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Any advertising above for ETS or ESB is NOT accepted by us as we are AGAINST ETS/ESB because of the side effects
I've had many questions about how the body is affected by ETS surgery and Reversal surgery. I will try and help you out by providing some basic information on the Sympathetic Nervous System and how it works. Forgive me, i'm not a scientist!
The spinal cord is divided into five sections: the cervical, thoracic, lumbar, sacral, and coccygeal regions.
The diagram below illustrates the connections between the major skeletal muscle groups and each level of the spinal cord. A similar organization exists for the spinal control of the internal organs.
In addition to the control of voluntary movement, the central nervous system contains the sympathetic and parasympathetic pathways that control the "fight or flight" response to danger and regulation of bodily functions - the involutary movements. These include hormone release (such as Cortisols), the release of insulin and glucagon in sugar control of the blood, movement of food through the stomach and intestines, and the sensations from and muscular control to all internal organs. These informational pulses executed in our nervous system allow us to do our daily functions. The processing of this information is done in the CNS, the brain, a highly developed mass of nerve cells. See towards the end for more explanation under Neurotransmission.
The sympathetic nervous system is located to the sympathetic chain, which connects to skin, blood vessels and organs in the body cavity. The sympathetic chain is located on both sides of the spine and consists of ganglias.
Here is a diagram that illustrates these pathways and the level of the spinal cord projecting to each organ.
thank you to the Christopher Reeve foundation webpage for these images
The sympathetic and the parasympathetic nervous system are parts of what is commonly called the autonomic nervous system. (Autonomic = can not be controlled by the mind). You can say that these systems work in balance with each other and directly or indirectly affect almost every structure in the body (e.g. heartfrequence, heartcapacity, lumbar function, kidneys, blood vessels, stomach and intestines). The sympathetic nervous system has an active "pushing" function, the parasympathetic has mainly a relaxing function.
The sympathetic and parasympatheic pathways control the gastrointestinal, reproductive, cardiovascular, respitory, and all sensory nerves of the body. For example, the T3 location directly affects sweat glands above the nipples, the heart, blood vessels and the respiratory system bronchi. The T4 location does the same, without affecting the sweat glands above the nipples. The T5 location is connected to the Celiac Ganglion, which controls the stomach's pylorus, adrenal medulla, kidneys, intestines, and anal sphincter. The surgeons state they don't "directly control these functions so they are not affected", but the entire system is connected. Every signal in the system is passed through, so clipping one area of the nerve ganglion affects every signal throughout the entire system. For example, by cutting T2, T1 is unable to send messages to the other levels because of the downward flow. Therefore, T1 is unable to function (which is incharge of blood pressure and heart rate increase). Each location (T1, T2, T3...) continually communicates back and forth (I know this has something to do with the fact that T1 to T12 has both a white and grey rami...but I don't enough about this yet). There is an incredible overlap within the sympathetic nervous system and these organs will continue to function, but these overlapped nerves become extremely sensitized in a process called "...denervaton supersensitivity of sympathetic organs"(see in denervation sensitivity paragraph for more detail). In essence, the remaining skin signal nerves become extremely sensitized to any stimulation (heat, cold, sweat, etc.), due to the loss of the cut or clipped nerves, and this is why people are having such severe problems with adjusting to changes in heat or physical exercise. This sensitivity decreases slowly with time (1-4 years), but it never returns back to normal - it will always stay sensitive to about 140% of the original state - 80 degree weather now feels like 112 degree weather to the brain.
When the environmental temperature is raised on a hot summers day, the increased temperature initiates several automatic responses from the Sympathetic Nervous System. Thermal receptors convey stimuli to sympathetic control centers of the brain from which inhibitory messages travel along the sympathetic nerves to the blood vessels of the skin resulting in dilatation of the cutaneous blood vessels, thereby greatly increasing the flow of blood to the surface of the body from where heat is lost by radiation from the surface of the body. Dilatation of the blood vessels in this way tends to lower the blood pressure and to promote oozing or transudation of the fluid from the capillaries, which may result in swelling of the dependent limbs. Therefore, fine adjustments in sympathetic control of vascular contraction and "tone" are required to prevent excessive vascular dilatation and undue reduction in blood pressure. Otherwise, this might result in severe gravitational pooling of blood in the lower limbs thereby reducing blood flow to the brain and causing fainting spells, to which individuals with impaired sympathetic nervous functions are very susceptible. The sympathetic nervous system responds to environmental heat in another important way. The rise in body temperature is sensed by the hypothalamic center from which stimuli emanate via sympathetic nerves to the sweat glands, resulting in appropriate sweating. This serves to cool the body by the loss of heat resulting from evaporation of the sweat, aided by a cool breeze. The only really voluntary input that we have to facilitate cooling in a warm environment is to get into a pool, a cold shower, or an air-conditioned room. We cannot voluntarily influence the dilatation of our blood vessels or the adequacy of our sweating in response to heat in other ways.
As mentioned there is a physiological process called "Tone" or "Sympathetic Tone", which is the manner in which the nervous system decides to essentially send signals at it's baseline, where functions of the body are at a normal limit. If a stimulous (such as warm weather) acts on the skin nerves of the body, the nervous system knows, based on the "normal tone", that this weather is warmer than usual, and tells the skin's sweat glands to begin sweating. It's the same thing as a household thermostat - based on knowing the temperature of the house and the temperature setting in which you want the house to stay, the device knows to either turn on the air conditioning (sweat for the body) or turn on the heat (constrict blood vessels and conserve heat within the body to raise body temperature). For the body, the temperature control centre (essentially the thermostat) is located in the hypothalmus of the brain. The main fuction of the hypothalmus is homeostasis, or maintaining the body's status quo. Factors such as blood pressure, body temperature, fluid and electrolyte balance and body weight, are held to a precise value called the set-point. It continually monitors temperature readings from the body by nerve signals passing from temperature nerves on the skin to the brain. These temperature sensors travel through the T2/T3 locations of the sympathetic nervous system before reaching the hypothalmus. The T2 location specifically is the centre for the "Sympathetic Tone" for the bodies temperature. The T3 location also plays a secondary role in this Tone, but the T2 location is the primary focal point. (It has to be pointed out that Dr Lin, Dr Telaranta and Dr Reisfeld now realise this, and by using the Lin-Telaranta classification they lower the clamping to T4 or below to avoid this phenomenon - see Lin's site for verification). This is the reason why people who had the T2 and T3 sympathectomies are having so many problems. Once the T2/T3 locations are cut/clamped from access by the hypothalmus of the brain, the brain can no longer disinguish what the "Tone" for the bodies temperature is. What the body used to know as 80 degrees felt like it is no longer valid, because the brain has no reference point. Using the thermostat example: if the thermostat couldn't read what the house temperature was, now would it know to either turn on the heat or air conditioning? Not only that, if it decided to turn on the heat, how would it know to stop? It wouldn't, it would remain on until the user turned off the device. This is exactly what the body is feeling when the T2/T3 locations are lost. It has no reference. However, the brain and body knows how to survive.
For the body to survive and function properly, the body needs to stay around 98.6 degrees. In defence to the sudden loss of the "Sympathetic Tone", the body responds by turning on the cooling mechanisms. This is where the CS problems arise, because the body no longer knows where to "turn off" the sweating! What does 98.6 degrees feel like now? It no longer knows, so it just leaves on the "air conditioning" and hopes the body will survive. The body decides to put itself into full body sweats (where it can, below the nipples...) and to dilate (open up) the skin's blood vessels to release heat from the bloodstream. This is why people are having the problems with hot skin, because the blood vessels remain dilated inevitably and the hypothalmus doesn't know when to turn itself off. Only when the body temperature drops dramatically (by sitting in cold baths and air-conditioning) does the body decide it's time to shut off the cooling mechanisms of the body by a process called "Intrinsic tone" - where the skin itself knows its limits and overrides the signals from the brain. It decides to stop the dilating of the blood vessels and sweating under extreme cases as a "self-protector" to protect the life of the skins cells. (thanks to Koeglerp for this info from the BFS forum)
INNERVATION OF THE HEART
The strength and frequency of the heart beat is controlled by the autonomic nervous system. Both parasympathetic and sympathetic parts of the autonomic nervous system are involved in the control of the heart.
The sympathetic fibers arise from segments T2-T4 of the spinal cord and are distributed through the middle cervical and cervico-thoracic (or stellate) ganglia and the first four ganglia of the thoracic sympathetic chain. The sympathetic fibers pass into the cardiac plexus and from there to the SA node and the cardiac muscle. The effect of the sympathetic nerves at the SA node is an increase in heart rate. The effect on the muscle is an increase in rise of pressure within the ventricle, thus increasing stroke volume.
The vagus provides the parasympathetic control to the heart. The effect of the vagus at the SA node is the opposite of the sympathetic nerves, it decreases the heart rate. It also decreases the excitability of the junctional tissue around the AV node and this results in slower transmission. Strong vagal stimulation here may produce AV block.
My theory is that if the heart rate can be increased to raise blood pressure so we don't feel so faint, vague and therefore feel better. I have checked out a site, which is about people who have side effects similar to ours (feel faint or have fatigue and pain.) Some patients take salt tablets and water to raise blood pressure and volume. There are no blood pressure lowering medications at the moment in Australia. Their internet address is: http://www.potsplace.com/what_helps.htm.
REGULATION OF INTERNAL BODY TEMPERATURE AFTER CUTTING THE SPINAL CORD
After cutting the spinal cord in the neck above the sympathetic outflow from the chord, regulation of body temperature becomes extremely poor because the hypothalmus can no longer control either skin blood flow or the degree of sweating anywhere in the body. This is true even though the local temperature reflexes originating in the skin, spinal cord, and intra-abdominal receptors still exist. These reflexes are extremely weak in comparison with hypothalmic control of body temperature. In people with this condition, body temperature must be regulated principally by the patient's psychic response to cold and hot sensations in the head region - that is, by behavioural control of clothing and by moving into an appropriate warm and cold environment.(reference to be added later)
EFFECTS OF SYMPATHETIC & PARASYMPATHETIC STIMULATION ON ETS PATIENTS
Many patients have suffered from light sensitivity since ETS/ESB. I have often wondered why I am sensitive towards the light now. In fact, sympathetic stimulation contracts the meridional fibers of the iris that dilates the pupil, whereas parasympathetic stimulation contracts the circular muscle of the iris to constrict the pupil. The parasympathetics that control the pupil are reflexly stimulated when excess light enters the eyes; this reflex reduces the pupillary opening and decreases the amount of light that strikes the retina. So this is why we are always squinting now!
Sympathetic stimulation also has multiple metabolic effects such as release of glucose from the liver, increase in blood glucose concentration, increase in glycogenolysis in both liver and muscle, increase in skeletal muscle strength, increase in basal metabolic rate, and increase in MENTAL ACTIVITY. Yes (apparantly) there is no affect on physical performance and mental activity (according to the ETS experts). (reference to be added later)
DENERVATION SUPERSENSITIVITY OF SYMPATHETIC AND PARASYMPATHETIC ORGANS AFTER DENERVATION
During the first week or so after a sympathetic or parasympathetic nerve is destroyed, the innervated organ becomes more sensitive to injected norepinephrine or acetylchoine, respectively. This effect, seen in a test, shows the blood flow in the forearm before removal of the sympathetics to be about 200 ml/min, a test dose of norepinephrine causes only a slight depression in flow. Then the stellate ganglian is removed, and normal sympathetic tone is lost. At first, the blood flow rises markedly because of the lost vascular tone, but over a period of days to weeks the blood flow returns to almost normal because of progressive increase in intrinsic tone of the vascular musculaure itself, thus compensating for the loss of sympathetic tone. Then, another test dose of norepinephrine is administered, and the blood flow decreases much more than before, demonstrating that the blood vessels have become about 2 to 4 times as responsive to norepinephrine as previously. This phenomena is called 'denervation supersensitivity'. It occurs in both sympathetic and parasympathetic organs, but to a far greater extent in some organs than in others, occasionally increasing the response more than 10-fold. (reference to be added later)
PHARMACOLOGY OF THE AUTONOMIC NERVOUS SYSTEM. DRUGS THAT ACT ON ADRENERGIC EFFECTOR ORGANS - THE SYMPATHOMIMETIC DRUGS
Many ETS/ESB patients have suffered badly from fatigue. I've often been looking out for different types of medication that might help us, but is not addictive. Read on:
Intravenous injection of norepinephrine causes essentially the same effects throughout the body as sympathetic stimulation. Therefore, norepinephrine (American term is adrenaline or noradrenaline) is called a sympathomimetic or adrenergic drug. Epinephrine and methoxamine are also sympathomimetic drugs, and there are many others. They differ from one another in the degree to which they stimulate different sympathetic effector organs and in their duration of action. Norepinephrine and Epinephrine have actions as short as 1 to 2 minutes, whereas the actions of other commonly used sympathomimetic drugs last for 30 minutes to 2 hours. So what are these drugs? Important drugs that stimulate specific adenergic receptors but not the others are 'phenylephrine'- alpha receptors (An example is 'sudafed', which is a cough medicine available freely over the counter in Australia. It's not even stocked in Norway, but may be available in England and posted over), 'isoproterenol' - beta receptors, and 'albuterol' - only beta2 receptors (ventalin and caffeine are good examples of this, as they have an effect on the smooth muscle and a dialating effect on the bronchi). (reference to be added later)
THE ENDOCRINE SYSTEM AND THE AUTONOMIC SYSTEM WORKING TOGETHER
The 'endocrine system' regulates metabolic activities in certain organs and tissues of the body, thereby helping to bring about homeostatis. The autonomic nervous system regulates certain organ and tissues via impulses that cause release of neurotransmitter substances, which produce rapid responses in the tissues affected. The endocrine system, on the other hand, produces a slow and diffused effect via chemical substances called 'hormones', which are released into the blood-stream to influence target cells at remote sites. Although the nervous and endocrine system function in different ways, the two interact to modulate and coordinate the metabolic activities of the body.
Secretion of nearly all the hormones produced by the pituatory gland is controlled by either hormonal or nerve signals from the hypothalmus. It is interesting to note that in addition to controlling the pituatory, the hypothalmus also receives input from various areas of the CNS, including controls form the autonomic system; therefore, it is the brain centre for the maintenance of homeostatis.
A lack of the thyroid hormone can have a very negative impact on the body. If you have a severe lack of thyroid it can lead to Hypothyroidism. Symptoms include fatigue, extreme somnalance with sleeping up to 14 hours a day, extreme muscular sluggishness, slowed heart rate, decreased cardiac output, decreased blood volume, sometimes increased body weight, constipation, mental sluggishness, failure of many trophic functions of the body evidenced by depressed growth of hair and scaliness of skin and decreased libido. This sound like the effects of ETS! I've spoken to a general practioner and she is not sure of the link, but this still needs investigating. (reference to be added later)
NEUROTRANSMISSION AND HOW IT'S AFFECTED BY ETS
As mentioned before informational pulses executed in our nervous system allow us to do our daily functions. The processing of this information is done in the CNS, the brain, or in other parts of the body, such as the ANS. This process of Neurotransmission allow neurons to receive, process and send Chemical "Messages". These chemicals or neurotransmitters are released by up-take sites or nerve cells (such as the Adrenergic receptors found in the sympathetic system) .There are perhaps 100 or so different neurotransmitter varieties in the brain. There are also a number of different neurotransmitters found in sympathetic nerves in the Autonomic Nervous System. Each neurotransmitter plays some role in most behaviors, but often we identify a key behavior with each neurotransmitter. For e.g. 5-HT or Serotonin is a transmitter involved in sleep, mood and arousal. 5-HT is also normally involved in temperature regulation and sensory perception. This is not surprising when you realise that MDMA (ecstasy) releases large amounts of serotonin affecting temperature control (the user can become dehydrated and their brains can 'fry'- leading to death) and also affects their arousal levels. However, 5-HT plays a major role in emotional disorders such as depression, suicide, impulsive behavior, and aggression. It is particularly linked to Obsessive Compulsive Disorder. This disorder is effectively treated by serotonin reuptake inhibitors (to release more 5-HT), suggesting that this condition may be due to dysregulation in serotonin synapses (not enough chemical in the up-take site). Basically they are theorising that sufferers may not naturally have enough serotonin. I disagree with this though. I believe that this condition is borne out of fear, not out of naturally having too much of one chemical because you were born that way. The patient has learned to fear germs, being harmed etc. and their nervous system has learned to react with fear every time they confront what they want to resist. The SNS raises the heart-rate, the blood pressure and the neurons send the chemical messages, through the process of neurotransmission, to release chemicals, but not 5-HT. If you are anxious you will not release this feel-good chemical. This is why I believe most illness is psychosomatic. We can literally kill ourselves from worry or emotional pain. This is why the Lin-Telaranta classification claims to cure psychotic illness, such as schizophrenia; anxiety disorders, such as obsessive compulsive disorder and anorexia nervosa; phobias and shyness. All of these apparently stop because the fear is 'clamped'. They don't feel the fear that drives these illnesses and causes the release of all those chemicals causing anxiety and deep emotional pain. Too little chemical release can also make us ill. For e.g. serotonin has the fundamental role in placticity of the central nervous system. In addition to normal nervous system development, changes in 5-HT mediated responses have been identified following injury to the brain or as a consequence of neurochemical-induced lesions of this transmitter system. 5-HT has also been indentified as important in age-related changes in central nervous system function. Receptor binding studies have revealed significant decreases in the number of 5-HT binding sites with age in the brain regions involved with cognitive processes, such as the cortex and hippocampus. However, Dr T.T has found by SPECT scan that ETS patients show more serotonin than average. Madonna (another ETS patient) has also done a great deal of research in this area and has found evidence, through her reading, as well. We infact have more feel-good chemicals being released than the normal person, probably because our we are not releasing other chemicals that cause anxiety and energy and so we are releasing more 5-HT. But this is not good. It leads to an inbalance of chemicals. It can lead to illness like Serotonin Syndrome, where you can actually get depressed because serotonin becomes the major antagonist and there is no adrenaline being released to balance it out.
Another mood-altering chemical is norepinephrine (NA), which essentially has the same effect as sympathetic stimulation - it accelerates the heart rate and speeds up metabolism. Norepinephrine is the principal neurotransmitter of sympathetic postganglionic endings. Both norepinephrine and the methylated derivative, epinephrine are stored in synaptic knobs of neurons that secrete it, however, epinephrine is not a mediator at postganglionic sympathetic endings. Epinephrine (adrenaline)is a hormone secreted by the adrenal medulla, is released into the bloodstream in response to physical or mental stress, and is a vasoconstrictor that increases heart rate and blood pressure. Adenosine triphosphate (ATP) is a purine and is known as an excitatory neurotransmitter. ATP, a source of metabolic energy and a neurotransmitter substance acting on neuronal receptors is released in high concentrations from nerve terminals synaptically. All these chemicals are released at sympathetic sites.
Many ETS patients claim to have decreased sex drive, depression and cognitive delay. It is no wonder when you think about how our neuronal pathway is blocked because of ETS. It has essentially decreased all these neurotransmitters. I don't care what the doctors say on that one. It's a fact.
Dr Lin has mentioned in one email to a patient that "A very important concept [is], neuro-transmitters play the most important role in reconstructive surgery. Anatomic restoration plays less role in it." He obviously is referring to the fact that neurotransmission is important because of the release of chemicals which affect thermoregulation, energy and mood. The ability for this to work is more important than to be anatomically exactly like we were pre-ETS.
To be able to detect neurotransmission and the repair of ganglia in a Reversal patient has been an issue. Measurement of activity of the sympathetic nervous system may be done by PET scan. PET scan or Positron Emission Tomography is an advanced form of an X-ray. It can be used to detect radioactive substances in the body. If small amounts of the radioactive drug fluorodopamine are injected into patients, which is very similar to the chemicals found in the sympathetic nervous system, it can attach to sympathetic nerve endings and allow researchers to view them with the aid of a PET scan. I have to investigate this further though. See www.clinicalstudies.info.nih.gov/detail/A_1994-N-0186.html.
Therefore, based on the points i've brought up, essentially the brain and the sympathetic nervous system work together. The CNS as well as the ANS contain nerves or sites that release neurotransmitters. ETS blocks the release of these chemicals and can affect us mentally and physically. No wonder ETS patients are tired when sympathetic nerves are no longer releasing as many of these chemicals (even though scientist say our body adjusts for the lack of sympathetic pressure by producing more chemicals) for energy.
LACK OF STRESS AND WHAT IT DOES TO OUR BODY
Acute stress actually improves our brain's attention and increases our capacity to store important and life-protecting information. But what happens when the body cannot mount an adequate response to an acute stress? Clearly, many of the good things that stress hormones do will not occur, like enhancing memory, replenishing energy reserves or moving immune cells to where they are needed. Which probably explains why i'm not as 'bright' as I used to be. One other consequence, seen most clearly in the immune system, is that systems that are normally "contained" by cortisol become hyperactive. In the immune system, we find inflammatory agents (cytokines) and self-generated responses ("autoimmune") are no longer contained by circulating cortisol. As a result, disorders like arthritis and autoimmune diseases, for example, lupus, become worse. One treatment for such disorders, as we will discuss later on, is to treat the patient with cortisone or another glucocorticoid steroid.
People with long-term histories of persistent and relatively small elevations or deficiencies in stress hormone levels may show accelerated progress toward pathophysiology and disease. In the case of excess hormone production, these disorders include atherosclerosis, obesity, type 2 diabetes and cognitive impairment. For relative hormone insufficiency, the pathophysiology includes autoimmune and inflammatory disorders, chronic pain and chronic fatigue.
In the case of relative hormone deficiency, there are experimental programs to treat with low dose glucocorticoids in the case of chronic fatigue syndrome and chronic pain but these have had mixed results. Admittedly, the medical community is still not certain how to treat these conditions.
Now, we even know that stress can sometimes cause us problems by making us react too little. As noted above, underarousal (insufficient allostatic response) to a stressor is potentially as damaging to the body as prolonged arousal.
Interestingly, some people with infectious episodes go on to develop the Chronic Fatigue Syndrome (CFS) which is often characterized by intermittent feverishness and malaise like that occurring with an infection, even though the person has no infection. It appears that this is a disorder where an inappropriate "allostatic" response is being made and this includes an insufficiency of the production of stress mediators like cortisol. Treatment will likely center on how to make the allostatic responses mounted by the CFS patient more appropriate. As we have already noted, this may include giving low dose cortisol treatment to supplement what the body produces.
Cortisol is also known as hydrocortisone. I think it may be a steroid. It comes in various forms including creams. I'd be wary of this though, with all of it's side-effects.
WHAT HAPPENS WHEN A NERVE IS CLAMPED?
When the clamps are applied to the nerves, considerable pressure is applied between the two ends of the clamps to the nervous tissue. This pressure prevents nerve signals from passing through the tissue, due to the blocking of calcium/potassium/sodium channels which nerves use to transmit electricity. This pressure over time (possibly only a day or two) will destroy the nerve cells and leave a dead patch of scar tissue beneath the clamps. In order for the nerve cells to survive, a constant flow of fresh blood is required (as is ever other cell in our bodies). The pressure from the clamps prevents any blood flow from getting to th enerve cells to maintain the life of the cells.
If the clamps are removed, according to Dr Telaranta and Dr Reisfeld there is a chance to go back to the original state (it's a true reversal). However, it has to be remembered, that a Reversal after the nerve has been cut can not be a true reversal to the original situation, they only are alleviations of the bad side effects and restoration of some sweating and thermoregulation.
WHAT HAPPENS IN A REVERSAL?
1.Excision of the scar around the nerves and a neurolysis around the healthy nerve ends. This gives immediate, considerable relief in the compensatory reflexive hyperhidrosis by stopping the harmful neuropathic (badly functioning) feedback hypersensitivity*.
2.Reconstruction of the neural connectivity between intact nerve ends by microsurgical nerve grafting technique. The best suitable donor for this purpose is the sural nerve from the ankle and calf region. The resulting residual numbness on the lateral side of the foot is negligible and normally causes no significant distress. The procedure adds to the possibility of positive thermoregulatory feedback between the lower sympathetic chain and the midbrain ganglia**(where the hypothalmus (temperature control) is located). This result is also partly immediate, but most of it is due to regeneration of the neurons by axoplasm migration* along the grafted nerve so a full-blown recovery can take more than a year.
* Axoplasm migration is not the same as axonal migration, though very near it: axoplasm migration happens when there are axonal nerve sheaths intact and the cytoplasm, which in the neural cells is called axoplasm, slowly fills the empty axonal sheaths. The axonal migration means cut nerve ends, which contain thousands of cut axons, which then grow in many directions to find some recipient nerve end and to then grow along. If there is none found, then the axonal migration form into a bundle, or glomus, agglomerate forming a neurome, which has no positive function but may cause neuropathic hypersensivity.
** The mid-brain ganglia are located up, around and in thalamus, mainly superiorly to hypothalamus. There are many of bassal nuclei: globus pallidum, nucleus caudatus, putamen, amygdala, corpus callosum, Hippocampus, nucleus lentiformis, corpus geniculatum, Pulvinar, substantia nigra, striatum, reticular formation etc. Each of these work together in highly delicate network fashion, and it seems that the changes in sympathetic tone as well as parasympathetic tone intricate influence them. Their malfunction is noticeable in Parkinson's disease (substantia nigra), in Alzheimer's disease, in sleep disorders, in epilepsy, in psychotic, neurotic, depressive and phobic states.
(this was quoted from Dr Telaranta)
CAN WE SCIENTIFICALLY DETERMINE IF THE REVERSAL WORKS OVER TIME?
"Finding out about nerve regeneration is usually most reliably achieved through demonstrated return of function. In the case of something like the nerves to a muscle, or to skin sense receptors, the return of function is usually easy to quantify. It is also possible to record electrical signs of active nerves, and those in the limbs are amenable to such recording with minimal invasion.
Assessment of sympathetic activity is difficult at best, but to demonstrate regenerated function would be quite difficult I think. (I say I think as I have no experience in trying to so this.) Recording electrical signals (or lack thereof) is theoretically possible, but only through quite invasive techniques in the case of something like the sympathetic chain. Electron microscopy could give some indication of anatomical outcomes, but this would be extremely invasive, as part of the graft would have to be removed for histological processing - the electron microscope cannot be used to observe living tissue, not even tissue removed from the body. So you might consider arranging for a post-mortem microscropic study of your grafts (or those of other interested people), but I don't think you should think about it until then.
A further complication of microscopic studies is that the presence of anatomically normal neuron processes within the graft could not be taken as evidence that those processes were functional. Many studies have shown that peripheral nerve grafts, such as the sural nerve, implanted into the central nervous system will cause sprouting of central neurons leading to "normal" peripheral nerve structure. But the same sorts of studies have shown little evidence for functional connections of the processes which grown through the grafts with other neurons. Use of these peripheral nerve implants as bridges to bypass injured parts of the spinal cord remain of considerable interest, because of the "innervation" of the bridges that occurs, but there is little evidence that any restoration of function results from the neuron processes reaching the other end of the graft. The problem of provoking functional connections remains the big challenge.
So overall I think the most valuable answer to your question about whether there has been regeneration is one that you can answer: whether the negative side-effects of the orginal surgery have been alleviated by the grafting.