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DSM-5 Changes For Anxiety Disorders • New category of Obsessive-Compulsive and Related Disorders • Removes obsessive-compulsive disorder from category of Anxiety Disorders • Recognizes a spectrum of obsessive-compulsive type disorders • including body dysmorphic disorder; • Anxiety remains the core feature of OCD • New category of Trauma and Stressor-Related Disorders – – – – Removes Acute Stress Disorder (ASD) from Anxiety Disorders Removes PTSD from Anxiety Disorders Groups all stress-related psychological disorders together Adjustment Disorders may now be coded in context of traumatic stressors Anxiety Disorders Examples • • • • • • Specific Phobia Social Anxiety Disorder (Social Phobia) Panic Disorder Agoraphobia Generalized Anxiety Disorder Separation Anxiety Disorder Obsessive-Compulsive and Related Disorders • • • • • Obsessive-Compulsive Disorder Body Dysmorphic Disorder Hoarding Disorder Hair-Pulling Disorder (Trichotillomania) Excoriation (Skin-Picking) Disorder Trauma and Stressor Related Disorders • • • • • Adjustment Disorders Acute Stress Disorder Posttraumatic Stress Disorder Reactive Attachment Disorder Disinhibited Social Engagement Disorder Prevalence of Any Anxiety Disorder Among Adults http://www.nimh.nih.gov/health/statistics/prevalence/any-anxiety-disorder-among-adults.shtml Prevalence of Anxiety Disorders by Type • “Specific phobia is consistently estimated to be the most common lifetime anxiety disorder, with prevalence estimates usually in the 6–12% range. • Social phobia is typically found to be the next most common anxiety disorder, with lifetime prevalence sometimes as high as 10%. • Panic disorder (2–5%) • Generalized anxiety disorder (GAD; 3–5%).” Epidemiology of Anxiety Disorders, (2010) Ronald C. Kessler. in M.B. Stein and T. Steckler (eds.), Behavioral Neurobiology of Anxiety and Its Treatment, Current Topics in Behavioral Neurosciences Comorbidity between Anxiety and Other Mental Disorders • “Comorbidity among anxiety disorders is quite common, with up to half of the people with a lifetime anxiety disorder in some surveys meeting criteria for two or more such disorders. “ (Kessler 2010) • “Three-quarters (75%) of people with a lifetime anxiety disorder also had at least one other lifetime mental disorder.” (Kessler 2010) • Early-onset anxiety disorders are powerful predictors of the subsequent onset and persistence of other mental and substance use disorders. Age-of-onset • Anxiety disorders begin much earlier than other mental disorders, including mood disorders, disruptive behavior disorders, nonaffective psychoses, and substance use disorders. – Tic disorders and most specific phobia in childhood, most by the age of 18 – Social phobia and OCD in adolescence or early adulthood, mostly beginning by their twenties. – Panic disorder, agoraphobia, and GAD are later and more widely dispersed, in the early-mid twenties up to mid forties – PTSD has the latest and most variable age of onset • Epidemiology of Anxiety Disorders, (2010) Ronald C. Kessler, p 21-35. M.B. Stein and T. Steckler (eds.), Behavioral Neurobiology of Anxiety and Its Treatment, Current Topics in Behavioral Neurosciences Age-of-onset • “Anxious temperament (AT) in human and non-human primates is a trait-like phenotype evident early in life that is characterized by increased behavioural and physiological reactivity to mildly threatening stimuli1, 2, 3, 4. Studies in children demonstrate that AT is an important risk factor for the later development of anxiety disorders, depression and comorbid substance abuse5. “ – Amygdalar and hippocampal substrates of anxious temperament differ in their heritability. Jonathan A. Oler, Nature 466, 864–868 (12 August 2010) • Aggressive treatment of child-adolescent anxiety disorders might be effective in preventing the onset of the secondary disorders Role of genetics in Anxiety • The heritability of anxiety disorders is from 30-67% however heritability varies by subcategory of anxiety disorder • No single gene but a variety of genes related to function of 5-HT1A, 5-HTT, MAO-A, COMT, CCK-B, ADORA2A, CRHR1, FKBP5, ACE, RGS2/7 and NPSR1 (Domschke, 2013) • Genes for anxiety disorders overlap and transcend diagnostic boundaries (Smoller , 2008) • Genetics for anxiety disorders are related to endotypes such as behavioral inhibition, anxiety sensitivity, increased startle reactivity or dysfunctional corticolimbic activity during emotional processing (Domschke, 2013) • Anxiety is similar to temperament and personality traits in that it is a general phenotypes that predispose for anxiety disorders Na (2011) Panic Disorder • Recurrent, unexpected panic – – – • attacks followed by at least 1 month of persistent concern about having another attack worry about the possible implications of the panic attacks significant behavioral change related to the attacks. Biological Influences – – – – – Oversensitive respiratory control center in brain stem Minor oxygen debt (high CO2) false alarm of suffocation Decreased temporal lobe volumes Increased activity in parahippocampal gyrus Decreased activity in anterior temporal cortex & amygdala Social Phobia: criteria • Marked and persistent fear of one or more social or performance situations in which a person is exposed to unfamiliar people or possible scrutiny by others • Exposed to the feared social situation invariably provokes anxiety • The person realizes that the fear is excessive or unreasonable • The feared situation is avoided or endured with great distress • Characterized by fear of humiliation by either performing badly or by displaying visible symptoms of anxiety. • More than shyness • If the fears include most social situations, it is considered generalized social phobia Social Phobia: etiology • Cognitive biases – – – Attentional bias: what people attend to Memory bias: what people remember Two kinds of judgment biases in anxiety disorders • Exaggerated estimates of the occurrence of negative events • Exaggerated estimates of the cost (valence) of negative events • Social phobia is more distinguished by exaggerated cost. Social Phobia: etiology • There is also evidence that social phobia runs in families – Modeling of socially anxious parents has an effect on children – In particular, overprotective and rejecting behavior increase the odds of developing social phobia – Weak evidence for specific genetic influence – However: recall very high comorbidity rate for all anxiety disorders – There is an overall genetic influence for anxiety disorders • Neurobiological characteristics – Hyper arousal similar to Panic but not hypersensitive to CO2 – Norepinephrine or Dopamine neurotransmitters implicated – Basal Ganglia and Striatum circuits Specific Phobia • Excessive or unreasonable fear related to a specific object/situation – Most common are snakes & heights – Some anxiety is adaptive to avoid danger from snakes or falling off cliffs – Often have associated panic attacks • Behavioral Explanation – Classical conditioning example from Little Albert • However not just classical conditioning – Evolutionary: Selectivity of phobias • Why spider but not lamb phobia? • Why dark but not electric outlet phobia? – Cognitive: Susceptibility to phobias • Physiological vulnerability (higher neurological activity) • Lack of history with stimuli • Threat-enhancing cognitive set • Expect threat in environment • Selective attention to threats • Selective recall of threats Generalized Anxiety Disorder • DSM criteria for GAD include: – – – – Excessive worry occurring more days than not Anxiety focuses on everyday events Person finds it difficult to control the worry Restlessness, easy fatigue, muscle tension, sleep disturbance • Biological Influences – Low GABA levels produces low inhibitory neuron activity – Lack of inhibition results in high neuronal activity in limbic system – High arousal can enhance conditioning – Anxiolytics increase GABA and decrease anxiety Posttraumatic Stress Disorder In posttraumatic stress disorder (PTSD, also called combat fatigue, war neurosis, or shell shock), unpleasant memories repeatedly plague the victim. PTSD victims show: – Memory changes, such as amnesia – Flashbacks – Deficits in short-term memory • Exposure to actual or threatened death, serious or sexual violence in one or more of the following ways: – Direct experiencing of traumatic event(s) – Witnessed in person the events as it occurred to others – Learning that the traumatic events occurred to person close to them – Experiencing repeated or extreme exposure to aversive details of trauma • Lifetime prevalence of PTSD is estimated to be only 1–2% in Western Europe, 6–9% in North America, and over 10% in countries that have been exposed to long-term sectarian violence. A Neural Model of Posttraumatic Stress Disorder Obsessive-Compulsive Disorder • Typical obsessions include contamination, aggressive impulses, sexual content, somatic concerns, symmetry • People with OCD may have early life experience with unacceptable thoughts • Onset early adolescence to young adulthood, course typically chronic • Biological Influences – Higher activity Orbitofrontal, cingulate and caudate nucleus – Serotonin dysregulation ? • Antidepressants (SSRIs) effective for 50% OCD • Dogs with OCD like behavior improve with Prozac – At least 2 gene polymorphisms: • BDNF • 5-HT2A receptor Obsessive-Compulsive Disorder • Obsessive-Compulsive as a distinct disorder – Because OCD does not result from anxiety – Compulsions: repetitive thoughts and behaviors – Similar to: • body dysmorphic disorder • Tourette’s syndrome • Glutamate involvement – Decision making brain circuits involved • Immune system (microglia) over activity – Damage neuronal circuits predisposing some people to OCD – Cortical - basal ganglia circuit Symptoms of Obsessive-Compulsive Disorders Biological Treatments for Anxiety Disorders • Benzodiazapines: Bind to GABA receptors – Valium “Diazepam” for GAD and Phobias – Xanax “Alprazolam”: for Panic – 70% individuals show symptom reduction • Antidepressants: Serotonin agonists – Paxil, Prozac for GAD, Panic, Agoraphobia, – Anafranil “Clomipramine” for OCD – 20-40 % reduction in symptoms for OCD patients • Neurosurgery – Cingulotomy–lesions of the cingulate cortex to treat anxiety, depression, and OCD. • partially cut cingulate gyrus • connects lower brain structures with orbitalfrontal cortex • effective in 50% of cases – Capsulotomy–lesions of the internal capsule, to treat anxiety disorders. Psychological Treatments • Behavioral Treatments – Extinction of anxiety through exposure and development of incompatible responses • Systematic Desensitization • Progressive muscle relaxation • Exposure to fear hierarchy • Cognitive-Behavior Therapy (CBT) – Challenge threat-magnifying cognitive sets Psychological Treatment Effectiveness • Generalized Anxiety Disorder – CBT more effective than Valium – CBT + Valium most effective • Panic Disorder studies – 75-95% panic-free after 3 months of CBT • OCD – Exposure + response prevention • 50% patients improve