Romanian Journal of Psychopharmacology (2013) 13, 50-62 [615397]

Romanian Journal of Psychopharmacology (2013) 13, 50-62

IS AROUSAL A VALID THEORY
IN EXPLAINING PSYCHIATRIC ILLNESS?
Florina Rad1, Cristina Petrescu -Ghenea2, Cristina Petrescu -Ghenea2,
Elena Tudora che2, Carmen Trutescu2, Cristina Gianina Anghel2, Iuliana Dobrescu1
1University Medicine and Pharmacy "Carol Davila" Bucharest , Romania
2Clinical Psychiatry Hospital "Prof. Dr. Al. Obregia", Bucharest, Romania

Abstract
In the scientific literature, ever since the beginning of the 20th century, there
have been vechiculated a lot of different theories concerning arousal.
Understanding and elaborating on this concept may help scientists develop pharmacological and psychotherapeutical methods to understand and treat some of the psychiatric disease and syndromes in which arousal is involved. In this article we tried to do a review of the literature about arousal using mainly medical search engines. During last years we could witness an alarming raise in the incidence of Autism and Attention Deficit Hyperactivity Disorder (ADHD) that led to the takeover of modern day Pediatric Psychiatry services by this kind of pathology. Hyperarousal is viewed as the explanation for sensory overactivity in Autism Spectrum Disorders and ADHD. A future better understanding of arousal could be the key in explaining and controlling some challenging behaviors involved in child developmental disorders. For the moment, arousal is used for explaining the paradox of treating ADHD with stimulant medication. Implications of arousal have also been found in mood
disorders or illicit drug use like amphetamines, cocaine or MDMA or in anxiety disorders. This review is not intended to adhere to or strictly support one or another theory about arousal but to enumerate and make a brief synopsis of each idea the literature. The years to come, with the new advances in neurosciences and neuroimaging, will lead to more evidence to support the implication of arousal in different psychiatric pathologies and to the use of this information in different methods of treatment .
Key words : arousal, child developmental disorders.

During last years we could whitness an alarming raise in the incidence of Autism and ADHD that
led to the takeover of modern day Pediatric Psychiatry services by this kind of pathology. If two
decades ago, Child Psychiatrists were predominantly seeing psychotic episodes and quite a
handfull of hysteria – as it was called then, nowadays a major clinic like „Prof. Al. Obregia” in
Buchare st diagnoses 3 to 5 children with ASD and/or ADHD every day according to "Prof. Dr. Al.
Obregia" Data Base.
1 Correspondence: Florina Rad, Clinica de de Psihiatrie a Copilului si Adolescentului, Spitalul Clinic de Psihiatrie
”Prof Dr Al Obregia”, Sos Berceni, nr 10, sector 4, Bucuresti, Romania.
Tel.: +[anonimizat]; e -mail: [anonimizat].

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Is Arousal a Valid Theory in Explaining Psychiatr ic Illness?

Of course we could pin this on the higher adresabillity to psychiatric services acomplished through
the numerous awareness campaignes or to the development of new and specific diagnostic tools
such as the ADI -R and ADOS that are now available for specialists in Romania through Ministry of
Health's 3.1 Programme. But if we take a closer look, in fact it is not typical Autism Disorder that had this recent boom but what we call PDD-NOS or Atypical Autism Disorder and can be described
more like a mix of early onset ADHD with autistic -like features.
This is the reason why we are trying to think about some etiopathogenic hypothesis behind this
disorder. There are many theories taken into consideration by scientist and one of them is the involvement of arousal in both autism and ADHD. (Sthal, 2008) We will make a review of this
theories as they can be found in the literature and also try to show how researchers thought about
aplications of arousal to other frequent psychiatric disorders. The operational definition of arousal proposed by the Rockefeller University researchers states that
an aroused animal or human will be more sensitive to sensory stimuli, be physically more active,
and react more emotionally. (Pfaff, 2003) Until this moment, arousal is defined as a physiological and psychological state of being awake or
reactive to stimuli. It involves the activation of the Reticular Activating System in the brain stem ,
the Autonomic Nervous System and the Endocrine System , leading to increased heart rate and
blood pressure and a condition of sensory alertness, mobility and readiness to respond. There are many different neural systems involved in what is collectively known as the arousal system. Four major systems originating in the brainstem, with connections extending throughout the
cortex, are based o n the brain's neurotransmitters, acetylcholine, norepinephrine , dopamine , and
serotonin. When these systems are in action, the receiving neural areas become sensitive and
responsive to incoming signals. Arousal is important in regulating consciousness , attention, and information processing. It is crucial
for motivating certain behaviours, such as mobility, the pursuit of nutrition, the fight -or-flight
response and sexual activity . It is also very important in emotion , and has been included as a part of
many influential theories such as the James -Lange theory of emotion. (Arousal, 12 January 2013)
According to Hans Ey senck , differences in baseline arousal level lead people to be either extraverts
or introverts . (Eysenck, 1973) Later research suggest it is most likely that extroverts and introverts
have different arousability . Their baseline arousal level is the same, but the response to stimulation
is different which means they have different potentials for arousal. (Sthal, 2008)
The Yerkes -Dodson Law states that there is a relationship between arousal and task performance,
essentially arguing that there is an optimal level of arousal for performance, and too little or too
much arousal can adversely affect task performance.
One interpretation of the Yerkes -Dodson Law is the Easterbrook Cue -Utilisation hypothesis.
Easterbrook states that an increase of arousal leads to a decrease in number of cues that can be

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utilised. (Arousal, 12 January 2013) However, many sport psychology researchers have challenged
this relationship, and the current trend is a shift toward a more "multidimensional" view of arousal –
anxiety and its effects on performance.
In 2003, Arent and Landers published “Arousal, anxiety, and performance: A reexamination of the
inverted -U hypothesis” study. As predicted by the Inverted -U-hypothesis, optimal performance on
the simple task was seen at 60 to 70 % of maximum arousal. Furthermore, for the simple task used in this study, only somatic anxiety accounted for significant variance in performance beyond that
accounted for by arousal alone. These findings support predictions of the Inverted- U hypothesis and
raise doubts about the utility of theories that rely on differentiation of cognitive and somatic anxiety to predict performance on simple tasks that are not cognitively loaded (Arent at al, 2003).
On the other hand, a study published by Basler et. all states that „The intercorrelation matrix of all
variables – gymnastic ability, pulse rate, pa lmar sweating, state and trait anxiety, and gymnastic
performance – revealed limited relationships between gymnastic performance and arousal/anxiety
measures. As expected, gymnastic ability was the best correlate of gymnastic performance.”
(Basler, 1976)
There have been proposed and studied many theories concerning the implication of arousal in
different psychopatologies such as Autist Spectrum Disorder, Attention Defficit Hyperactivity Disorder, Mood Disorders or Anxiety Disorders as well as in everyday normal life.
For many years, high arousal has been regarded as an unpleasant and unwanted state. With an anxious patient we are most likely to try and reduce arousal in order make them feel better. One may
acomplisch this by useing different techniques for i nduceing relaxation. But now, after years of
research and controversy, scientists have reached the idea that high arousal is not necesarrily bad. As Svebak and Stoyva concluded in their paper „In a broad segment of human behavior, especially in the
areas o f sports and entertainment, people seem clearly to be looking not for low arousal but for its
opposite. People seek out high arousal and enjoy it!”. At the time they have writen The Theory of Psichological Revelsals, a motivational theory had been developed to explain the relation between
arousal and hedonic state. According to this theory, there are people who prefer to function in a
hyperaroused state, called paratelic and those who function mostly in the so called telic mode defined
by low arousal. It is also well known that, for the normal individual, both high and low arousal can be
good and desirable raported to the activity that one performes. (Svebak & Stoyva, 1981)
Arousal states strongly influence behavioral decisions. In general, arousal promotes activity and enhances responsiveness to sensory stimuli. Earlier work has emphasized the nonspecific effects of
arousal on multiple classes of behaviors. However, contemporary work indicates that arousal has
quite specific effects on behavior. Neural subst rates for both general and specific effects of arousal
have been identified.

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Based on the scope of their actions, we can distinguish two major classes of arousal elements:
localized versus general. Actions of localized arousal elements are often limited to one class of
behavior, and may thereby mediate specific effects of arousal. In contrast, general arousal elements
may influence multiple classes of behaviors, and mediate both specific and nonspecific effects of
arousal. One common way in which general a rousal elements influence multiple behaviors is by
acting on localized arousal elements of distinct networks. Often, effects on distinct networks have different time courses that may facilitate formation of specific behavioral sequences. Jing’s review
from 2009 highlights prominent roles of serotonergic systems in arousal. The studies also indicate
that the serotonergic elements can act as either localized or general arousal elements. (Jing, 2009)

1. Arousal and Autism Spectrum Disorder
Arousal was initially discussed as a concept involved in the pathology of Autistic Spectrum
Disorders (ASD) stating that these patients are more reactive to sensory stimuly than the rest of the
population, due to hyperarousal.
Hyperarousal is not universally accepted by all researchers; in a review of sensorial patterns in
autistic patients from 2005, Rogers and Ozonoff concluded that the rezults are mixed. (Rogers &
Ozonoff, 2005)
The reasons for hyperarousal not standing up as a general explanatory theory for autism are the
folllowing: ASD is a heterogenous condition and the hyperarousal explanation would be to broad to
justify such a broad spectrum of simptoms. On the other hand, sensitivity to arousing stimuly is not constant in this individuals. And third, the stimuly employed in habituation paradigms cannot be the
same as real life non -laboratory based events.
Hypoarousal has also been proposed as a theory for explaining autistic simptomatology in the 1960s by Rimland, although he had limited laboratory evidence. Shore in 2006 talks about unusual
sensory experiences in autobiographical reports of people with ASD. (Rimland, 1964)
Nevertheless at this moment hyperarousal is viewed as the explanation for sensory over -activity in
ASD and that is why a better undersatanding of arousal could be the key for explaining and handeling some forms of chalanging behaviours.
Some individuals with ASD have difficulties in regulating their emotional responses or
comunicating them to carers. The implication of arousal in mediating stress may be a factor in
chalanging behaviours in ASD.
After analising the literature available at this time, we could conclude that there are two categories of
individuals with ASD with different arousal patterns. The group of hyperaroused people who are over –
reactive to stimuly and often present challenging behaviours and the hypoaroused ones. (Sthal, 2008)

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2. Arousal and ADHD
The „Low arousal theory” is a psychological theory which tries to explain the ADHD
simptomatology by arguing that this individuals are hyperac tive because they need self -stimulation
in order to increase their abnormally low arousal which keeps them from performing at their best
capacity. (http://en.wikipedia.org/wiki/Low_arousal_theory, 1 January 2013 )
ADHD is related to an insuficency of dopa mine system. The problem with ADHD patients is that
they cannot self -moderate and their attention can only be focused by external over -stimulation. This
theory seems to be the best fit for both attention defficit and the hyperactivity simptoms in ADHD.
According to Hare, a person with low arousal is „in a chronic state of stimulus hunger”. (Hare,
1970) In 1977, Mawson and Mawson complete this idea by adding that an individual with low
arousal needs more sensorial input to gain a certain equillibrium.This is why, without enough
environmental stimulation, an ADHD patient will try to self -stimulate by walking, running,
fidgeting, talking and so on. (Mawson&Mawson, 1977) ADHD is described as a defficency in information processing in the prefrontal cortex linked to
under or over -stimulation of the arousal networks through defficencies in the receptors for
Dopamine (DA) and Norepinefrine (NA).
The key in ADHD treatment is to find the „optimal tuning of signal -to-noise ratio”. (Stahl, 2008) It
is important to know if we have a hypo or a hyper -activated brain because the pharmacological
approach can varry from case to case: either by augmenting or by decreasing DA and NE.
With regard to attention defficits, in ADHD patients, studies have shown an abnormal pattern of
cortical activation in other brain regions than controls who, for problem solving activate the anterior cingulate cortex. This aberant pattern makes individuals perform, but with a pour, inefficient result.
Substances that increase DA or alpha 2A adrenergic receptors – stimulants, atomoxetine, guanfacine
or modafinil, can be used to reestablish a normal neurotransmition. This abnormal arousal can be
also found in sleep disorders and therefore treated with stimulant drugs. Normal arousal means „tonic firing of DA and NE neurons” and leads to normal levels of attention. (Sthal, 2008)
When arousal mechanisms are low, not only are the tonic firing rates low in arousal neurons utilizing
NE and DA, but pyramidal neurons in the prefrontal cortex are "out of tune" and unable to distinguish
important neuronal signals from unimportant "noise". This patients cannot focus on one thing more
than another because all signals are the same. They cannot sustain attention because it is easy to be
distracted from one signal to another and that is why they may move or act impulsively. Increasing
DA may diminish the level of the noise, whereas NE may enhance the size of the signal. (Sthal, 2008)
On the other hand, some ADHD patients can present excessive arousal but have the same s ymptoms
as ADHD patients with deficient arousal. They have a high incidence of comorbidities linked to this
overstimulation by NE and DA: mood disorders, anxiety disorders, sleep disorders and substance

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abuse. In the case of overarousal we can observe “phasic firing of NE and DA neurons”. It is
believed that this is the reason for which in some ADHD patients major neural alterations can be
observed to such extent as brain atrophy due to overactivation of the HPA axis in the presence of
chronic stress. Here, stimulation of DA and NE is not appropriate.
Treatments that slowly reduce overarousal in time by desensitizing postsynaptic NE and DA receptors
but also steadily downregulate neuronal activity in order to return NE and DA neurons to normal
phasic firing might be the answer. Norepinephrine reuptake inhibitors (NRIs) that block NET
constantly around the clock desensitize overarousal systems in time and return them to faster tonic NE and DA firing with basicly the same result as treatments that enhances defi cient arousal systems.
It is somewhat of a paradox that agents that increase DA and NE, even tonically, could reduce excessive DA and NE activity over time. That is why this treatments can “make conditions as anxiety somewhat worse before they make them better but it was observed that the therapeutic
effects of such agents in the treatment of ADHD and its comorbidities increase over the first few
months as NE and DA systems theoretically desensitize” (Stahl).
The hypo or hyperarousal aproach is more a theoretical model used with an educational purpose because in real life conditions we can find that “different circuits have different states of arousal in
the various areas of prefrontal cortex” and in complex cases, “some circuits maybe understimulated,
while others are simultaneously overstimulated”. This mixed hypo and hyperarousal can be found in
patients where ADHD is comorbid with tics, conduct disorders, oppositional disorders, psychotic disorders, and affective disorders which makes the psychopharmacological approach much more
difficult. Theoretically, we can use stimulants in combination with atypical antipsychotics because
“atypical antipsychotics simultaneously release DA in prefrontal cortex to stimulate Dl receptors reducing ADHD symptoms, while acting in limbic areas to block D2 receptors to prevent worsening of mania or psychosis”.
When ADHD is comorbid with anxiety, depression or substance abuse augmenting antidepressant
or anxiolytic therapies with a tonic activator of DA and/or NE systems such as long -lasting
norepinephrine reuptake inhibitors (NRIs), or alpha 2A adrenergic agonist rather than a stimulant can be an effective long -term approach. Some studies of NRIs report improvement in both ADHD
and anxiety symptoms, and others report improvement in both ADHD and heavy drinking. “It is interesting that ADHD is rarely the focus of treatment in adults unless it presents with no comorbid conditions. Since lack of comorbidity in adults with A D H D is rare, this may explain
why the majority of adults with AD FID are not treated.” (Stahl, 2008)
“Adults with ADHD smoke as frequently as adults with schizophrenia, at about twice the rate of the normal adult population in the United States. This may be because nicotine subjectively improves ADHD symptoms, especially in patients who are not treated for their ADHD. Nicotine enhances DA
release and arousal, so it is not surprising that it may be effective for ADHD symptoms.” (Stahl, 2008)

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3. Arousal in Mood Disorders
In a research published in 2008 in the Annals of the New York Accademy of Science, MacKinnon
try to explain Bipolar Disorder in terms of arousal saying that "Bipolar disorder can be understood as a disorder of behavioral regulation. Manic and depressed individuals are impaired in the titration
of appetitive arousal, possibly at the level of neuronal plasticity". (MacKinnon, 2008)
Mania is a state of excessive or abnormally high arousal, mood and energy levels. Mania is often in
association with bipolar disorder, which was known as manic -depressive diso rder in the past.
People with bipolar disorder experience cycling periods of mania with alternating periods of major
depression. The symptoms and severity of mania can vary. Some experience only mild symptoms
known as hypomania, in which they tend to need less sleep, have elevated energy levels and show
an increased metabolism. In more severe cases of mania, people may sometimes display psychotic
symptoms that can include delusions and hallucinations.
The major area of the brain affected in mania is the lim bic system through allterations of
neurotransmitters such as adrenaline and dopamine. These modifications lead to abnormally high
levels of arousal that take the form of sexual desinhibition, excessive spending or even shoplifting,
agitation, gambling and all kinds of risky behaviours encountered in mania.
Illicit drugs that that raise arousal levels and have effects that mimic a manic episode are
amphetamines, diet pills – containing diferent mixtures of amphetamines and other substances,
cocaine and MDMA – also known as Extasy. (Turner, 1999)
Several lines of evidence show impaired right hemisphere function in depression. Lateralized simple reaction time tasks show impaired left visual field responses both in normals experiencing a
depressed mood and in patients with mild unipolar depression. One interpretation for these findings
that was prooved by Liotti and Tucker is that depression impairs right hemisphere function by
interfering with right hemisphere arousal and vigilance mechanisms. (Liotti&Tucker, 1992)
Byrne performed an experiment to investigate predictions of vigilance performance among
depressive patients, based on the assumptions that vigilance would vary in a predictable manner
with level of arousal, and that levels of arousal among diagnostic categories of depressive patients are well known. It was found that psychotic depressives, presumed to be hypo- aroused relative to
normals, exhibited poor signal detection performances and committed few false positive errors
relative to normals. Neurotic d epressives, presumed to be hyperaroused relative to normals,
detected fewer signals than did normals, but also made more false positive errors than normals.
Again this was consistent with predictions.
A measure of arousal in experimental subjects, namely barbiturate tolerance, was found to directly
relate to the false positive error rate in all subjects. The relationship between arousal and total signal
detection rate was significantly curvilinear, and an ‘inverted U ’ (quadratic) function provided the

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Is Arousal a Valid Theory in Explaining Psychiatr ic Illness?

best fit. This justified the conclusion that vigilance performance is a function of that component of
arousal measured by barbiturate tolerance. (Byrne, 1976)
Neuropsychological models of depression highlight temporoparietal hypofunction associated with
low le vels of arousal in major depressive disorder. These models were derived from indirect
measures such as neuropsychological tests and alpha band electroencephalography.
In 2008 Moratti et all wanted to determine if large excitatory stimuli directly modulate activity
in sensory regions of the brain involved in attention and arousal in patients with major
depressive disorder.
The study group included 15 women with low anxiety, patients with major depressive disorder. In
control group were also taken 15 girls and women. The groups were matched by age and compliance.
Although emotional images led to a dorsal visual stream in a greater extent than neutral pictures in
both study groups, only the control group showed a strong right temporoparietal cortex excitatory
modulation. Since the temporoparietal cortex is associated with emotional arousal, subjects with
depression may have difficulty in activating cortical areas involved in arousal while processing the
stimuli on activation of dorsal visual stream is intact. (M oratti, 2008)

4. Arousal in Anxiety Disorders
Anxiety sensitivity refers to beliefs that anxiety symptoms or arousal can have harmful
consequences. There is growing evidence for anxiety sensitivity as a risk factor for anxiety disorders. Anxiety sensitivity is elevated in panic disorder as well as other anxiety disorders. It is
thought to contribute to the maintenance and severity of anxiety symptoms. Studies have shown that
anxiety sensitivity more specifically predicts the future occurrence of panic attacks .
The Anxiety Sensitivity Index (ASI), which measures the construct of anxiety sensitivity, has three
subscales, namely, the ASI -Physical subscale, ASI -Social subscale and ASI -Mental Incapacitation
Concerns subscale. The dimension reflecting "fear of phys ical sensations" of anxiety sensitivity is
the most predictive one of panic attacks and panic disorder. Research on the ASI has demonstrated
that persons diagnosed with post -traumatic stress disorder, generalized anxiety disorder, obsessive –
compulsive disorder, and social anxiety disorder all had ASI scores higher than normal controls. (Mantar et all, 2011) Depression was speculated to hold a positive correlation to high anxiety sensitivity scores. The relationships between anxiety sensitivity, alcohol and substance use disorders are still unknown.
There is evidence that anxiety sensitivity is related with "drinking used as a way of coping". Since
anxiety sensitivity is a cognitive construct, it should be taken into consideration when evaluating patients with anxiety and psychotherapeutic formulations. In a complex review from 1957 called „Anxiety and Emotional Arousal”, Robert Malmo tries a
clarification of the concepts of motivation, emotion, and anxiety by 3 different approaches:

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physiological indicants of behavioral arousal such as EMGs and EEGs, experimental studies with
psychiatric patients which show that anxiety should be restricted to the chronic pathological
condition where the patient is physiologically overactive to every stimulating situation, and the
formulation of plausible hypotheses concerning the nature and etiology of anxiety. Like a conclusion he states that anxiety can be produced in organisms by keeping the arousal level very
high for long periods of time. On the basis of neurophysiological data, continuous overarousal may
result in damage of central inhibitory mechanisms. (Malmo, 1957)
In a research pubished in August 1975 in the the Journal for Counsulting and Clinical Psychology,
Gouldfried and Sobochinsky studied the relationship between the tendency to hold certain irrational
beliefs and the likelihood of becoming emotionally aroused in various types of situations. 77 female
undergraduates completed a battery of tests including Jones's Irrational Beliefs Test, the Social
Avoidance and D istress Scale, and Alpert -Haber Achievement Anxiety Test. Results show a
positive relationship between irrational beliefs and the measures of interpersonal, examination, and
public speaking anxiety. Another experiment performed by the same team focused on one specific
irrational belief: the importance of social approval. It was investigated the likelihood of emotional
arousal occurring among individuals who ascribed to this belief. When asked to imagine themselves
in social situations that might be interpre ted as involving rejection by others, subjects holding this
belief reported feeling significantly more anxious and angry than those who did not.
(Gouldfried&Sobochinsky, 1975)
On the other hand, it seems that compared to controls, individuals with generalized anxiety disorder
(GAD) often fail to exhibit expected changes in physiological arousal in response to laboratory
stressors. Nevertheless, individuals with GAD often report significant subjective arousal. Overall,
individuals with GAD exhibit no significant changes in arousal in response to an emotional
challenge. However, basal sympathetic arousal moderated degree of change such that non-comorbid
GAD patients low in baseline sympathetic arousal exhibit changes in arousal similar to controls in
response to a stressor. The fact that basal sympathetic arousal moderates both self -reported arousal
at baseline and sympathetic response to a stressor suggests important physiological heterogeneity in
GAD, wherein only those individuals with heightened tonic sympa thetic arousal report
accompanying symptoms and display diminished sympathetic reactivity. (Fisher et all, 2010)
According to “The Neuropsychology of Anxiety” by Gray and McNaughton, anxiolytic drugs of all types act on a behavioural inhibition system, the most important neural component of which is the
septo -hippocampal system. Anxiolytics affect septo- hippocampal function by impairing the
subcortical control of hippocampal ‘theta’ activity — the main response of the septo-hippocampal
system to arousal. Re cent experiments show that there are multiple systems controlling theta
activity and that anxiolytics act on several, but not all, of these systems. This pattern of results
implies that there are many different types of arousal, only some of which appear to contribute to

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the generation of anxiety in normal subjects and to the etiology of pathological anxiety.
(Gray&McNaughton, 2003)
A very interesting application of the concept of arousal in anxiety disorders is that found by Scott and Beidel in their study from 2011 where children with selective mutism were compared with children
with social phobia. Those with social phobia and selective mutism had chronically higher levels of
arousal as reflected by respiratory sinus arrhythmia and skin conductance levels. This may help
explain why children with selective mutism may appear to others to not be overtly anxious; their
silence may serve to decrease outward signs of anxiety observable by others. (Scott&Beidel, 2011)

5. Arousal in PTSD
Hyperarousal is one of the core carachteristics of Postraumatic Stress Disorder. PTSD is now defined as a pathological anxiety that usually occurs after an individual experiences or witnesses severe trauma that constitutes a threat to the physical integrity or life of the individual o r of another
person. The individual initially responds with intense fear, helplessness, or horror. The person later
develops a response to the event that is characterized by persistently reexperiencing the event, with
resultant symptoms of numbness, avoida nce, and hyperarousal.

These symptoms result in clinically significant distress or functional impairment. To meet the full criteria for PTSD, these symptoms should be present for a minimum of 1 month following the
initial traumatic event. (Risser, 2006)
In a 1997 study, Michael Maes staits that “it is appropriate to express PTSD in terms of general
severity of PTSD and severity of the deppression-avoidance and anxiety-arousal dimensions”. The amygdala is a key brain structure implicated in PTSD. Research ha s shown that exposure to
traumatic stimuli can lead to fear conditioning, with resultant activation of the amygdala and
associated structures, such as the hypothalamus, locus ceruleus, periaqueductal gray, and parabrachial nucleus. This activation and the accompanying autonomic neurotransmitter and
endocrine activity produce many of the symptoms of PTSD. (Maes, 1997)
The hippocampus also may have a modulating effect on the amygdala. However, in people who develop PTSD, the orbitoprefrontal cortex appears to be less capable of inhibiting this activation,
possibly due to stress-induced atrophy of specific nuclei in this region. (Sthal, 2011)
Posttrauma factors that influence whether PTSD develops include availability of social support,
emergence of avoidance o r numbing, hyperarousal, and reexperiencing symptoms.
In a study publicated in 1998 by Maes et all, who tried to define the DSM -IV criteria for PTSD,
concluded that “PTSD is not a well -delimited clinical entity, as there is a clinical continuum from
PTSD non-cases to cases with less and more severe depression -avoidance and anxiety -arousal
symptoms. It is more appropriate to express PTSD in terms of general severity of PTSD and
severity of the depression -avoidance and anxiety-arousal dimensions”. (Maes, 1998)

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Conclusions
Althow a concept that has been dealt with for decades now, arousal still leaves the scientific world
under the impression that it is quite more to it than we know yet. Understanding and elaborating on this concept may help scientists develop pharmacololical methods to enhace alertness, regulating
consciousness, attention and information and stimulus processing. What we know for sure is that arousal is a major component of motivation, and participates through
this in pursuit of nutrition, sex ual activity or fight-or- flight response and it also has an important
role in performance driven activity. After much debate, researchers have reached the conclusion that baseline arousal is the same in all
people, but each individual can response differe ntly to the same level of stimulation. This means
that each of us has different potentials for arousal. A very popular hipothesys in sport psychology, for years, was that too little or too much arousal can
adversly affect task performance. On the other hand, in recent yars, has been prooved that high
arousal is not necesarely bad at certain moments when people seem to be looking for it. For the
normal individual, both high and low arousal can be good and desirable raported to the activity that
one performes .
In psychopathology, hyperarousal is viewed as the explanation for sensory overactivity in Autism Spectrum Disorders and Attention Deficit Hyperactivity Disorder. Maybe this is why, a future
better understanding of arousal could be the the key in explaining and handeling some chalanging
behaviorsthat manifest in this disorders. For the moment, arousal is used for explaining the paradox
of treating ADHD with stimulant medication.
Implications of arousal have also been found in mood disorders, where high l evels seem to be
responsible for risky behaviors encountered in mania like gambling, sexual desinhibition, excessive spending or shoplifting. This effects can be also mimiqued by illicit drugs like amphetamines,
cocaine or MDMA.
In anxiety, arousal kept at a very high level can acount for the etiology of these disorders because
continous overarousal results in damage of the central inhibitory mechanisms.
The limitation of this review is that the main source of information was that of articles published in
online libraries such as Medline, Medscape, PubMed or PsycINFO and that is why it is not intended
to adhere to or strictly support one or another theory about arousal.
We think that the years to come, with the new advances in neurosciences and neuroimaging, will
lead to more and more evidence to support the implication of arousal in different psychiatric pathologies and to use this information in different methods of treatment.

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