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Anxiety Disorders Dr Ali Kheradmand M.D. Assistant Professor of Shahid Beheshti Medical University When does anxiety become a disorder? Anxiety is a normal human response to objects, situations or events that are threatening Anxiety is different from fear due to its cognitive component (i.e. fear of the future) Anxiety can be helpful and adaptive (e.g. anxiety about giving lectures!) Anxiety becomes a disorder when out of proportion or when it significantly interferes with life. Anxiety disorders… Highly treatable yet also resistant to extinction Often begins early in life Reported more by women than men Reported more in Western countries Often comorbid both with other anxiety diagnoses and with other disorder groups (e.g. Mood disorders, psychoses) General considerations for anxiety disorders Often have an early onset- teens or early twenties Show 2:1 female predominance Have a waxing and waning course over lifetime Similar to major depression and chronic diseases such as diabetes in functional impairment and decreased quality of life There Are Two Types Of Anxiety: Anticipatory: feeling of distress occurring while studying for or thinking about the exam. Situational: feeling of distress occurring while taking the exam. It is important to be aware of when anxiety attacks you so that you may use strategies in and out of the exam situation to manage the anxiety. How does test anxiety affect you? Test anxiety affects you in three ways: Physiologically Behaviorally Psychologically 4. More considered response based on cortical processing 1. Thalamus receives stimulus and sends to both amygdala and cortex Sensory Input 2. Amygdala registers danger 3. Amygdala triggers fast response • Parts of the brain involved in fear response = thalamus, amygdala, hypothalamus, which then instruct the endocrine glands and autonomic nerv.sys. • Evolved fear module (pink) versus considered response (green) = “fight or flight” versus “feel the fear and do it anyway (or do it differently)”! 8 Physiological reactions may include: - increased heartbeat - tensed muscles - perspiration - dry mouth Behavioral reactions may include: - Inability to make decisions, act, or express yourself. - Difficulty reading and understanding questions on an exam. - Difficulty organizing your thoughts. - Difficulty recalling or retrieving terms and concepts. Psychological reactions may include: - Feeling apprehensive or uneasy. - Feeling upset. - Having self-doubt or negative self-talk. 12 Primary versus Secondary Anxiety Anxiety may be due to one of the primary anxiety disorders OR secondary to substance abuse (Substance-Induced Anxiety Disorder), a medical condition (Anxiety Disorder Due to a General Medical Condition), another psychiatric condition, or psychosocial stressors (Adjustment Disorder with Anxiety) The differential diagnosis of anxiety. Psychiatric and Medical disorders. Psychiatr Clin North Am 1985 Mar;8(1):3-23 The Anxiety Disorders Specific Phobia Social Phobia Panic Disorder without agoraphobia Panic Disorder with agoraphobia ObsessiveCompulsive Disorder Substance induced Anxiety Disorder Post-traumatic Stress Disorder Generalized Anxiety Disorder Anxiety Disorder due to a general medical condition Anxiety Disorder Not otherwise specified Epidemiology of anxiety disorders Damsa C. et al. Current status of brain imaging in anxiety disorders. Curr Opin Psychiatry 2009;22:96-110 Specific Phobias Selective, persistent and out of proportion Includes cognition that leads to behavioural response, whether or not the threat is present May be genetically, neurologically or experientially based Maintained through the processes of classical and operant conditioning. Specific Phobia Epidemiology Etiology Up to 15% of general population Onset early in life Female:Male 2:1 Learning, contextual conditioning Treatment Systematic desensitization Social Phobia A more pervasive, highly cognitive type of phobia Distinguishing feature is the fear of doing something in front of others May be situation or context (e.g. performance versus interaction anxiety) specific Fear of one’s own behaviour causing negative attention from others Social Phobia Epidemiology 7% of general population Age of onset teens; more common in women. Stein found half of SAD patients had onset of sx by age 13 and 90% by age 23. Causes significant disability Increased depressive disorders Incidence of social anxiety disorders and the consistent risk for secondary depression in the first three decades of life. Arch Gen Psychiatry 2007 Mar(4):221-232 What is going on in their brains?? Both groups ↑ medial prefrontal cortex activity in response to intentional relative to unintentional transgression. SAD patients however showed a significant response to the unintentional transgression. SAD subjects also had significant increase activity in the amygdala and insula bilaterally. Blair K. Et al. Social Norm Processing in Adult Soical Phobia: Atypical Increased Ventromedial Frontal cortex Responsiveness to Unintentional (Embarrasing) Trasgressions. Am J Psychiatry 2010;167:1526-1532 What is going on in their brains?? Blair K. Et al. Social Norm Processing in Adult Soical Phobia: Atypical Increased Ventromedial Frontal cortex Responsiveness to Unintentional (Embarrasing) Trasgressions. Am J Psychiatry 2010;167:1526-1532 Agoraphobia Marked fear or anxiety for more than 6 months about two or more of the following 5 situations: Using public transportation Being in open spaces Being in enclosed spaces Standing in line or being in a crowd Being outside of the home alone Agoraphobia The individual fears or avoids these situations because escape might be difficult or help might not be available The agoraphobic situations almost always provoke anxiety Anxiety is out of proportion to the actual threat posed by the situation The agoraphobic situations are avoided or endured with intense anxiety The avoidance, fear or anxiety significantly interferes with their routine or function Prevalence 2% of the population Females to males:2:1 Mean onset is 17 years 30% of persons with agoraphobia have panic attacks or panic disorder Confers higher risk of other anxiety disorders, depressive and substance-use disorders Panic Disorder Two major types: with or without agoraphobia Consists of a pattern of recurring panic attacks Emotional, physical, cognitive and behavioural components Main fear is of losing control (consequence = dying, going crazy, embarrassment, not being able to get help) The fear of having a panic attack becomes a problem of itself, possibly leading to agoraphobia (fear of open spaces, crowds etc. Any place where escape or finding help is difficult or embarrassing) or other phobias A Panic Attack is: A discrete period of intense fear in which 4 of the following Symptoms abruptly develop and peak within 10 minutes: Palpitations or rapid heart rate Sweating Trembling or shaking Shortness of breath Feeling of choking Chest pain or discomfort Nausea Chills or heat sensations Paresthesias Feeling dizzy or faint Derealization or depersonalization Fear of losing control or going crazy Fear of dying Panic disorder epidemiology 2-3% of general population; 5-10% of primary care patients ---Onset in teens or early 20’s Female:male 2-3:1 Things to keep in mind A panic attack ≠ panic disorder Panic disorder often has a waxing and waning course Post Traumatic Stress Disorder Is it an anxiety disorder? Main diagnostic criteria: Witness or experience of an event that (a) involved actual or threatened death or injury, and Feelings of intense fear, horror, or helplessness Person must relive the event in some way (e.g. dreams, “flashbacks”, internal distress, physiological reactions) Avoidance (subconscious and/or conscious) Hyperarousal or mood instability Usually persisting for at least three months Generalized Anxiety Disorder Excessive worry more days than not for at least 6 months about a number of events and they find it difficult to control the worry. 3 or more of the following symptoms: Restlessness or feeling keyed up or on edge, easily fatigued, difficulty concentrating, irritability, muscle tension, sleep disturbance Causes significant distress or impairment Generalized Anxiety Disorder Epidemiology 4-7% of general population Median onset=30 years but large range Female:Male 2:1 OCD Comorbidities >70% have lifetime dx of an anxiety disorder such as PD, SAD, GAD, phobia >60% have lifetime dx of a mood disorder MDD being the most common Up to 30% have a lifetime Tic disorder 12% of persons with schizophrenia/ schizoaffective disorder Obsessive Compulsive Disorder Classified as anxiety disorder, but with unique presentation Characterised by obsessions and compulsions (in most cases) Compulsions may be physical or mental Types of presentation: contamination fear; doubt/checking; magic thinking; symmetry; hoarding Severity = frequency + capacity to resist + interference with normal functioning OCD Etiology Genetics Serotonergic dysfunction Cortico-striatothalamo-cortical loop AutoimmunePANDAS Treatment 40-60% treatment response Serotonergic antidepressants Behavior therapy Adjunctive antipsychotics, psychosurgery PANDAS – penicillin, plasmapharesis, IV immunoglobulin Functional imaging studies Increased activity in the right caudate is found in pts with OCD and Cognitive behavior therapy reduces resting state glucose metabolism or blood flow in the right caudate in treatment responders. Similar results have been obtained with pharmacotherapy Baxter L. et al. Caudate glucose metabolic rate changes with both drug and behavioral therapy for obessive-compulsive disorder. Arch Gen Psych 1992;49:681-689 Anxiety Disorders Possible Causes • Tourette’s syndrome is characterized by muscular and vocal tics: facial grimaces, squatting, pacing, twirling, barking, sniffing, coughing, grunting, or repeating specific words (especially vulgarities). • Tourette’s Syndrome a neurological disorder characterized by tics and involuntary vocalizations and sometimes by compulsive uttering of obscenities and repetition of the utterances of others 37 Trauma- and Stressor-Related Disorders Acute Stress Disorder Adjustment Disorders Posttraumatic Stress Disorder PTSD continued Presence of 1 or more intrusive sx after the event Recurrent, involuntary and intrusive memories of event Recurrent trauma-related nightmares Dissociative reactions Intense physiologic distress at cue exposure Marked physiological reactivity at cue exposure Persistent avoidance by 1 or both: Avoidance of distressing memories, thoughts or feelings of the event(s) Avoidance of external reminders of that arouse memories of event(s) e.g. people, places, activities Negative alterations in cognitions and mood associated with the traumatic event(s) as evidenced by 2 or more of the following: Inability to remember an important aspect of the traumatic event(s) Persistent distorted cognitions about cause or consequence of event that lead to blame of self or others Persistent negative emotional state Marked diminished interest Feeling detached from others Persistent inability to experience positive emotions Marked alterations in arousal and reactivity with 2 or more of: Irritable behavior and and angry outbursts Reckless or self-destructive behavior Hypervigilance Exaggerated startle response Problems with concentration Sleep disturbance Duration of disturbance is more than one month AND causes significant impairment in function Specifiers: With dissociative sx (derealization or depersonalization) With delayed expression (don’t meet criteria until >6 months after event) PTSD Epidemiology 7-9% of general population 60-80% of trauma victims 30% of combat veterans 50-80% of sexual assault victims Increased risk in women, younger people Risk increases with “dose” of trauma, lack of social support, pre-existing psychiatric disorder Comorbidities Depression Other anxiety disorders Substance use disorders Somatization Dissociative disorders Functional neuroimaging in PTSD Increased amygdal activation is seen in PTSD pts compared to controls Hypoactivation of the medial prefrontal cortex including the orbitofrontal cortex and anterior cingulate cortex (area implicated in affect regulation) Francati V. et al. Functional Neuroimaging Studies in Posttraumatic Stress Disorder:Review of Current methods and Findings. Depression and Anxiety 2007;24:202-218 Study found treatment of PTSD with paroxetine resulted in increased anterior cingulate cortex function Fani N. et al. Increased neural response to trauma scripts in posttraumatic stress disorder following paroxetine treatment: A pilot study. Neurosci Letters 2011;491:196-201 Acute Stress Disorder Similar exposure as in PTSD Presence of >9 of 5 categories of intrusion, negative mood, dissociation, avoidance, and arousal related to the trauma. Duration of disturbance is 3 days to 1 month after trauma Causes significant impairment General treatment approaches Pharmacotherapy Antidepresssants Anxiolytics Antipsychotics Mood stabilizers Psychotherapy- Cognitive Behavior Therapy Crank up the serotonin Cornerstone of treatment for anxiety disorders is increasing serotonin Any of the SSRIs or SNRIs can be used How to use them Start at ½ the usual dose used for antidepressant benefit i.e citalopram at 10mg rather than the usual 20mg WARN THEM THEIR ANXIETY MAY GET WORSE BEFORE IT GETS BETTER!! May need to use an anxiolytic while initiating and titrating the antidepressant Other options Hydroxyzine- usually 50mg prn. Helpful for some patients but has prominent anticholinergic SEs Buspirone-For GAD- 60mg daily Propranolol-Effective for discrete social phobia i.e. performance anxiety Atypical antipsychotics at low doses for augmentation in difficult to treat OCD pts Anticonvulsants Valproic acid 500-750 mg bid (ending dose) carbamazepine 200-600 mg bid (ending dose) Gabapentin 900-2700 mg daily in 3 divided doses (ending dose) Atypical antipsychotics at low doses for augmentation in difficult to treat OCD pts Mothers little helpers Benzodiazapines are very effective in reducing anxiety sx however due to the risk of dependence must use with caution Depending on the patient may either use on a prn basis or scheduled DO NOT USE ALPRAZOLAM- talk about a reinforcing drug! For patients with a history of addiction or active drug/ETOH abuse or dependence benzodiazepines are not an option Alternative Treatments Acupuncture Aromatherapy Breathing Exercises Exercise Meditation Nutrition and Diet Therapy Vitamins Self Love