Muscle & Nerve
Published Online: 7 Dec 1998
"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
Published Online: 7 Dec 1998
Spinal and Epidural AnesthesiaBy Cynthia Wong |
Publication Date: 2007-01-01 Publisher: MCGRAW-HILL EDUCATION - EUROPE Country of origin: UNITED STATES
The pathogenesis of angina and myocardial infarction pain involves the activation of the afferent sympathetic pathway. A frequent and important consequence of pain (especially when severe) is the `flight or fight' response through activation of sympathetic efferents. The clinical image of the patient with an acute myocardial infarction (cold, clammy, sweaty, anxious, tachycardic) is secondary to this adrenergic activation. Therefore, angina might be regarded as the sensory component of a positive feedback loop, which cannot under these circumstances be conceived as resulting in benefit, and which may be considered to be a maladaption.
The angina-relieving effects of sympathetic blockade might be due to interference with this maladaptive feedback loop, in a similar manner to the way in which adenosine interrupts a re-entrant tachycardia. If such a loop exists, it may partly explain chronic refractory angina and the fact that temporary interruption of this pathway has a prolonged effect on pain14. Beneficial amelioration of angina can be achieved with repeated blocks14. There does not appear to be any predictability in the length of time a patient remains pain-free after successive blocks.
http://www.angina.org/source/pro/symp_block.htm
Moya-Moya Syndrome
Moya Moya syndrome is a vasculopathy of the cranial arteries, usually the carotids, leading to progressive intracranial occlusion with distal collateral vessels. This is a very frequent cause of pediatric stroke in India(10,11). Children usually present with an acute focal deficit such as hemiplegia, whereas in later years sub-arachnoid hemorrhage is a common presenta-tion. Due to bilateral carotid involvement sometimes alternating hemiplegia is seen. The outcome varies widely without treatment. Moya Moya disease is usually idiopathic, although same radiographic pattern is seen in some patients with sickle cell disease, neuro-fibromatosis, postcranial irradiation and in various other conditions(15). There is no proven treatment of Moya Moya disease. Medical management involves use of aspirin but needs further testing. Surgical treatment involves cervical sympathectomy, intracranial graft of omentum or temporalis muscle and bypass of superficial temporal artery to the middle cerebral artery(34).
http://indianpediatrics.net/feb2000/personal.htm
Answered by Barak Goodman:
The quantitative analysis of lobotomy was meager. The obstacles to a good study of lobotomy were numerous: the patients were often abandoned in mental hospitals and therefore hard to access; controlled studies were of course impossible; and no two patients got the same operation (Freeman's operation was truly "a stab in the dark"). The stigma attached to the operation made it a less than desirable area of research and study. Perhaps the most thorough analysis was done by Freeman himself, who kept in touch with hundreds of his patients and tried to assemble data to support lobotomy's efficacy. I think we have to regard that data as suspect.
Occasionally, after the fact, lawsuits are launched attempting to secure damages for the victims. This occurred in Canada, for instance, after the death of Ewen Cameron, former president of the American, Canadian, and World Psychiatric Associations, and a member of the Nuremberg medical tribunal which had investigated Nazi doctors. Cameron, practicing at McGill University, had experimented with "depatterning" and "psychic driving," extraordinary experiments where, inter alia, he wiped out patients' memories with repeated electroshocks designed to reduce those subjected to them to the status of helpless, incontinent "infants," whose psyches he then purported to rebuild. Cameron at his death was a highly respected figure in his profession. Only after it emerged that much of this work had been secretly supported by the CIA were lawsuits brought, some of which were successful in securing monetary damages for his victims and/or their families. Whether money could ever adequately compensate for what has been done, for suicides and ruined lives, is very doubtful, as I'm sure you would agree. But the legal acknowledgement of the depth of the wrong that has been wrought is, of course, worth something.
Andrew Scull
My father was aiming to disconnect the thalamus from the frontal cortex
The positive(sic!) consequences of cutting between thalamus and frontal cortex were loss of fear and anxiety. The negative consequences of cutting were loss of social inhibition (loss of guilt, shame, fear of disapproval) and loss of the ability to think ahead (no ambition, eating to excess, inability to read the minds of others).
" People who start taking Prozac, Miltown, or other tranquilizers no longer suffer anxiety and fear of the future, but they lose ambition, libido, and the capacity for deep feelings. That is the cost of treatment. Neither surgery nor drugs cure the mental illness. They only relieve the suffering, and the cost is high.
Most patients who are not suffering too much prefer to continue to suffer than to accept the loss. Other patients suffer so intensely that they kill themselves rather than continue living.
Walter Freeman III
So, could something like this happen today? Could psychiatry -- or some other branch of medicine -- adopt a form of care that we would later come to see as harmful? The history of medicine certainly warns us that doctors can be deluded about the merits of their therapies, and today that whole decision-making process is greatly influenced by pharmaceutical companies' money, which only increases the possibility of medicine going astray. The lobotomy story really should remind us of that possibility.
Robert Whitaker
http://www.pbs.org/wgbh/amex/lobotomist/forum/day1.htmlWe present a case of orthodeoxia (postural hypoxaemia) which resulted from a combination of lung collapse/consolidation and blunted hypoxic pulmonary vasoconstriction due to partial interruption of the sympathetic nerve supply to the lung by bilateral thoracic sympathectomy.
Less common associations with orthodeoxia are atypical pneumonia3, trauma8, organophosphate poisoning10 and progressive autonomic failure12.
The surgical procedure, which interrupted both sympathetic trunks, probably resulted in "sympathectomy" of the lung with consequent vasoplegia of the pulmonary circulation and blunting of the HPV response.
The combination of areas of reduced ventilation in the lung, together with blunted HPV, resulted in profound oxygen desaturation in our patient when she sat up in bed.
As antibiotics and chest physiotherapy improved the collapse/consolidation of the lungs, the patient became less dependent on artificial means of maintaining pulmonary vascular tone, so that the noradrenaline and then the almitrine could be weaned without incident. Presumably there will be some return of sympathetic tone to the pulmonary circulation with time.
It was not the intention of the authors to describe all the physiological consequences of thoracotomy or thoracoscopy, with or without one-lung ventilation, in this short communication. Clearly these procedures on their own can have significant effects on lung physiology, quite apart from the unique confluence of factors producing orthodeoxia in the patient presented in this case report.
| E. Marley ALTERED RESPONSE TO SMALL DOSES OF INSULIN ASSOCIATED WITH ELECTROPLEXY AND HYPOGLYCAEMIC THERAPIES J. Neurol. Neurosurg. Psychiatry, Feb 1956; 19: 57 - 61. |
Abstract:
Background: A patient developed severe, continuous, unilateral headache that was "vascular" in nature, following cervical sympathectomy.
Objective: To determine the changes in cranial blood flow in the cat following lesioning and stimulation of the cervical sympathetic nerve.
Method: Carotid blood flow was determined by electromagnetic flowmetry and its tissue distribution by intra-arterial injection of 15-[mu]m radioactive microspheres.
Results: Following sympathetic lesioning, an increase in carotid blood flow was observed and reversed with stimulation. The distribution of carotid blood flow changed for the brain only, maintaining relatively constant tissue perfusion.
Conclusion: An increase in cerebral blood flow could not have accounted for the sympathectomy-induced headache. Dilation of major cerebral arteries and cranial noncerebral vasodilation probably constitutes its mechanism.
| Journal | Journal of Anesthesia |
| Publisher | Springer Japan |
| ISSN | 0913-8668 (Print) 1438-8359 (Online) |
| Issue | Volume 10, Number 3 / September, 1996 |
Category: Neurology & Clinical Neurophysiology
Publication Date: 1999-12-16 Publisher: Elsevier - Health Sciences Div
H. J. Romijn1
| (1) | Present address: Department of Electron Microscopy, Netherlands Central Institute for Brain Research, Amsterdam, The Netherlands |
Received: 3 March 1975
| |
Techniques in Regional Anesthesia and Pain Management, Volume 5, Issue 3, Pages 99-101
N.Mekhail, O.Malak
J Anat. 1984 October; 139(Pt 3): 449–461. | PMCID: PMC1165060 |
Science 3 September 1971: |
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-- 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-
-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-
-hydroxylase activity arises from sympathetic nerve terminals.
Measurements: Heart rate recovery was defined as the change from peak heart rate to that measured 2 minutes later (heart rate recovery was defined as 42 beats/min).
Results: During 12 years of follow-up, 312 participants died. Abnormal heart rate recovery predicted death (relative risk, 2.58 [CI, 2.06 to 3.20]). After adjustment for standard risk factors, fitness, and resting and exercise heart rates, abnormal heart rate recovery remained predictive (adjusted relative risk, 1.55 [CI, 1.22 to 1.98]) (P <>
Conclusion: Even after submaximal exercise, abnormal heart rate recovery predicts death.
4 April 2000 | Volume 132 Issue 7 | Pages 552-555
Clinically, chemical inhibition of the PNS is used to manage joint pain. Chemical blockade of the sympathetic nervous system is often accomplished through the administration of guanethidine. Guanethidine blocks the release and subsequent reuptake of norepinephrine (NE) (a major sympathetic neurotransmitter) in patients with osteoarthritis, rheumatoid arthritis, and reflex sympathetic dystrophy (12, 13, 24, 38, 40). This treatment, while effective in relieving pain, may have undesirable effects on connective tissues, because it alters the normal concentration of neurogenic factors.
Growing anatomic and physiological evidence suggest that the PNS is important to ligament and joint homeostasis.Department of Physiology, Henri Mondor Hospital, Creteil, France.
Objective assessment of the results of surgical sympathectomy and sympathetic block (both temporary and permanent) are not widely practised. This article comments briefly on the available methods, and describes the use of the abolition of the skin potential response (formerly known as the psychogalvanic reflex) to assess the abolition of sympathetic function. This method of assessment has proved useful in clinical practice.
PMID: 525760 [PubMed - indexed for MEDLINE]
• Idiopathic orthostatic hypotension
• Multiple sclerosis
• Parkinsonism
1 Department of Neuroanaesthesiology, All India Institute of Medical Sciences (A.I.I.M.S.), New Delhi, India. 2 University Department of Anaesthesia and Intensive Care, Queen's Medical Centre, Nottingham, UK
* Corresponding author. E-mail: pkbithal@hotmail.com
Accepted for publication July 11, 2005.
Service of Cardiothoracic Surgery, Hospital de Santa Maria, Lisbon, Portugal. costacruzjorge@gmail.com
PMID: 19258086 [PubMed - indexed for MEDLINE]
| | Our findings suggest that peripheral autonomic denervation ( ETS= peripheral autonomic denervation) is associated with grey matter loss in cortical regions encompassing areas that we have previously shown are functionally involved in generation and representation of bodily states of autonomic arousal. http://www.ncbi.nlm.nih.gov/pubmed/12725766
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Clinical Imaging Sciences Centre, Brighton and Sussex Medical School, University of Sussex, Brighton, East Sussex BN1 9RR, United Kingdom. m.a.gray@bsms.ac.uk
Central nervous processing of environmental stimuli requires integration of sensory information with ongoing autonomic control of cardiovascular function. Rhythmic feedback of cardiac and baroreceptor activity contributes dynamically to homeostatic autonomic control. We examined how the processing of brief somatosensory stimuli is altered across the cardiac cycle to evoke differential changes in bodily state. Using functional magnetic resonance imaging of brain and noninvasive beat-to-beat cardiovascular monitoring, we show that stimuli presented before and during early cardiac systole elicited differential changes in neural activity within amygdala, anterior insula and pons, and engendered different effects on blood pressure. Stimulation delivered during early systole inhibited blood pressure increases. Individual differences in heart rate variability predicted magnitude of differential cardiac timing responses within periaqueductal gray, amygdala and insula. Our findings highlight integration of somatosensory and phasic baroreceptor information at cortical, limbic and brainstem levels, with relevance to mechanisms underlying pain control, hypertension and anxiety.
J Neurosci. 2009 Feb 11;29(6):1817-25.
Author/s: Critchley, Hugo D (HD); Mathias, Christopher J (CJ); Dolan, Raymond J (RJ);
Affiliation: Department of Imaging Neuroscience, 12 Queen Square, Institute of Neurology and Institute of Cognitive Neuroscience, UCL, WC1N 3BG, London, United Kingdom.
Reference: 2002-Feb; vol 33 (issue 4) : pp 653-63
Wellcome Department of Imaging Neuroscience, Institute of Neurology, UCL, 12 Queen Square, London WC1N 3BG, UK. j.critchley@fil.ion.ucl.ac.uk