PTSD.net !

CRACKING THE CODE OF PTSD

Fresh clinical evidence telling us about the probable

biological nature of PTSD: u understanding, managing and
treating PTSD rationally.

The empirical clinical evidence base gained from a 35 year

clinical investigation into the neurobiology of PTSD.

Dr Bob Tym, Clinical Neuro-psychiatrist, formerly an A/Professor of

Neurosurgery. (Now retired from active clinical practice.)

(Abstract of a forthcoming book “Cracking the Code of PTSD”)

Contents

Introduction The fresh clinical evidence

Section One The two different PTSDs, and so-called complex PTSD
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 Section Two The nature of PTSD-A and PTSD-B and so-called Complex PTSD

Section Three The neurobiology of PTSD-A and its response to EMDR

Section Four The diagnosis of PTSD-A and PTSD-B & The Visual Test for PTSD-A

Section Five The treatment of PTSD-A, PTSD-B and Complex PTSD

Section Six Performing EMDR for the treatment of PTSD-A

Section Seven Addendum

INTRODUCTION.

Novel twenty-!rst century clinical evidence shows “PTSD” to be a lot

more biologically complicated than previously thought. The novel 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 bene!t 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 (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) e"ect 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
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 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 o", 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 Classi!cation of Diseases’. (ICD, latest edition).

The new clinical evidence on PTSD has emerged from a thirty-!ve 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 de!ned in the !rst 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, speci!c 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 !ve 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
4.3). The simple Visual Test can be performed
by any adult on anyone who is older than !ve 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 persiting anxiety disorder following the experience of a mentally
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 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 su"ering 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 !elds 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 !elds 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
symptom,
always reported an intrusive and distressing abnormally formed
#ashing-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
#ashback of PTSD). Those people with a PTSD but without the visual
symptom, had only normally formed memories of the mentally
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 traumatic event or events that had caused their PTSD, intrusive, yes, but
not ‘#ashing back’ and not ‘re-experiencing’ memories.

A scienti!c paper entitled “EMDR,

EMDR, A Cure for PTSD
PTSD” appeared in 1989.
The paper was by the American psychologist, Dr Francine Shapiro.
(EMDR is described brie#y in Section 3.0 and in detail in Section 6.
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 n one 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 di"erent 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
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 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
nique 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
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. 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

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 e"ects on the developing personality of
having to live for many years with extremes of inescapable mentally
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 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. PTSD-A is a “categorical”
categorical” anxiety disorder
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

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 brie#y 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’
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 clinical symptoms constitute an invariant ‘complex memory and vision
symptom’ unique to PTSD-A, and together the two features in e"ect
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 di"erent experiences of mental
shock from multiple di"erent experiences of mentally traumatic events.
(There can be no de!nable module of a PTSD-B or of Complex PTSD.)

PTSD-A can be diagnosed in people of any age over !ve or six years, and
PTSD-A can be treated with EMDR in people of any age over !ve 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 !eld when one eye is steadily focussing on a
stationary object straight ahead. The symptom is called ‘persisting
persisting
peripheral oscillopsia
oscillopsia‘. (This is described in detail in Section 4.2
.2, and
the simple visual test for the presence or absence of persistent
peripheral oscillopsia is described in Section 4.3
4.3.) For most people with
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 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 #ashback, 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.
4.5.)

2.4 PTSD-B
PTSD-B. PTSD-B is a “dimensional”
dimensional” anxiety disorde
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
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 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 di"erent clinical entities

neurobiologically, but they can have many non-speci!c anxiety-related
symptoms in common, they can appear super!cially clinically
indistinguishable. The two neurobiologically di"erent anxiety disorders
PTSD-A and PTSD-B can be present alone, or, being di"erent
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 de!ned as emotional dysregulation,
interpersonal di$culties, 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
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 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 !rst 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; #uctuating 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

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
#ashback memory (described above and in detail in Section 4.5
.5). Then
(ii), immediately asking them to follow with their eyes the moving hand
and !nger of the therapist as the therapist sweeps the hand and !nger
to and fro from far left to far right at 1 to 2 sweeps per second in front of
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 them (rapid side to side eye movements are called “saccades
saccades“.) And
then (iii), asking the person to stop moving their eyes as soon as the
evoked re-experiencing #ashing-back memory goes. Then, repeating (i),
(ii) and (iii), perhaps several times, until the abnormal #ashing-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 e"ective 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 di$cult
for them to tolerate, because of their intense anxiousness on evoking a
#ashback, or for some other reason.

For some people with PTSD-A the EMDR, although well tolerated, turns
out to be totally ine"ective, no matter for how long EMDR sessions are
continued. It is not possible to predict for whom EMDR treatment will be
ine"ective 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
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 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 inde!nitely, and
intermittently recalled abnormally. A second senior geneticist, who
subsequently had PTSD-A eliminated by EMDR treatment, agreed with
the !rst geneticist’s views.

3.2
3.2. An ‘epigenetic
epigenetic mechanism
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
#ashback.

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
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 movements seen in the visual !elds. This area of the anterior insular
cortex it is part of the vestibulo ocular re#ex system (the system that
maintains a steady focus of the eyes when the head moves by re#exly
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
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, con!rmable 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
But, EMDR is not e"ective
for everyone with a PTSD-A.

3.3 But, there is signi!cant 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 e"ect on many aspects of the clinical manifestations of PTSD-A.
For example, those people with the genes for ADHD appear to have a
signi!cantly 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 signi!cant
comorbidity that cannot be attributable to chance or behaviour. Also,
those people with genes for dark eyes and or olive skin appear to have
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 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 in#uences 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 di"erent treatments.

Having the same non-speci!c anxiety symptoms they can appear
virtually clinically indistinguishable. Being neurobiologically two di"erent
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 con!rmed 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 !eld
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 !xated 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 #ashbacks).

This visual symptom was !rst 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 su"ering 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 speci!c for
the presence or absence of persistent peripheral oscillopsia, hence The
Visual Test is reliable, sensitive and speci!c for the presence and
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 absence of a module of PTSD-A. This was !rst 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 Re!nement of Construct PTSD and Its Visual State Marker.
Traumatology. 15(3): 22-33 (2009). ]

4,4 Performing the simple Visual Tes

Test for the presence or
absence of PTSD-A.

The test can be performed by anyone on anyone over the age of !ve 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 !xation,
some part of the outstretched left arm, the hand or just the !ngers,
appeared to swing up and down or round and round, to shiver, to
oscillate, at about two to !ve 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 !xated 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 signi!cance 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
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 other form of abnormal oscillopsia disorder.

Figure
Figure. How the examiner appears to the person being examined.
The oval line is the outer edge of the visual !eld 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 !ngers must just reach
the very outer edge of the right visual !eld 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 #ashback. 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 #ashback is not a dissociative phenomenon and not a

dream and not a nightmare
nightmare. Dreams and nightmares are not
characteristics of PTSD-A or PTSD-B but they are common non-speci!c
anxiety symptoms of PTSD-A, regardless of their content.

Abnormal #ashbacks 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 #ashback is a ‘#ashing 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 #ashback 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 #ashing-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 #ashback 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
:
 #ashbacks 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 e"ect on PTSD-B.) If properly performed EMDR treatment
has no e"ect 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 e"ective 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
certi!ed 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
:
 signi!cant 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 speci!c 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
e"ectiveness 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.

SECTION SIX: Performing EMDR

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 #ashbacks. Children over the age of !ve or six years with
proven PTSD-A can be treated with EMDR. Since the e"ectiveness of
EMDR in eliminating PTSD-A is determined by, amongst many other
factors, the person’s genome, it’s e"ectiveness 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 quali!ed 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 di"erent) abnormal re-experiencing #ashback, and then
“hold” that “visual picture” (if there is one) or whichever sensation is the
most characteristic of his #ashback. 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 !rst 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 #ashback 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 #ashback
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 #ashback image re-evoked, and each run of
saccades is continued until the #ashback image or other sensation goes.
YYY

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 #ashing
back image or other sensation is degrading in intensity step-by-step. If
and only if there is no other #ashback, then on re-doing the Visual Test
the persistent peripheral oscillopsia will be lessening in range over the
visual !eld 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 #ashback

image or other sensation can be re-evoked. It may take as few as one,
two or three runs of saccades at his !rst 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 #ashback image or other sensation can be voluntarily re-
evoked.

If he had one or more other #ashbacks (more PTSD-A modules) from

one or more other experiences of traumatic events, then each #ashback
(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.

SECTION SEVEN: Addendum.

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

7.2 There is readily con!rmable 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 !ve 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 !ve 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 a"ecting 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 a"ect 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.

THE END
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