sugiura2
(1) Department of Anesthesiology, Fukushima Medical College, 1 Hikarigaoka, 960-12 Fukushima, Japan
(2) Department of Anatomy, Fukushima Medical College, 1 Hikarigaoka, 960-12 Fukushima, Japan
Received: 24 August 1994 Accepted: 16 December 1994
Hiroshi Iwama1 Contact Information, Choichiro Tase1, Yoshikazu Tonosaki2 and Yasuo Sugiura2
(1) Department of Anesthesiology, Fukushima Medical College, 1 Hikarigaoka, 960-12 Fukushima, Japan
(2) Department of Anatomy, Fukushima Medical College, 1 Hikarigaoka, 960-12 Fukushima, Japan
Received: 24 August 1994 Accepted: 16 December 1994
Sympathectomy decreases and adrenergic stimulation increases the release of tissue plasminogen activator (t-PA) from blood vessels
Our recent morphologic studies indicated that peripheral nervous system (PNS) adrenergic neurons synthesize, transport, and store the serene protease, tissue plasminogen activator (t-PA) in axon terminals, many of which innervate vessel walls. Sympathoadrenal stimulation induces a surge of t-PA from vessel walls into the blood. The vascular endothelium, which constitutively secretes t-PA into blood also has long been widely assumed to be the principal source of this stress-induced release, but has not been verified as such. A neurologically regulated release from adrenergic stores could thus augment the known constitutive endothelial release. To functionally test this possibility, we quantitated the effects of guanethidine-induced systemic sympathectomy on the basal and stimulated release of t-PA from isolated vessel explants in superfused organ cultures. Moment-to-moment changes in the release rate were plotted from serial assays of the t-PA free activity. The effects of endothelial and adventitial nerve plexus ablations were also tested. Sympathectomy induced 30-50% reductions in t-PA release from both arterial and microvascular explants. An acute release induced by alpha-1 adrenergic receptor stimulations was also strongly suppressed, as were basal levels of the circulating enzyme in vivo. Adventitial and endothelial ablations from normal large vessel explants produced greater reductions than small vessel endothelial ablations. Ganglion electrical stimulation also induced an acute microvascular release in vivo. These and past morphologic findings indicate a physiological infusion of t-PA into the vessel walls, blood, and other innervated matricesby sympathetic neurons. J. Neurosci. Res. 57:680-692, 1999. © 1999 Wiley-Liss, Inc.
Tao Peng 1, Xi Jiang 1, Yafei Wang 1, Arthur Hand 2, Concettina Gillies 1, Robert E. Cone 1, James O'Rourke 1 *
1Department of Pathology, University of Connecticut Health Center, Farmington
2Central Electron Microscope Facility, University of Connecticut Health Center, Farmington
Tao Peng 1, Xi Jiang 1, Yafei Wang 1, Arthur Hand 2, Concettina Gillies 1, Robert E. Cone 1, James O'Rourke 1 *
1Department of Pathology, University of Connecticut Health Center, Farmington
2Central Electron Microscope Facility, University of Connecticut Health Center, Farmington
Wednesday, May 7, 2008
Sympathectomy - surgical treatment for endometriosis
Pre-sacral neurectomy: An operation in which the nerves that transmit pain from the uterus to the brain are cut. Very rarely done in Australia. Also known as pre-sacral sympathectomy.
Influence of preganglionic cervical sympathectomy
Thus, the dilating effect of the sympathectomy on
the skin vessels appeared to predominate in our
experiments, representing an extracranial steal from
the cerebral circulation.
Cerebral infarction due to carotid occlusion and
carbon monoxide exposure
II. Influence of preganglionic cervical sympathectomy
JORG IGLOFFSTEIN, RUDOLF LAAS
From the Department of Neuropathology, Eppendorf Hospitals, University of Hamburg, H,-mburg, FederalRepublic of Germany
Journal of Neurology, Neurosurgery, and Psychiatry 1983;46:768-773
the skin vessels appeared to predominate in our
experiments, representing an extracranial steal from
the cerebral circulation.
Cerebral infarction due to carotid occlusion and
carbon monoxide exposure
II. Influence of preganglionic cervical sympathectomy
JORG IGLOFFSTEIN, RUDOLF LAAS
From the Department of Neuropathology, Eppendorf Hospitals, University of Hamburg, H,-mburg, FederalRepublic of Germany
Journal of Neurology, Neurosurgery, and Psychiatry 1983;46:768-773
HR as indicator of arrousal
A Neuropsychological Model Relating Self-Awareness to
Hostility
Heath A. Demaree1,2 and David W. Harrison1,3
Neuropsychology is an approach that may be
beneficial in the attempt to relate mental proc-
esses—awareness, behaviors, cognitions, and emo-
tions—to the brain, its structures, and processes
including arousal of brain systems (Heilman and Va-
lenstein, 1993). Rather than ignore the role of the
cortex, view the brain as a "black box," or vaguely
describe different cortical processes, neuropsychol-
ogy purportedly evaluates how and where compo-
nents of mental processes occur. In accordance with
Mill, this approach assumes that all mental processes
result from physical processes within the central
nervous system. Accordingly, a change in any mental
process is associated with changes in the brain's
physical state. Conversely, an altered brain state simi-
larly affects mental processes.
Hostility
Heath A. Demaree1,2 and David W. Harrison1,3
Neuropsychology is an approach that may be
beneficial in the attempt to relate mental proc-
esses—awareness, behaviors, cognitions, and emo-
tions—to the brain, its structures, and processes
including arousal of brain systems (Heilman and Va-
lenstein, 1993). Rather than ignore the role of the
cortex, view the brain as a "black box," or vaguely
describe different cortical processes, neuropsychol-
ogy purportedly evaluates how and where compo-
nents of mental processes occur. In accordance with
Mill, this approach assumes that all mental processes
result from physical processes within the central
nervous system. Accordingly, a change in any mental
process is associated with changes in the brain's
physical state. Conversely, an altered brain state simi-
larly affects mental processes.
The effect of sympathectomy on blood flow in bone
Sympathectomy as a therapeutic modality has been
employed for a variety of pathological states. It first
gained popularity in the 1920’s and 1930’s for improving
peripheral circulation, but soon its limitations began to be
apparent. The initial vasodilation after sympathectomy de-
creases some days after the procedure is performed. Results
for denervation of the upper extremity are not as long-lasting
as those for denervation of the lower extremity. A variety
of mechanisms have been proposed for the apparent return
of vasomotor tone, including: (1) development of intrinsic
tone in smooth muscle, (2) partial anatomical denervation
at the time of the operation, (3) post-denervation sensiti-
zation, (4) post-denervation sprouting, (5) hypertrophy of
the extraganglionic sympathetic nervous system, and (6)
cross-over of the lumbar sympathetic systems30. The pres-
ence or absence of inflow obstruction appears to be impor-
tant. The work of Rutherford and Valenta indicated that
while sympathectomy may increase flow in the resting state
and after exercise, the presence of inflow obstruction in a
patient who has a sympathectomy might actually interfere
with the increased distribution of the flow of blood to ex-
ercising muscle.
1987;69:1384-1390. J Bone Joint Surg Am.RF Davis, LC Jones and DS Hungerford
The effect of sympathectomy on blood flow in bone. Regional distribution and effect over time
employed for a variety of pathological states. It first
gained popularity in the 1920’s and 1930’s for improving
peripheral circulation, but soon its limitations began to be
apparent. The initial vasodilation after sympathectomy de-
creases some days after the procedure is performed. Results
for denervation of the upper extremity are not as long-lasting
as those for denervation of the lower extremity. A variety
of mechanisms have been proposed for the apparent return
of vasomotor tone, including: (1) development of intrinsic
tone in smooth muscle, (2) partial anatomical denervation
at the time of the operation, (3) post-denervation sensiti-
zation, (4) post-denervation sprouting, (5) hypertrophy of
the extraganglionic sympathetic nervous system, and (6)
cross-over of the lumbar sympathetic systems30. The pres-
ence or absence of inflow obstruction appears to be impor-
tant. The work of Rutherford and Valenta indicated that
while sympathectomy may increase flow in the resting state
and after exercise, the presence of inflow obstruction in a
patient who has a sympathectomy might actually interfere
with the increased distribution of the flow of blood to ex-
ercising muscle.
1987;69:1384-1390. J Bone Joint Surg Am.RF Davis, LC Jones and DS Hungerford
The effect of sympathectomy on blood flow in bone. Regional distribution and effect over time
Imbalances of sympathetic nervous system - autoimmune inflammatory diseases
Interruptions of the HPA axis at any level
and through multiple mechanisms, whether on a genetic
basis, through surgical means such as adrenalectomy or
hypophysectomy, or with pharmacological interventions
such as treatment with the glucocorticoid receptor antag-
onist RU 486, can render an inflammatory resistant host
susceptible to inflammatory disease (Sternberg 1997a,b).
Imbalances of sympathetic nervous system responses are
also associated with autoimmune inflammatory diseases
such as arthritis in both humans and rodents. Human
juvenile rheumatoid arthritis has been associated with both
abnormal HPA axis and sympathoneuronal responses (Kuis
et al. 1996). Inflammatory susceptible LEW/N rats show
not only blunted HPA axis responsiveness, but also
blunted sympathoneuronal activity in response to gluco-
privic stress (Goldstein et al. 1993). This raises the question
of whether in such susceptible hosts multiple factors may
account for overall susceptibility to autoimmune/ inflammatory disease.
While this review has focused on the HPA axis and
glucocorticoids and their role in susceptibility to inflam-
matory disease, estrogen is known to play an extremely
important role in immune modulation, and contributes to
the approximately two- to tenfold higher ratio of most
autoimmune diseases in females of all species (Wilder
& Sternberg 1990, Ahmed et al. 1999, Lahita 1999).
Ovariectomy has been shown to reduce, while replace-
ment of estrogen re-constitutes, this di
and through multiple mechanisms, whether on a genetic
basis, through surgical means such as adrenalectomy or
hypophysectomy, or with pharmacological interventions
such as treatment with the glucocorticoid receptor antag-
onist RU 486, can render an inflammatory resistant host
susceptible to inflammatory disease (Sternberg 1997a,b).
Imbalances of sympathetic nervous system responses are
also associated with autoimmune inflammatory diseases
such as arthritis in both humans and rodents. Human
juvenile rheumatoid arthritis has been associated with both
abnormal HPA axis and sympathoneuronal responses (Kuis
et al. 1996). Inflammatory susceptible LEW/N rats show
not only blunted HPA axis responsiveness, but also
blunted sympathoneuronal activity in response to gluco-
privic stress (Goldstein et al. 1993). This raises the question
of whether in such susceptible hosts multiple factors may
account for overall susceptibility to autoimmune/ inflammatory disease.
While this review has focused on the HPA axis and
glucocorticoids and their role in susceptibility to inflam-
matory disease, estrogen is known to play an extremely
important role in immune modulation, and contributes to
the approximately two- to tenfold higher ratio of most
autoimmune diseases in females of all species (Wilder
& Sternberg 1990, Ahmed et al. 1999, Lahita 1999).
Ovariectomy has been shown to reduce, while replace-
ment of estrogen re-constitutes, this di
Influence of Endoscopic Thoracic Sympathectomy on Baroreflex Control of Heart Rate
Before and after the ETS, there were no significant differences in resting SBP (105.0±8.7 and 105.3±13.7 mmHg, respectively)
and heart rate (88.9±14.4 and 86.0±15.1 beats/min, respectively). In the pressor test, the ETS produced a significant
suppression of baroreflex response in all petient studied; baroreflex sensitivity before and after the ETS were 7.6±2.8 and
3.4±2.5 msec/mmHg, respectively (P<0.05). In the depressor test, the ETS also suppressed baroreflex response. In two of
eight patients, baroreflex response was completely suppressed after the ETS. Baroreflex sensitivity before and after the ETS
were 3.8±0.4 and 1.2±1.4 msec/mmHg, respectively (P<0.05). All patients showed the increase in skin temperatures of bilateral
palmars and arms, and the ceasing sweat after the ETS, indicating successful T2-3 sympathectomy.
Conclusion
Our results indicated that T2-3 sympathectomy suppressed baroreflex control of heart rate in both pressor and depressor tests
in the patients with palmar hyperhidrosis. We should note that baroreflex response for maintaining cardiovascular stability is
suppressed in the patients who received the ETS.
Anesthesiology 2001; 95:A160
Yurie T. Kawamata, M.D.; Eiji Homma, M.D.; Tomoyuki Kawamata, M.D.; Kiichi Omote, M.D.; Akiyoshi Namiki, M.D.
Anesthesiology, Sapporo Medical University, Sapporo, Hokkaido, Japan
and heart rate (88.9±14.4 and 86.0±15.1 beats/min, respectively). In the pressor test, the ETS produced a significant
suppression of baroreflex response in all petient studied; baroreflex sensitivity before and after the ETS were 7.6±2.8 and
3.4±2.5 msec/mmHg, respectively (P<0.05). In the depressor test, the ETS also suppressed baroreflex response. In two of
eight patients, baroreflex response was completely suppressed after the ETS. Baroreflex sensitivity before and after the ETS
were 3.8±0.4 and 1.2±1.4 msec/mmHg, respectively (P<0.05). All patients showed the increase in skin temperatures of bilateral
palmars and arms, and the ceasing sweat after the ETS, indicating successful T2-3 sympathectomy.
Conclusion
Our results indicated that T2-3 sympathectomy suppressed baroreflex control of heart rate in both pressor and depressor tests
in the patients with palmar hyperhidrosis. We should note that baroreflex response for maintaining cardiovascular stability is
suppressed in the patients who received the ETS.
Anesthesiology 2001; 95:A160
Yurie T. Kawamata, M.D.; Eiji Homma, M.D.; Tomoyuki Kawamata, M.D.; Kiichi Omote, M.D.; Akiyoshi Namiki, M.D.
Anesthesiology, Sapporo Medical University, Sapporo, Hokkaido, Japan
Tuesday, May 6, 2008
Sympathectomy - extracranial steal phenomenon
Unilateral cerebral infarcts were produced in the rat by ligation of one common carotid artery and subsequent exposure to carbon monoxide. The incidence and extension of brain infarcts was increased in animals with additional ipsilateral cervical preganglionic sympathectomy. Sympathectomy did not affect markedly the respiration and systemic circulation. The effect of sympathectomy was attributed to a cutaneous vasodilation, leading to an extracranial steal phenomenon.
Cerebral infarction due to carotid occlusion and carbon monoxide exposure. II. Influence of preganglionic cervical sympathectomy.
J Igloffstein and R Laas
J Neurol Neurosurg Psychiatry. 1983 August; 46(8): 768–773.
Cerebral infarction due to carotid occlusion and carbon monoxide exposure. II. Influence of preganglionic cervical sympathectomy.
J Igloffstein and R Laas
J Neurol Neurosurg Psychiatry. 1983 August; 46(8): 768–773.
Cerebral blood flow is no longer constant after sympathectomy
Cerebral blood flow remains relatively constant and is in-
dependent of modest fluctuations in arterial pressure,
presumably because of its capacity for autoregulation.22-23
After cervical sympathectomy, however, one group reported
that cerebral blood flow rate is no longer constant but varies
with arterial pressure.
The demonstration that non-uniform changes in blood flow
between cortical lobes and between hemispheres could be in-
duced by ischemia26 and neurogenic stimulation26 probably
implicates neurogenic factors. There is some evidence for
heterogeneity of the function of the sympathetic neurons
originating from the superior cervical ganglion.
Adrenergic lnnervation of Large Cerebral Blood
Vessels of the Rabbit Studied by Fluorescence Microscopy
Absence of Features That Might Contribute to Non-Uniform Change
in Cerebral Blood Flow
RALPH E. PURDY, PH.D.,* AND JOHN A. BEVAN, M.D.
STROKE VOL 8, No 1, JANUARY-FEBRUARY 1977
dependent of modest fluctuations in arterial pressure,
presumably because of its capacity for autoregulation.22-23
After cervical sympathectomy, however, one group reported
that cerebral blood flow rate is no longer constant but varies
with arterial pressure.
The demonstration that non-uniform changes in blood flow
between cortical lobes and between hemispheres could be in-
duced by ischemia26 and neurogenic stimulation26 probably
implicates neurogenic factors. There is some evidence for
heterogeneity of the function of the sympathetic neurons
originating from the superior cervical ganglion.
Adrenergic lnnervation of Large Cerebral Blood
Vessels of the Rabbit Studied by Fluorescence Microscopy
Absence of Features That Might Contribute to Non-Uniform Change
in Cerebral Blood Flow
RALPH E. PURDY, PH.D.,* AND JOHN A. BEVAN, M.D.
STROKE VOL 8, No 1, JANUARY-FEBRUARY 1977
Sympathetic regulation of cerebral blood flow
AJP - Heart and Circulatory Physiology, Vol 249, Issue 3 672-H680, Copyright © 1985 by American Physiological Society
Sympathetic regulation of cerebral blood flow during reflex hypertension
P. Lacombe, M. C. Miller and J. Seylaz
Sympathetic regulation of cerebral blood flow during reflex hypertension
P. Lacombe, M. C. Miller and J. Seylaz
Sympathectomy may result in profound hypotension
Regional anesthetic techniques such as
spinal or epidural anesthesia, though efficacious in
providing surgical anesthesia and sensory deafferenta-
tion, are often avoided because they produce bilateral
sympathectomy. This may result in profound hypoten-
sion that can be difficult to treat in HOCM patients.
Paravertebral somatic nerve blocks for breast
surgery in a patient with hypertrophic obstructive
cardiomyopathy
Chester C. Buckenmaier III MD, Susan M. Steele MD, Karen C. Nielsen MD, Stephen M. Klein MD
CAN J ANESTH 2002 / 49: 6 / pp 571–574
spinal or epidural anesthesia, though efficacious in
providing surgical anesthesia and sensory deafferenta-
tion, are often avoided because they produce bilateral
sympathectomy. This may result in profound hypoten-
sion that can be difficult to treat in HOCM patients.
Paravertebral somatic nerve blocks for breast
surgery in a patient with hypertrophic obstructive
cardiomyopathy
Chester C. Buckenmaier III MD, Susan M. Steele MD, Karen C. Nielsen MD, Stephen M. Klein MD
CAN J ANESTH 2002 / 49: 6 / pp 571–574
Monday, May 5, 2008
Follow-up surgery after ETS to reduce axillary HH
Many of the patients attend after thorascopic sympathectomy which resolved their palmar, but not axillary, hyperhidrosis. Surgical excision of axillary tissue remains an important treatment modality for a large proportion of hyperhidrotic patients. It has the ability to provide a permanent and satisfactory solution to a frustrating problem. It is not as yet a redundant method of treatment.
J L Atkins, senior house officer, plastic surgery.
P E M Butler, consultant plastic surgeon.
Royal Free Hospital, London NW3 2QG
BMJ 2000;321:702 ( 16 September )
Letters
Treating hyperhidrosis
Excision of axillary tissue may be more effective
J L Atkins, senior house officer, plastic surgery.
P E M Butler, consultant plastic surgeon.
Royal Free Hospital, London NW3 2QG
BMJ 2000;321:702 ( 16 September )
Letters
Treating hyperhidrosis
Excision of axillary tissue may be more effective
Skin in 'overdrive' following sympathectomy
I. Kelman Cohen1 Contact Information and Barbara J. McCoy1
(1) Division of Plastic Surgery, Department of Surgery, Medical College of Virginia, 23298 Richmond, Virginia, USA
Lesions of “surface overhealing” include keloid, hypertrophic scar, and burn scar. All are characterized by overabundant collagen deposition. The biology of these lesions is reviewed, suggesting that abnormal collagen metabolism results from alterations in the inflammatory/immune response. Practical and theoretical treatment plans are outlined based on methods that alter collagen metabolism, the inflammatory/immune system or rely on physical alterations (surgery, pressure).
(1) Division of Plastic Surgery, Department of Surgery, Medical College of Virginia, 23298 Richmond, Virginia, USA
Lesions of “surface overhealing” include keloid, hypertrophic scar, and burn scar. All are characterized by overabundant collagen deposition. The biology of these lesions is reviewed, suggesting that abnormal collagen metabolism results from alterations in the inflammatory/immune response. Practical and theoretical treatment plans are outlined based on methods that alter collagen metabolism, the inflammatory/immune system or rely on physical alterations (surgery, pressure).
Saturday, May 3, 2008
Structural changes and in situ aortic pressure-diameter relationship
These results suggest that intact sympathetic nerves are necessary to maintain normal functional and structural properties of large arteries in rat. The reduction in aortic distensibility, in long-term sympathectomized rats, could have resulted from complex interactions between local aortic denervation, change in the set point of distending pressure, and changes in aortic smooth muscle tone and/or wall composition.
Auteur(s) / Author(s)
LACOLLEY P. ; GLASER E. ; CHALLNDE P. ; BOUTOUYRIE P. ; MIGNOT J.-P. ; DURIEZ M. ; LEVY B. ; SAFAR M. ; LAURENT S. ;
American journal of physiology. Heart and circulatory physiology ISSN 0363-6135 COD
1995, vol. 38, no2, pp. H407-H416 (36 ref.)
Auteur(s) / Author(s)
LACOLLEY P. ; GLASER E. ; CHALLNDE P. ; BOUTOUYRIE P. ; MIGNOT J.-P. ; DURIEZ M. ; LEVY B. ; SAFAR M. ; LAURENT S. ;
American journal of physiology. Heart and circulatory physiology ISSN 0363-6135 COD
1995, vol. 38, no2, pp. H407-H416 (36 ref.)
Friday, May 2, 2008
Sequential cerebrospinal fluid and plasma sampling in humans: 24-hour melatonin measurements in normal subjects and after peripheral sympathectomy
In the patient with hyperhidrosis, a prominent melatonin rhythm was observed preoperatively in the CSF and plasma. After bilateral T1-T2 ganglionectomy, however, melatonin levels were markedly reduced, and the diurnal rhythm was abolished. These results provide direct evidence in humans for a diurnal melatonin rhythm in CSF and plasma as well as regulation of this rhythm by sympathetic innervation.
J Bruce, L Tamarkin, C Riedel, S Markey and E Oldfield
Surgical Neurology Branch, National Institute of Neurologic Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892.
Journal of Clinical Endocrinology & Metabolism, Vol 72, 819-823, Copyright © 1991 by Endocrine Society
J Bruce, L Tamarkin, C Riedel, S Markey and E Oldfield
Surgical Neurology Branch, National Institute of Neurologic Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892.
Journal of Clinical Endocrinology & Metabolism, Vol 72, 819-823, Copyright © 1991 by Endocrine Society
Melatonin - Circadian Cycle - Delayed sleep phase syndrome
Main article: Circadian rhythm sleep disorder
Delayed sleep-phase syndrome (DSPS), also known as delayed sleep-phase disorder (DSPD) or delayed sleep-phase type (DSPT), is a circadian rhythm sleep disorder, a chronic disorder of the timing of sleep, peak period of alertness, core body temperature, hormonal and other daily rhythms. People with DSPS tend to fall asleep well after midnight and have difficulty waking up in the morning.
DSPS is a disorder of the body's timing system - the biological clock. Individuals with DSPS might have an unusually long circadian cycle, or might have a reduced response to the re-setting effect of light on the body clock.
People with normal circadian systems can generally fall asleep quickly at night if they slept too little the night before. Falling asleep earlier will in turn automatically advance their circadian clocks due to decreased light exposure in the evening. In contrast, people with DSPS are unable to fall asleep before their usual sleep time, even if they are sleep-deprived. Research has shown that sleep deprivation does not reset the circadian clock of DSPS patients, as it does with normal people.[10]
People with the disorder who try to live on a normal schedule have difficulty falling asleep and difficulty waking because their biological clocks are not in phase with that schedule. Normal people who do not adjust well to working a night shift have similar symptoms.
People with the disorder also show delays in other circadian markers, such as melatonin-secretion and the core body temperature minimum, that correspond to the delay in the sleep/wake cycle. The timing of sleepiness, spontaneous awakening, and these internal markers are all delayed by the same number of hours. Non-dipping blood pressure patterns are also associated with the disorder when present in conjunction with socially unacceptable sleeping and waking times.
In most cases, it is not known what causes the abnormality in the biological clocks of DSPS patients. DSPS tends to run in families,[11] and a growing body of evidence suggests that the problem is associated with the hPer3 (human period 3) gene.[12][13] There have been several documented cases of DSPS and non-24 hour sleep-wake syndrome developing after traumatic head injury.[14][15]
There have been a few cases of DSPS developing into non 24-hour sleep-wake syndrome, a more severe and debilitating disorder in which the individual sleeps later each day.[16]
In humans, melatonin is produced by the pineal gland, a gland about the size of a pea, located in the center of the brain. The melatonin signal forms part of the system that regulates the circadian cycle by chemically causing drowsiness and lowering the body temperature, but it is the central nervous system that controls the daily cycle in most components of the paracrine and endocrine systems[23][24] rather than the melatonin signal (as was once postulated).
Delayed sleep-phase syndrome (DSPS), also known as delayed sleep-phase disorder (DSPD) or delayed sleep-phase type (DSPT), is a circadian rhythm sleep disorder, a chronic disorder of the timing of sleep, peak period of alertness, core body temperature, hormonal and other daily rhythms. People with DSPS tend to fall asleep well after midnight and have difficulty waking up in the morning.
DSPS is a disorder of the body's timing system - the biological clock. Individuals with DSPS might have an unusually long circadian cycle, or might have a reduced response to the re-setting effect of light on the body clock.
People with normal circadian systems can generally fall asleep quickly at night if they slept too little the night before. Falling asleep earlier will in turn automatically advance their circadian clocks due to decreased light exposure in the evening. In contrast, people with DSPS are unable to fall asleep before their usual sleep time, even if they are sleep-deprived. Research has shown that sleep deprivation does not reset the circadian clock of DSPS patients, as it does with normal people.[10]
People with the disorder who try to live on a normal schedule have difficulty falling asleep and difficulty waking because their biological clocks are not in phase with that schedule. Normal people who do not adjust well to working a night shift have similar symptoms.
People with the disorder also show delays in other circadian markers, such as melatonin-secretion and the core body temperature minimum, that correspond to the delay in the sleep/wake cycle. The timing of sleepiness, spontaneous awakening, and these internal markers are all delayed by the same number of hours. Non-dipping blood pressure patterns are also associated with the disorder when present in conjunction with socially unacceptable sleeping and waking times.
In most cases, it is not known what causes the abnormality in the biological clocks of DSPS patients. DSPS tends to run in families,[11] and a growing body of evidence suggests that the problem is associated with the hPer3 (human period 3) gene.[12][13] There have been several documented cases of DSPS and non-24 hour sleep-wake syndrome developing after traumatic head injury.[14][15]
There have been a few cases of DSPS developing into non 24-hour sleep-wake syndrome, a more severe and debilitating disorder in which the individual sleeps later each day.[16]
In humans, melatonin is produced by the pineal gland, a gland about the size of a pea, located in the center of the brain. The melatonin signal forms part of the system that regulates the circadian cycle by chemically causing drowsiness and lowering the body temperature, but it is the central nervous system that controls the daily cycle in most components of the paracrine and endocrine systems[23][24] rather than the melatonin signal (as was once postulated).
Reduced melatonin production has been proposed as a likely factor in the significantly higher cancer rates in night workers
Reduced melatonin production has been proposed as a likely factor in the significantly higher cancer rates in night workers,[28] and the effect of modern lighting practice on endogenous melatonin has been proposed as a contributory factor to the larger overall incidence of some cancers in the developed world.
^ Schernhammer E, Rosner B, Willett W, Laden F, Colditz G, Hankinson S (2004). "Epidemiology of urinary melatonin in women and its relation to other hormones and night work". Cancer Epidemiol Biomarkers Prev 13 (62): 936-43. PMID 15184249
^ Schernhammer E, Rosner B, Willett W, Laden F, Colditz G, Hankinson S (2004). "Epidemiology of urinary melatonin in women and its relation to other hormones and night work". Cancer Epidemiol Biomarkers Prev 13 (62): 936-43. PMID 15184249
CCS alone significantly decreased melatonin concentrations in serum at the time of highest secretory activity of the pineal gland
J. GORSKI, D. KAJDANIUK, J. GLOGOWSKA-SZELAG, Z. OSTROWSKA, M. NOWAK, B. BUNTNER
I Department of Pathophysiology and Medical Analytics, Silesian University School of Medicine, 41-800 Zabrze, Poland
The study showed that morphine alone significantly increased melatonin concentrations in serum. CCS alone significantly decreased melatonin concentrations in serum at the time of highest secretory activity of the pineal gland. Long-term morphine treatment of rats subjected to CCS significantly increased the serum concentration of melatonin. Therefore, it may be concluded that the central adrenergic system does not take part in the morphine-stimulated secretion of melatonin.
I Department of Pathophysiology and Medical Analytics, Silesian University School of Medicine, 41-800 Zabrze, Poland
The study showed that morphine alone significantly increased melatonin concentrations in serum. CCS alone significantly decreased melatonin concentrations in serum at the time of highest secretory activity of the pineal gland. Long-term morphine treatment of rats subjected to CCS significantly increased the serum concentration of melatonin. Therefore, it may be concluded that the central adrenergic system does not take part in the morphine-stimulated secretion of melatonin.
procarbazine
Sensitivity to procarbazine
»Caution should be used also in patients who have had previous cytotoxic drug therapy or radiation therapy. »In addition, caution should be used in patients who have undergone sympathectomy, who may be more sensitive to the hypotensive effects of MAO inhibitors.
Other medical problems, especially active alcoholism, bone marrow depression, cardiac arrhythmias, chickenpox or recent exposure, congestive heart failure, coronary insufficiency, severe or frequent headaches, hepatic function impairment, herpes zoster, other infection, paranoid schizophrenia or other hyperexcitable personality states, pheochromocytoma, sympathectomy, or renal function impairment
Indications
Systemic
Lymphomas, Hodgkin's (treatment) or [Lymphomas, non-Hodgkin's (treatment)]
Procarbazine is indicated, in combination with other agents, for treatment of Hodgkin's disease (Stage III and IV) and some non-Hodgkin's lymphomas .
[Tumors, brain, primary (treatment)]
Procarbazine is indicated for treatment of primary brain tumors .
[Multiple myeloma (treatment)]
Procarbazine is indicated for treatment of multiple myeloma.
»Caution should be used also in patients who have had previous cytotoxic drug therapy or radiation therapy. »In addition, caution should be used in patients who have undergone sympathectomy, who may be more sensitive to the hypotensive effects of MAO inhibitors.
Other medical problems, especially active alcoholism, bone marrow depression, cardiac arrhythmias, chickenpox or recent exposure, congestive heart failure, coronary insufficiency, severe or frequent headaches, hepatic function impairment, herpes zoster, other infection, paranoid schizophrenia or other hyperexcitable personality states, pheochromocytoma, sympathectomy, or renal function impairment
Indications
Systemic
Lymphomas, Hodgkin's (treatment) or [Lymphomas, non-Hodgkin's (treatment)]
Procarbazine is indicated, in combination with other agents, for treatment of Hodgkin's disease (Stage III and IV) and some non-Hodgkin's lymphomas .
[Tumors, brain, primary (treatment)]
Procarbazine is indicated for treatment of primary brain tumors .
[Multiple myeloma (treatment)]
Procarbazine is indicated for treatment of multiple myeloma.
Thursday, May 1, 2008
neuroaxial block may produce profound bradycardia and hypotension
A high level of neuroaxial block may produce profound bradycardia and hypotension, possibly as a result of an imbalance between sympathetic and parasympathetic control of heart rate.
Our results indicate that cervical, but not lumbar, epidural anesthesia depresses phasic and tonic dynamic modulation of the cardiac cycle by the vagal nerve in conscious humans.
IMPLICATIONS: Cervical epidural anesthesia with lidocaine produces depressed heart rate variability and baroreflex control of heart rate, whereas lumbar epidural anesthesia exerts minimal effects on autonomic nervous system activity in conscious humans.
Anesth Analg 2004;99:924-929
© 2004 International Anesthesia Research Society
doi: 10.1213/01.ANE.0000131966.61686.66
REGIONAL ANESTHESIA
The Effects of Cervical and Lumbar Epidural Anesthesia on Heart Rate Variability and Spontaneous Sequence Baroreflex Sensitivity
Makoto Tanaka, MD, Toru Goyagi, MD, Tetsu Kimura, MD, and Toshiaki Nishikawa, MD
Our results indicate that cervical, but not lumbar, epidural anesthesia depresses phasic and tonic dynamic modulation of the cardiac cycle by the vagal nerve in conscious humans.
IMPLICATIONS: Cervical epidural anesthesia with lidocaine produces depressed heart rate variability and baroreflex control of heart rate, whereas lumbar epidural anesthesia exerts minimal effects on autonomic nervous system activity in conscious humans.
Anesth Analg 2004;99:924-929
© 2004 International Anesthesia Research Society
doi: 10.1213/01.ANE.0000131966.61686.66
REGIONAL ANESTHESIA
The Effects of Cervical and Lumbar Epidural Anesthesia on Heart Rate Variability and Spontaneous Sequence Baroreflex Sensitivity
Makoto Tanaka, MD, Toru Goyagi, MD, Tetsu Kimura, MD, and Toshiaki Nishikawa, MD
Influence of sympathectomy in humans on the rhythmicity of 6-sulphatoxymelatonin urinary excretion
The amount of 6-sulphatoxymelatonin, the chief metabolite of melatonin, in the urine was measured in nine patients, who were subjected to bilateral sympathectomy at the second thoracic ganglionic level for treatment of hyperhidrosis of the palms. All patients showed before surgery a normal 6-sulphatoxymelatonin excretion with a peak in the excretion during the night time. After the sympathectomy, the high night time excretion was clearly abolished in five patients but remained high in four patients. This indicates that the segmental locations of the preganglionic sympathetic perikarya in the spinal cord, stimulating the melatonin secretion in the pineal gland in humans, vary between individuals. An increase in daytime melatonin excretion was observed in the patients responding to the sympathectomy with an abolished 6-sulphatoxymelatonin rhythm. This increase could indicate that the final sympathetic neurons innervating the pineal gland might have a both stimulatory and inhibitory function.
Morten Møllera, Corresponding Author Contact Information, E-mail The Corresponding Author, Ole Osgaardb and Michael Grønbech-Jensenc
aInst. Med. Anatomy, University of Copenhagen, Panum Institute, Blegdamsvej 3, DK-2200 Copenhagen, Denmark
bDepartment Neurosurgery, Rigshospitalet, Copenhagen, Denmark
cNeurological Specialist Clinic Copenhagen, Christianshavns Torv 2, Copenhagen, Denmark
Morten Møllera, Corresponding Author Contact Information, E-mail The Corresponding Author, Ole Osgaardb and Michael Grønbech-Jensenc
aInst. Med. Anatomy, University of Copenhagen, Panum Institute, Blegdamsvej 3, DK-2200 Copenhagen, Denmark
bDepartment Neurosurgery, Rigshospitalet, Copenhagen, Denmark
cNeurological Specialist Clinic Copenhagen, Christianshavns Torv 2, Copenhagen, Denmark
Does the pineal gland have a role in the psychological mechanisms involved in the progression of cancer?
Department of Anatomical Sciences, University of Adelaide, Adelaide, Australia
Received 9 November 2001;
accepted 13 February 2002.
Available online 28 August 2002.
Psychological factors, e.g., depression and psychological stress have been implicated in the progress of cancer. Similarly, the pineal gland and its principal secretion, melatonin, are known to influence the initiation and progress of cancer. Furthermore, changes in melatonin secretion have been linked with psychological stress and depression, and both the pineal gland and the cerebral cortex act via the limbic system in producing their effects. Both psychological stress and melatonin affect the immune system, as does the hypothalamus and the autonomic nervous system. The pineal gland has both a direct effect on cancer, and via the immune system. Psychological treatment and melatonin treatment have both been found to alleviate the course of cancer clinically. It is thus hypothesized that the pineal gland, and melatonin, are involved in the mechanism of psychological effects in the promotion of the progress of cancer.
Received 9 November 2001;
accepted 13 February 2002.
Available online 28 August 2002.
Psychological factors, e.g., depression and psychological stress have been implicated in the progress of cancer. Similarly, the pineal gland and its principal secretion, melatonin, are known to influence the initiation and progress of cancer. Furthermore, changes in melatonin secretion have been linked with psychological stress and depression, and both the pineal gland and the cerebral cortex act via the limbic system in producing their effects. Both psychological stress and melatonin affect the immune system, as does the hypothalamus and the autonomic nervous system. The pineal gland has both a direct effect on cancer, and via the immune system. Psychological treatment and melatonin treatment have both been found to alleviate the course of cancer clinically. It is thus hypothesized that the pineal gland, and melatonin, are involved in the mechanism of psychological effects in the promotion of the progress of cancer.
Two cases of symptomatic cluster-like headache suggest the importance of sympathetic/parasympathetic balance
Despite several reports on symptomatic cluster-like headache, there is no clear explanation of how different lesions thought to be causative are related to cluster-like headache. On the basis of two additional cases of symptomatic cluster headache, we discuss the possibility that an acute imbalance of the autonomic nervous system, namely a net overactivity of the parasympathetic system, may be able to trigger these headache attacks in patients who probably have an additional individual predisposition to react with a cluster-like headache. Such an imbalance can be due to an increase in parasympathetic tone (e.g. stimulation of parasympathetic fibres) or to a reduction of the sympathetic tone (e.g. a lesion of the sympathetic fibres).
Two cases of symptomatic cluster-like headache suggest the importance of sympathetic/parasympathetic balance
* A Straube,
* T Freilinger,
* T Rüther &
* C Padovan
*
Department of Neurology, Klinikum Großhadern, Ludwig-Maximilians-University Munich, Germany
----------------------------------
A chronobiological study of melatonin, cortisol growth hormone and prolactin secretion in cluster headache
Results from this study suggest a neuroendocrine dysregulation in cluster headache in the endogenous clock which controls the pineal rhythmicity.
* Guy Chazot11Unite Neurométabolique, Hôpital Neurologique. 59 boulevard Pinel, 69003 Lyon, France; ,
* Bruno Claustrat22Service de Radiopharmacie et Radioanalvse. Centre de Médecine Nucléaire, 59 boulevard Pinel, 69003 Lyon, France; ,
* Jocelyne Brun22Service de Radiopharmacie et Radioanalvse. Centre de Médecine Nucléaire, 59 boulevard Pinel, 69003 Lyon, France; ,
* Daniel Jordan33Laboratoire de Médecine Expérimentale, INSERM U. 197-UER, Médecine Alexis Carrel, rue Guillaume Paradin. 69008 Lyon, France; ,
* Geneviève Sassolas44Unite de Soins, Centre de Médecine Nucléaire, 59 boulevard Pinel, 69003 Lyon, France,
* Bernard Schott
Cephalalgia
Volume 4 Issue 4 Page 213-220, December 1984
Although migraineurs appear in general to be hypersensitive to external stimuli, they maybe also have increased daytime sleepiness and complain of fatigue. Neurophisiological studies between attacks have shown that for a number of different sensory modalities the migrainous brain is characterised by a lack of habituation of evoked responses. Whether this is due to increased cortical hyperexcitability, possibly due to decreased inhibition, or to an abnormal responsivity of the cortex due a decreased preactivation level remains disputed. Studies using transcranial magnetic stimulation in particular have yielded contradictory results. We will review here the available data on cortical excitability obtained with different methodological approaches in patients over the migraine cycle. We will show that these data congruently indicate that the sensory cortices of migraineurs react excessively to repetitive, but not to single, stimuli and that the controversy above hyper- versus hypo-excitability is merely a semantic misunderstanding. Describing the migrainous brain as ‘hyperresponsive’ would fit most of the available data. Deciphering the precise cellular and molecular underpinnings of this hyperresponsivity remains a challenge for future research. We propose, as a working hypothesis, that a thalamo-cortical dysrhythmia might be the culprit.
Is the cerebral cortex hyperexcitable or hyperresponsive in migraine?
* G Coppola11G.B. Bietti Eye Foundation-IRCCS, Department of Neurophysiology of Vision and Neurophthalmology, ,
* F Pierelli2,32University of Rome ‘La Sapienza’ Polo Pontino—I.C.O.T., Rome and 3IRCCCS-Neuromed, Pozzilli (IS), Italy, &
* J Schoenen4,5
Two cases of symptomatic cluster-like headache suggest the importance of sympathetic/parasympathetic balance
* A Straube,
* T Freilinger,
* T Rüther &
* C Padovan
*
Department of Neurology, Klinikum Großhadern, Ludwig-Maximilians-University Munich, Germany
----------------------------------
A chronobiological study of melatonin, cortisol growth hormone and prolactin secretion in cluster headache
Results from this study suggest a neuroendocrine dysregulation in cluster headache in the endogenous clock which controls the pineal rhythmicity.
* Guy Chazot11Unite Neurométabolique, Hôpital Neurologique. 59 boulevard Pinel, 69003 Lyon, France; ,
* Bruno Claustrat22Service de Radiopharmacie et Radioanalvse. Centre de Médecine Nucléaire, 59 boulevard Pinel, 69003 Lyon, France; ,
* Jocelyne Brun22Service de Radiopharmacie et Radioanalvse. Centre de Médecine Nucléaire, 59 boulevard Pinel, 69003 Lyon, France; ,
* Daniel Jordan33Laboratoire de Médecine Expérimentale, INSERM U. 197-UER, Médecine Alexis Carrel, rue Guillaume Paradin. 69008 Lyon, France; ,
* Geneviève Sassolas44Unite de Soins, Centre de Médecine Nucléaire, 59 boulevard Pinel, 69003 Lyon, France,
* Bernard Schott
Cephalalgia
Volume 4 Issue 4 Page 213-220, December 1984
Although migraineurs appear in general to be hypersensitive to external stimuli, they maybe also have increased daytime sleepiness and complain of fatigue. Neurophisiological studies between attacks have shown that for a number of different sensory modalities the migrainous brain is characterised by a lack of habituation of evoked responses. Whether this is due to increased cortical hyperexcitability, possibly due to decreased inhibition, or to an abnormal responsivity of the cortex due a decreased preactivation level remains disputed. Studies using transcranial magnetic stimulation in particular have yielded contradictory results. We will review here the available data on cortical excitability obtained with different methodological approaches in patients over the migraine cycle. We will show that these data congruently indicate that the sensory cortices of migraineurs react excessively to repetitive, but not to single, stimuli and that the controversy above hyper- versus hypo-excitability is merely a semantic misunderstanding. Describing the migrainous brain as ‘hyperresponsive’ would fit most of the available data. Deciphering the precise cellular and molecular underpinnings of this hyperresponsivity remains a challenge for future research. We propose, as a working hypothesis, that a thalamo-cortical dysrhythmia might be the culprit.
Is the cerebral cortex hyperexcitable or hyperresponsive in migraine?
* G Coppola11G.B. Bietti Eye Foundation-IRCCS, Department of Neurophysiology of Vision and Neurophthalmology, ,
* F Pierelli2,32University of Rome ‘La Sapienza’ Polo Pontino—I.C.O.T., Rome and 3IRCCCS-Neuromed, Pozzilli (IS), Italy, &
* J Schoenen4,5
Comparison of the Emotional Effects of a Beta-Adrenergic Blocking Agent and a Tranquilizer
This study investigated the emotional effects of the beta-adrenergic blocking agent oxprenolol (40 mg, p.o.) and the tranquilizing agent diazepam (5 mg, p.o.) in healthy subjects under three situational conditions:an emotionally neutral control situation and two situations designed to arouse different levels of anxiety. Both oxprenolol and diazepam induced positive emotional changes only in the more strongly anxiety-arousing situation. Significant differences between oxprenolol and diazepam in inducing emotional stabilization were not demonstrable.
Gisela Erdmann, Wilhelm Janke, Sigrid Köchers, Brunhild Terschlüsen
Institut fur Psychologie, Technische Universität Berlin; Lehrstuhl fur Psychologie I, Universität Würzburg, BRD
Neuropsychobiology 1984;12:143-151 (DOI: 10.1159/000118129)
Gisela Erdmann, Wilhelm Janke, Sigrid Köchers, Brunhild Terschlüsen
Institut fur Psychologie, Technische Universität Berlin; Lehrstuhl fur Psychologie I, Universität Würzburg, BRD
Neuropsychobiology 1984;12:143-151 (DOI: 10.1159/000118129)
when sympathectomy results in excessive hypotension, vasoconstrictor drugs may be needed
High spinal anaesthesia may block the
nociceptive and haemodynamic responses to common
surgical events such as sternotomy. The extensive sym-
pathectomy provided by high spinal anaesthesia has po-
tential benefits and risks. If cardiac sympathectomy is achieved, there may be improvements in coronary per-
fusion. Stress response may be diminished. However,
when sympathectomy results in excessive hypotension, va-
soconstrictor drugs may be needed. These agents may
have detrimental effects on the coronary circulation, by-
pass grafts, and other organs.30"32
11 Parsonnet V, Dean D, Bernstein AD. A method of uni-
form stratification of risk for evaluating the results of
surgery in acquired adult heart disease. Circulation 1989;
79 (Suppl I): 13-112.
12 Robbins GR, Wynands JE, Whalley DG, et al.
nociceptive and haemodynamic responses to common
surgical events such as sternotomy. The extensive sym-
pathectomy provided by high spinal anaesthesia has po-
tential benefits and risks. If cardiac sympathectomy is achieved, there may be improvements in coronary per-
fusion. Stress response may be diminished. However,
when sympathectomy results in excessive hypotension, va-
soconstrictor drugs may be needed. These agents may
have detrimental effects on the coronary circulation, by-
pass grafts, and other organs.30"32
11 Parsonnet V, Dean D, Bernstein AD. A method of uni-
form stratification of risk for evaluating the results of
surgery in acquired adult heart disease. Circulation 1989;
79 (Suppl I): 13-112.
12 Robbins GR, Wynands JE, Whalley DG, et al.
Heart rate, heart rate variability and skin conductance as indicators of arousal
Arousal is a physiological and psychological state of being awake. It involves the activation of the reticular activating system in the brain stem, the autonomic nervous system and the endocrine system, leading to increased heart rate and blood pressure and a condition of sensory alertness, mobility and readiness to respond.
There are many different neural systems involved in what is collectively known as the arousal system. Four major systems originating in the brainstem, with connections extending throughout the cortex, are based on the brain's neurotransmitters, acetylcholine, norepinephrine, dopamine, and serotonin. When these systems are in action, the receiving neural areas become sensitive and responsive to incoming signals.
Importance
Arousal is important in regulating consciousness, attention, and information processing. It is crucial for motivating certain behaviours, such as mobility, the pursuit of nutrition, the fight or flight response and sexual activity (see Masters and Johnson's human sexual response cycle, where it is known as the arousal phase). It is also very important in emotion, and has been included as a part of many influential theories such as the James-Lange theory of emotion. According to Hans Eysenck, differences in baseline arousal level lead people to be either extraverts or introverts.
There are many different neural systems involved in what is collectively known as the arousal system. Four major systems originating in the brainstem, with connections extending throughout the cortex, are based on the brain's neurotransmitters, acetylcholine, norepinephrine, dopamine, and serotonin. When these systems are in action, the receiving neural areas become sensitive and responsive to incoming signals.
Importance
Arousal is important in regulating consciousness, attention, and information processing. It is crucial for motivating certain behaviours, such as mobility, the pursuit of nutrition, the fight or flight response and sexual activity (see Masters and Johnson's human sexual response cycle, where it is known as the arousal phase). It is also very important in emotion, and has been included as a part of many influential theories such as the James-Lange theory of emotion. According to Hans Eysenck, differences in baseline arousal level lead people to be either extraverts or introverts.
Adrenaline or peripheral noradrenaline depletion and passive avoidance in the rat
Physiol Behav. 1972 Jun;8(6):1059-62.
Adrenaline or peripheral noradrenaline depletion and passive avoidance in the rat.
Di Giusto EL.
J Comp Physiol Psychol. 1972 Dec;81(3):491-500.Links
Chemical sympathectomy and avoidance learning in the rat.
Di Giusto EL, King MG.
Adrenaline or peripheral noradrenaline depletion and passive avoidance in the rat.
Di Giusto EL.
J Comp Physiol Psychol. 1972 Dec;81(3):491-500.Links
Chemical sympathectomy and avoidance learning in the rat.
Di Giusto EL, King MG.
Heart rate and blood pressure responses to signaled and unsignaled shocks: effects of cardiac sympathectomy
J Comp Physiol Psychol. 1969 Jun;68(2):163-74.Links
Heart rate and blood pressure responses to signaled and unsignaled shocks: effects of cardiac sympathectomy.
Katcher AH, Solomon RL, Turner LH, LoLordo V, Overmier JB, Rescorla RA.
Heart rate and blood pressure responses to signaled and unsignaled shocks: effects of cardiac sympathectomy.
Katcher AH, Solomon RL, Turner LH, LoLordo V, Overmier JB, Rescorla RA.
adrenergic nerve degeneration after sympathectomy of the pineal gland
Electron microscopic evidence that bretylium and pargyline delay adrenergic nerve degeneration after sympathectomy of the pineal gland
Journal Naunyn-Schmiedeberg's Archives of Pharmacology
Publisher Springer Berlin / Heidelberg
ISSN 0028-1298 (Print) 1432-1912 (Online)
Issue Volume 319, Number 2 / May, 1982
Journal Naunyn-Schmiedeberg's Archives of Pharmacology
Publisher Springer Berlin / Heidelberg
ISSN 0028-1298 (Print) 1432-1912 (Online)
Issue Volume 319, Number 2 / May, 1982
Effects of thoracoscopic upper dorsal sympathicolysis for essential hyperhidrosis on bronchial responsiveness
Respirology. 1996 Sep;1(3):195-9.Links
Effects of thoracoscopic upper dorsal sympathicolysis for essential hyperhidrosis on bronchial responsiveness to histamine: implications on the autonomic imbalance theory of asthma.
Noppen MM, Vincken WG.
Respiratory Division, Academic Hospital AZ-VUB, Free University of Brussels, Belgium.
Three of the 26 patients (12%) without pre-operative bronchial hyperresponsiveness became hyperresponsive after TS, whereas 1 of the 9 patients with pre-operative BHR lost hyperresponsiveness. Upper dorsal thoracoscopic D2-D3 sympathicolysis performed for the treatment of EH has no significant effects on mean PD20 His and individual loss (11%) or development (12%) of BHR occurs only in 12% of patients.
Effects of thoracoscopic upper dorsal sympathicolysis for essential hyperhidrosis on bronchial responsiveness to histamine: implications on the autonomic imbalance theory of asthma.
Noppen MM, Vincken WG.
Respiratory Division, Academic Hospital AZ-VUB, Free University of Brussels, Belgium.
Three of the 26 patients (12%) without pre-operative bronchial hyperresponsiveness became hyperresponsive after TS, whereas 1 of the 9 patients with pre-operative BHR lost hyperresponsiveness. Upper dorsal thoracoscopic D2-D3 sympathicolysis performed for the treatment of EH has no significant effects on mean PD20 His and individual loss (11%) or development (12%) of BHR occurs only in 12% of patients.
beta 1-adrenoreceptor-mediated change in pulmonary capillary membrane permeability
Respir Med. 1997 Oct;91(9):537-45.Click here to read Links
Partial pulmonary sympathetic denervation by thoracoscopic D2-D3 sympathicolysis for essential hyperhidrosis: effect on the pulmonary diffusion capacity.
Noppen MM, Vincken WG.
Respiratory Division, Academic Hospital, University of Brussels, Belgium.
In patients with essential hyperhidrosis (EH), a pathological condition characterized by increased activity of the upper dorsal sympathetic ganglia D2-D3, anatomical interruption at the D2-D3 level by thoracoscopic sympathicolysis (TS) is a safe and effective treatment. The D2 and D3 ganglia, however, are also in the pathway of sympathetic lung innervation, which may influence the pulmonary diffusion capacity for carbon monoxide (expressed as transfer factor for CO:TLCO, and as transfer coefficient for CO:KCO). We therefore studied the effect of TS on TLCO and KCO in 50 EH patients: compared with pre-operative values, both TLCO (-6.7%, P < 0.001) and KCO (-4.2%, P = 0.002) were significantly decreased at 6 weeks after bilateral TS, an effect which was independent of the smoking status of the patients. In order to explain this phenomenon, the following pharmacological interventions were studied: (1) oral beta 1 + 2-adrenoreceptor blockade with propranolol caused a comparable decrease of TLCO (-6.3%) and KCO (-7.5%) in matched normal subjects, but had no effect on TLCO and KCO in EH patients prior to TS; and (2) subsequent inhalation of the beta 2-adrenoreceptor agonist salbutamol in a dosage suspected to cause alveolar beta-receptor stimulation had no effect on TLCO and KCO, neither in the normal subjects, nor in EH patients (before and after TS). Although the exact mechanism of the TS-induced decrease in TLCO and KCO remains speculative, these findings suggest that they may be related to a beta 1-adrenoreceptor-mediated change in pulmonary capillary membrane permeability, although TS-induced changes in pulmonary blood flow or an interplay of both mechanisms cannot be excluded.
Partial pulmonary sympathetic denervation by thoracoscopic D2-D3 sympathicolysis for essential hyperhidrosis: effect on the pulmonary diffusion capacity.
Noppen MM, Vincken WG.
Respiratory Division, Academic Hospital, University of Brussels, Belgium.
In patients with essential hyperhidrosis (EH), a pathological condition characterized by increased activity of the upper dorsal sympathetic ganglia D2-D3, anatomical interruption at the D2-D3 level by thoracoscopic sympathicolysis (TS) is a safe and effective treatment. The D2 and D3 ganglia, however, are also in the pathway of sympathetic lung innervation, which may influence the pulmonary diffusion capacity for carbon monoxide (expressed as transfer factor for CO:TLCO, and as transfer coefficient for CO:KCO). We therefore studied the effect of TS on TLCO and KCO in 50 EH patients: compared with pre-operative values, both TLCO (-6.7%, P < 0.001) and KCO (-4.2%, P = 0.002) were significantly decreased at 6 weeks after bilateral TS, an effect which was independent of the smoking status of the patients. In order to explain this phenomenon, the following pharmacological interventions were studied: (1) oral beta 1 + 2-adrenoreceptor blockade with propranolol caused a comparable decrease of TLCO (-6.3%) and KCO (-7.5%) in matched normal subjects, but had no effect on TLCO and KCO in EH patients prior to TS; and (2) subsequent inhalation of the beta 2-adrenoreceptor agonist salbutamol in a dosage suspected to cause alveolar beta-receptor stimulation had no effect on TLCO and KCO, neither in the normal subjects, nor in EH patients (before and after TS). Although the exact mechanism of the TS-induced decrease in TLCO and KCO remains speculative, these findings suggest that they may be related to a beta 1-adrenoreceptor-mediated change in pulmonary capillary membrane permeability, although TS-induced changes in pulmonary blood flow or an interplay of both mechanisms cannot be excluded.
Wednesday, April 30, 2008
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.
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.
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.
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.
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
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
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)...."
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
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...
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
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]
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
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
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.
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.
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,
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,
Monday, April 28, 2008
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
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.
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.
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
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
Sunday, April 27, 2008
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
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.
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)
[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
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
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.
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.
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
* 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
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