Saturday, January 26, 2008
Australian Story2 (rant)
quote from the ets forum:
"I do realise there are sweat tests conducted after a reversal but my point is that doctors do not do these tests on ETS patients. Therefore how can they generalise and say that after ETS CS will be mild or severe?? They do not do follow ups on ETS patients and if a patient complains of heavy CS the doctor may see it as mild and normal CS for statistical purposes."
http://etsandreversals.yuku.com/topic/3016/t/Eastern-Surgical-Australia.html
My question is: did anybody ever made an attempt at quantifying the scale of the 'compensatory sweating" after the surgery? Is there an attempt made to measure the amount of sweating before and after the surgery? Surely not, it would provide the proof that Sympathectomy causes profound sweating. What else could be the reason for not measuring this very significant side-effect? And then, - based on what!!!? - are the surgeons making the sweeping statements about the % of the people and the severity or scale of sweating after the surgery? Or about patient satisfaction rates??? How are these figures made up? Surely nobody bothered to ask any questions from me...
Why are the surgeons not accountable by providing statistical information on the side-effects after the surgery??? Don't they want to know how effective their surgery is? If it is safe ?! Reliable? Does more good then harm???
My surgeon did not schedule a follow up consultation. If I would have not called him (which I almost didn't), he would have never been told about the side-effects I have experienced. Did he file a report on my condition/case? Of course not. It would harm the statistics. (What statistics?!)
"I do realise there are sweat tests conducted after a reversal but my point is that doctors do not do these tests on ETS patients. Therefore how can they generalise and say that after ETS CS will be mild or severe?? They do not do follow ups on ETS patients and if a patient complains of heavy CS the doctor may see it as mild and normal CS for statistical purposes."
http://etsandreversals.yuku.com/topic/3016/t/Eastern-Surgical-Australia.html
My question is: did anybody ever made an attempt at quantifying the scale of the 'compensatory sweating" after the surgery? Is there an attempt made to measure the amount of sweating before and after the surgery? Surely not, it would provide the proof that Sympathectomy causes profound sweating. What else could be the reason for not measuring this very significant side-effect? And then, - based on what!!!? - are the surgeons making the sweeping statements about the % of the people and the severity or scale of sweating after the surgery? Or about patient satisfaction rates??? How are these figures made up? Surely nobody bothered to ask any questions from me...
Why are the surgeons not accountable by providing statistical information on the side-effects after the surgery??? Don't they want to know how effective their surgery is? If it is safe ?! Reliable? Does more good then harm???
My surgeon did not schedule a follow up consultation. If I would have not called him (which I almost didn't), he would have never been told about the side-effects I have experienced. Did he file a report on my condition/case? Of course not. It would harm the statistics. (What statistics?!)
Slowly the surgeons admit to more and more side-effects
Go to Dr Reisfeld's web site to read his new comments about ETS: www.sweaty-palms.com/blushing.html
"Another clinical observation which will need more time for verification is the thought that the higher failure rate of sympathectomy when ETS is done only for facial blushing has to do with the fact that when the sympathectomies were done in the past for vascular problems the success rate was very minimal. At this time we know that higher failure rate was due to a clinical situation which we call denervation hypersensitivity. In essense the blood vessels become very sensitive to certain circulating hormones within the blood system. Dr. Reisfeld believes that the same phenomenon happens in this facial blushing presentation. More time and more clinical experience is needed before there can be a more definite conclusion."
Hopefully this may assist court cases but it sounds like Reisfeld is trying to cover his legal liability in his "at the time we thought..." comments.
Also see how the Australian site www.easternsurgical.com.au (click on blushing) have now admitted "some failures" and had to remove their biased comments about 500 consecutive successes.
Unfortunately the more people who have ETS side effects, the more the statistics become 'significant' to such doctors.
Madonna
"Another clinical observation which will need more time for verification is the thought that the higher failure rate of sympathectomy when ETS is done only for facial blushing has to do with the fact that when the sympathectomies were done in the past for vascular problems the success rate was very minimal. At this time we know that higher failure rate was due to a clinical situation which we call denervation hypersensitivity. In essense the blood vessels become very sensitive to certain circulating hormones within the blood system. Dr. Reisfeld believes that the same phenomenon happens in this facial blushing presentation. More time and more clinical experience is needed before there can be a more definite conclusion."
Hopefully this may assist court cases but it sounds like Reisfeld is trying to cover his legal liability in his "at the time we thought..." comments.
Also see how the Australian site www.easternsurgical.com.au (click on blushing) have now admitted "some failures" and had to remove their biased comments about 500 consecutive successes.
Unfortunately the more people who have ETS side effects, the more the statistics become 'significant' to such doctors.
Madonna
Australian Story1
ETS studies are not done in the Australian climate and resulting CS means ETS should never have been allowed here without a review. One conducted by Monash University concluded not enough evidence on ETS is available and that existing ETS studies are flawed.These boards are accountable.
.....Madonna Aussie
.....Madonna Aussie
Norepinephrine Turnover - increase in plasma NE=increase in brain NE
Norepinephrine Turnover Is Increased in Suprabulbar Subcortical Brain Regions and Is Related to Whole-Body Sympathetic Activity in Human Heart Failure
From the Baker Medical Research Institute, Melbourne, Australia.
© 2002 American Heart Association, Inc.
This study, for the first time, demonstrates elevated suprabulbar subcortical noradrenergic activity in human CHF and identifies a positive correlation between this and the level of whole-body NE spillover. The findings suggest that the activation of noradrenergic neurons projecting rostrally from the brain stem mediates sympathetic nervous stimulation in CHF.
cerebrovascular CO2 reactivity
- Acta Physiol Scand. 1977 Sep;101(1):122-5.
Effects of intraventricular 6-hydroxydopamine on cerebrovascular CO2 reactivity in anesthetized rats.
Regional cerebral blood flow was measured by the 14C-ethanol technique in anesthetized rats before and after intraventricular injection of 6-hydroxydopamine. This treatment reduced the fluorescence of the central noradrenaline and dopamine nerve terminals, as well as of the perivascular nerve terminals in cerebral vessels. The administration of 6-hydroxydopamine had no significant effect on cerebral blood flow at normocapnia. The cerebrovascular reactivity to hypercapnia was significantly increased in the 6-hydroxydopamine treated animals. The results indicate an involvement of central catecholamine pathways in the cerebrovascular reactivity to hypercapnia.
PMID: 906856 [PubMed - indexed for MEDLINE]
catecholamine neuron in cerebral circulation
J Neurosurg. 1986 Sep;65(3):370-5
A role of the central catecholamine neuron in cerebral circulation.
The effect of the central catecholaminergic neurons on the cerebral microcirculation was investigated by means of a unilateral intracerebral injection of 6-hydroxydopamine (6-OHDA) which produced the degeneration of catecholamine (CA) nerve terminals. Subsequent observation with CA histofluorescence revealed an absence of CA fibers in the vicinity of the 6-OHDA injection site. A significant increase in regional cerebral blood flow (rCBF), measured by the hydrogen clearance method, was demonstrated in the CA-depleted cortex under normocapnia as compared with rCBF in the control cortex (CA-depleted cortex 47.0 +/- 2.8 ml/100 gm/min; control cortex 38.5 +/- 3.5 ml/100 gm/min; p less than 0.005). The increased rCBF in the cortex treated with 6-OHDA was suppressed by the iontophoretic replacement of noradrenaline (NA) to the CA-depleted cortex. An iontophoretic replacement of 10(-5) M dopamine (DA) mildly suppressed the increased rCBF in the 6-OHDA-treated cortex. The CO2 reactivity in the CA-depleted cortex was significantly lower than that of the control cortex (CA-depleted cortex 2.13% +/- 0.6%/mm Hg; control cortex 3.53% +/- 0.70%/mm Hg). No change was noticeable in the cerebral glucose metabolism in the CA-depleted cortex in an investigation based on tritiated (3H)-deoxyglucose uptake. It is suggested that the 6-OHDA-induced change in cerebral blood flow (CBF) is not secondary to alterations in cerebral metabolic rate, and that the central NA neuron system innervating intraparenchymal blood vessels regulates CBF through a direct vasoconstrictive effect on the cerebral blood vessels. The central DA neuron system may modulate the cerebral circulation as a mild vasoconstrictor.
Why many patients who undergo SYMPATHECTOMY complain about stuffy nose/a cold for life...?!
AJP - Regulatory, Integrative and Comparative Physiology, Vol 253, Issue 3
494-R500, Copyright © 1987 by American Physiological Society
Articles by Haxhiu, M. A.
Articles by Cherniack, N. S.
A role for the ventral surface of the medulla
in regulation of nasal resistance
M. A. Haxhiu, K. P. Strohl, M. P. Norcia, E. van Lunteren,
E. C. Deal Jr and N. S. Cherniack
Nasal resistance is known to be affected by changes in nasal blood volume
and hence to depend on sympathetic discharge to nasal blood vessels.
Structures located superficially near the ventrolateral surface of the medulla
significantly affect respiratory and sympathetic activity and the tone of the
trachea. To assess the importance of these structures on nasal patency, we
measured transnasal pressure at a constant flow and examined the change in
pressure produced by topically applied N-methyl-D-aspartic acid (NMDA).
Experiments were performed in chloralose-anesthetized, paralyzed, and
artificially ventilated cats. NMDA administered on the intermediate area of
the ventral surface of the medulla decreased transnasal pressure and increased phrenic nerve activity. The response to
NMDA could be diminished or abolished by application to the ventral medullary surface of the NMDA antagonist
2-amino-5-phosphonovalerate (2-APV) or the local anesthetic lidocaine. Carotid sinus denervation and
posthypothalamic decerebration did not alter the nasal and phrenic nerve responses to NMDA; however, cervical
sympathetic denervation decreased these responses, both in intact and in bilaterally adrenalectomized animals. Therefore,
activation of NMDA receptors on structures near the ventral surface of the medulla increases tone in the nasal
vasculature and leads to a response pattern that includes changes in not only phrenic nerve activity and blood pressure
but also nasal patency.
494-R500, Copyright © 1987 by American Physiological Society
Articles by Haxhiu, M. A.
Articles by Cherniack, N. S.
A role for the ventral surface of the medulla
in regulation of nasal resistance
M. A. Haxhiu, K. P. Strohl, M. P. Norcia, E. van Lunteren,
E. C. Deal Jr and N. S. Cherniack
Nasal resistance is known to be affected by changes in nasal blood volume
and hence to depend on sympathetic discharge to nasal blood vessels.
Structures located superficially near the ventrolateral surface of the medulla
significantly affect respiratory and sympathetic activity and the tone of the
trachea. To assess the importance of these structures on nasal patency, we
measured transnasal pressure at a constant flow and examined the change in
pressure produced by topically applied N-methyl-D-aspartic acid (NMDA).
Experiments were performed in chloralose-anesthetized, paralyzed, and
artificially ventilated cats. NMDA administered on the intermediate area of
the ventral surface of the medulla decreased transnasal pressure and increased phrenic nerve activity. The response to
NMDA could be diminished or abolished by application to the ventral medullary surface of the NMDA antagonist
2-amino-5-phosphonovalerate (2-APV) or the local anesthetic lidocaine. Carotid sinus denervation and
posthypothalamic decerebration did not alter the nasal and phrenic nerve responses to NMDA; however, cervical
sympathetic denervation decreased these responses, both in intact and in bilaterally adrenalectomized animals. Therefore,
activation of NMDA receptors on structures near the ventral surface of the medulla increases tone in the nasal
vasculature and leads to a response pattern that includes changes in not only phrenic nerve activity and blood pressure
but also nasal patency.
Noradrenaline (NA) has been shown to influence astrocytic and vascular functions related to brain homeostasis
Journal of Cerebral Blood Flow & Metabolism (1997) 17, 894–904;
doi:10.1097/00004647-199708000-00008
Astroglial and Vascular Interactions of Noradrenaline Terminals
in the Rat Cerebral Cortex
Noradrenaline (NA) has been shown to influence astrocytic and vascular functions related
to brain homeostasis, metabolism, local blood flow, and blood-brain barrier permeability.
In the current study, we investigate the possible associations that exist between
NA-immunoreactive nerve terminals and astrocytes and intraparenchymal blood vessels
in the rat frontoparietal cortex, both at the light and electron microscopic levels. As a
second step, we sought to determine whether the NA innervation around intracortical
microvessels arises from peripheral or central structures by means of injections of
N-(2-chloroethyl-N-ethyl-2-bromobenzylamine) (DSP-4), a neurotoxin that specifically
destroys NA neurons from the locus ceruleus. At the light microscopic level, 6.8% of all
NA-immunoreactive nerve terminals in the frontoparietal cortex were associated with
vascular walls, and this perivascular noradrenergic input, together with that of the cerebral
cortex, almost completely disappeared after DSP-4 administration. When analyzed at the
ultrastructural level in control rats, NA terminals in the neuropil had a mean surface area
of 0.53 0.03 m2 and were rarely junctional (synaptic incidence close to 7%). Perivascular
terminals (located within a 3-m perimeter from the vessel basal lamina) counted at the
electron microscopic level represented 8.8% of the total NA terminals in the cortical tissue.
They were smaller (0.29 0.01 m2, P < 0.05) than their neuronal counterparts and were
located, on average, 1.34 0.08 m away from intracortical blood vessels, which consisted
mostly of capillaries (65%). None of the perivascular NA terminals engaged in junctional
contacts with surrounding neuronal or vascular elements. The primary targets of both
neuronal and perivascular NA nerve terminals consisted of dendrites, nerve terminals,
astrocytes, and axons, whereas in the immediate vicinity (0.25 m or less) of the
microvessels, astrocytic processes represented the major target. The results of the current
study show that penetrating arteries and intracortical microvessels receive a central NA
input, albeit parasynaptic in its interaction, originating from the locus ceruleus.
Particularly, they point to frequent appositions between both neuronal and perivascular
NA terminals and astroglial cells and their processes. Such NA neuronal-glial and
neuronal-glial-vascular associations could be of significance in the regulation of local
metabolic and vascular functions under normal and pathologic situations.
doi:10.1097/00004647-199708000-00008
Astroglial and Vascular Interactions of Noradrenaline Terminals
in the Rat Cerebral Cortex
Noradrenaline (NA) has been shown to influence astrocytic and vascular functions related
to brain homeostasis, metabolism, local blood flow, and blood-brain barrier permeability.
In the current study, we investigate the possible associations that exist between
NA-immunoreactive nerve terminals and astrocytes and intraparenchymal blood vessels
in the rat frontoparietal cortex, both at the light and electron microscopic levels. As a
second step, we sought to determine whether the NA innervation around intracortical
microvessels arises from peripheral or central structures by means of injections of
N-(2-chloroethyl-N-ethyl-2-bromobenzylamine) (DSP-4), a neurotoxin that specifically
destroys NA neurons from the locus ceruleus. At the light microscopic level, 6.8% of all
NA-immunoreactive nerve terminals in the frontoparietal cortex were associated with
vascular walls, and this perivascular noradrenergic input, together with that of the cerebral
cortex, almost completely disappeared after DSP-4 administration. When analyzed at the
ultrastructural level in control rats, NA terminals in the neuropil had a mean surface area
of 0.53 0.03 m2 and were rarely junctional (synaptic incidence close to 7%). Perivascular
terminals (located within a 3-m perimeter from the vessel basal lamina) counted at the
electron microscopic level represented 8.8% of the total NA terminals in the cortical tissue.
They were smaller (0.29 0.01 m2, P < 0.05) than their neuronal counterparts and were
located, on average, 1.34 0.08 m away from intracortical blood vessels, which consisted
mostly of capillaries (65%). None of the perivascular NA terminals engaged in junctional
contacts with surrounding neuronal or vascular elements. The primary targets of both
neuronal and perivascular NA nerve terminals consisted of dendrites, nerve terminals,
astrocytes, and axons, whereas in the immediate vicinity (0.25 m or less) of the
microvessels, astrocytic processes represented the major target. The results of the current
study show that penetrating arteries and intracortical microvessels receive a central NA
input, albeit parasynaptic in its interaction, originating from the locus ceruleus.
Particularly, they point to frequent appositions between both neuronal and perivascular
NA terminals and astroglial cells and their processes. Such NA neuronal-glial and
neuronal-glial-vascular associations could be of significance in the regulation of local
metabolic and vascular functions under normal and pathologic situations.
Subscribe to:
Posts (Atom)