The Etiology of Panic Disorder

By John C Goodman

Introduction

The etiology of panic disorder (PD) remains a mystery. This paper will
explore, compare and contrast the historical and current thinking behind
the possible etiologies of PD. There is much conflict, contradiction and
overlap between existing theories. These theories tend to fall within one
of the following three categories: biological/physiological, psychological,
and psychobiological causation (which tends to be the current school of
thought).

PD will first be examined for a historical perspective, where it was

considered to be of biological origin. Then PD will be examined in terms
of its influence on the psychic structure and its defense mechanisms. This
will be explained from the psychoanalytical perspective. Then the
biological and psychological implications of PD on human growth and
development will be explored.

From it earliest reference the etiology of what has come to be know as PD

was considered to be biologic, more specifically cardiovascular in nature
(Raj & Sheehan, 1990). More recently PD has been considered to be
caused by abnormalities in the sympathetic nervous system (SNS).
DaCosta, in 1871 (Heninger, 1998) observed a condition among soldiers
during the American Civil War, which he referred to as “irritable heart.”
This condition consisted mainly of palpitations, chest pains and dizziness
with no apparent trigger (Barlow, 1988). DaCosta attributed it to a
“hyperaesthesia of the cardiac nerve centers” (Heninger, 1998, p.522). In
1919, during World War I, Lewis described a very similar syndrome he
called effort syndrome.” This condition had the same exact symptoms.
Lewis observed that a large number of soldiers developed this syndrome
during physical activity or combat. The symptoms appeared to manifest
themselves in soldiers with either a nervous or physical weakness in their
character or those that had been exposed to stress. Lewis hypothesized
that blood acidosis generated by changes in carbon-dioxide (C02) or
lactate acid levels was responsible for these attacks (Barlow, 1988). It is
interesting to note that Lewis was making a psychological distinction
between those who experience “effort syndrome’ and those who did not,
e.g. nervous characteristics and exposure to stress. Though this condition
was presented from a biological/physiological prospective it appears to
indicate the presents of a psychological trigger and/or predisposition.

In 1941, Wood determined that “irritable heart” and “effort syndrome”

was the same condition and named them neurocirculatory asthenia or
cardiac neurosis, referring to an anxiety state with pronounced
cardiovascular characteristics. Other names given to these same disorders
over history were vasoregulatory asthenia, vasomotor neurosis, nervous
tachycardia, and nervous exhaustion, all reflecting the same biological
origin (Barlow, 1988).

In 1959 Roth discovered a separate condition referred to as phobic

anxiety-depersonalization syndrome. “Roth proposed that
“depersonalization and the underlying psychophysiology of the regulation
of awareness associated with depersonalization might be important keys
to the disorder” (Barlow, 1988, p. 90). Roth’s explanation was the first to
distinguish between panic attacks and anxiety neurosis (Barlow, 1988).

Pitts and McClure were credited for defining PD as a disease. In 1967

they infused sodium lactate into subjects with a histories of spontaneous
PAs to demonstrate that this would trigger a PA. Subjects with no history
of PAs were unaffected by the infusion. Sims & Snaith believed this
experiment substantiated that psychiatric symptoms could be induced
through chemical means (1988).

In 1976 Wooley proposed that PD and mitral valve prolapse were the
same illness. He found the symptoms of the two to be very similar (Raj &
Sheehan, 1990). This appears to be an oversimplification. Wooley likely
confused similarities, and cause and effect between symptoms of MVP
and PD. Hamada, Koshino, Misawa, Isaki, and Gejyo, (1998) studied the
relationship of MVP and autonomic PD. Studying 121 subjects with PD,
they found the occurrence of MVP was higher in these subjects (32.2%)
than in the control group(16.7%), yet they determined the difference to be
insignificant. In a subgroup of PD subjects with depression, the MVP rate
was 58.1%, significantly higher than the value of 25.7% observed in the
PD patients without depression. These findings appear to indicate a
strong relationship with the parasympathetic nervous system (Hamada, et
al., 1998, p.143).

Research supports the theory that the brain chemistry of panickers may be
out of balance or different then non-panickers, yet the reason remains
unclear. The biological view of growth and development within the PD
sufferer may be best understood by the word “predisposition.” A 1990
study by Rosenhaum revealed that:

children of parents with panic disorder and agoraphobia have particularly

high rates of behavioral inhibitions to the unfamiliar compared with
controls. . . . [He found] that about 15% of the normal population
manifests early in life (as young as 21 months) a temperamental quality
known as behavioral inhibition to the unfamiliar (Rosenbaum, 1990, p.
464).

This quality appears to heighten inhibition and arousal in times of

uncertainty and challenge and may be a marker for PD later in life. There
appears to be increased locus ceruleus firing and a possible lower limbic
threshold to arousal and inhibition caused by unfamiliar situations
(Rosenbaum, 1990). However this appears to ignore the influence of
environment cues the child may be internalizing through learning or
modeling, e.g. parental anxiety.

Several studies using twins also imply a genetic factor for PD (Barlow,
1988). One study (Andrews et al., 1990) on twins concludes that although
there was no inheritance of specific disorders . . . there was a genetic
contribution to the predisposing trait(p. 23).
Battaglia et al (1998) conducted a study to detect possible genetic or
familial relationship to the onset and severity of PD. Their findings
suggest:

a significant decrease in the time before the first episode of panic and
onset of panic disorder from the older to the younger generation. No
evidence of a generational effect on the index of severity of agoraphobia
was found. Corrections for possible biases suggested that these results are
not likely to be simple artifacts. (p.595)

Battaglia et al (1998) concluded that if their findings are correct then

trinucleotide repeat sequences might account for the familial aggregation
of PD.

Much research continues to point towards a dysfunction of the central

nervous system (CNS) as the cause of PD. Though the specific
dysfunctions are unknown, it appears that the midbrain structure and the
noradrenegic and serotonergic neurotransmitter system may play a major
role (Taylor & Arnow, 1988). The speculation that PD is caused by a
neurobiological problem is supported by the consistency with which
lactate, caffeine, isoproterenol, yohimbine, and epinephrine induce panic
(Barlow, 1988), as well as evidence that C02 inhalation, hyperventilation,
and behavior also trigger PAs (Taylor & Arnow, 1988). Reiman (1987)
used a PET to identify several abnormalities in subjects with PD.
Creating lactate-induced anxiety attacks in them he found they “had
abnormal hemispheric asymmetries of parahippocampal blood flow,
blood volume, and oxygen metabolism; abnormally high whole brain
metabolism; and abnormal susceptibility to episodic hyperventilation”.
(p.87) Reiman et al. (1989) again utilizing PET measurements and
lactate-induced panic this time finding:

significant blood flow increases bilaterally in the temporal poles;

bilaterally in insular cortex, claustrum, or lateral putamen; bilaterally in
or near the superior colliculus; and in or near the left anterior cerebellar
vermis. Lactate infusion was not associated with significant changes in
regional blood flow incontrol subjects. Thus, the identified regions
seemed to be involved in an anxiety attack. (p.493)

Another study found that PD patients sensitive to sodium lactate who

were observed with a MRI scan had neuroanatomical abnormalities that
usually involved the right temporal lobe. It was reported that “(s)ubjects
with temporal abnormalities were significantly younger at the onset of PD
and had more panic attacks compared with patients with normal MRI
scans” (Ontivero et al., 1989, p. 404). Although it is clear that the
neurological change can be trigger by injecting foreign substances, which
unfortunately there remains no consensus as to why these agents cause
panic.

It is interesting to note that many panickers trace the onset of their PD to

the use of cocaine, amphetamine, or caffeine. These all increase central
nervous system (CNS), noradrenergic activity, supporting the theory that
noradrenergic dysfunction may be a key to the development of PD. If this
theory is correct:

the main neuroanatomic structures involved with panic disorder would

include the locus coeruleus and other noradrenergic midbrain sites and
their ascending pathways. Yet, again, abnormalities in other
neurotransmitter systems cannot be ruled out (Taylor & Arnow, 1988, p
150).

In recent clinical trials Bell & Nutt (1998) provide evidence that
Serotonin has an instrumental role in PD and serotoergic dysfunction.
Their study indicated the effectiveness of Serotonin reuptake inhibitors
(SSRIs) in the management of PD. In conjunction with previous research
showing the effectiveness of tricyclic and monoamine oxidase inhibitors
in treating PD indicates a clear biological connection to PD. However
they admit their findings do not fit a single theory. They concluded that it
is likely different brain regions and 5-HT receptors are involved in
specific ways (1998).
Recent research conducted by Wilkinson et al (1998) reveals a marked
increase in the total body epinephrine-appearance rate and a smaller
increase in the norepinephrine-appearance rate in subjects during
spontaneous PAs.

These findings support the idea that the core abnormalities in panic
disorder will be found in those central neurobiological systems that
regulate SNS function. These data suggest that the panic attack originates
in the brain and only secondarily is there an excessive SNS discharge.
There is an increasingly detailed and differentiated body of knowledge
describing the brain regions, neuroanatomical pathways, and
neurotransmitter systems relevant to fear and anxiety. [3] These are an
essential aspect of the complex circuitry mediating the central pathology
of panic disorder-the spontaneous panic attack-thought to be the result in
appropriately triggered alarm systems. [4]

It has been shown that patients with panic disorder have a lower threshold
for panic attacks to agents that stimulate several different neurobiological
systems, including alterations of electrolyte balance (e.g., carbon dioxide
and sodium lactate infusion [5,6]), increased adrenergic system function
(e.g., yohimbine [7]), increased cholecystokinin, [8] and impaired
gamma-aminobutyric acid (GABA) function (e.g., flumazenil [9]).
(Wilkinson, 1998, p515)

Heninger believes the GABAA system is the most likely candidate for the
central neurobiologic system regulating SNS function, where an
abnormality could explain the etiology of PD (1998). Malizia et al. (1998)
found supporting evidence an association with the
benzodiazepine-GABA (A) receptor to PD and demonstrated that
decreased flumazenil binding at this site might underlie PD.

Yet around the same time Crowe et al (1997) failed to support these
findings. “Within the limitations of the candidate gene linkage method,
panic disorder does not appear to be caused by mutation in any of the
eight GABAA receptor genes tested”(Crowe et al., p.1098, 1997). In his
admittedly limited and restricted study, no evidence was found
connecting PD and eight of the 13 known human GABAA receptor
subunit genes, thus DISCounting this as an indicator of familial panic
disorder (Crowe et al, 1997). As he failed to investigate five of the 13
GABAA receptor subunit genes he many have only succeeded in
narrowing down the scope of possible subunit genes.

Clearly external biochemical agents can trigger a PA in some individuals

who may be biological or genetic predisposition to with PD. Substance
abuse or use (e.g. cocaine, marijuana, and alcohol) appears in many to
play an important role as a trigger, byproduct, or symptom of PD. Louie,
Lannon, and Ketter (1989) found a significant relationship between
cocaine use and PD. They speculated that repeated cocaine use might
gradually deepen panic pathways in the brain over time having a
cumulative affect, which could lead to PD.

There has also been research showing a relationship between marijuana

abuse and the occurrence of PA’s and/or PD (e.g. Weil, 1970; Michelson,
1990; Strohle, Muller, & Rupprecht 1998). It has been reported that
marijuana abuse may provoke panic attacks. A strong association
between agoraphobia and the consumption of marijuana have been found,
as well as an increased risk of anxiety reactions in patients with PD who
smoke marijuana. Complicating the diagnosis of PD in marijuana users is
that depersonalization (often a symptom of PD) is often the most
noticeable feature of marijuana precipitated psychopathology.

In an antidotal case study an adolescent experienced onset of a PD with

agoraphobia after a single PA during marijuana intoxication. Although
there was no family history of PD both parents had been abstinent
alcoholics for over 10 years. They suggest the possibility of a genetic link
of an increased risk for PD and that there many be a greater chance of
adverse subjective experiences during intoxication for those who
experience depersonalization during marijuana intoxication (Strohle,
Muller, & Rupprecht 1998).

A study conducted by George, Nutt, Dwyer, & Linnoila (1990) on

alcoholic patients found a very high degree of PD in alcoholics. There
was a positive correlation between the amount of alcohol they consumed
and the degree of their anxiety. Also, they found an increased amount of
alcoholism in first-stage relations of people with PD:

Common, or overlapping, neurochemical perturbations may play a role in

the etiology of both disorders. This is supported by biochemicals
measured in both disorders that show similar changes in the
noradrenergic and GABA Systems in alcohol withdrawal and during
panic attacks (George et al., 1990, p. 103).

George et al. also questions whether alcoholism may increase the chance
of PD in predisposed people. Although this study implies that there might
be the same type of genetic predisposition as found in alcoholism (1990),
it really is not known whether psychological factors (e.g. weak ego
structure, cognitive, modeled or learned factors) could also predispose
one to similar neurochemical changes and PD.

Some panickers were found to have low exercise tolerance and higher
than normal blood lactate levels preceding exercise (Taylor & Arnow,
1988). As mentioned earlier, Lewis first made a lactate/exercise
connection in 1919. Lactate is produced naturally through physical
exercise and this increase in lactate through exercise as well as when
injected induces PAs in the panickers (Barlow, 1988).

In 1988, Gorman countered these theories by pointing out that some

panicker’s panic while breathing normal room air, which would not alter
the chemoregulatory centers in the way suggested (Taylor & Arnow,
1986). This would imply a cognitive expectation. Barlow conducted an
experiment where he gave panickers CO2 mixed air to inhale and a
nonfunctioning control dial to regulate the intake of the CO2 and air
mixture. Although the dials did not work, the subjects rarely panicked
(1988). This study will be discussed later.

Conflicting biological theories continue to abound in attempting to

determine the etiology of PD. Rosenblat proposed that some PD might
actually be an epileptiform phenomenon. This theory is based on the use
of phobic stimulation to induce PA (1989), thus supporting a
psychobiological causation. Bouwer and Stein’s research indicates there
may be a direct relationship between PD and a history of traumatic
suffocation, which primarily consists of respiratory symptoms and
nocturnal PAs. They hypothesized such a history of may play a part
instrumental in the etiology of PD (1997). These findings also suggest a
psychobiological relationship of PD.

Examining the etiology of PD in terms of gender differences Yonkers et

al. conducted a longitudinal study, which indicated no significant
differences between gender in panic symptoms or degree of severity
initially. Although women run a higher risk of have PD with agoraphobia
and are more likely than men to have a recurrence of panic symptoms
following remission of panic. Their study was not able to determine what
types of biological and psychosocial substrates contribute to the more
chronic course women often experience (1998).

In examining how men and women cope with PD, Chambless and Mason
(1986) found women tend to manage panic through the defense of
avoidance, while men usually used external coping mechanisms, i.e.
alcohol. They also found that in testing for masculinity the less masculine
a subject tested the greater the likelihood of using avoidance as a defense
for coping with stress and anxiety, regardless of gender. George (1990)
postulates that it is possible that separation anxiety, particularly in women,
may be the early form of a defense, which will later manifest itself as PD
or agoraphobia. [The relationship between separation anxiety and PD will
be explored later in this paper.] Also, cultural and social factors may
influence the type of avoidance chosen i.e. agoraphobia for women and
alcoholism and drug abuse for men.

The psychological perspective of PD offers a diversity of explanations for

its etiology. In examining the psychic structure of PD it is generally
believed that PAs are not truly spontaneous. Psychoanalysts believe that
these seemingly spontaneous attacks are related to the unconscious mind.
Freud, who approached psychology from a medical perspective, offers
what may be more accurately described as a psychobiological interpreted
what has now become known as PD. Freud believed unconscious
thoughts, ideas, and fantasies, which were usually related to events during
childhood, were the cause for anxiety. In Freud’s model sexual instinct
also played a key role in the causation of anxiety. He also believed that
PAs were triggered by both past and present events (Taylor & Arnow,
1988). Freud considered anxiety as the ego’s response to the threat of a
traumatic situation. The dangers triggering anxiety entail fantasized
situations with respect to separation from, or loss of, a loved object or a
loss of its love (Taylor & Arnow, 1988). The particular fantasies that
create anxiety are determined by a developmental progression that is
influenced both by maturation and by learning (Taylor & Arnow, 1988, p.
19).

In 1917 Freud described an anxiety model distinguishing three types of

anxiety: expected anxiety, phobic anxiety, and anxiety attacks. It is
anxiety attacks that are now referred to as PA (Barlow, 1988). Even
before that, in 1895 Freud first described what we now know as PD,
referring to it as anxiety neurosis (Holland, 1989); but even for Freud,
panic was not clear-cut. He found a connection between PA and
agoraphobia.

In the case of agoraphobia . . . we often find the recollection of an anxiety

attack and what the patient actually fears is the occurrence of such an
attack under the special conditions from which he believes he cannot
escape it. (Sims & Snaith, 1988, p.26).

In 1919 Freud hypothesized that “defenses against impulses toward …

parental figures resulted in panic attacks (Taylor & Arnow, 1988, p. 18).
These PAs may have been caused by suppressed rage. (Taylor & Arnow,
1988)

In 1920 Freud again wrote about the difficulty of defining panic:

Sometimes it is used to describe any collective fear, sometimes even fear
in an individual when it exceeds all bounds, and often the name seems to
be reserved for cases in which the outbreak of fear is not warranted by the
occasion. Fear in an individual is provoked either by the greatness of a
danger or by the cessation of emotional ties (libidinal cathexes); the latter
is the case of neurotic fear or anxiety (Sims & Snaith, 1988, p. 26).

Fenichel wrote that postponement of affects or delayed emotional

outbursts are often related to incidents of grief and rage as well as being
used by the ego in dealing with issues of shame, disgust and danger.
When the ego needs to protect itself from fear it can defer feelings to a
later time. This postponement may later return as a PA (1945).

Most psychoanalysts view inhibition, symptoms, and anxiety as being

inherently connected. Inhibitions restrict instinctual expression in order to
avoid the anxiety occasioned by the associated unconscious dangers. The
symptom is a sign of, and a substitute for, instinctual satisfaction or
conflict (Taylor & Arnow, 1988, p. 17).

Psychoanalytical theories also focus on the significance of interpersonal

relationships, current experiences, narcissistic disasters, i.e., fear of
humiliation and loss of self-esteem and troubles with self-identity, as
triggering anxiety and panic (Taylor & Arnow, 1988).

Psychoanalytical theory describes how the psychic structure attempts to

use defense mechanisms to ward off PA in people with PD. Typically
defense mechanisms reduce anxiety by regulating or inhibiting the desires
related to the perceived danger (Taylor & Arnow, 1988). Panic occurs
when the ego becomes overwhelmed by anxiety causing a failure in its
ability to regulate and control. Instead of using its defense mechanisms to
avoid a traumatic state it may actually create one. PAs occurs when these
defenses become overwhelmed and are unable to defend against
disturbing memories, images, or feelings, although the actual content
often remains unconscious (Taylor & Arnow, 1988).
In individuals with PAs affect becomes overpowering, causing
[seemingly] spontaneous and random anxiety (Fenichel, 1945). Normally
the ego uses its defenses to cope with anxiety. Fenichel explains:

Defenses against instinctual drives are used by the ego:

to avoid the pain of traumatic panic or of loss of self-esteem. Thus… any

defense is a defense against affect…. They are used so as not to feel pain.
But because the anxiety, which motivates instinctual drive defenses, can
be so painful itself there are defenses used directly toward the avoidance
of the very feeling of anxiety (Fenichel, 1945, p. 161).

Powerful quantities of counter cathexes are often invested in the defense

against anxiety. Many defensive attitudes are not directed against the
situation in which the anxiety may arise but only against the appearance
of the anxiety itself (Fenichel, l945, p. 479). This concept of anticipatory
anxiety is a key focus for treatment in cognitive and behavioral therapies.

“The egos signal fails when the person is, as a result of previous
repression, in a dammed-up state, the slight anxiety added by the
judgment of danger acts like a lighted match in a powder keg (Fenichel,
1945, p. 133).

Other psychological theories define the etiology of PD and how it relates

to growth and development within their paradigms. Learning theory,
dating back to 1917 points to anxiety as a conditioned response to a
fearful situation. As recently as 1998 a study conducted by Larson,
Asmundson, and Stein substantiated previous studies showing that the
resting heart rate of patients with PD is higher than a group with social
phobia and a control group deemed healthy. Their findings imply that the
subject with PD appeared to suffer from anticipatory anxiety (Larson et al.
1998).
The use of modeling may explain why those with panic often have at
least one parent with an anxiety or depressive disorder. As children they
may have picked up cues and attributes from their over-protective,
abusive or neurotic parents (Taylor & Arnow, 1988). Although this
argument can also be used to imply a genetic predisposition, a
conditioned behavior, or ineffective parents who lacked the ability to
meet the needs of their child.

Learning and behavior therapists believe that PAs are not spontaneous.
Rather, a PA is a conditioned response to stimulus conditioned to elicit a
panic, which is unknown to the panicker. The fact that PA is experienced
as spontaneous makes it devastating to the sufferer and often leads to
avoidance behavior.

Cognitive therapy differs from the learning or behavioral models in that it

suggests panickers have fear of fear, they learn to anticipate danger in the
presence of certain cues. It is these terrifying thoughts that produce PD
(Taylor & Arnow, 1988). This cognitive explanation appears to be
consistent with psychoanalytical theorists such as Freud and Fenichel as
to the concept of PAs being a fear of fear, anxiety over anxiety, or panic
over panic. In other words PA appears to be a response to anticipatory
fear or anxiety of a consciously unknown nature. Taylor & Arnow, refer
to Clark’s research in 1986, which indicated that lactate-induced panic in
PD sufferers might be due to their interpretation of somatic sensations
catastrophically. This would support the notion that lactate-induced panic
might be psychologically caused. The physiologic symptoms caused by
lactate infusion may cause subjects to interpret these as signaling the
onset of a panic attack (1988). The difference is the psychoanalytic
theorists believe the response to be due to ineffective ego strength and
defense regulation, whereas the cognitive therapist believe it to based on
learned responses or cognitive distortions.

Mechanic, in 1972, found that stressors may alter how separate events are
evaluated, e.g., illness, death of a relative or witnessing an accident can
increase awareness of the same events occurring in those with panic.
Illness, for example, may direct attention toward somatic sensations, and
if they are perceived as threatening they may trigger anxiety (Hallam,
1985). Preoccupation of these somatic sensations may intensify them,
reinforcing the fears of illness and/or death. The somatic sensations
occurring during times of panic and anxiety are similar to those of many
illnesses, i.e., weakness, rapid heart beat, breathing problems and
dizziness. This may create an over identification with others on both an
affective and somatic level. This could be explained psychoanalytically as
over identification; behaviorally as modeling, cognitively as catastrophic
thinking, cause and effect, or other cognitive distortions; through learning
theory as a learned response or relationship; or biologically as a
predisposed hypersensitive autonomic nervous system.

Many psychological theories recognized control, loss, and separation

issues to be primary issues within the psychic structure of those with PA
and PD (e.g. Hallam, 1995; Barlow, 1988; Taylor & Arnow,1988) This
can be observed by how unfamiliar perceptual experiences can cause
panic, i.e., drug experiences, anesthesia, and depersonalization. What
these seem to have in common is a fear of a perceived loss of control
(Hallam, 1985). Mellman and Uhde found that for people with sleep
panic (which occurs in 1 in 3 panickers), PA often occurs when entering
the stage of deep sleep. They believe that the degree of relaxation
experienced at this level can cause PA and that the panic sufferer’s
mechanisms due to hypersensitivity (1990). In addition it has been shown
that panic can also be induced through relaxation exercises and
meditation. This too could be associated to the feeling of loss of control.
The significance of these findings is that panic can be triggered without
any neurobiological alteration, such as pharmacological or respiratory
influences (Barlow, 1988), implying involvement of the psychological or
cognitive influence.

Barlow found that panickers were hypervigilant about their body

functions and had an overall feeling of helplessness and a sense of being
out of control. In an experiment panickers were given CO2 mixed air to
inhale and a control dial to regulate the amount of CO2 in the mixture.
Although the dials did not work, the subjects rarely panicked because
they had the illusion of control (1988). This appears to suggest that the
psychi, based on its subjective interpretation can override a biological
predisposition for panic.
Kelly (1971) found that by just being reassuring, doctors could keep some
PD patients from having attacks (Taylor & Arnow, 1988). Their
reassurance may interrupt the autonomic and/or cognitive chain reaction
through distraction or by providing a more desirable outcome. These
studies appear to indicate a mind-body or psychobiological connection
between the strength and impact of one’s subjective beliefs and how they
can trigger or prevent a PA. Again this can be accounted for in multiple
ways depending on the paradigm one uses.

The impact on PD caused by issues of loss can be seen in terms of loss of

control; loss of a significant other; loss of a job; or loss of self-esteem,
self worth, or identity. “Problems with attachment and separation are
linked, genetically, developmentally, and causally withpanic disorder in
adults. (Taylor & Arnow, 1988, p. 24) Developmentally PD in adults
appears to be related to separation anxiety in childhood. Neurotic anxiety
or separation anxiety results from insecure bonding to the attachment
figure, brought about by real life experiences of unavailable or
unresponsive caregivers (Taylor & Arnow, 1988, p. 22). Taylor & Arnow
pose an interesting question: Do the parents have trouble separating from
their children, thereby teaching them to be phobic, and, if so, are both the
problems of the parents and the children partly genetic? (1988, p. 23)
Children experiencing panic and trauma upon separation from their love
object may 1ater find it later manifesting itself as panic and/or
agoraphobia, which is thought to be an adult expression of those
childhood stresses. This hypothesis is supported by the “similarity of drug
treatment effects for separation anxiety and adult agoraphobia; family
concordance for separation anxiety and agoraphobia; and history of
childhood separation anxiety in agoraphobia adults (Barlow, 1988, p.
212). Taylor & Arnow (1988) found that in adults most PDs begin as a
spontaneous PA within six months after a major stressful event. Of these
events, the number one stressful situation was separation, followed by job
changes and pregnancy. Yet all of these examples can be explained in
multiple ways: psychologically as an early development deficit, as a
learned/modeled behavior, or a conditioned response, as well as a genetic
predisposition.
Rosenbaum (1990) found that children of panickers were substantially
more inhibited in novel situations than their peers. They also tended to be
more fearful about normal stressful events such as going to the doctor,
speaking in class or riding in elevators (p. 464).

Rosenbaum, (1990) admits it is unknown whether people are genetically

predisposition to PD or if it is learned from nervous parents, yet he
agreement that something must happen to trigger Pas. In addition to the
feelings associated with separation anxiety in childhood and the disrupted
attachment bonds from adults, child abuse, negative developmental
experiences, physiological triggers such as substance abuse and major life
events (i.e., college, moving to a new home, job changes and marital
stress) appear to cause PD.

In conclusion, the original thinking on the etiology of PD was divided

between a biological (neurological or cardiovascular) causation and a
psychological (psychic defense overload or learned behavior) causation.
Current thought takes the perspective of a multi-dimensional etiology.
There appears to be a variety of pharmacological agents, which have been
shown to induce panic, which are associated with several different
neurobiological processes. Some of these processes appear mutually
exclusive. Exploring the psychic structure of the panicker we see during
PD the ego becomes overwhelmed by anxiety. It turns to its defense
mechanisms for relief. These defenses become overwhelmed and somatic
symptoms appear, thus producing a PA. The overwhelmed ego is
expending all of its psychic energy on coping, leaving little energy to use
for growth and development. It appears that loss is a psychological key to
anxiety. e.g. love loss, love object loss, and loss of control. As
development, growth and life proceed, various developmental,
environmental or psychobiological events may cue any genetic or learned
predisposition one may have and influence when and how one experience
and copes with such situations. “These feelings of loss of control may be
associated (learned) with specific patterns of somatic symptoms” (e.g.
Lindemann & Finesinger, 1938) and may also be present in healthy
individuals at less severe levels. More likely the answer will be found in a
complex psychobiological interaction (Barlow, 1988). Although there is
no definitive etiology to PD it is important to realize how common PD
and PA is, what are there likely triggers, and to be aware of there
prevalence with other psychiatric disorders.

Biologically, PD sufferers may have a genetic time bomb waiting to go

off, yet it appears there must be some trigger to ignite the fuse. Whether
the trigger is genetically set or environmentally, psychologically,
experientially, cognitively, or behaviorally triggered. With the knowledge
and theories, which have evolved over time it is now possible to defuse,
dismantle, or even dispose of this bomb through effective biological,
cognitive, behavioral, and other interventions.