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.
Wednesday, April 30, 2008
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,
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