Neuropsychology of Anxiety Disorders

NEUROPSYCHOLOGY OF
ANXIETY DISORDERS
SHRUTI LAHOTI
GUIDED BY: MRS. AMRITHA S.
 Anxiety disorders are common with the prevalence varying between
2% and 5% in population-based studies (APA, 1994).

 During the past decade, an increasing number of studies addressing
neuropsychological functioning in anxiety disorders have been

published.
 However, the majority of this research has focused on the less
prevalent obsessive–compulsive disorder (OCD), whereas less

attention has been paid to the DSM defined anxiety disorders, such
as panic disorder (PD) and social phobia (SP)
Role of the Amygdala in Fear Learning
and Expression
 Neural activity within the amygdala is modulated by cortisol,
norepinephrine (NE), and other neurotransmitters and by

mnemonic input related to previous conditioning and
reinforcement experiences conveyed by projections from
mesiotemporal and prefrontal cortical structures.
 Electrical stimulation of the amygdala can evoke emotional
experiences (especially fear or anxiety) and the recollection of

emotionally charged life events from remote memory
 The amygdala also appears to play important roles in mediating innate fear and in
processing affective elements of social interactions (Weiskrantz, 1956)
 Amygdala lesions cause rats to lose their fear of cats and monkeys to lose their fear of
snakes (LeDoux, 1998)
 In monkeys, amygdala lesions reduce aggression as well as fear and cause animals to
become more submissive to dominant animals (Murray et al.,1999)
 In humans, blood flow increases in the amygdala as subjects view faces expressing
fear or sadness (Murray et al., 1999)
 and amygdala lesions impair the ability to recognize fear or sadness in facial
expression ; and fear and anger in spoken language

Role of Prefrontal Cortical Structures in
Modulating Fear and Anxiety Behavior
 PFC structures are thought to participate in interpreting the
higher-order significance of experiential stimuli, in modifying

behavioral responses based on competing reward versus
punishment contingencies, and in predicting social outcomes
of behavioral responses to emotional events
 These areas share extensive, reciprocal projections with the
amygdala, through which the amygdala can modulate PFC

neuronal activity and the PFC can modulate amygdala-
mediated responses to emotionally salient stimuli
 They also participate in modulating peripheral responses to stress,
including heart rate, blood pressure, and glucocorticoid secretion

 The neuronal activities within these areas are, in turn, modulated by
various neurotransmitter systems that are activated in response to

stressors and threats. For example, the noradrenergic, dopaminergic,
and serotonergic systems play roles in enhancing vigilance,
modulating goal-directed behavior, and facilitating decision making
about probabilities of punishment versus reward by modulating
neuronal activity in the PFC
Medial Prefrontal Cortex (mPFC)
The reciprocal projections between the amygdala
and the mPFC are hypothesized to play critical roles

in attenuating fear responses and extinguishing
behavioral responses to fear conditioned stimuli that
are no longer reinforced
 Humans with mPFC lesions show abnormal autonomic responses to
emotionally provocative stimuli, inability to experience emotion related
to concepts, and inability to use information regarding the probability
of aversive social consequences versus reward in guiding social
behavior (Damasio, 1990).
 Physiologic activity also increases in more dorsal mPFC areas in
healthy humans as they perform tasks that elicit emotional responses
or require emotional evaluations

 During anxious anticipation of an electrical shock, CBF
increases in the rostral mPFC, and the magnitude of CBF

correlates inversely with changes in anxiety ratings and heart
rate
 In rats, lesions of the rostral mPFC result in exaggerated heart
rate responses to fear-conditioned stimuli, and stimulation of

these sites attenuates defensive behavior and cardiovascular
responses evoked by amygdala stimulation
Orbital and Anterior Insular Cortex
 Physiologic activity increases in these areas during experimentally
induced anxiety states in healthy subjects and in subjects with

obsessive- compulsive disorder (OCD), simple phobia, and panic
disorder (PD)
 Humans with orbital cortex lesions show impaired performance on
tasks requiring application of information related to punishment or

reward, perseverate in behavioral strategies that are unreinforced,
and exhibit difficulty in shifting intellectual strategies in response to
changing task demands .
Dysfunction of the orbital cortex may contribute to
pathologic anxiety and obsessional states by

impairing the ability to inhibit non-reinforced or
maladaptive emotional, cognitive, and behavioral
responses to social interactions.
FUNCTIONAL ANATOMIC CORRELATES
OF SPECIFIC ANXIETY DISORDERS
Panic Disorder
The baseline state in PD is characterized by mild to
moderate levels of chronic anxiety (termed anticipatory

anxiety)
abnormalities of CBF and glucose metabolism
have been reported in the vicinity of the

hippocampus and parahippocampal gyrus
Phobias
An aversive conditioning paradigm (in which the US
was an aversive odor and the CS was a picture of a

human face) showed that hemodynamic activity
decreased in the amygdala and the hippocampus
during presentations of the CS in healthy controls,
but it increased in social phobic subjects.
Given the role of hippocampal-amygdalar
projections in mediating contextual fear there is a
possibility that deficits in the transmission of
information regarding context may be involved in
the pathogenesis of phobias
Posttraumatic Stress Disorder
PTSD is hypothesized to involve the emotional-
learning circuitry associated with the amygdala,

because the traumatic event constitutes a fear-
conditioning experience, and subsequent exposure to
information related to the event elicits psychological
distress and sympathetic arousal
Obsessive-Compulsive Disorder
A broad consensus for widely distributed structural
abnormalities involving frontostriatal circuits in

OCD (e.g. Jenike et al. (1996) and Pujol et al. (2004))
 Brambilla et al. (2002) : orbitofrontal and basal ganglia
regions are frequently reported to be anatomically
abnormal in OCD.
The Cortico-Striatal Model of OCD -
Structural and functional neuroimaging studies

implicate the striatum, orbitofrontal cortex (OFC)
and anterior cingulate (ACC) in the pathophysiology
of OCD.
Studies using positron emission tomography (PET)
and single photon emission computed tomography
(SPECT) in OCD have found increased regional
brain activity within the OFC, ACC and the
striatum (specifically, caudate nucleus)
The provocation of checking symptoms in a study
by Mataix-Cols et al. (2004) yielded predominant
activations in brain regions important for
motor and attentional functioning (e.g.
thalamus, dorsolateral cortical regions including
dorsal ACC), whereas provocation of washing
symptoms was overall more associated with
activation in ventromedial prefrontal regions.
Neuropsychological studies in OCD have been
conducted for over two decades.
While intellectual function in individuals with OCD
appears to be preserved (Mataix-Cols et al., 2002;
Savage et al., 1999, 2001), studies point to
neuropsychological impairments in three cognitive
domains:
(1) visuospatial skills,

(2) memory and
(3) executive functioning.
Memory
OCD patients show impaired performance on a number
of different memory tasks

behaviour seen in people with OCD might be argued to
be suggestive of memory problems.

many patients engage in repetitive checking behaviour—
e.g. that the gas stove is off—arguably suggestive of

attentional problems or a failure to appropriately
encode memories for self-actions.
Executive Functions
 On Complex figure test and BVRT, an impairment exists in recall performance,
but many have argued that this impairment is due to failures in the employment
of appropriate organisational strategies (Kuelz et al., 2004; Martinot et al., 1990;
Savage et al., 1999; Savage and Rauch, 2000; Deckersbach et al., 2000; Kim et al.,
2002).
 Verbal memory is generally unimpaired in OCD patients (Christensen et al., 1992;
Martin et al., 1995; Mataix-Cols et al., 1999), except in tasks requiring stimuli to
be semantically clustered (Savage and Rauch, 2000; Cabrera et al., 2001)
 Concluded that their findings were suggestive of executive dysfunction rather
than a deficit in spatial working memory system per se.

Decision-making
 the compulsive behaviours in OCD may be conceptualised as failures in
decision-making (Cavedini et al., 2002).
The Iowa Gambling Task (Bechara et al., 1994)

 several decks of cards and the goal is to maximise profit by making a series of card
selections. The examiner schedules rewards and punishments such that decision
making can be objectively quantified by examining the tendency of the subject to
select advantageous versus disadvantageous card decks overall.
 The available studies utilising this task in individuals with OCD provide mixed
findings (Cavedini et al., 2002; Nielen et al., 2002), and there is some evidence that
decision-making impairments on this task may represent a marker for treatment
resistant forms of the disorder (Cavedini et al., 2002).
Set-shifting
 Given the perseveration and repetition demonstrable in the clinical behaviour,
set-shifting impairments might be expected to represent a core feature of the

neurocognitive profile of OCD.
 The object alternation test (OAT; Freedman, 1990) and delayed alternation test
(DAT; Freedman and Oscar-Berman, 1986) measure a distinct aspect of set-
shifting: behavioural reversal, in which a rule is learnt and then subsequently
needs to be inhibited and reversed in order to maintain good performance.
 Set-shifting performance (in terms of behavioural reversal) in OCD sufferers has
been found to be impaired on both of these tasks (Abbruzzese et al., 1997;
Aycicegi et al., 2003).

Response inhibition
In Go/No-Go tasks, OCD patients made significantly
more commission errors than matched panic

disorder control subjects in a computerised task
Attentional bias and vigilance
 The clinical symptoms of OCD are suggestive of processing

biases, such as fixations with potential contamination
sources or stimuli that would not normally evoke emotional
responses.
 Impairments have been noted in visual attention tests

(Dirson et al., 1995; Nelson et al., 1993), selective attention
tests (Clayton et al., 1999), self-paced working-memory
tests (Martin et al., 1995), Stroop (Hartston & Swerdlow,
1999) etc.
Airaksinen , Larsson, Forsell (2004) did a
study to examine whether persons diagnosed with an

anxiety disorder show neuropsychological
impairments relative to healthy controls in tasks
tapping episodic memory, verbal fluency,
psychomotor speed, and executive functioning
Neuropsychological tests
used in the study
 In task of assessing episodic memory persons affected by an anxiety disorder
remembered fewer words in both free and cued recall as compared with healthy
controls.
 Separate analyses of the respective anxiety diagnosis showed that persons
affected by PD with and without agoraphobia, or agoraphobia, recalled
significantly fewer words as compared with healthy controls in both free and
cued recall.
 Specific phobia and GAD did not affect episodic memory performance
Verbal Fluency
Also, persons affected by SP had a tendency to
generate fewer words totally in FAS

Verbal fluency proficiency was of equal size in the
total group of persons affected by anxiety, and in PD

and GAD groups, and in specific phobias as
compared with healthy controls
Perceptual-motor speed and executive
functioning
 TMT-A completion time revealed no significant differences between the total group
of anxiety persons or for any of the anxiety subgroups and controls

 The analyses on TMT-B completion time showed that persons affected by an anxiety
disorder needed significantly more time to complete the TMT-B as compared with
healthy controls.
 persons affected by PD with and without agoraphobia, or agoraphobia needed more
time to complete the TMT-B than controls

 persons diagnosed with OCD were slower than controls in their performance on
TMT-B completion time

 Persons diagnosed with SP, GAD or specific phobia showed no reliable effects on
TMT-B completion time as compared with healthy controls.

Neuropsychology of Anxiety Disorders

Uploaded by

Copyright:

Available Formats

Neuropsychology of Anxiety Disorders

Uploaded by

Document Information

Original Description:

Original Title

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

Neuropsychology of Anxiety Disorders

Uploaded by

Copyright:

Available Formats

NEUROPSYCHOLOGY OF

2% and 5% in population-based studies (APA, 1994).

neuropsychological functioning in anxiety disorders have been

prevalent obsessive–compulsive disorder (OCD), whereas less

 Neural activity within the amygdala is modulated by cortisol,

norepinephrine (NE), and other neurotransmitters and by

experiences (especially fear or anxiety) and the recollection of

processing affective elements of social interactions (Weiskrantz, 1956)

snakes (LeDoux, 1998)

become more submissive to dominant animals (Murray et al.,1999)

fear or sadness (Murray et al., 1999)

expression ; and fear and anger in spoken language

 PFC structures are thought to participate in interpreting the

higher-order significance of experiential stimuli, in modifying

amygdala, through which the amygdala can modulate PFC

including heart rate, blood pressure, and glucocorticoid secretion

various neurotransmitter systems that are activated in response to

The reciprocal projections between the amygdala

and the mPFC are hypothesized to play critical roles

emotionally provocative stimuli, inability to experience emotion related

to concepts, and inability to use information regarding the probability

of aversive social consequences versus reward in guiding social

behavior (Damasio, 1990).

 Physiologic activity also increases in more dorsal mPFC areas in

healthy humans as they perform tasks that elicit emotional responses

or require emotional evaluations

increases in the rostral mPFC, and the magnitude of CBF

rate responses to fear-conditioned stimuli, and stimulation of

 Physiologic activity increases in these areas during experimentally

induced anxiety states in healthy subjects and in subjects with

tasks requiring application of information related to punishment or

pathologic anxiety and obsessional states by

The baseline state in PD is characterized by mild to

moderate levels of chronic anxiety (termed anticipatory

have been reported in the vicinity of the

An aversive conditioning paradigm (in which the US

was an aversive odor and the CS was a picture of a

PTSD is hypothesized to involve the emotional-

learning circuitry associated with the amygdala,

A broad consensus for widely distributed structural

abnormalities involving frontostriatal circuits in

Structural and functional neuroimaging studies

(1) visuospatial skills,

OCD patients show impaired performance on a number

of different memory tasks

be suggestive of memory problems.

e.g. that the gas stove is off—arguably suggestive of

 On Complex figure test and BVRT, an impairment exists in recall performance,

of appropriate organisational strategies (Kuelz et al., 2004; Martinot et al., 1990;

 Verbal memory is generally unimpaired in OCD patients (Christensen et al., 1992;

be semantically clustered (Savage and Rauch, 2000; Cabrera et al., 2001)

 Concluded that their findings were suggestive of executive dysfunction rather

than a deficit in spatial working memory system per se.

decision-making (Cavedini et al., 2002).

The Iowa Gambling Task (Bechara et al., 1994)

 Given the perseveration and repetition demonstrable in the clinical behaviour,

set-shifting impairments might be expected to represent a core feature of the

(DAT; Freedman and Oscar-Berman, 1986) measure a distinct aspect of set-