Heart and Circulatory Physiology, Vol 260, Issue 3 827-H831, Copyright © 1991 by American Physiological Society
A. Iwai, W. W. Monafo and S. G. Eliasson
Department of Surgery, Washington University School of Medicine, St. Louis, Missouri 63110.
"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
A. Iwai, W. W. Monafo and S. G. Eliasson
Department of Surgery, Washington University School of Medicine, St. Louis, Missouri 63110.
MARTIN LUSTER PRESIDING
NYC, May 18, 2001
http://www.healthyplace.com/Communities/Depression/ect/news/newyork/friedbergtest.asp
1 Laboratory of Clinical Science, National Institute of Mental Health, Bethesda, Maryland 20014
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.
VOL. 31, NOS. 5 & 6, 2000 JOURNAL OF MEDICINE
JOURNAL OF MEDICINE, 2000
ENHANCEMENT OF NORADRENERGIC NEURAL TRANSMISSION: AN EFFECTIVE THERAPY OF
MYASTHENIA GRAVIS
Fuad. Lechin1,2, Bertha van der Dijs1,2, Betty Pardey-Maldonado1,
Eduardo Jahn1, Vladimir Jimenez1, Beatriz Orozco1,Scarlet Baez2 and Marcel E. Lechin3
After ETS, heart rate, systolic, diastolic, and mean blood pressures, rate-pressure product, and NOR decreased,whereas left ventricular end-systolic volume index, cardiac index, and ejection fraction did not change in the 2 groups.Among percent changes in all hemodynamic parameters and NOR occurring after ETS, only the percent decrease in systolic blood pressure in group Th2–4 was larger than that in group Th2–3 (–15 ± 12 % vs.–4±8%, respectively, p <>
Yukio Nakamura1, Shin-ichiro Muramoto1, Rira Kato1, Takahiro Saeki1, Manabu Fujimoto1, Hiroshi Kida1 and Yasushi Matsumoto2
| (1) | Dept. of Cardiology, Kanazawa National Hospital, 1-1 Shimoishibiki-machi, Kanazawa, Ishikawa, 920–8650, Japan |
| (2) | Dept. of Cardiovascular Surgery, Kanazawa National Hospital, Kanazawa, Ishikawa, Japan |
Tampere City Mental Health Care Centre, Finland. paipoh@koti.soon.fi
Social phobia is a neglected disorder, which can cause very debilitating consequences in patients' lives. The patients tend to isolate and suffer from comorbid disorders such as depression, other anxiety disorders, and drug and alcohol abuse. Traditional treatment methods such as medication and psychotherapy do not help everyone. A prospective, uncontrolled follow-up study with 169 social phobic patients was performed by uni- or bilateral endoscopic sympathetic block of the upper thoracic ganglia.University of Oulu, Oulu, Finland. timo.telaranta@privatix.fi
In addition to more widely and longer known indications of ETS, various neurological disorders and psychologically stressful situations in their worst expressions might be alleviated by the reversible ESB procedure. The patients with social phobia, especially those who have also blushing and/or stage fright type of heart racing, benefit from the ESB. The disturbances of the sympathetic nervous system, e. g. in Parkinson's disease and multiple system atrophy might be alleviated with sympathetic block, especially the extrapyramidal symptoms in these diseases. In migraine, sympathetic surgery has been noted to give some help. The unilateral left-sided block has been effective in long QT-syndrome type arrhythmias. In schizophrenia, the phobic, paranoic or confusional reactions have been tentatively treated by the sympathetic block.
http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=Retrieve&db=PubMed&list_uids=14673667&dopt=AbstractPlus
Authors: Joyner, M. J.1; Dietz, N. M.1
Source: Acta Physiologica, Volume 177, Number 3, March 2003 , pp. 329-336(8)
Publisher: Blackwell Publishing
| By Philippa Newfield, James E. Cottrell |
| Contributor Philippa Newfield, Stephen Onesti, James E. Cottrell |
| Published 2006, Lippincott Williams & Wilkins |
The time course of ultrastructural and electrophysiological disorders and their role in sudden death of ventricular fibrillation at various intervals of desympathization caused by reserpine administration were studied. Early in the effect of reserpine (up to 30 min), glycogen granules were found to accumulate in the sarcoplasm of cardiomyocytes. At later intervals (1-24 hours), along with glycogen accumulation destructive lesions of organoids were observed in the form of myofibrillar recontraction, destruction of mitochondria, degeneration of sarcolemma. These changes are morphologic reflections of metabolic disorders developing in the myocardium under conditions of acute desympathization of the patient, and may be one of the causes of increased vulnerability of the heart in fibrillation.
Department of Physiology, Southern Illinois University School of Medicine, Carbondale, IL 62901, United State, 2005.
| By Otto Appenzeller, P. J. Vinken, G. W. Bruyn, |
| Contributor Otto, Appenzeller, P. J. Vinken, G. W. Bruyn |
| Published 2000 Elsevier Health Sciences |
| Autonomic nervous system / Pathophysiology |
Department of Physiology, Biochemistry and Immunology, School of Medicine, University of São Paulo, 14049-900 Ribeirão Preto, São Paulo, Brazil
Submitted 18 August 2003 ; accepted in final form 28 November 2003
Thoracic Department, Institut Mutualiste Montsouris, Paris, France
Department of Surgery, Mansoura Faculty of Medicine, Mansoura University, Mansoura, Egypt.
Surgery. 2008 Jun;143(6):784-9. Epub 2008 Mar 20
Received 2 November 1998; received in revised form 14 May 1999; accepted 9 July 1999.
U. I. Tuor
Division of Neonatology, Hospital for Sick Children Research Institute, Toronto, Ontario, Canada.
Am J Physiol Heart Circ Physiol 263: H511-H518, 1992;
Department of Pharmacology, Institut National de la Santé et de la Recherche Médicale U. 337, Paris, France.
Am J Physiol. 1995 Aug;269(2 Pt 2):H407-16.
Clinical Anesthesiology, Chapter 17
Peripheral Nerve Blocks, p. 298~ 8/22/2004 3:07 PM
Increased Ocular Blood Vessel Numbers and Sizes Following Chronic Sympathectomy in Rat
Author: Lychkova, A.
Source: Bulletin of Experimental Biology and Medicine, Volume 140, Number 5, November 2005 , pp. 486-488(3)
Publisher: Springer
Depression accompanying compensatory hyperhidrosis following endoscopic thoracic sympathectomy
Authors: Hashim, N.; Wilson, N. J. E.
Source: Clinical & Experimental Dermatology, Volume 31, Number 6, November 2006 , pp. 818-819(2)
Publisher: Blackwell Publishing
| Published 2006 Lippincott Williams & Wilkins |
| Human anatomy |
| 1209 pages |
| ISBN:0781736390 |
Departments of Physiology and Zoology, University of Toronto, Toronto, Ontario, Canada.
Over several years of experience in treating patients with recurrent and/or persistent sweating of the face after undergoing T2 sympathectomy, Dr. Nielson has found that persistence of any sympathetic nerve innervation across the second rib level, just above the T2 ganglion, plays a significant role in persistent sweating conditions of the face after undergoing a T2. T3, or T4 sympathectomy.
It is apparent in some patients that there are neuronal contributions from lower levels such as the T3 that pass up over the second rib level on their way to the face that participate in the sweating symptoms of the face. Some physicians misunderstand the sympathetic nerve innervation of the face and believe in order to cure facial sweating it is important to cut the sympathetic nerve at the T1 level or above, thereby causing the dreaded Horner’s Syndrome. In Dr. Nielson's experience, he has found this not to be the case.
In summary, for successful treatment of facial sweating, it is imperative that all sympathetic nerve innervation crossing the second rib level be divided as opposed to clamped or having lower levels cut or clamped. Also, accessory nerve branch pathways bypassing the T2 ganglion can or may contribute to persistent facial symptoms.
Department of Psychology, 6 Washington Place, 8(th) floor, New York, New York 10003, USA. liz.phelps@nyu.edu
The amygdala and hippocampal complex, two medial temporal lobe structures, are linked to two independent memory systems, each with unique characteristic functions. In emotional situations, these two systems interact in subtle but important ways. Specifically, the amygdala can modulate both the encoding and the storage of hippocampal-dependent memories. The hippocampal complex, by forming episodic representations of the emotional significance and interpretation of events, can influence the amygdala response when emotional stimuli are encountered. Although these are independent memory systems, they act in concert when emotion meets memory.
Curr Opin Neurobiol. 2004 Apr;14(2):198-202.http://www.ncbi.nlm.nih.gov/pubmed/15082325?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_Discovery_RA&linkpos=3&log$=relatedarticles&logdbfrom=pubmed
Orthostatic hypotension is commonly associated with prolonged bed rest (24 hours or longer). It may also result from sympathectomy, which disrupts normal vasoconstrictive mechanisms. http://www.wrongdiagnosis.com/m/multiple_system_atrophy_msa_with_orthostatic_hypotension/causes.htm
Negative amplitude shifts of cortical potential are related to seizure activity in epilepsy. Regulation of the cortical potential with biofeedback has been successfully used to reduce the frequency of some patients' seizures. Although such behavioural treatments are increasingly popular as an alternative to pharmacotherapy, there has been no investigation of the mechanisms that might bridge the behavioural index of peripheral autonomic activity and the central regulation of arousal. Galvanic Skin Response (GSR) is a sensitive measurement of autonomic arousal and physiological state which reflects one's behaviour. Thus we investigated the effect of peripheral autonomic modulation on cortical arousal with the future intention of using GSR biofeedback as a therapeutic treatment for epilepsy. http://www.ncbi.nlm.nih.gov/pubmed/15120749?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_Discovery_RA&linkpos=1&log$=relatedarticles&logdbfrom=pubmed