There is fresh empirical clinical evidence telling us about the most probable biological nature of PTSD.  The implications of this fresh clinical evidence, clinical evidence that anyone involved with PTSD can readily confirm, helps us now to better understand, to diagnose with more certainty, to better manage and to more rationally treat PTSD.

This empirical fresh clinical evidence has been gained from a thirty five year long exploratory clinical investigation into a specific aspect of the abnormal neurobiology of PTSD. The ‘specific aspect’ is a subtle visual abnormality first (first as far as we know) reported by an ophthalmologist in 1946.  The ophthalmologist had been examining the vision of ex-soldiers from WWII who were suffering  from Traumatic Neurosis.  The soldiers were each reporting to the ophthalmologist that they experienced a strange and persisting visual abnormality whenever they they had to stare with one eye for more than ten seconds or so at a stationary object — something they were routinely being asked to do during the particular eye examination. These ex-soldiers all said that after a few seconds of staring, the stationary objects that were seen in the periphery of their vision started to appear to wave about, and continued to wave about for as long as the ex-soldiers continued to stare at the stationary object in the centre of their visual field.  This notable London  ophthalmologist, a Dr Ross Traquair, performed this same visual test on many if not all his many patients, year in year out, but only patients with Traumatic Neurosis were reporting to him the wavy vision in the periphery.  The ex-soldiers themselves appeared to notice this abnormality only during that particular eye 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 people who aren’t ex-soldiers.  Dr Traquair didn’t investigate this odd visual symptom but did mention it very briefly in a book he was writing on Visual Fields.

        It has been the clinical findings of a thirty five year long  exploratory clinical investigation into the nature of  this  seemingly insignificant visual symptom, and the most probable neurological and genomic  implications of those clinical  findings, that the book is about — the understanding of PTSD.


Author:  Dr Bob Tym, Clinical Neuro-psychiatrist, formerly an  A/Professor of Neurosurgery. (Now retired from active clinical practice.)


(What follows is in essence an abstract of a forthcoming book “Cracking the Code of PTSD”)


Novel twenty-first century clinical evidence shows “PTSD” to be a lot more biologically complicated 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 and for the PTSD expert alike.

For the benefit of the common sense of the everyday person, a “post-traumatic stress disorder”, a PTSD, has to be what the four simple words say it is. So, a PTSD is a “disorder”, meaning a mental (a brain) 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 of anxiety (fear) or disgust) on the brain.  For many people with a PTSD the PTSD lasts for the rest of their life, and the clinical evidence suggests that for them their brain has been permanently damaged by the experience of the sudden fear or sudden disgust that caused the PTSD.  For others with a PTSD the disorder can resolve spontaneously over time.   The trouble has always been trying to understand just how sudden anxiety (fear) or sudden disgust can, for some people, permanently damage their brain and their brain cannot recover spontaneously.

The former name for PTSD was Traumatic  Neurosis, given in 1889 by the Prussian neurologist, Hermann Oppenheim. He thought there must be some “molecular damage to the brain” caused by “fright”, to cause Traumatic Neurosis, but he couldn’t envisage how the damage could come about. In 1980 the name was changed to PTSD  by the American Psychiatric Association (the APA). They couldn’t envisage how a permanent damage could come about either.

By chance, some fresh bits of empirical clinical evidence about PTSD have been turning up, on and off, since 1889. The implications of the fresh bits of evidence, once they had all been joined up, now throw some light on the possible neurobiology of PTSD — what can go wrong inside the brain in in some people in response to a sudden  surge of high anxiety from a fright or sudden disgust.

What is written  here must be understandable to the everyday person.   And, the fresh clinical evidence about the neurobiological nature of a PTSD must be clinically provable, reproducible, for any PTSD expert.  The implications of the new and fully testable clinical evidence, testable by anyone, means that some of what is written here has to be at odds with the currently “authorised” versions of a PTSD given in the AMA’s ‘Diagnostic and Statistical Manual’ (DSM, latest edition ) and the WHO’s  ‘International Classification of Diseases’. (ICD, latest edition).

The new clinical evidence on PTSD has emerged from a thirty-five year long exploratory clinical investigation.   The investigation, initially, was into the nature of a persisting subtle and unique visual symptom that was being reported by some people with a PTSD (a PTSD as is defined in the first paragraph above, by its four simple words).  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 about it “.  A unique visual symptom means that the symptom is only present in some people with a PTSD, not otherwise.   The people experiencing the visual symptom report their own experience of having it.  The more people who spontaneously report the same experience of a particular persisting visual symptom following a mentally traumatic experience, the more credible, convincingly “real”, it has sounded to other people, the rest of us, who don’t experience the same visual symptom.  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 test can be performed  on anyone who is older than five or six years of age.  We come to this Visual Test and the visual symptom that it tests for, latter. (Sections 4.2 and 4.3). The simple Visual Test  can be performed  by any adult on anyone who is older than five or six.

(It is certainly counter to most people’s intuition, their common sense, that a visual test could have anything to do with a PTSD.  But, empirical clinical evidence about PTSD, like PTSD itself,  has never been under any obligation to be intuitive, commonsensical, to anyone.) 

In the later stages of the 30 year clinical investigation this visual symptom had been reported to be persistently present by some people with a persisting anxiety disorder following the experience of a mentally traumatic event,  that is, present in people with a PTSD.  But,  the visual symptom was reported to be persistently absent in other people with an anxiety disorder following the experience of a mentally traumatic event, that is, absent in other people with a PTSD.  So, some people with a PTSD reported that they always had the visual symptom and some people with a PTSD said they never had the visual symptom.

Ten years into the clinical investigation it had been found that in 1946 this same visual symptom had been reported by some ex-soldiers from WWII who were suffering from what was then called Traumatic Neurosis (the name changed to PTSD  1980). It was reported to an eye doctor, the London ophthalmologist, Dr Ross Traquair.  Dr Traquair was examining the visual fields of these ex-soldiers at the time the ex-soldiers reported the symptom.  He took notice of the many reports of the symptom by the ex-soldiers with Traumatic Neurosis and mentioned the symptom in the textbook he wrote in 1946, a text book on Visual Fields.  There is no known evidence that Dr Traquair investigate the visual symptom — and presumably the symptom was only noticed incidentally by the ex-soldiers while they were having their visual fields tested..  There were very many ex-soldiers with Traumatic Neurosis from WWII.

During the ongoing clinical investigation being reported here, it was found that those people with a PTSD and the visual symptom, always reported an intrusive and distressing  abnormally formed flashing-back “re-experiencing” memory of the mentally  traumatic event that had caused the their PTSD.   (See Sections 2.3, and in for more detail in 4.5, of this abnormally formed memory, the abnormal flashback of PTSD). Those people with a PTSD but without the visual symptom, had only normally formed memories of the mentally traumatic event or events that had caused their PTSD, intrusive, yes, but not ‘flashing back’ and not ‘re-experiencing’ memories.

A scientific paper entitled “EMDR, A Cure for PTSD” appeared in 1989. The paper was by the American psychologist, Dr Francine Shapiro. (EMDR is described briefly in Section 3.0 and in detail in Section 6.)

During the ongoing clinical investigation being reported here 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  EMDR.   It was also found that none of  those people with a PTSD with no visual symptom and a normal form of memory of the mentally traumatic event could be helped with EMDR either.


SECTION ONE    Two forms of PTSD and so-called Complex PTSD

1.1   It is apparent, from the observations given just above,  that  there must be two different forms of  the anxiety disorder PTSD.  One form of PTSD 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 mentally traumatic event that caused their PTSD.  Some of the cases could be clinically proven to respond to EMDR but not all. The other form of PTSD 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.

1.2  One form of PTSD can now be called PTSD-A (see Section 2 below)It has a subtle and unique visual abnormality and an abnormal form of memory of the causal event or events that caused it.  PTSD-A cannot recover spontaneously over time. Some people with PTSD-A can  be clinically proven to be cured by EMDR.  Some people with exactly the same PTSD-A cannot respond to EMDR at all. (See below and Sections  2.2 and in detail in Section 4.2 for the visual symptom and Sections 4.2 and in detail in Section 4.5. for the abnormal memory symptom.)

The other form of PTSD can now be called PTSD-B (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-B could respond to EMDR.

The so-called Complex PTSD  (described in detail in Section 2.6) 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 the developing personality of having to live for many years with extremes of inescapable mentally traumatic situations, combined with persisting PTSD-A and or PTSD-B.


SECTION TWO  The nature of PTSD-A, PTSD-B and Complex PTSD. 

2.1 PTSD-A.  PTSD-A is a “categorical” anxiety disorder, “categorical” meaning it has two unique clinical symptoms that characterise the disorder.  Only if both those two unique clinical features are present is the  disorder present; neither of the two unique clinical features  occurs in any other mental of physical disorder.    The disorder 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 fear or disgust triggered in turn by the experience of a sudden  mentally traumatic event.

The two unique clinical symptoms are invariant, implying the two symptoms are unchanging and always there together in PTSD-A.  The two symptoms  can be subtle, implying that one or the other or both are not always obvious or noticed. The two symptoms are unique, implying that neither is found in any other mental or physical disorder.  PTSD-A forms “in real time”, contemporaneously during the moment of  a “traumatic mental shock” causing the PTSD-A, and hence the two unique symptoms come together at the outset.  If and only if  PTSD-A 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 simultaneously,  together. When neither of the symptoms is present then the PTSD-A is completely cured, eliminated. So, these two unique ‘stuck together’ clinical symptoms  constitute an  invariant ‘complex memory and vision symptom’ unique to PTSD-A, and together the two features in effect constitute a module of PTSD-A.  Hence, someone with PTSD-A may have one module of PTSD-A or multiple modules of PTSD-A: a multi-modular PTSD-A is caused by multiple different experiences of mental shock from multiple different experiences of mentally traumatic events. (There can be no definable module of a PTSD-B or of Complex PTSD.)

PTSD-A can be diagnosed in people of any age over five or six years, and PTSD-A can be treated with EMDR in people of any age over five or six years —people from all walks of life. For some people with PTSD-A  it had been caused by the experience of an event that would terrify anyone, and for some people with PTSD-A it had been caused 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.  From person to person the susceptibility to getting PTSD-A varies widely (See Section 3.3 for the increased susceptibility of developing PTSD-A for those with genes for ADHD).  The spectrum of severity of PTSD-A extends from not at all severe to severely incapacitating.

2.2 The abnormal visual symptom of PTSD-A.   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 one eye is steadily focussing on a stationary object straight ahead. The symptom is called ‘persisting peripheral oscillopsia‘.  (This 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 Section 4.3.) For most people with PTSD-A the symptom is only noticed when it is tested for.  Its presence always indicates the presence of PTSD-A, regardless of the presence of other mental or physical disorders.

2.3 The abnormal memory symptom of PTSD-A, the recurrent abnormal flashback, is a recurrent abnormal re-experiencing memory recall of what was emotionally and sensorially experienced during that moment of the mental shock that had caused the PTSD-A.  Its presence always indicates the presence of PTSD-A, regardless of the presence of other mental or physical disorders.     (This is described in detail in Section 4.5.)

 2.4 PTSD-B.  PTSD-B is a “dimensional” anxiety disorder, “dimensional” implying it has no unique clinical symptom or symptoms that characterise the disorder, it is a generic anxiety disorder caused by experiencing mental trauma.  PTSD-B can be caused by the experience of a sudden traumatic mental shock, as can PTSD-A, but unlike PTSD-A, PTSD-B 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 damages 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 common anxiety symptoms that are common to both anxiety disorders PTSD-A and PTSD-B.   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 periods of dissociation, periods of derealization. There can be sleeplessness, frightening nightmares of the event or of anything else, emotional withdrawal, hypervigilance—being easily startled over anything,  being inattentive;  lacking in concentration; failing to remember things; recurrent tension headaches; recurrent 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 self harm and suicide.

Since PTSD-A and PTSD-B are distinctly different clinical entities neurobiologically, but they can have many non-specific anxiety-related symptoms in common, they can appear superficially clinically indistinguishable.  The two neurobiologically different anxiety disorders PTSD-A and  PTSD-B can be present alone, or, being different disorders, both can be present together. 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, with personality disorders, and together with ADHD and other autism spectrum disorders.

2.6. The nature of Complex PTSD.   This is not a third form of PTSD, it is a “dimensional” personality disorder. The resulting personality symptoms are similar to 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 symptoms of C-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 having multiple modules of PTSD-A from multiple traumatic mental shocks as a combatant or other first responder. C-PTSD usually has but not necessarily has followed interpersonal trauma.  The spectrum of severity of the personality disorder, C-PTSD, extends from not at all severe to severely incapacitating and can be of any duration.

(The features of Borderline Personality Disorder  include impulsive and risky behavior; 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 behavior or threats of self-injury; fear of being alone or abandoned, pervading sense of emptiness.)


SECTION THREE: The plausible speculation of the neurobiology of PTSD A and its elimination by EMDR treatment, based on abductive reasoning from the fully testable clinical evidence.

[ 3.0 First, a brief explanation of  EMDR treatment. (Given in more detail in Section 6.).  Eye Movement Desensitisation and Reprocessing treatment, EMDR, consists of (i), asking a person with a PTSD-A to voluntarily evoke and hold the abnormal form of re-experiencing flashback memory (described above and in detail in Section 4.5). Then (ii), immediately asking them to follow with their eyes the moving hand and finger of the therapist as the therapist sweeps the hand and finger to and fro from far left to far right at 1 to 2 sweeps per second in front of them (rapid side to  side eye movements are called “saccades“.) And then (iii), asking the person to stop moving their 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 form of memory of the same moment of the 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, EMDR may be effective in permanently changing the abnormal form of memory to a normal normal form within ten seconds of starting saccades, 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. For some people 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-A the EMDR, although well tolerated, turns out to be totally ineffective, no matter for how long EMDR sessions are continued.  It is not possible to predict for whom EMDR treatment will be ineffective without trying EMDR treatment and persevering.]

3.1. Neurobiology of PTSD.  A senior geneticist, well acquainted with all the clinical evidence given here (and in the book referred to in the title of this document), who had experienced multi-modular PTSD-A, had also experienced successful EMDR treatment. He said that some of his abnormally formed memories (some of his PTSD-A modules) were changed to permanent normally formed memories within ten seconds of starting the saccades of the EMDR. He also said that in his experience as a senior research geneticist, only some epigenetic mechanism could explain such a fast action on 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 can cause an instant change in the brain’s DNA (instantly forming a module of PTSD-A) 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. A second senior geneticist, who subsequently had PTSD-A eliminated by EMDR treatment, agreed with the first geneticist’s views. 

3.2. An ‘epigenetic mechanism’ in this context implies one or more chemical methyl groups (CH3) being tagged-on to some of the the brain’s DNA molecules, tagged-on via the action of the enzyme methyl-transferase. The DNA molecules that are tagged function (express themselves) abnormally.  They form a PTSD-A module, that is, they form an abnormal combination of an abnormally formed memory of the emotional, sensorial and or physical experiences during that moment, a second or so, during the sudden surge of anxiety, combined with persistent peripheral oscillopsia.  The module of PTSD-A gives rise to persisting anxiety. The abnormally formed memory can only be recalled in the abnormal form of the recurrent abnormal re-experiencing flashback. 

A possible site and mechanism:  It is known that in the region of the brain where this “module of PTSD-A” is believed to be stored 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 areas of cortex that can be electrically activated by movements seen in the visual fields.  This area of the anterior insular cortex it is part of the vestibulo ocular reflex system (the system that  maintains a steady focus of the eyes when the head moves by reflexly moving the eyes).  It is postulated that voluntary saccades, combined with voluntary activation of the  abnormal form of memory, that is, EMDR treatment, can bring about a step by step epigenetic reversal—the methyl groups  are detached from the DNA molecules.  This allows the no longer tagged DNA molecules to function (express themselves) normally and they convert the abnormally formed re-experiencing memory, step by step, to a normal form of non-re-experiencing memory.  Simultaneously, the abnormal form of wavy vision, persistent oscillopsia, is step by step and in step converted to normal stable peripheral vision, confirmable on simple visual testing. 

So much for the abductive reasoning, the plausible speculation, of the clinically involved geneticists,  based on their knowledge of genetics, their clinical experience, and, the clinical evidence.  But, EMDR is not effective for everyone with a PTSD-A.

3.3 But, there is significant clinical evidence taken from the cohort of 9000 or so randomly referred people examined in the thirty year clinical investigation, that a person’s genome, their total genetic makeup, has a marked effect on many aspects of the clinical manifestations of PTSD-A.  For example, those people with the genes for ADHD appear to have a significantly  increased risk of developing PTSD-A in response to the experience of a mental shock, and making it appear that PTSD-A is heritable (which it obviously cannot be, even when PTSD-A appears to cluster in certain extended families).  There us a statistically significant comorbidity that cannot be attributable to chance or behaviour. Also, those people with genes for dark eyes and or olive skin appear to have more severe persistent peripheral oscillopsia, and, an increased risk of being relatively or absolutely EMDR-treatment-resistant. It might be reasonable to speculate that there are some people whose genes prevent them from developing PTSD-A under any circumstances.

(There is no speculation forthcoming for the mechanism whereby the person’s genome influences these clinical manifestation of their PTSD-A: for example,  the ease or otherwise of epigenetic insertion being triggered by a surge of anxiety, and, the possibility or impossibility of an epigenetic reversal via EMDR.)

SECTION FOUR: The diagnosis of PTSD-A and PTSD-B and The Visual Test for PTSD-A        

4.1 Obviously, PTSD-A and PTSD-B require very different treatments.  Having the same non-specific anxiety symptoms they can appear virtually clinically indistinguishable.  Being neurobiologically two different disorders they can both be present at the same time.  Either or both can be together with other disorders, including Complex PTSD. The  presence  or absence of PTSD-A can only be confirmed by the presence or absence of one or other or both of the symptoms unique to PTSD-A, that is., by the presence of a module of PTSD-A.

4.2 The unique visual symptom of PTSD-A:  Persisting Peripheral Oscillopsia.  (‘osi-lop-sia’, a Greek word for ‘wavy vision’)

Persistent peripheral oscillopsia is an illusory perception (meaning a false perception) of stationary objects seen in the periphery of the field of vision appearing to be moving about —  waving up and down, side to side or round and round .  For most people with PTSD-A this visual symptom is seen to be present only when the head is held still, and with one eye closed, the other eye is held fixated on some stationary object straight ahead for 5 to 10 seconds.  Once 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.

This symptom (this form of oscillopsia) is unique to PTSD-A.  It does not occur in any other physical or mental disorder.  It is always present in those PTSD-A  ( that is, in anyone with the other unique feature of PTSD-A, the recurrent abnormal re-experiencing flashbacks).

This visual symptom was first described (as far as we know) in 1946 by a London  ophthalmologist, Dr Harry Moss Traquair*.   It had been reported to him by ex-soldiers  suffering from Traumatic Neurosis from WWII.  Traumatic Neurosis was 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.

4.3 The simple Visual Test for persistent peripheral oscillopsia, hence  for the presence or absence of PTSD-A.

The visual test is a simple test but is reliable, sensitive and specific for the presence or absence of persistent peripheral oscillopsia, hence The Visual Test is reliable, sensitive and specific for the presence and absence of a module of PTSD-A.    This was first published in 2009.

[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). ]

4,4 Performing the simple Visual Test for the presence or absence of PTSD-A. 

The test can be performed by anyone on anyone over the age of five or six years who is not blind and is fully co-operative. For those not understanding the language an interpreter will be needed.

Let us suppose here that the person being examined is female.

The test cannot be performed if she is acutely anxious—there are many transient and chaotic visual abnormalities 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.

  1. Throughout the test she remains seated.
  2. One of her eyes is covered (let us say her left).
  3. She is asked to focus with her right eye on the pupil of the examiner’s left eye.
  4. The examiner stands a metre or so in front, and will have the right eye covered.
  5. The examiner’s left eye is then focussed 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.
  6. The examiner’s left arm is held out rigid and horizontal. The fingertips of the left hand must just reach the outer periphery of her right visual field—the examiner’s distance from her has to be adjusted so that she can just see the fingertips but no further out: this is an essential detail.
  7. 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.
  8. During the ten seconds of the test she is asked to pay strict attention to what, if anything, appears to happen to the examiner’s left arm, hand or fingers while her right eye remains fixated on the examiner’s left eye.
  9. After 10 seconds the examiner lowers the left arm and asks her to demonstrate with her right arm, how the examiner’s left arm appeared to her at any time during the 10 seconds of keeping her right eye fixated on the examiner’s 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 the outstretched left arm, the hand or just the fingers, appeared 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 the examiner’s left eye and the examiner’s 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 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-A. The jerks do not persist, and they are not part of persistent peripheral oscillopsia or any other form of 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: the 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 the authors experience these are extremely rare.

4.5  The unique memory symptom of PTSD-A.  The  nature of the recurrent abnormal re-experiencing flashback.  A recurrent abnormal re-experiencing form of memory recall of what emotional, sensorial and or physical experience was noticed  during that moment of a second or so of the mental shock, the sudden surge of high anxiety, that had triggered the PTSD-A.

An abnormal flashback is not a dissociative phenomenon and not a dream and not a nightmare. Dreams and nightmares are not characteristics of PTSD-A or PTSD-B but they are common non-specific anxiety symptoms of PTSD-A, 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-A 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 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-A, hence persistent peripheral oscillopsia will be always present on testing.   If abnormal flashbacks recur at all, then at anytime in between them, at any time, the Visual Test will give a positive test result for persistent  peripheral oscillopsia.


SECTION FIVE: Treatment of PTSD-A. 

5.1 Treatment of PTSD-A.  PTSD-A cannot spontaneously resolve over time.   Properly performed EMDR (see Section 6.1 and 6.2 ) has the best chance, but no certainty, of permanently eliminating (curing) PTSD-A.  (EMDR has no effect on PTSD-B.) If properly performed EMDR treatment has no effect on PTSD-A, and sadly it cannot be successful for everyone with PTSD, then PTSD lasts life long unless successfully cured by something else, but as yet nothing else is known to permanently cure PTSD-A. No one knows whether a person with PTSD-A  will or will not respond to properly performed EMDR until it has been tried and persisted with for some time. The clinical evidence is that properly performed EMDR is only effective in eliminating PTSD-A in persons of certain genotypes (genetic makeups).

Most of the people with PTSD-A who do not respond to properly performed EMDR can be helped considerably by treatment that reduces the severity of the anxiety and anxiety related symptoms. 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 certified therapists.  As yet there is no proof  that these other treatments have permanently cured PTSD-A (or PTSD-B). They do give some hope of significant alleviation of severity to those with PTSD-A for whom EMDR has failed,  (and for those with severe PTSD-B).

The clinical proof of success or otherwise of EMDR treatment having eliminating PTSD-A (eliminating all modules of multimodular PTSD-A)  is easily determined by having a positive Visual Test result before treatment and a negative Visual Test result immediately after treatment. Similarly, by having one or more abnormal re-experiencing form of memory recall of the moment of mental shock before treatment and only normal form of non-re-experiencing memories immediately after treatment.  The Visual Test is the quicker and more accurate of the two tests — The Visual Test remains sensitive, reliable and specific regardless of the presence of other mental or physical disorders.

Following the successful treatment of PTSD-A, then PTSD-B and or Complex PTSD, and or any other mental disorder may remain, and be in need of separate treatment.

5.2 Treatment of PTSD-B and Complex PTSD.   Both disorders are “dimensional disorders”, that is, neither has any unique clinical feature that alone characterises the disorder (that is, there is no feature that alone has to be always present to make a diagnosis):  at the lower end of the spectrum of severity the disorders merges imperceptibly with a normal mental state and an unremarkable personality.

Both disorders are treated with extensive social support and standard short or long-term psychotherapy techniques and or anxiety relieving medication or other anxiety relieving substance.  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-A 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-A therapies will be needed.


6.1 Properly Performed EMDR for the treatment of PTSD-A. 

First of all,  one has to be sure the person has PTSD-A, that is, the person has  persistent peripheral oscillopsia and has recurrent abnormal re-experiencing flashbacks. Children over the age of five or six years with proven PTSD-A can be treated with EMDR. Since the effectiveness of EMDR in eliminating PTSD-A is determined by, amongst many other factors, the person’s genome, it’s effectiveness cannot be predicted with certainty before attempting treatment. There is no proven clinical evidence that EMDR cures any disorder other than PTSD-A.  (It might be a helpful placebo treatment for some disorders).

6.2 The treatment. 

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).   The person being treated sits comfortably in a chair; the therapist sits or stands in front, a metre 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 sensation 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.

As soon as the abnormal experiential flashback image is “held”, he has a run of saccades, that is,  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 three 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 goes, and then the therapist stops also.  This temporary disappearance of the image 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  hand-sweeps (and his saccades).

The procedure is repeated.  Each repeated run of his saccades has the abnormal experiential flashback image re-evoked, and each run of saccades is continued until the flashback image or other sensation goes.

If EMDR is being successful, then following every few runs of saccades, he senses that, step by step, the the anxiety is lessening and the flashing back image or other sensation is 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 step-by-step likewise, lessening in amplitude of oscillation and or lessening in frequency of oscillation.

The runs of saccades must continue until no fragment of that flashback image or other sensation 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.

If he had one or more other flashbacks (more PTSD-A modules) from one or more other experiences of traumatic events, then each flashback (each PTSD-A module) must be treated by EMDR until eliminated before PTSD-A has been fully cured, eliminated. Only then will there be a negative result from the Visual Test, no hint of any peripheral oscillopsia on testing.

If  other mental disorders are present at the same time, for example, PTSD-B, Complex PTSD, then they will be left to be treated in some other way after PTSD-A has been cured.


7.1 No one can be born with PTSD-A.  It appears that PTSD-A cannot occur in those under five or six years old.

7.2 There is readily confirmable clinical evidence that those people with the genes for ADHD are at markedly extra risk of developing PTSD-A in response to experiencing a mental shock at any age over five or so years than are those without the genes for ADHD.  What a mental shock, a sudden surge of anxiety, can or cannot do to the brain of those younger than five years old children, particularly to those with the genes for ADHD, is not known.

7.3  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.  This is presently unknowable.

7.3 Oscillopsia, “wavy vision”, is just one of many physiological disorders that high anxiety can produce. In a panic attack “wildly wavy vision” is a common symptom that is present in those with or without without PTSD-A. 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 and trigger an epigenetic insertion and PTSD-A.

7.4 There is a lot we do not know, cannot intuitively grasp, about the patho-physiological mechanisms of anxiety.

7.5 A book entitled ‘Cracking the Code of PTSD’ may soon be published, giving more details of what is known about PTSD-A and PTSD-B and how it became known from the 30 year long clinical investigation.