Anecdotal accounts of lowered mental alertness, and loss of strong emotions abound in the oral history of ETS. For example, airline pilot and ETS patient "Britton Johnson" writes:
I have throughout my life always been gifted with a creative edge. From the time I was an infant I had a free flowing stream of creative thoughts and ideas. Sometimes this is in the form of witty insight other times the ability to grasp deep thought provoking ideas on the fly. If anything I may have entered the wrong career field even though I do like the challenges of flying and wouldn-t trade it for the world. I now feel that a part of the creative me has been lost and is dead. I feel certain emptiness now where there used to be an intensity that could rarely ever be diminished. The 'killer instinct' and 'flight or flight' impulses no doubt benefited me during my competitive years as a swimmer. I miss this part of me and am sad when I have to consciously think of what I am going to say without the 'instinct' kicking in. Music (something I have always loved dearly everything from rock to classical) has also become less rewarding. I feel this is partly due to the many distractions related to side effects but also a diminished response to the excitement and "feeling" that music used to bring to me. Yes I attribute these losses all to a "simple 30 minute procedure that will reduce sweating on the face and hands with very few side effects". Britton Johnson 2003It's not difficult to imagine ETS leading to lowered alertness. After ETS, catecholamines are low, there is a loss of sympathetic tone on the cerebral artery, and baroreflex is low. This means less blood to the brain, and less adrenaline in the blood that is there. But what about this subjective loss of strong emotions? Music less rewarding? Could it be?
Roz Carroll MA, is supervisor at Chiron Centre for Body Pshychotherapy. She has given a series of lectures, one entitled "The Autonomic Nervous System: Barometer of Emotional Intensity and Internal Conflict". Carrol presents the concept of "autonomic splitting", in which misdirected autonomic signals are blamed for a variety of psychological dysfunction. She gives a nice overview of the ANS role in psychophysiology, and is masterful at integrating information from various disciplines.
"I believe that the functioning . . . of the autonomic nervous system is fundamentally bound up with preserving the dynamic integrity of the self." Carroll2001Carrol's thesis offers strong theoretical support for a crucial role of the sympathetic nervous system in human emotion.
Brain Studies After Pure Autonomic Failure
A team of British scientists led by Hugo Critchley is interested in the role of the autonomic nervous system in human emotion, and have been doing very interesting studies on people with pure autonomic failure (PAF). Certain diseases can eat away at the autonomic nervous system, causing the gradual loss of more and more autonomic nerve function.As we might expect, the PAF patients reported feeling unemotional. "On statements designed to probe subjective emotional experience, there was a trend for PAF patients to rate themselves as feeling less emotional than controls". (Critchley et al. 2001) Later we will discuss if, and to what extent data on PAF patients might apply to ETS patients.
Normal and PAF subjects were asked to perform four different sets of tasks effortless exercise, effortful exercise, effortless arithmetic, and effortful arithmetic. The researchers took PET scans of their brains. When compared to controls, the PAF patients showed significantly less activity in the posterior cingulate and medial parietal lobe, while at the same time showed significantly greater activity in the anterior cingulate.
PET Scans Showing Differences in Brain Activity Between (a) PAF and (b) Controls During Interaction with Effort.
PAF patients do not have brain damage. They have damage to their autonomic nervous systems. What these PET scans show us then, is that loss of autonomic nerve function down in the effector organs somehow changes how the brain works. What is known about the function of these particular brain areas?(a) Significantly greater anterior cingulate activity (circled, peak x, y, z coordinates, 8, 10, 36, Z= 4.48, p <0.05, corrected for volume of regions predicted by the theoretical model to support second-order representations of bodily states, that is, cingulate, thalamus, superior colliculi) in PAF subjects compared to controls, mapped onto three consecutive axial sections of a standard template image derived from one subject. Vertical (z) coordinates are shown above each slice image.
(b) Significantly greater posterior cingulate/medial parietal lobe activity (circled, peak x, y, z coordinates, 56, 38, Z= 4.51, p <0.05, corrected for predicted regions) in controls relative to PAF subjects, mapped onto three consecutive axial sections of a standard template image derived from one subject.
Activity in the posterior cingulate is thought to prevent distractibility. "This function of the posterior cingulate cortex appears to entail an inhibition of parietal cortices, probably for preventing distractibility." (Small et al. 2003) Activity in the medial parietal lobe, on the left side, is associated with language receptiveness. So the PAF patients could be expected to be more distractible, and less receptive to language.
The anterior cingulate is known to be associated with autonomic responses. (see Bush et al. 2000). Could the increased activity in this area observed in PAF patients be a hyperactive response to the loss of input signals from effectors?
Obviously emotion-driven brain changes bring about body state changes. What Critchley and colleagues discovered is that the body state changes, in turn, feedback this information to various brain centers. Emotions are dependent upon body state changes. These scientists came right out and said so. The opening sentence in their report was:
Changes in bodily states, particularly those mediated by the autonomic nervous system, are crucial to ongoing emotional experience(Critchley et al. 2001, emphasis added)The British researchers had more questions, so the next year they did another study. This time they did classic fear conditioning on PAF patients and controls, and took pictures of their brains with Magnetic Resonance Imaging (MRI).
Classic fear conditioning is done by combining a painful sensation, such as an electric shock, with a neutral sensation, such as the sound of a tone. The subject becomes conditioned to fear the tone, even when the shock is not present. It has been shown from earlier rat studies that the brain organs amygdala and insula show greater electrical activity and characteristic electrical patterns after fear conditioning. (see Ledoux website).
So Critchley took MRI pictures of the patients' amygdalas and insulas before and after the fear conditioning, and showed that in humans, like rats, normal subjects would show increased activity of the amygdala after fear conditioning. The PAF patients, however, failed to develop the characteristic changes observed in control subjects. Again, we see that the brain-ANS interface is very much a "two-way street". The brain informs the ANS, but the ANS informs the brain also.
"Absent autonomic responsivity, and therefore blunting of arousal-related representations, is associated with attenuated conditioning-related activity in insula, amygdalae, and right anterior hippocampus." (Critchley, et al. 2002)Reduced Activity in PAF Patients Relative to Controls After Classic Fear Conditioning Reduced Activity in PAF patients, relative to controls, during conditioning to unmasked stimuli. The influence of autonomic arousal on conditioning was determined by random effects comparison of regional brain activity associated with positive conditioned stimulus versus negative conditioned stimulus in controls and PAF subjects who demonstrated behavioral conditioning. Significant differential activity between the groups is shown superimposed upon a normalized structural template image.
Pure Autonomic Failure vs. ETS
Bear in mind now that these brain studies were done on Pure Autonomic Failure patients, not ETS patients. PAF patients have a (more or less) complete loss of autonomic function, compared with the regional loss of sympathetic function in ETS. Still, recall Goldstein's neurocardiology work.Goldstein studies both PAF and ETS, and plots ETS patients just where we would expect - in the middle - more functional than PAF, but less functional than normal. It seems reasonable to think the changes in brain function documented by Critchley would follow the same pattern - that ETS would produce the same types of brain changes as seen in PAF, but to a lesser degree. Perhaps Dr. Critchley would like to study ETS patients, and we call on him to do so.
ETS as Psychosurgery
In consideration of Critchley then, and accepting the notion that his results are applicable to the corposcindosis model, two more predictions are made.
Empirical Status: Confirmed.
Empirical Status: Confirmed.
The empirical confirmation for the previous two predictions comes from Finland, where we find the Privatix psychiatric clinic. Founded by surgeon/psychiatrist Timo Telaranta, Privatix specializes in performing ETS surgery to treat psychiatric conditions such as anxiety and panic disorders. (Teleranta 2003)
Paivi Pohjavaara, a researcher at the University of Oulu, Finland, did a statistical analysis on 169 Telaranta patients who had undergone ETS surgery to treat psychiatric conditions from 1995-2000. Patients were given subjective questionnaires before, and then at various points in time after surgery (1 month, 6 months, 1 year, and annually after that). The questions were designed to quantify the patients' subjective experience of concepts such as "alertness", and "fear of observation". The changes produced by sympathectomy were derived by simply subtracting the "after" numbers from the "before" numbers.
The simple table conveys what has happened. These patients are less alert, less embarrassed, experience less fear, and less anxiety than they did before ETS. (see Pohjavaara 2004)Changes in Psychic Symptoms after ETS Changes in the psychic symptoms of social phobia presented as remainders of equation: (preoperative symptom severity) minus (postoperative symptom severity).
Los Angeles surgeon Farshad Malekmehr also offers ETS surgery for social phobia and anxiety. (Malekmehr website) His website presents a diagram which is instructive.
Whether intended or not, Malekmehr's diagram makes for a simple schematic representation of the concepts empirically explored by Critchley and the British team. "COGNITIVE SYMPTOMS" would occur in the brain, and "PHYSICAL SIGNS" would occur in the effectors. ETS would indeed "break the cycle", interrupting not only the brain signals to effectors, but also the (now diminished or non-existent) feedback information from effectors back to the brain.Cycle of Social Phobia
In December 2006, Bracha et al. have published a paper whose title makes a very insightful analogy:
"A surgical treatment for anxiety-triggered palmar hyperhidrosis is not unlike treating tearfulness in major depression by severing the nerves to the lacrimal glands."Bracha's analogy is harshly critical of ETS, to be sure, but does not go far enough. It would be a better analogy if severing the nerves to the lacrimal glands also affected a dozen other body systems. Still, the authors sound alarm bells:
"Referring an anxious patient with palmar hyperhidrosis to surgery without first completing a proper trial of psychotropic medication may constitute malpractice especially if the patient experiences some of the more severe surgical complications which can occur during sympathectomy" (Bracha et al. 2006 emphasis added)
