THE LADIES WITH STAMMERING VISION, and how their observation finally solved the Genomic Codes of PTSD .
There is novel clinical observational evidence on the neurobiology, genomics and epigenomics of the anxiety disorder called PTSD. What does the new evidence imply about what must have gone wrong in the brain? What can and can’t be done about it? The findings, coming from a 35 year-long exploratory observational clinical investigation. One can make the same observations and convince oneself yea or nay
Dr Robert Tym,
NEURO-Psychiatrist, previously ASSist Prof Neurosurgeon.
At last, enough evidentiary observational clinical evidence about the biological nature of PTSD has turned up. This novel clinical evidence can be confirmed by anyone who is clinically involved with PTSD. The implications that can be drawn from this collated clinical evidence tell us more about the most probable neurobiological, epigenomic and genomic nature of PTSD –- a nature more complicated than ever imagined. There can now be a better understanding of PTSD; there can be more certainty to the clinical diagnose of PTSD; the complicated management and treatment regimens of PTSD can now be more rational.
(Reporting on “PTSD” without describing its visual test and the effects of EMDR treatment, would be like reporting on bone fractures without describing their X-rays and the effects of orthopaedic surgery. And, since no two people have the same genome, then nothing can be always and nothing can be never in any branch of medical science.)
*This web page (9k words) is the kernel of an E-book of the same name’ soon to be available. The E-book gives a step-by-step account of the 35-year-long exploratory investigation: its separate evidentiary clinical findings, and the argument for their inferences on the biological nature of PTSD.
SECTION 1 — Two different types of PTSD.
SECTION 2 — The Nature of PTSD type-1, PTSD type-2 and Complex PTSD.
SECTION 3 — The neurological, epigenomic and genomic nature of PTSD type-1.
SECTION 4 — Persistent peripheral oscillopsia and the simple visual test for the presence or absence of PTSD type-1.
SECTION 5 — The treatment of PTSD type 1, PTSD type-2 and Complex PTSD.
SECTION 6 — The proper performance of EMDR.
SECTION 7 — Addendum.
This fresh empirical clinical evidence came bit by bit during a 30 to 40 year-long exploratory clinical investigation into a chance clinical observation of a subtle abnormality of vision, a visual symptom hitherto thought to be of no clinical significance, best ignored. This subtle abnormality of vision, now seemingly a transformative clinical observation, was first (first as far as we know) reported in a book by a London ophthalmologist, Dr Ross Traquair, in 1946. He had been examining the vision of some British ex-soldiers from WWII who were suffering from Traumatic Neurosis — the pre-PTSD name.
During Dr Traquair’s examination of the visual fields of these ex-soldiers, each of them was reporting to him, the ophthalmologist, that they were experiencing a strange, subtle and persisting visual abnormality: When they were staring with one eye for more than ten seconds or so at a stationary object — something these ex-soldiers and anyone else were routinely asked to do during a visual field examination at that time –- the ex-soldiers were reporting that after a few seconds of staring, all the stationary objects that they were seeing in the periphery of their vision were appearing to wave about, and were continuing to wave about for as long as they continued to stare at the stationary object in the centre of their vision. The stationary object they were staring at did not appear to wave about, only the things out in the periphery. This notable ophthalmologist performed this same visual test on most of his many patients year in year out — visual fields was his specialty — but only his ex-soldier patients with Traumatic Neurosis were reporting to him the wavy vision in the periphery of the visual field during the test. The ex-soldiers themselves noticed this abnormality only during that visual field test, and it didn’t trouble them otherwise — in everyday life they didn’t stare for long periods with one eye, the other held closed, at stationary objects, and at the same time take notice of stationary objects in their peripheral vision, and nor do everyday people who aren’t ex-soldiers. Dr Traquair didn’t investigate this reported odd visual symptom of a group of ex-soldiers with Traumatic Neurosis, but he did mention it as a ‘Stammering of vision in the periphery of the visual field in ex-soldiers with Traumatic Neurosis’ very briefly in his textbook on Visual Fields *.
*Traquair, H.M., Introduction to Clinical Perimetry’, 5th Edition, 1946, London: Henry Kimpton. Page 121.
Most people reading this, including most doctors of any specialty, would reasonably assume that the subtle observation of the ex-soldiers could not be of any clinical significance — it certainly didn’t seem to worry anyone. However, the seventeenth century English physician, known universally as The Father of Observational Medicine, Thomas Sydenham, in 1666, had made a never-to-be-forgotten point of saying to all doctors, “. . . nothing (no observation) in medicine is so insignificant as not to merit attention . . .”. This author found the visual observation of these ex-soldiers when he first came across Dr Traquair’s book in 1987 –- twenty-one years after it had been written. Traumatic Neurosis had been renamed to PTSD by the American Psychiatric Association (the APA) in 1980.
But by chance, this author had been investigating this same subtle visual abnormality since 1977. In 1977, just after opening his psychiatric practice, and having retired from neurosurgery, several women patients had been referred to him who were immigrants to Australia from southern European countries. They were all suffering from Traumatic Neurosis caused by various frightening accidents at work some years before, soon after their arrival in Australia. From the time of their accidents, they had all been reporting not only various aches and pains and constant anxiety, but in addition they were all reporting wavy vision throughout most of their visual fields and present all the time, wavy vision that seriously interfered with their vision and added to their being unable to return to work. These women didn’t know each other. By chance they all had the same lawyer, and all had been applying for Workers Compensation. But various ophthalmologists and psychiatrists to whom they had been referred by their lawyer had diagnosed them all as being hysterical, implying that there was nothing wrong with their vision, and meaning they were either grossly exaggerating their disabilities, including their visual difficulties, or they were imagining them – either way they should not be compensated for their supposed work-related visual and other disabilities. This perspicacious lawyer strenuously disagreed with the medical specialists. He had observed his women clients for the several years since their accidents and believed in the authenticity of their disabilities, including their visual disabilities. The lawyer decided to seek the opinion of the author, a psychiatrist who had previously been a neurological surgeon, and certainly interested in the visual system. This author, likewise, could not agree that the abnormal vision of these women was hysterical, rather that there must be some real organic reason for their several years of long-persisting visual abnormality — but he did not know, nor could he envisage, just what organic reason there could possibly be. His psychiatric training had been in London, UK. He had seen few patients with Traumatic Neurosis and very, very few psychiatric patients who had been born in southern Europe or the Middle East. He decided there and then that he would need to exploratorily investigate any-and-all visual abnormalities in any-and-all the psychiatric patients he would be seeing over the following thirty to forty years of his psychiatric practice in Australia, a country with an ethnically more diverse population than the then UK. Thus began the 30-year or so long exploratory clinical investigation into abnormal visual symptoms in psychiatric patients. (All clinical knowledge depends on observation; with complex phenomena there is often an awful lot of observation needed.)
A visual symptom is a visual phenomenon that is seen to exist by the person who experiences it. A subtle visual symptom means the visual symptom is not immediately obvious or comprehensible to the person experiencing it or to anyone they may tell of it. As we shall come to later, a unique visual symptom means the symptom is always present in some people, in this case it was found to be always present in some people with a PTSD, but never to be found in any other people. In the later stages of the 30-year clinical investigation this visual symptom was being reported to be persistently present by some people with a persisting PTSD but persistently absent in other people with a persisting or not persisting PTSD. So, as we shall come to, some people with a PTSD reported that they always had this unique visual symptom and some people with a PTSD said they never had this visual symptom. It was soon becoming obvious that PTSD is a lot more complicated than it first appeared to be. There was, also, a first hint that people of different ethnicities who had PTSD had this same symptom but of characteristic different severities.
This subtle visual symptom has subsequently become a linchpin for the understanding of PTSD. There is now a very simple, reliable, specific and sensitive visual test for detecting the presence or absence of this unique and subtle visual symptom. The simple visual test can be performed by any one on anyone who is older than five or six years of age who is not blind and is cooperative. (The details of how to perform this simple Visual Test and the details of the visual symptom for which it tests we come to in Sections 4.2 and 4.3 below.)
The novel clinical findings, the clinical evidence coming from that exploratory investigation, combined with other novel clinical evidence coming from others over the 30 to 40 years since the exploratory investigation began, confirmed that PTSD is neurobiologically, epigenetically and genomically (not culturally) complicated –- much more than previously thought. The novel empirical clinical evidence is counterintuitive, not surprisingly, but can be understood and tested out by anyone involved with PTSD. This webpage is for the everyday person as well as for any PTSD expert, sceptical or curious.
For the benefit of the common sense of the everyday person, a PTSD, a post-traumatic stress disorder, must be what the four simple words say it is. So, a PTSD is a disorder, meaning a mental (a brain, a mind) state characterised by personal distress and impairment in multiple areas of life. It is a disorder caused by experiencing mentally traumatic stress, meaning it caused by the traumatising (damaging) effect on the brain’s functioning of experiencing anxiety (fear or disgust). For many people with a PTSD their PTSD lasts for the rest of their life, and the clinical evidence suggests that for them some specific aspect of their brain has been permanently traumatised (organically damaged, organically changed) by the experience of a mental shock — a sudden surge of intensely high anxiety from a sudden fear or a sudden disgust. For others with a PTSD the disorder can resolve spontaneously over time – for them there had been no permanent damage or change caused by the experience of anxiety.
This simple empirical fact alone and confirmed by further empirical clinical evidence we come to later, shows there must be two different (but only two) biologically distinct forms of PTSD. The trouble has always been trying to understand just how sudden anxiety (fear) or sudden disgust can, for some people, not all people, permanently damage their brain — and their brain cannot recover spontaneously.
The former name for PTSD was Traumatic Neurosis, a name given in 1889 by the Prussian neurologist, Hermann Oppenheim. He posited, seemingly presciently so, that there must be some molecular damage to the brain caused by fright, to cause Traumatic Neurosis, but he couldn’t envisage what the damage was or how the damage could come about. In 1980 the name Traumatic Neurosis was changed to PTSD by the American Psychiatric Association (the APA). They couldn’t envisage how permanent damage could come about from fright either – they made no distinction between two distinct forms of PTSD. (The term epigenetics that we come to later, was introduced in 1942 by an embryologist, Conrad Waddington.)
The second transformative clinical observation was in 1989 by psychologist Dr Francine Shapiro. She published a paper saying that her newly discovered EMDR treatment (described below) could permanently cure some people with PTSD.( “Cure” in this context meaning “permanently eliminate”) This was confronting to the PTSD psychiatric experts, the psychiatric cognoscenti. Their general response was to, incuriously, ignore or deny Dr Shapiro’s highly counterintuitive-to-them clinical observation rather than investigate it — their denial virtually amounting to an act of agnotology (culturally induced ignorance) amongst the world psychiatric community. The practice of EMDR treatment was virtually left to the psychologists, with no medical training. As we shall see below, EMDR treatment plays a large part in our appreciation of the complexity of the neurobiology and genomics of PTSD. And as we shall also come to, what EMDR treatment can and cannot do is complex — certainly not a panacea for all with PTSD.
More clinical evidence slowly emerged: During the author’s ongoing 30 year-long clinical investigation, it was found that those people with a PTSD and the visual symptom always reported in addition a circumscribed intrusive and distressing abnormally formed flashing-back re-experiencing memory of the mentally traumatic event that had caused their PTSD, i.e., they also had abnormal flashbacks of the momentary causal event. Also the reverse: those with an abnormally formed flashing-back re-experiencing memory always reported the presence of the abnormal visual symptom when they performed the simple Visual Test. (See Sections 2.3, and for more detail 4.5, of this abnormally formed memory, the abnormal re-experiencing flashback of PTSD).
So: Some people with PTSD reported both the abnormal flashbacks and the visual symptom on visual testing. Other people with PTSD reported no abnormal flashbacks and no visual symptom on visual testing. Those people with a PTSD but without the visual symptom, had only normally formed distressing memories of the mentally traumatic event or events that had caused their PTSD, intrusive memories, yes, but not flashing back memories in abnormal re-experiencing form.
During the ongoing clinical investigation, it was found that only some people with a PTSD plus the visual symptom and the abnormal form of memory, could be permanently and clinically provably cured of their PTSD with properly performed EMDR. But, other people with a PTSD plus the visual symptom and the abnormal form of memory could not be helped at all with properly performed EMDR. It was also found that EMDR did not cure any people with a PTSD but no visual symptom and no abnormal flashback. (properly performed EMDR is explained briefly in Section 3 and in more detail in Section 6.)
When EMDR cured the people with PTSD it was reported that their visual symptom and the abnormal flashback were both slowly eliminated simultaneously, step by step and in step. When there was no longer any remnant of the visual symptom on repeated visual tests, then there was no remnant of any form of abnormal memory recall on repeated attempts to recall the causal event — the causal event could only be recalled in normal non-re-experiencing form: their PTSD had been cured.
For many of those people with a PTSD that is resistant to EMDR treatment then talking therapies, psychotherapy in the form of Cognitive Behaviour Therapy and Exposure Therapy, can greatly reduce the anxiety, but neither could eliminate the symptom of the abnormal flashback or the symptom of the abnormal vision. The visual test is simple but reliable, sensitive and specific for the presence and absence of persistent peripheral oscillopsia, hence it is reliable, sensitive and specific for the presence and absence of a module (see later) of PTSD type-1 –see Section 1 below. All this was first published, somewhat inchoately and anecdotally, in 2009**.
**Tym, R., 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).
Being anecdotal, inchoate and wildly counterintuitive the paper was ignored. There has since been significant progress, but the information remains necessarily anecdotal and certainly too long and involved for journal-publication form. Hence the need for a book.
SECTION ONE: Two different forms of PTSD and the Personality Disorder, so-called Complex PTSD.
1.1 It is obviously apparent, from the observations given just above, that there must be two different forms of the anxiety disorder PTSD.
One form of PTSD is a unique mental disorder, unlike any other. It has a persisting visual symptom that is always found to be present on testing, together with, an abnormally formed emotionally and sensorially re-experiencing memory of the experiences during the moment of the mentally traumatic event that caused their PTSD, i.e., ‘an abnormal flashback’. Some of the cases could be clinically proven to respond to properly performed EMDR, but by no means all –– there were early hints that the persons’ different genomes were playing a part in determining whether a person has a PTSD that might respond to properly performed EMDR.
The other form of the anxiety disorder PTSD is a generic anxiety disorder. It has no visual symptom and has only normally formed memories of the mentally traumatic event or events that caused their PTSD. None of those cases of PTSD could respond to EMDR at all. So, following one or more very frightening experiences of mentally traumatic events, some people develop one form of PTSD, other people develop the other form of PTSD. Obviously, many people don’t develop either form of PTSD following one or more very frightening experiences of mentally traumatic events. The two different forms of PTSD must be given different names.
1.2 So, one form of PTSD can now be called, for the sake of simplicity, PTSD type-1 (in detail see Section 2 below). It always has a subtle and unique visual abnormality and an abnormal form of memory of the causal event or events that triggered the mental shock, the sudden surge of intense anxiety. PTSD type-1 cannot recover spontaneously over time. Some people with PTSD type-1 can be clinically proven to be cured by properly performed EMDR; some people with the same form of PTSD type-1 cannot respond to properly performed EMDR at all. Exposure therapy can help to significantly lower the anxiety but not eliminate the two unique symptoms of vision and memory.
The other form of the anxiety disorder PTSD can now be called PTSD type-2 (see Section 2 below). It has no visual abnormality and has no abnormal form of memory of the causal event or events that caused it. It can recover spontaneously over time, but may not, depending on circumstances that might delay or prevent its recovery. No case of PTSD type-2 could respond curatively to properly performed EMDR. It can respond to psychotherapy (above).
1.3 Since PTSD type-1 and PTSD type-2 are neurobiologically very different, there is no reason why PTSD type-1 and PTSD type-2 cannot be present in the same person at the same time, having developed them from the same experience or from different experiences at different times.
Either or both types of PTSD can coexist with other mental disorders and diseases, including traumatic brain injury (TBI) — as well as with grief and ADHD and . . . etc.
Since PTSD type-1 results from one experience, there is no reason why further PTSD type-1 may arise from one or more later experiences, resulting in PTSD type-1 with two or more different abnormal flashbacks from two of more experiences of different causal events — i.e., with two or more distinct modules of PTSD type-1 (see later).
1.4 The so-called Complex PTSD (described in detail in Section 2.6 below) is not a third form of PTSD, it is a form of personality disorder. It is the name given to the long-term effects on a person’s developing personality from having to live for many years with extremes of inescapable mentally traumatic situations, combined with persisting one or more modules of PTSD type -1 and or PTSD type -2.
SECTION TWO: The nature of PTSD type-1, PTSD type-2 and Complex PTSD.
2.1 PTSD type-1 is a categorical anxiety disorder, categorical meaning it has (in this case two) unique clinical symptoms that characterise the disorder. One of the unique symptoms is the abnormal form of vision: persistent peripheral oscillopsia (Section 2.2 below). The other unique symptom is the abnormal form of re-experiencing memory, an abnormal flashback, of the experiences during the moment of onset of the PTSD type-1 (Section 2.3 below). Only if both unique clinical features are present is the disorder present. PTSD type-1 can only be caused by the experience of a sudden traumatic mental shock, mental shock meaning a sudden surge of intensely high anxiety triggered by an experience of sudden fear or disgust, triggered in turn by the experience of a sudden mentally traumatic event. These two unique clinical symptoms are invariant, implying the two symptoms are unchanging and always there together in PTSD type -1. The two symptoms can be subtle, implying that one or the other or both are not always obvious or noticed.
PTSD type-1 forms in real time, i.e., it is formed contemporaneously during the moment of the traumatic mental shock that causes the PTSD type-1: the two unique symptoms arise together during the moment of outset. If and only if PTSD type-1 is cured by EMDR treatment (described briefly in Section 3.0 and in detail in Section 6) will the two symptoms go, and when they go, they go step by step and in step simultaneously, together. When neither of the symptoms is present then PTSD type-1 is completely cured, permanently eliminated.
So, these two unique stuck-together clinical symptoms constitute an invariant complex memory and vision symptom that is unique to PTSD type-1. Stuck together, these two unique features in effect constitute a module of PTSD type-1. Hence, someone with PTSD type-1 may have one module of PTSD type-1 or may have two or more modules of PTSD type-1: a multi-modular PTSD type-1 is caused by multiple different experiences of mental shock from multiple different experiences of mentally traumatic events at different times.
PTSD type-1 can be diagnosed in people of any age over five or six years, and PTSD type-1 can be treated with EMDR in people of any age over five or six years — people from all walks of life. EMDR (described in Section 6) is effective in eliminating PTSD type-1 only in some people and not in all people with PTSD type-1. The responsiveness or otherwise to EMDR depends on the genome (the genetic make-up) of the person with PTSD type-1: just how or why is not fully understood.,
For some people with PTSD type-1 it had been caused by the experience of an event that would terrify anyone, and for some people with PTSD type-1 it had been caused by experiencing an event that frightened them but probably would not have frightened anyone else. For most people with PTSD type-1 the event that they experienced was somewhere between those two extremes. From person to person the susceptibility to getting PTSD type-1 in response to experiencing a mental shock varies widely (See Section 3.3 for the increased susceptibility of developing PTSD type-1 for those with the genome for ADHD). The spectrum of severity (the obtrusiveness) of PTSD type-1 extends from not at all severe to severely incapacitating.
2.2 The abnormal visual symptom of PTSD type-1. It is a symptom of persisting wavy vision (called oscillopsia: ‘osi-lop-sia‘, a Greek word for wavy vision). The waving about of stationary objects is seen in the periphery of the visual field when — with one eye closed while the other eye is steadily focusing on a stationary object straight ahead. It is an illusory (no objective reality) experience. This symptom is called persisting peripheral oscillopsia. It is a unique form of oscillopsia unrelated to other forms of wavy vision and unrelated to other forms of oscillopsia associated with neurological and vestibular disorders. (This symptom is described in detail in Section 4.2, and the simple visual test for the presence or absence of persistent peripheral oscillopsia is described in more detail in Section 4.3.) For most Northern European people with PTSD type-1 the symptom is only noticed when it is tested for. In most Southern European people with PTSD type-1 it is more likely to be somewhat more obtrusive, more extensive over the whole visual field and may interfere with everyday vision. In anyone, its presence always indicates the presence of PTSD type-1, regardless of genome or presence of mental or physical disorders or diseases other than blindness.
2.3 The abnormal memory symptom of PTSD type-1, the recurrent abnormal flashback, is a recurrent abnormal re-experiencing memory recall of what was emotionally and sensorially experienced (noticed) during that moment of the mental shock that caused the PTSD type-1. Its presence always indicates the presence of PTSD type-1, regardless of the presence of other mental or physical disorders. (This is described in more detail in Section 4.5.)
2.4 The anxiety disorder PTSD type-2 is a dimensional anxiety disorder, dimensional implying it has no unique clinical symptom or non-anxiety symptoms that characterise the disorder: it is a generic anxiety disorder caused by experiencing mental trauma. PTSD type-2 can be caused by the experience of a sudden traumatic mental shock, as can PTSD type-1, but unlike PTSD type 1, PTSD type-2 can also be caused by the experience or experiences of other forms of mental trauma, sometimes long-drawn-out mental trauma. The clinical evidence suggests that the experiences of mental trauma functionally but not physically damage the brain — the brain can recover from the functional damage spontaneously over time, though it not always does, depending on circumstances that can delay or otherwise hinder recovery.
2.5 There are many anxiety symptoms that are common to both anxiety disorders PTSD type 1 and PTSD type-2 and hence to the personality disorder Complex PTSD (see below). There can be recurring distressing traumatic memories of the event or events that caused the PTSD type-2, but they are memories that are not coming back in abnormal re-experiencing form (as does the abnormal flashback of PTSD type-1): they may be distressingly recalled but recalled in normal form. In both forms of PTSD there can be periods of extra high anxiety, hypervigilance, dissociation, periods of derealization, sleeplessness, frightening nightmares of the event or of anything else, emotional withdrawal, hypervigilance (being easily startled over anything), being inattentive due to the anxiety, lacking concentration, failing to remember important things, there can be recurrent tension headaches, recurrent frustrations, depressed moods, uncontrollable anger and sometimes violence, and avoidance of any reminders of the event that caused their PTSD. All too often there can be dangerous thoughts and actions of self-harm and suicide.
Since PTSD type-1 and PTSD type 2 are distinctly different clinical entities neurobiologically, and both can have many non-specific anxiety-related symptoms in common, then the two different disorders can appear superficially clinically indistinguishable. One or both can be present with any physical disorders, including traumatic brain injury (TBI), and with other mental disorders, including psychotic disorders such as schizophrenia, personality disorders, grief, ADHD and autism spectrum disorders.
2.6 Complex PTSD is not a third form of PTSD, it is a dimensional personality disorder. The symptoms of Complex PTSD can follow the mental traumas of long-lasting childhood abuse, of childhood abandonment, of long-lasting relationship abuse, of sexual slavery, of living along with long-lasting combat, of being tortured, of being interned alone and or for long periods, of having multiple modules of PTSD type-1 from multiple traumatic mental shocks as a combatant or other first responder. Complex PTSD usually has but not necessarily has followed interpersonal trauma. The spectrum of severity of the personality disorder, Complex PTSD, extends from not at all severe to severely incapacitating and can be of any duration.
Also, there is robust clinical evidence that those above five tears of age who have a genome for ADHD are significantly more likely to develop PTSD type-1 in response to experiencing one or more mental shocks than are those without that genome. (ADHD can be of any level of severity or obtrusiveness.)
The resulting personality symptoms, with or without ADHD in addition, can be somewhat like those of Borderline Personality Disorder. The personality symptoms of Complex PTSD include disturbances of self-organisation, symptoms defined as emotional dysregulation, interpersonal difficulties, and, negative self-concept. The end-result can be devastating to every aspect of social, emotional, economic and family life over decades.
(The features of Borderline Personality Disorder include impulsive and risky behaviour; unstable or fragile self-image; unstable and intense relationships; fluctuating moods, sudden bursts of anger, often as a reaction to interpersonal stress; stress-related paranoia behaviour or threats of self-injury; fear of being alone or abandoned, pervading sense of emptiness.)
SECTION THREE: The most plausible neuro-biological and epigenomic explanation for the pathological nature of PTSD type-1 and its elimination by EMDR treatment.
(It is based on the abductive-reasoning speculation of two senior academic geneticists –- the two quite independent and unknowing of each other. Both had experiences of having had PTSD type-1, of having had successful EMDR treatment, and of being fully acquainted with all the fully testable clinical evidence associated with PTSD type-1 mentioned here and in the book.).
3.0 But first, a brief explanation of properly performed EMDR treatment (given in more detail in Section 6). Eye Movement Desensitisation and Reprocessing treatment, EMDR, consists of (i), her, the therapist, asking him, the person with a PTSD type-1, to voluntarily evoke and hold his abnormal form of re-experiencing flashback memory of the causal incident (described above and in detail in Section 4.5). Then (ii), immediately asking him to follow with both his eyes her moving hand and finger as she repeatedly sweeps her hand and finger to and fro from far left to far right at one to two sweeps per second in front of him (rapid side to side eye movements are called saccades.) And then (iii), asking him to stop moving his eyes as soon as the evoked re-experiencing flashing-back memory goes. Then, repeating (i), (ii) and (iii), perhaps several times, until the abnormal flashing-back form of memory can no longer be voluntarily re-evoked, only the normal non-re-experiencing form of memory of the same moment of the causal event can be evoked. On visual testing at this stage there is no persistent peripheral oscillopsia: the PTSD has been permanently cured.
From person to person, and depending on the person’s genome, EMDR may be effective in permanently changing the abnormal form of memory to a normal form, i.e., curing the PTSD type-1, within ten seconds of starting saccades at one extreme, or, it takes repeated runs of saccades, perhaps repeated runs over half an hour, or over many half hour sessions of multiple runs over a period of a week or over a month or over three months at the other extreme. For some people with PTSD type-1, regardless of their genome, the EMDR treatment is too difficult for them to tolerate — because of their intense anxiousness on evoking a flashback, or for some other reason.
For some people with PTSD type-1 the EMDR, although well tolerated, turns out to be totally ineffective, no matter for how long EMDR sessions is continued. It is not possible to predict for whom EMDR treatment will be effective or ineffective without trying EMDR treatment and persevering.
3.1 The most probable neurobiology of PTSD type 1.
A senior geneticist, well acquainted with all the clinical evidence given here (and in the author’s forthcoming book, Cracking the Code of PTSD), had experienced his own multi-modular PTSD type-1 and had experienced successful EMDR treatment for each module. He said that some of his abnormally formed memories (some of his PTSD type-1 modules) were changed to permanent normally formed memories within less than ten seconds of starting the saccades of the EMDR — and immediately at the end of his final 10 second run for his last remaining module, finding that his peripheral vision had been reverted to normal stable peripheral vision. He also said that in his experience as a senior research geneticist, only an epigenetic mechanism could explain such a fast process effecting the elimination of such a complex neuro-physiological module. Similarly, he said, that in his view only an epigenetic mechanism could explain how a sudden surge of intense anxiety could cause an instant change in the brain’s DNA, i.e., virtually instantly forming a module of PTSD type-1, such that the memory of experiences during the moment of the sudden surge of anxiety is formed abnormally in real time, contemporaneously, and is thereafter stored indefinitely, and intermittently recalled abnormally, together with persistent peripheral oscillopsia. A second senior geneticist, quite independent of the first, who subsequently attended with PTSD type-1, and had the PTSD type-1succesfully eliminated by EMDR treatment, agreed with the first geneticist’s transformative views.
3.2 An epigenetic mechanism in this context implies one or more chemical methyl groups (CH3) being tagged-on to some of the brain’s DNA molecules, tagged-on via the action of the enzyme methyl-transferase. When the DNA molecules are tagged with CH3, they function (express themselves) abnormally — they form a PTSD type-1 module, that is, they form an abnormal combination of an abnormally formed memory of the emotional, sensorial and or physical experiences during that moment — lasting a second or so — of the sudden surge of anxiety, combined with persistent peripheral oscillopsia. The module of PTSD type-1 always gives rise to persisting higher than normal anxiety. The abnormally formed memory of the happenings and sensations experienced during that circumscribed moment of intense anxiety can only be recalled in the abnormal form of the recurrent abnormal re-experiencing flashback. The persistent peripheral oscillopsia is always present whenever tested for, independent of the time of the most recent abnormal re-experiencing flashback.
There is a possible brain site and pathological neuro-biological mechanism: It is known that in the region of the brain where this module of PTSD type-1 is believed to be located and from where the anxiety is maintained — in or around the anterior insular cortex closely connected with the amygdalae nuclei — there is (in animals) an area of cortex that can be electrically activated by movements seen in the visual fields. This area of the anterior insular cortex is part of the vestibulo-ocular reflex system (the system that maintains a steady focus of the eyes by a reflex contrary movement of the eyes when the head moves). It is postulated that voluntary saccades, combined with voluntary activation of the abnormal form of memory, i.e., during EMDR treatment, can effect a step-by-step epigenetic reversal — the methyl groups are detached from the tagged DNA molecules. This allows the no-longer-tagged DNA molecules to function (express themselves) normally and they can then convert the abnormally formed re-experiencing memory, step by step, to a normal form of non-re-experiencing memory — what they do normally in the absence of extreme anxiety. Simultaneously, the abnormal form of wavy vision, persistent oscillopsia, is step-by-step and in-step converted to normal stable peripheral vision, something that is immediately confirmable on simple visual testing. At the same time the persistent excessive level of anxiety lowers to an appropriate, or normal, level.
So much for the abductive reasoning, the plausible speculation, of the clinically involved geneticists, based on their knowledge of genomics and epigenomics, their personal clinical experience, and, the accumulated clinical evidence. All reasoning from evidence must be fallible. But alas: it is not known why EMDR is effective for only some with PTSD type-1, not effective for everyone with a PTSD type-1.
3.3 There is significant anecdotal clinical evidence, taken from the examinations of the cohort of 9000 or so randomly referred psychiatric clients (not all of whom, by any means, had any form of PTSD) during the thirty-year clinical investigation, that a person’s genome, their total genetic makeup (not their culture) has a marked effect on many aspects of the clinical manifestations of their PTSD type-1. (This anecdotal clinical evidence is given in the forthcoming book, Cracking the Code for PTSD.) For example (given also above) there is a statistically significant comorbidity between those with the genome for ADHD and the likelihood of the development of PTSD type -1 in response to the experience of a mental shock at some time of life after five years of age, a comorbidity that cannot be attributable to chance or behaviour. This might make it appear that PTSD type 1 is heritable when PTSD type 1 appears to cluster in certain extended families. Obviously, PTSD type-1 cannot be heritable any more than a broken leg can be heritable. Also, those people with the genotype of dark eyes and or olive skin appear to have more severe persistent peripheral oscillopsia, and, an increased risk of being relatively or totally EMDR-treatment-resistant. It might be reasonable to speculate that there are some people whose genotype prevents them from ever developing PTSD type-1 under any circumstances, but that could never be confirmed.
SECTION FOUR: The diagnosis of PTSD type-1 and PTSD type-2 and The Visual Test for the presence or absence of PTSD type-1.
4.1 The presence or absence of PTSD type-1 can only be confirmed by the presence or absence of one or other or both symptoms that are unique to PTSD type-1, i.e., by the presence of one or more modules of PTSD type-1.
4.2 The unique visual symptom of PTSD-A: Persisting Peripheral Oscillopsia. (osi-lop-sia is a Greek word for wavy vision).
Persistent peripheral oscillopsia is an illusory perception (i.e., with no objective reality) of stationary objects seen in the periphery of the field of vision appearing to be moving, waving, about — waving up and down, side to side or round and round at two or three or more cycles per second. For most people with PTSD type-1 this visual symptom is seen to be present only when the head is held still, one eye is held closed, and the other eye is held fixated, for up to five to ten seconds without blinking, on some stationary object straight ahead. Once the stationary objects in the periphery appear to start moving about, they continue to appear to be moving about for as long as the head and eye are kept perfectly still and there is no blinking.
4.3 The visual test is simple but is reliable, sensitive and specific for the presence and absence of persistent peripheral oscillopsia, hence it is reliable, sensitive and specific for the presence and absence of a module of PTSD type-1.
4.4 Performing the simple Visual Test for the presence or absence of PTSD type-1.
The test can be performed by anyone on anyone over the age of five or six years who is not blind and who is fully co-operative. For those not understanding the language an interpreter will be needed.
Let us suppose, here, that the examiner is male, the person being examined is female. The test cannot be performed if she is acutely anxious — there are many transient and chaotic visual abnormalities present during a panic attack or when in near-panic that can confuse the test result. The test should be delayed until any acute or near acute panic has passed.
The performance of the Visual Test:
· Throughout the test she (the person being tested) remains seated.
· One of her eyes is covered (let us say her left).
· She is asked to focus with her right eye on the pupil of the examiner’s left eye.
· The examiner stands a metre or so in front and will have his right eye covered.
· The examiner’s left eye is then focused on the pupil of her right eye, ensuring that during the ten seconds of the test she does not shift her focus the tiniest bit unnoticed: the visual axis (the examiner’s left eye fixation to her right eye fixation) is thereby held rigid and controlled throughout the test.
· The examiner’s left arm is held out rigid and horizontal. The fingertips of the examiner’s left hand must just reach the outer periphery of her right visual field — the examiner’s distance from her must be adjusted so that she can just see the fingertips of his of his outstretched arm but no further out. This is an essential detail.
· During the ten seconds of the test, she is asked not to shift the fixation of her right eye from his left eye, and not blink.
· During the ten seconds of the test, she is asked to pay strict attention to what, if anything, appears to happen to his left arm, hand or fingers while her right eye remains fixated on his left eye.
· After 10 seconds he lowers his left arm and asks her to demonstrate with her right arm, how his left arm appeared to her at any time during the 10 seconds of keeping her right eye fixated on his left eye.
· The Visual Test gives a positive test result when she reports: (a) that at some time within ten seconds of commencing her steady fixation, some part of his outstretched left arm, hand or just his fingers, appeared to start to swing up and down or round and round, to shiver, to oscillate, at about two to five up-and-down or round-and-round cycles per second; (b) that the oscillations continued uninterruptedly to the end of the ten seconds, or for as long as her right eye remained fixated on his left eye and his left arm remained extended and stationary.
· The Visual Test gives a negative test result when she reports she saw no movement, or, she may report she saw only one or two very brief jerks up or down of his, the examiner’s, left arm during the ten seconds, when in fact there were no such jerks. Under such circumstances these are normal visual illusions and of no known clinical significance on the part of anyone who does or does not have PTSD type-1. The jerks do not persist, and they are not part of persistent peripheral oscillopsia or any other form of known consistent abnormal oscillopsia disorder.
Figure. How the examiner appears to the person being examined. The oval line is the outer edge of the visual field of the person being examined. Where the dotted lines cross is the stationary visual axis between the examiner’s left eye and the person’s right eye.
Note, an important detail: The examiner’s fingers must just reach the very outer edge of the right visual field of the person being examined — before the test starts the examiner must adjust the distance away so that this is exactly so.
It is necessary for the examiner to be on the lookout for false negative or false positive test results that may be voluntary or involuntary — in this author’s experience these are extremely rare.
In some patients of Middle East and Southern European ethnicity with PTSD type-1 there is persistent oscillopsia over the whole of the visual field, not just in the periphery of the visual field. This author, not surprisingly, has not seen patients with or without PTSD type-1 of every ethnicity, genome; his patients were mostly of North European ethnicities, genomes. Many clinical features of PTSD of either form vary with ethnicity, genome, but not, apparently, with the essential features of the module of PTSD type-1.
4.5 The abnormal flashback of PTSD type-1. The nature of the unique abnormal form of memory symptom — t the recurrent abnormal re-experiencing memory flashback.
A recurrent abnormal re-experiencing form of memory recall of the emotional, sensorial and or physical experiences that were noticed during that moment of a second or so during the mental shock, i.e., during the sudden surge of high anxiety, that had triggered the PTSD type-1.
An abnormal flashback is not a dissociative phenomenon and not a dream and not a nightmare. Dissociation phenomena, dreams and nightmares are not characteristics of PTSD type-1 or PTSD type-2 but they are common non-specific anxiety symptoms of PTSD type-1 and PTSD type-2, regardless of their content.
Abnormal flashbacks can be of any severity, from near terrifying to a hardly noticeable twinge of anxiety that accompanies their appearance (and the same range of severity goes for PTSD type-1 itself).
An Abnormal flashback 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 emotional, sensory and physical sensations that had been noticed during that circumscribed moment of sudden mental shock, the sudden surge of high anxiety. With each flashback there is always an emotional, sensory and physical re-experiencing of the sudden surge of the mental and physical (shaking, sweating) anxiety that had been felt; there is usually, not always a flashing-out-there-in-front vivid picture or video-replay of what was seen, stationary or actively happening, during that moment; there is usually, not always a re-hearing of the sounds or words that had been heard; usually, not always a re-feeling of the physical pain that had been felt; usually, not always a re-smelling of the smell that was there . . ..
An abnormal flashback can last a few seconds or persist replaying for many minutes; it can come every few minutes, once an hour, once a day, once a month or much longer. It can come spontaneously or be triggered by any reminder of the event that caused it, or it can be recalled voluntarily. Its abnormal form is unique to a module of PTSD type-1, hence persistent peripheral oscillopsia will be always present on testing. If abnormal flashbacks recur at all, then at any time in between them, at any time, the Visual Test will always give a positive Visual Test result for persistent peripheral oscillopsia.
SECTION FIVE: Treatment of PTSD type-1.
5.1 There is no clinical evidence known to suggest that PTSD type-1 can resolve spontaneously over time. Properly performed EMDR (see Section 6.1 and 6.2) has the best chance, but no certainty, of permanently eliminating (curing) PTSD type-1 (EMDR has no curative effect on PTSD type -2.) The clinical evidence suggests that if properly performed EMDR treatment has no effect on PTSD type-1, and sadly it cannot be successful for everyone with PTSD type-1, then PTSD type-1 lasts lifelong unless successfully cured by something else yet unknown. No one knows whether a person with PTSD type-1 will or will not respond to properly performed EMDR until it has been tried and persisted with for some time. The clinical evidence confirms that properly performed EMDR is only effective in eliminating PTSD type-1 in persons of certain genotypes (genomes, genetic makeups), about which little is known at present, though from the anecdotal clinical evidence it has appeared that those with blue eyes and fair skin appear to be more likely to respond than are those with dark eyes and olive skin.
Most of the people with PTSD type-1 who do not respond to properly performed EMDR can be helped considerably by treatments that reduces the severity of the anxiety and anxiety related symptoms. Most importantly, talking therapies and exposure therapies, together with or without medication or other anxiety-relieving substances are needed. This includes, for some people, MDMA (Ecstasy)-assisted psychotherapy conducted by certain certified therapists.
Presently there is no clinical proof that these other (non EMDR) treatments that reduce the anxiety have permanently cured PTSD type-1, i.e., eliminated one or more pre-existing modules of PTSD type-1. They do give some hope of very significant alleviation of severity to those with PTSD type-1 for whom EMDR has failed (EMDR treatment resistant patients) and for those with severe PTSD type-2.
Confirmation of the biological mechanism whereby EMDR can, in some people with PTSD type-1 and not in others with PTSD type-1, effect an elimination of a module of PTSD type 1, i.e., can apparently effect an epigenetic reversal of a methyl group, and allow the brain to convert an abnormally formed memory of PTSD type-1 to a normal form of memory, eliminate persistent peripheral oscillopsia, and eliminate the excess anxiety of PTSD yype-1, is beyond our intuitive grasp.
Following the successful treatment of PTSD type-1, then PTSD type-2 and or Complex PTSD, and or any other mental disorder may remain, and need separate management and treatment.
5.2 Treatment of PTSD type-2 and Complex PTSD.
Both these disorders are dimensional disorders, i.e., neither has any unique clinical feature that alone specifically characterises the disorder. At the lower end of the spectrum of severity the two disorders merge imperceptibly with a normal mental state and an unremarkable personality. Their diagnoses and severities depend on the number and severity of their symptoms.
As with all Anxiety Disorders, these are caused by experiences of mental trauma, and are treated with extensive social support and standard short or long-term, cognitive behaviour therapy, exposure therapy and or anxiety relieving medication or other anxiety relieving substances. The ease and effectiveness of treatment is part-determined by the severity of the symptoms and the duration of the disorder. Obviously, if one or more modules of PTSD type-1 are still present in Complex PTSD then attempts to eliminate them with EMDR will be needed, and if the modules are EMDR-treatment-resistant, other PTSD type-1 psychotherapies will be needed.
SECTION SIX: Performing EMDR.
6.1 Properly Performed EMDR for the treatment of PTSD type-1.
One first must be sure the person has PTSD type-1, i.e., that the person has persistent peripheral oscillopsia and has recurrent abnormal re-experiencing memory flashbacks. Children over the age of five or six years with clinically proven PTSD type-1 (i.e., they report the wavy vision on the Visual Test and can describe an abnormal re-experiencing abnormal flashback) can be treated with EMDR. Since the effectiveness of EMDR in eliminating PTSD type-1 is determined by, amongst other factors, the person’s genome, its effectiveness cannot be predicted with certainty before attempting treatment — perhaps the patient should be made aware of this before starting. There is no proven clinical evidence that EMDR cures any disorder other than PTSD type-1 in some people but not all people with PTSD type-1. (EMDR might be used by some therapists as a helpful placebo treatment, a “cure”, but meaning in this context “transiently eliminating some anxiety and or depressed mood symptoms that are unrelated to specified mental disorders”.)
Let us say that the person being treated is a male. The person doing the EMDR will be called the therapist (a qualified therapist or just a friend, parent or helpful neighbour — there is nothing special about physically providing the treatment). The person being treated sits comfortably in a chair; the therapist sits or stands in front, a meter or so away. The person being treated is asked to re-evoke just one (perhaps one of several different) abnormal re-experiencing flashback, and then hold that visual picture, if there is one, or whichever features and or sensations is the most characteristic of his flashback. This will raise his anxiety, possibly 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 session or sessions.
As soon as the abnormal experiential flashback image and or other feature or features is held, he has a run of saccades, i.e., a run of repeatedly moving his eyes from side-to-side. He does this by following the therapist’s moving hand as the therapist’s hand repeatedly sweeps from far-left-to-far-right-to-far-left . . . in front of him, at one to two to-and-fro sweeps per second.
He is told by the therapist to stop the run of his saccades, his side-to-side eye movements, as soon as his abnormal experiential flashback image or other feature goes, and then the therapist stops also. This temporary disappearance of the image or other feature may have taken a run of just several of the therapist’s hand-sweeps (and his saccades), or a run of ten or twenty or thirty or more to-and-fro hand-sweeps (and his saccades) before it goes, goes temporarily.
The procedure is repeated. Each repeated run of his saccades has the abnormal experiential flashback image or other feature re-evoked, and each run of saccades is continued until the flashback image or other feature goes temporarily.
If EMDR is being successful, then following every few runs of saccades he senses that, step-by-step, his anxiety is lessening, and the flashing back image or other feature is degrading in detail and intensity step-by-step. If and only if there is no other abnormal flashback, then on re-doing the Visual Test the persistent peripheral oscillopsia will be seen to be lessening in range over the visual field step-by-step likewise, lessening in range and or amplitude and or frequency of oscillation.
The runs of saccades must continue until no fragment of that flashback image or other feature can be re-evoked. It may take as few as one, two or three runs of saccades at his first session, or it might take several once or twice per week sessions of saccades over weeks or even several months of repeated sessions before no fragment of his abnormal experiential flashback image or other sensation can be voluntarily re-evoked – there is a range from ten seconds of EMDR to several months of repeated EMDR sessions (a wide range apparently determined by the inevitable wide range of people’s different genomes).
If he had one or more other abnormal flashbacks (more PTSD type-1 modules) from one or more other experiences of traumatic events, then each abnormal flashback (each PTSD type-1 module) must be treated by EMDR until eliminated, before his PTSD type-1 has been fully cured, eliminated. Only then will there be a negative result from the Visual Test — no hint of any persistent peripheral oscillopsia on testing.
If other mental disorders are present at the same time, e.g., PTSD type-2, Complex PTSD, another mental disorder, then they will remain until treated in some other way after PTSD type-1 has been cured.
SECTION SEVEN Addendum.
7.1 No one can be born with PTSD type-1. It appears that PTSD type-1 cannot occur in those under five or six years old. Those older than five or six years can be successfully diagnosed with PTSD type-1 via the visual test above and treated for PTSD type-1 with EMDR — similarly, they can be clinically proven to be cured.
7.2 What a mental shock, a sudden surge of anxiety, can or cannot do to the brain of those children younger than five years old, particularly to those with the genes for ADHD, is not known. Very few people with autism were seen in the investigation.
7.3 Having the genome for ADHD does not appear to affect the likelihood or otherwise of PTSD type-1 responding to EMDR treatment.
7.4 Perhaps there are people with genes that prevent them from ever getting PTSD type-1 when they are experiencing a sudden surge of high anxiety from a mental shock. This is unknowable.
7.5 Transient oscillopsia, wavy vision, is just one of many physiological disorders that high anxiety can cause. In a panic attack — transient wild wavy vision is a common symptom that is present in those with or without PTSD type-1. It goes away when the level of the anxiety subsides at the end of the panic attack. A sudden surge of high anxiety can cause sudden death from affecting the physiology of heart muscle, producing Takotsubo cardiomyopathy, a sudden a heart attack—so it is hardly surprising that a sudden surge of high anxiety can affect the physiology of the brain in some unique way in some people and effect an epigenetic insertion and PTSD type-1.
7.6 There is a lot we do not know, what we cannot intuitively grasp, about the patho-physiological mechanisms of anxiety alone.
7.7 A book entitled ‘The Soldiers with Stammering Vision and how their observation finally solved the Genomic Codes of PTSD’ may soon be published, giving more details of how what is known about PTSD type 1 and PTSD type-2 came about and of the many people involved in its provenance since Oppenheim, in 1889, first called it Traumatic Neurosis in defiance of the then psychiatrists who called it hysteria following trauma.
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