Week 3: Panic disorder
Barlow et al. (2000) – Cognitive-Behavioral Therapy, Imipramine, or their
combination for Panic Disorder
Why treating panic disorder (PD)is important
Individuals with PD frequently use emergency department and general medical services, presenting with
high rates of unexplained cardiac symptoms, dizziness, and bowel distress. These patterns continue
indefinitely. The social and economic costs of PD are considerable and successfully treating PD can
produce medical cost offsets as high as 94%. Therefore, efforts to ascertain effective treatment for PD is
important.
Imipramine was regarded as the pharmacological criterion standard for treatment of PD for over 20
years until SSRI’s emerged.
Study was conducted RCT comparing CBT alone, imipramine+medical management, combination of
CBT+imipramine, pill placebo+medical management, and CBT+placebo for patients with a diagnosis of
PD with or without agoraphobia.
Aims of the study + results:
Address of both CBT alone and imipramine alone performed better than placebo7
Results: Both CBT alone and imipramine alone were superior to placebo for the PDSS
continuous measure (=PD severity scale).
If either CBT or imipramine performed better relative to each other
Results: No significant difference between CBT alone and imipramine alone. Only higher
dropout-rate in the imipramine group because of adverse effects. Follow-up showed trends
favouring CBT over imipramine.
If there was an advantage to combining CBT and imipramine as evidenced by superiority of
CBT+Imipramine to CBT+placebo, imipramine alone, and CBT alone.
Results: CBT+imipramine was superior to CBT alone but was not superior to CBT+placebo.
Follow-up showed superiority to CBT alone and CBT+placebo compared to placebo.
Overall conclusion:
Both imipramine and CBT are better than pill placebo for treatment of PD. Imipramine produced
a superior quality of response, but CBT had more durability and was somewhat better tolerated.
Several difference between active treatments: imipramine patients showed more improvement
on the PDSS than patients who responded to CBT. However, at follow-up CBT-alone patients
maintained their improvement significantly better than those who received imipramine.
Roy-Byrne (2006) – Panic Disorder
Panic attack = sudden, sometimes unexpected paroxysmal bursts of severe anxiety, accompanied by
several physical symptoms. Such attacks are often striking in their initial presentation, affect the
individual’s function, and could be progressive and disabling, especially if complicated by agoraphobia.
Controversy continues about the nosological status of agoraphobia without panic attacks, which is
rarely seen in clinical settings.
, Difference between panic attack and specific phobia
The same physical and cognitive symptom constellation of a panic attack can occur in individuals with
specific phobias when exposed to the feared stimulus or in those with social phobia when faced with
situations where they might be scrutinised. The difference in such situations is that the individual is
keenly aware of the source of their fearful sensations, whereas in panic disorder, these same types of
sensations are unprovoked, unexplained, and often occur out of the blue.
Panic attacks can also occur in PTSD, for whom exposure to reminders of the traumatic event can
trigger panic attacks.
Panic attacks can also be a symptom of common conditions such as caffeine and stimulant use/abuse.
Characteristics of PD
Excess of PD in females
Modal age of onset in late adolescence or early adulthood
Strong associations with agoraphobia and MDD.
Rarely occurs in clinical settings without other psychopathological comorbidity.
Mostly comorbid with MDD, bipolar disorder, other anxiety disorders, and alcohol abuse.
In children and adolescents, the disease tends to have a chronic course and is often comorbid
with other anxiety, mood, and disruptive disorders.
A strong association is found between panic disorder (and anxiety disorders in general) and suicidal
ideation and suicide attempts, even after adjustment for affective comorbidity and other suicide risk
factors Therefore, clinician should be vigilant to the probability that their patients with PD are at
increased risk for suicide.
Risk factors for PD
Genetics, heritability about 40%.
Early life trauma or maltreatment
Anxious temperament characterised by neuroticism and anxiety sensitivity
Stressful live events contribute to the onset and maintenance of PD
In adolescence: cigarette smoking and nicotine dependence for later onset of PD
Whole neuropsychological part about genes and neurotransmitters associated with PD, however they
will definitely not have questions about this in the exam so, I skipped this part.
Psychopathological processes
Anxiety sensitivity is a factor that increases the salience of bodily sensations. Anxiety sensitivity is the
belief that anxiety could cause deleterious physical, social, and psychological consequences that extend
beyond any immediate physical discomfort during a panic attack. Moreover, panic attacks themselves
increase anxiety sensitivity. Insular cortex activation could mediate heightened anxiety sensitivity.
Anxiety sensitivity could be acquired through:
A lifetime of direct aversive experiences (i.e., personal history of severe illness or injury)
Vicarious observations (i.e., severe illnesses or death among family members)
Informational transmissions (i.e., parental warnings)
Parental reinforcement of attention to somatic symptoms and parental modelling of distressed
reactions to bodily sensations
Barlow et al. (2000) – Cognitive-Behavioral Therapy, Imipramine, or their
combination for Panic Disorder
Why treating panic disorder (PD)is important
Individuals with PD frequently use emergency department and general medical services, presenting with
high rates of unexplained cardiac symptoms, dizziness, and bowel distress. These patterns continue
indefinitely. The social and economic costs of PD are considerable and successfully treating PD can
produce medical cost offsets as high as 94%. Therefore, efforts to ascertain effective treatment for PD is
important.
Imipramine was regarded as the pharmacological criterion standard for treatment of PD for over 20
years until SSRI’s emerged.
Study was conducted RCT comparing CBT alone, imipramine+medical management, combination of
CBT+imipramine, pill placebo+medical management, and CBT+placebo for patients with a diagnosis of
PD with or without agoraphobia.
Aims of the study + results:
Address of both CBT alone and imipramine alone performed better than placebo7
Results: Both CBT alone and imipramine alone were superior to placebo for the PDSS
continuous measure (=PD severity scale).
If either CBT or imipramine performed better relative to each other
Results: No significant difference between CBT alone and imipramine alone. Only higher
dropout-rate in the imipramine group because of adverse effects. Follow-up showed trends
favouring CBT over imipramine.
If there was an advantage to combining CBT and imipramine as evidenced by superiority of
CBT+Imipramine to CBT+placebo, imipramine alone, and CBT alone.
Results: CBT+imipramine was superior to CBT alone but was not superior to CBT+placebo.
Follow-up showed superiority to CBT alone and CBT+placebo compared to placebo.
Overall conclusion:
Both imipramine and CBT are better than pill placebo for treatment of PD. Imipramine produced
a superior quality of response, but CBT had more durability and was somewhat better tolerated.
Several difference between active treatments: imipramine patients showed more improvement
on the PDSS than patients who responded to CBT. However, at follow-up CBT-alone patients
maintained their improvement significantly better than those who received imipramine.
Roy-Byrne (2006) – Panic Disorder
Panic attack = sudden, sometimes unexpected paroxysmal bursts of severe anxiety, accompanied by
several physical symptoms. Such attacks are often striking in their initial presentation, affect the
individual’s function, and could be progressive and disabling, especially if complicated by agoraphobia.
Controversy continues about the nosological status of agoraphobia without panic attacks, which is
rarely seen in clinical settings.
, Difference between panic attack and specific phobia
The same physical and cognitive symptom constellation of a panic attack can occur in individuals with
specific phobias when exposed to the feared stimulus or in those with social phobia when faced with
situations where they might be scrutinised. The difference in such situations is that the individual is
keenly aware of the source of their fearful sensations, whereas in panic disorder, these same types of
sensations are unprovoked, unexplained, and often occur out of the blue.
Panic attacks can also occur in PTSD, for whom exposure to reminders of the traumatic event can
trigger panic attacks.
Panic attacks can also be a symptom of common conditions such as caffeine and stimulant use/abuse.
Characteristics of PD
Excess of PD in females
Modal age of onset in late adolescence or early adulthood
Strong associations with agoraphobia and MDD.
Rarely occurs in clinical settings without other psychopathological comorbidity.
Mostly comorbid with MDD, bipolar disorder, other anxiety disorders, and alcohol abuse.
In children and adolescents, the disease tends to have a chronic course and is often comorbid
with other anxiety, mood, and disruptive disorders.
A strong association is found between panic disorder (and anxiety disorders in general) and suicidal
ideation and suicide attempts, even after adjustment for affective comorbidity and other suicide risk
factors Therefore, clinician should be vigilant to the probability that their patients with PD are at
increased risk for suicide.
Risk factors for PD
Genetics, heritability about 40%.
Early life trauma or maltreatment
Anxious temperament characterised by neuroticism and anxiety sensitivity
Stressful live events contribute to the onset and maintenance of PD
In adolescence: cigarette smoking and nicotine dependence for later onset of PD
Whole neuropsychological part about genes and neurotransmitters associated with PD, however they
will definitely not have questions about this in the exam so, I skipped this part.
Psychopathological processes
Anxiety sensitivity is a factor that increases the salience of bodily sensations. Anxiety sensitivity is the
belief that anxiety could cause deleterious physical, social, and psychological consequences that extend
beyond any immediate physical discomfort during a panic attack. Moreover, panic attacks themselves
increase anxiety sensitivity. Insular cortex activation could mediate heightened anxiety sensitivity.
Anxiety sensitivity could be acquired through:
A lifetime of direct aversive experiences (i.e., personal history of severe illness or injury)
Vicarious observations (i.e., severe illnesses or death among family members)
Informational transmissions (i.e., parental warnings)
Parental reinforcement of attention to somatic symptoms and parental modelling of distressed
reactions to bodily sensations
