THE WEB SITE: CRACKING THE CODE OF PTSD
Fresh clinical evidence telling us about the nature of PTSD.
How to set about treating PTSD rationally.
Dr Bob Tym, Clinical Psychiatrist, formerly an Assistant Professor of Neurosurgery — now retired from active clinical practice.
Extracts of the book of this title, waiting to be published.
THERE IS CONSIDERABLE CLINICAL CONFUSION AFFECTING ANY RATIONAL DIAGNOSIS AND TREATMENT OF “PTSD” RESULTING FROM TERMINOLOGY GIVEN ELSEWHERE INVOLVING “PTSD and C-PTSD”. THAT TERMINOLOGY AND THOSE CRITERIA ARE CONTRADICTED BY THE FRESH CLINICAL EVIDENCE GIVEN HERE, FRESH CLINICAL EVIDENCE THAT ANYONE CAN TEST.
The book tells of a long drawn out exploratory investigation into some long-ignored obscure clinical phenomena: some unexplained visual symptoms. Surprisingly, the new findings throw light on the nature of PTSD: clinical evidence for what PTSD is, and for what goes wrong inside the brain in response to sudden and severe mental stress. e. Yes, the evidence says there are two different PTSDs – superficially very similar clinically; neuro-biologically very different. One PTSD has unique and subtle clinical features; it cannot resolve on its own, it appears to be caused by an acute stress-induced epigenetic insertion into the brain — given the clinical evidence, geneticists consider no other explanation to be as plausible. The other PTSD has no unique clinical features and it can resolve on its own, but it not always does. The two PTSD’s require very different treatments: there is a simple visual test to distinguish them. In 2009 a scientific paper was written, peer reviewed and published in the international literature*. but mostly unnoticed. Everyday people with PTSD and mental health workers alike can easily understand the new evidence, can confirm it for themselves and put it to good use clinically for themselves and others.
- Tym, B., Beaumont, P., Lioulios, T. Two Persisting Pathophysiological Visual Phenomena following Psychological Trauma and their Elimination with Rapid Eye Movements: A Possible Refinement of Construct PTSD and Its Visual State Marker. Traumatology. 15(3): 22-33 (2009). ]
PTSD had always been a mystery: What exactly is PTSD? What goes wrong in the brain? Why can some people recover and not others? Why is it so severe for some people that they prefer to die rather than put up with it, and for others it is far less troublesome? Why do certain treatments work for some people and not for other people? Why are some people more likely to get PTSD than others? What more can be done about it?
Exploratory clinical investigations can take a long time. This clinical investigation started in 1977, three years before Traumatic Neurosis, as it was called then, re-named to PTSD in 1980. The investigation lasted over thirty years, and involved briefly examining the vision of 9000 or so psychiatric clients over those thirty years.
At the present time the descriptions of PTSD and C-PTSD make kittle clinical sense in the light of this new clinical evidence
PTSD has turned out to be a lot more complicated than it has been thought to be. The new evidence goes a long way to explain what PTSD is and what can best be done about it. Complicated issues cannot be explained simply, cannot be fitted into quick sound bites.
This website attempt to explain the gist of it all in the simplified Sections One to Five .
At any stage the reader can skip from one Section to any other Section. Each Section has to give a lot of detail because the detail has to be given somewhere. Section One describes the final results, ‘what PTSD is’, in simple-as-possible terms for the everyday person to understand, but without giving all the complicated clinical evidence for ‘what PTD is’ in that section. All the complicated detail of the evidence is given in other sections.
What is written has to be at odds with the “official” versions of “PTSD” in the American Psychiatric Association Diagnostic and Statistical Manual (DSM) and the WHO’s International Classification of Diseases. (ICD). Their ad hoc clinical criteria were not intended to describe the biological nature of PTSD, just criteria needed for their administratively useful classifications of disorders.
SECTION ONE. What the clinical evidence and its implications have told us.
There are two forms of PTSD. There is a PTSD-A and a PTSD-B (so called C-PTSD does not clinically fit any categorical, clear-cut, clinical entity) . Both PTSD-A and PTSD-B are different and distinct disorders, each having been caused by experiencing a frightening event. The two different disorders look very much alike superficially, but they are not alike neuro-biologically. Since they look very much alike clinically, and no one knew about the biological difference, it had always been assumed there was only one disorder, so the two have always been getting mixed up. (As already noted, the clinical criteria for a “PTSD and a C-PTSD”do not describe two clinically distinct disorders.)
It is the trauma induced anxiety disorder PTSD-A that is very complicated. In PTSD-A something ‘physical’ had gone wrong inside the brain. The anxiety disorder PTSD-B is like any other Anxiety Disorder, with nothing ‘physical’ having gone wrong inside the brain.
PTSD-A is caused by a sudden and unexpected surge of high anxiety (fear), a sudden ‘mental shock’. Obviously, not everyone who has experienced a sudden surge of high anxiety, a sudden ‘mental ‘shock’ has a PTSD-A, just some unfortunate people have.. (Anxiety in one form or another can cause many different forms of damage to the physical workings of the body in ways we do not understand.)
PTSD-A has two invariant (meaning they are always there in PTSD-A) abnormal symptoms that are subtle (meaning not always obvious or noticed) and unique (meaning they are not found in any other mental or physical disorder). They are inseparable symptoms: PTSD-A comes during the moment of the “mental shock” causing the PTSD-A and the two symptoms are there together from the outset. As PTSD-A is cured the the two symptoms go together.
The first of the two invariant abnormal symptoms is a subtle but abnormal visual symptom. It is called ‘persistent peripheral oscillopsia‘ (osi-lop-sia, is a Greek word for ‘wavy vision’). Persistent peripheral oscillopsia’ is described in Section Two, just below.
The second of the two invariant abnormal symptoms is usually more obvious: a constantly recurring abnormal form of memory-recall, an abnormal reliving, re-experiencing, of what had been experienced during the moment of the frightening event that had caused PTSD-A This is described in detail in Section Three.
Both of these abnormal symptoms are directly caused by that ‘something physical’ that went wrong in the brain, triggered by the sudden surge of high anxiety. The most plausible explanation for that ‘something physical that went wrong in the brain, and how it give rise to the two symptoms, is explained in Section Five.
PTSD-A can occurs in people of any age over five or six years, people from all walks of life. For some people with PTSD-A it was caused by the experience of an event that would terrify anyone, and for some people, by experiencing an event that frightened them but probably would not have frightened anyone else. For most people with PTSD-A the event that they experienced was somewhere between those two extremes. The susceptibility of people to getting PTSD-A varies widely. The severity of PTSD-A varies widely.
Both anxiety disorders PTSD-A and PTSD-B can have the same ‘ordinary’ anxiety symptoms. The anxiety symptoms vary widely in number and severity from person to person in both disorders (which is why the two different disorders so often look so alike clinically):
There can be distressing traumatic memories that keep coming back distressingly, but they are memories that are not coming back abnormally, just distressingly in normal form. There can be sleeplessness, frightening nightmares of the event or of anything else (these nightmares are not limited to PTSD-A), jumpiness over anything, being easily startled, being inattentive, lacking in concentration, failing to remember things, tension headaches, emotional withdrawal, frustrations, depressed moods, uncontrollable anger and sometimes violence, and avoidance of any reminders of the event that caused their PTSD. There can be dangerous thoughts of suicide.
The presence or absence of PTSD-A can be specifically, sensitively and reliably diagnosed clinically by a simple visual test.
The test detects the presence or the absence of ‘persistent peripheral oscillopsia’. Because ‘persistent peripheral oscillopsia’ only occurs in PTSD-A, the simple Visual Test detects the presence or absence of PTSD-A in anyone over five or six years old. It is a simple test that can be performed by anyone on anyone who is over five or six years old. The test is sensitive, reliable and specific for the presence or absence of PTSD-A despite the possible presence or absence of any other mental disorder. If that test is ‘positive’ before PTSD-A is treated, and negative after PTSD-A has been treated, then PTSD-A has been permanently cured. (A description of the visual symptom and the simple test for it are in Section Three.)
Treatment of PTSD-A
PTSD-A cannot get better on its own over time, it requires very special treatment, e.g., properly performed EMDR. If EMDR treatment is not successful, and sadly it cannot be successful for everyone with PTSD-A, then PTSD-A lasts life long unless successfully treated by something else. EMDR is explained and explained how anyone can try it on anyone over five or six who has PTSD-A, in Section Four. No one knows whether a person with PTSD-A will or will not respond to properly performed EMDR until it has been tried.
Most of the people with PTSD-A who do not respond to properly performed EMDR can be helped considerably by talking therapies and some medications (including for some people, ‘MDMA (Ecstasy)-assisted psychotherapy’, a not-to-be-tried-by-one’s-self treatment not likely to be readily available for most people at present). As yet there is no proof that these other treatments have permanently cured PTSD-A. They give hope to those for whom EMDR has failed.
PTSD-B (confusingly referred to as C-PTSD by some)
PTSD-B is far less complicated (less difficult) than PTSD-A. PTSD-B is far less complex (has fewer components) than PTSD-A.
PTSD-B is caused by either experiencing a sudden mental shock, as just above for PTSD-A, or by experiencing a less sudden dangerous or otherwise shocking event or series of events over time.
PTSD-B can resolve, get better, on its own over time, but it not always does, depending on the circumstances.
Treatment of PTSD-B.
PTSD-B is treated with talking therapies and or with anxiety-relieving medication.
Because PTSD-A and PTSD-A are similar but biologically different disorders, either can be there alone, or, both can be there together in the same person, having been caused by the same sudden mental shock. If just one of the two disorders there together is cured by treatment, the other will still be there, and needing to be treated next. Several different mental disorders can be present at the same time.
So called ‘Complex PTSD’ (C-PTSD) is NOT a seperate disorder. It is when PTSD-A and or PTSD-B are mixed together with one or more other mental of physical disorders, e.g., with traumatic brain injury, a psychotic schizophrenic illness etc. I.e., when there are many different components of disorders.
Persisting Peripheral Oscillopsia
Peripheral Oscillopsia (osi-lop-sia, a Greek word for ‘wavy vision’), is an illusory (false) perception of objects appearing to be moving up and down, or side to side in the periphery (the outer part) of the field of vision. It is present only with head and eyes held still, and after staring at something straight ahead for 5 to 10 seconds. Once it starts, and the head and eyes are kept perfectly still, then it persists. It was first described in 1946 by a London ophthalmologist, Dr Harry Moss Traquair*. Several ex-soldiers from WWII whose vision he was testing reported it to him. The ex-soldiers were all suffering from with Traumatic Neurosis from the war. Traumatic Neurosis is the name given by a neurologist, Hermann Oppenheim, in 1889. The name was changed to PTSD in 1980.
*Traquair, H.M., Introduction to Clinical Perimetry’, 5th Edition, 1946, London: Henry Kimpton. Page 121.
This abnormal visual phenomenon was reported but not investigated by Traquair. The same abnormal visual phenomenon was reported to the author in 1977. The author at the time was unaware of Traquair’s report. The author had independently and exploratorily investigated the visual phenomenon throughout his clinical psychiatric practice 1977 and 2008. The result of the findings and their implications is that persistent peripheral oscillopsia only occurs in people with PTSD-A, not in PTSD-B or in any other disorder.
The Visual Test
The person being tested sits in a chair, The person testing stands in front, At the start of the test the person being tested covers his left eye and stares at the left eye of the person doing the test for ten seconds, without moving their eye. The person doing the test has his right eye covered and makes eye to eye contact to ensure there is no eye movement. He has his left arm stretched out and holds it rigid and still for the ten seconds. At the end of the ten seconds he lowers his left arm and asks the person being tested to demonstrate with their right arm how the examiner’s left arm, hand or fingers appeared to them during the ten seconds.
Figure One. How the examiner appears to the person being examined. The oval line is the outer edge of the visual field. Where the dotted lines cross is the stationary visual axis between the examiner’s left eye and the right eye of the person being examined.
Note the important detail: the examiner’s fingers must just reach the very outer edge of the right visual filed of the person being examined. The examiner must adjust his distance away so that this is exactly so before the test starts.
A Recurrent abnormal re-experiencing form of memory recall of what was seen and felt during that moment of the mental shock that had triggered the PTSD-A.
It is a ‘flashing back’ re-experiencing, a ‘re-living’, ‘as though the event is happening over again’. There is a sudden return of all the sensations that had been experienced during that circumscribed moment of sudden mental shock. With each flashback there is a mental and physical re-experiencing of the sudden surge of the mental and physical (shaking, sweating) anxiety that had been felt; a flashing-out-there-in-front vivid ‘picture’ or ‘video-replay’ of what was seen happening during that moment; a re-hearing of the ‘sounds’ of what had been heard; a re-feeling of the ‘pain’ that had been felt; a re-smelling of the ‘smell’ that was there . . .. It is not a dream or a nightmare. It lasts a few seconds or a few minutes. It can come once an hour, once a day, once a month or longer. It can come spontaneously, or triggered by any reminder, or recalled voluntarily.It is not a ‘dissociative’ phenomenon, its abnormal form is unique to PTDD-A.
If they recur at all, then at anytime in-between, and the Visual Test is performed, there will be Persistent Peripheral Oscillopsia.
During successful properly performed EMDR (Section Four, below), as the picture of flashback goes bit by bit during the EMDR, then the peripheral oscillopsia, if it is tested for in between sessions of EMDR, gets less and less. Once the flashback has gone for good the peripheral oscillopsia has gone for good. They come together, stay together and go together simultaneously: what had gone wrong with the brain has been (somehow, inexplicably) corrected with EMDR.
Properly Performed EMDR.
First of all one has to be sure the person has PTSD-A — that they have persistent peripheral oscillopsia and have recurrent abnormal flashbacks. There is no proven evidence that EMDR helps with any other disorder than PTSD-A (but it might be, but not proven that it can be more than, a placebo treatment for other disorders).
Let us say ‘he’ is the person being treated, and ‘she’ is the person doing the EMDR. He sits comfortably in a chair, she sits or stands in front, a metre or so away. He is asked to re-evoke one (perhaps just one of several different) abnormal experiential flashback, and then ‘hold’ that ‘picture’ of the flashback. This may raise his anxiety to a near-unbearable level, and he will need reassurances that his anxiety will be at its most severe only with the first trial or two of EMDR, and he must do whatever he can to tolerate the discomfort at the beginning of the EMDR.
As soon as the abnormal experiential flashback image is ‘held’, he has a run of repeatedly moving his eyes from side to side by following her moving hand as she repeatedly sweeps her hand from far left to far right to far left… at one to three sweeps per second in front of him.
He is told to stop the run of his eye movements as soon as his abnormal experiential flashback image goes, and she stop also. This disappearance of the image may have taken a run of just several of her hand-sweeps, or a run of ten or twenty or thirty or more of her hand-sweeps.
The procedure is repeated. Each repeated run of eye movements has the abnormal experiential flashback image re-evoked , and each run is continued until it goes.
If EMDR is being successful, then following every few runs of side to side eye movements, he senses that, step by step, the flashback image and the other sensations are degrading in intensity step by step. If and only if there is no other flashback, then on re-doing the Visual Test the persistent peripheral oscillopsia will be lessening in range over the visual field, lessening in amplitude of oscillation and or lessening in frequency of oscillation.
The runs of eye movements must continue until no fragment of that flashback image can be re-evoked. It may take as few as two or three runs of eye movements at his first session, or it might take several once or twice per week sessions of repeated runs of eye movements over weeks or even several months of repeated sessions before no fragment of his abnormal experiential flashback image can be re-evoked and is permanently eliminated.
If he had one or more other flashbacks from one or more other traumatic events, then each flashback must be treated by EMDR until eliminated before PTSD-A has been cured. Only then will there be no more peripheral oscillopsia on testing for it.
If there are other disorders are present at the same time, the they will be left to be treated in some other way after PTSD-A has been cured.
EMDR is, for some inexplicable reason, never successful for some people with exactly the same sort of PTSD-A. It appears that peoples’ genes somehow or other determine whether it is to be successful or not.
What is the most probable explanation for what has gone wrong in the brain in PTSD-A.
These suggestions are from some senior geneticists who have had PTSD-A themselves, have been cured after many decades of having their PTSD-A by properly performed EMDR, and are fully aware of the nature of all the new clinical evidence.
In some people, they themselves included, a sudden momentary surge of high anxiety can trigger an epigenetic insertion into the DNA molecules, the genes, that are forming, laying down, the memory of what is happening at that moment. What gets inserted into the genes are methyl groups, a simple chemical group (CH 3) that tags onto those molecules and disrupts their normal functioning and they function abnormally — forming the recurrent re-experiencing abnormal flashback of PTSD-A. This epigenetic change isn’t passed on to the next generation. PTSD-A cannot be inherited.
(There is provable clinical evidence that for some people, particularly those people with the genes for ADHD, an increased risk of developing PTSD-A in response to the experience of a sudden mental shock can be inherited, sometimes making it look as if PTSD-A is inherited when PTSD-A appears in several members of the same genetic extended-family, each of them having inherited the genes for ADHD.)
When PTSD-A successfully responds to properly performed EMDR, it is suggested that in some equally inexplicable way the methyl group goes back to wherever it came from and the brain DNA can then continue forming that memory into a normal form of memory, and from then on it is remembered normally, without re-experiencing it.
It appears that whether PTSD-A will respond or not to properly performed EMDR also depends on the person’s genes.
Perhaps there are people with genes that prevent them from ever getting PTSD-A when they are experiencing a sudden surge of high anxiety from a mental shock.
Oscillopsia, ‘wavy vision’, is one of many bodily disorders that anxiety can produce. In a panic attack ‘wildly wavy vision’ is a common symptom that is present. It goes away when the level of the anxiety subsides at the end of the panic attack. Since the time of Hippocrates, anxiety symptoms that fade away when the anxiety fades away have always been regarded as ‘hysterical symptoms’, of no clinical importance. More recently they are called ‘somatoform symptoms’, bodily-like symptoms. In the past, when wild wavy vision was there with Traumatic Neurosis, it confirmed in the minds of many people that Traumatic Neurosis itself was a ‘hysterical’ condition.
Persistent peripheral oscillopsia of PTSD-A appears to be caused by the anxiety that is persistently ‘locked-in’ with the abnormal form of memory of the frightening mental shock that caused the PTSD-A. It gives rise to the sudden anxiety that comes when the flashback suddenly comes. That ‘locked-in’ anxiety only goes when that abnormal form of memory goes to normal form in response to EMDR. The two together constitute an invariant ‘complex clinical symptom’.
There is a lot about the workings of anxiety that we don’t know and can’t even start to imagine — except that the word ‘hysteria’ isn’t a good word to apply to any of its clinical manifestations.
The book: ‘ Cracking the Code of “PTSD” ‘ is shortly to be published. It explains in detail the way the fresh clinical evidence came from different sources and slowly came together.