Week 4 Mood and Anxiety Disorders

Week 4 Mood and Anxiety Disorders **\ Required readings** Barlow, D. H., Durand, V. M., & Hofmann, S. G. (2022). Psychopathology: An Integrative Approach to Mental Disorders. Cengage. - Chapter 5: Anxiety, Trauma- and Stressor-Related, and Obsessive-Compulsive and Related Disorders. -...

Week 4 Mood and Anxiety Disorders **\ Required readings** Barlow, D. H., Durand, V. M., & Hofmann, S. G. (2022). Psychopathology: An Integrative Approach to Mental Disorders. Cengage. - Chapter 5: Anxiety, Trauma- and Stressor-Related, and Obsessive-Compulsive and Related Disorders. - **Just the anxiety disorders part.** - Chapter 7: Mood Disorders and Suicide. **Recommended reading** LeDoux, J. (2016). *Anxious: Using the Brain to Understand and Treat Fear and Anxiety*. Penguin Books. - Chapter 1: The Tangled Web of Anxiety and Fear - Available via the Reading List. **Mood Disorders** **Dr Daniel Zuj** 1. Those that only include depressive symptoms (unipolar depression) 2. Those that involve manic symptoms (bipolar disorders) - Major depressive episode - Mania - Hypomanic episode Major depressive disorder -- DSM-5 criteria ================================================================ Think of it as two ends of a pole, one end depression, the other end manic. - Most people will experience both depression and manic episodes Major depressive disorder -- DSM-5 criteria =========================================== Sad mood or loss of pleasure in usual activities (anhedonia) Additional criteria includes experiencing at least five of the following symptoms (counting sad mood and loss of pleasure): - Sleeping too much or too little (VERY BIG SIGN) - Psychomotor retardation or agitation - Weight loss or change in appetite - Loss of energy - Feelings of worthlessness or excessive guilt - Difficulty concentrating, thinking or making decisions - Recurrent thoughts of death or suicide (persistent thoughts) Symptoms are present nearly every day, most of the day, for at least two weeks. Symptoms are distinct and more severe than a normative response to significant loss - *People who experience an episode have a 16% increase of having another episode* Persistent depressive disorder -- DSM-5 criteria ================================================ \^used to be called dysthymia Having a depressed mood for most of the day more than half of the time for two years (or one year for children and adolescents). Individuals will experience at least two of the following symptoms during that time: - Poor appetite or overeating - Sleeping too much or too little - Low energy - Poor self-esteem - Trouble concentrating or making decisions - Feelings of hopelessness Persistent depressive disorder can be diagnosed if symptoms do not clear for more than two months at a time and bipolar disorders are not present New to the DSM-5 (used to be in DSM-IV appendix) Premenstrual dysphoric disorder ------------------------------- - Marked affective lability symptoms (irritability, depression) that develop in the final week before the onset of menses; - Start to improve within a few days after the onset of menses; and - Become minimal/absent in the week post-menses Disruptive mood dysregulation disorder -------------------------------------- - Mood disorder in childhood - Extreme affective lability (typ. Irritability and temper outbursts) - Was originally believed to be a form of manic-depression (old name for bipolar). But did not have the manic episodes, so they researched it and found it is distinguished from bipolar because something? determined it was different... leading onto next dot point - Increased risk for development of anxiety and (unipolar) depression Mania/hypomania =============== The person displays increased activity or energy, and at least three of the following are noticeably changed from baseline (four, if mood is irritable): - Increase in goal-directed activity or psychomotor agitation - Unusual talkativeness (lots of fast talking) - Flight of ideas (can't keep up with own thoughts) - Decreased need for sleep (sometimes only need 30mins of sleep) - Increased self-esteem (do the point of psychoticism, believing they are invincible, everyone wants to have sex with them) - Distractibility (anything can distract them, and send their thoughts wild) - Excessive involvement in risk-taking behaviours (gambling, excessive sex/masturbation, excessive drug use) - Symptoms are present most of the day, nearly every day Can be hard to maintain therapeutic relationship as psych wants to stay on topic while, patient wants to go off on tangents, putting strain on relationship. Client thinks therapist isn't on their side and stops going to therapy. People experiencing mania get annoyed that others can't keep up with them and they will cut off important relationships e.g. friends and family - Symptoms last one week, require hospitalization or include psychosis (often acknowledge they are different but believes its because God had blessed them or they are God) - Symptoms cause significant distress or functional impairment Hypomania (hypo means under, so less than mania) - Symptoms last at least four days - Clear changes in functioning are observable to others, but impairment is not marked - No psychotic symptoms present - Some people see hypomania as a good thing due to the high focus, increased goal directed behaviour, high energy, reduced need for sleep, but can still function/blend in (not psychotic). Some people try to induce it through caffeine and drug use - \^Dan has heard stories that completed PHDs in 12 months while inducing hypomanic episodes Bipolar I vs. Bipolar II ======================== Bipolar I At least one experience of manic symptoms (no need for a depressive episode, but often there is) - \^if high particularly high, low is particularly low (has depressing coming down from such a high) Bipolar II At least one major depressive episode and one episode of hypomania (no history of a manic episode) Cyclothymic disorder For at least two years (or one year in children and adolescents): - Numerous periods with hypomanic symptoms that do not meet criteria for a hypomanic episode - Numerous periods with depressive symptoms that do not meet criteria for a major depressive episode \^Walking the line for hypomania and depression \^ asked people about their hypomania experience. Increased spending (maxing out multiple credit cards), excessive drinking, excessive risk taking sex, interpersonal conflict. After they felt high levels of guilt for their behaviour and ruined friendships. Suicide ======= ^Suicide:\ Behaviours\ intended\ to\ cause\ death\ and\ do\ so^ Non-suicidal self-injury: Behaviours meant to cause immediate bodily harm, but not death. (a tension reduction behaviour, release the intense negative emotions). Cutting, burning, scratching. **^Epidemiology:^** In Australia, suicide rate is 12.6 per 100 000 people Men are three times more likely to die by suicide than women - Why? Men are likely to use more deadly means of suicide The rate of death by suicide for First Nations people is almost double the rate of non-Indigenous people (25.5 per 100 000)  Preventing suicide ================== Risk assessment is key for determining risk of suicide (remember slap acronym) Specificity of plan Lethality of means (OD compared to over drinking) Access to means Protective factors (family, friends, thinks they enjoy Development of a safety plan: what - What are dangers/ warning signs - how can they prevent access \* make environ safe - who can they talk to, Hospitalisation if risk imminent some argue that forcing someone into hospitalisation is taking away their autonomy. However, they report gratitude for still being alive and being emitted. - Used to do anti-suicide agreements where client signs a paper agreeing to not commit suicide. - \^side steps a thorough risk assessment - Impacts best care by ignoring a likely issue by saying "they signed they wouldn't" Please take care of yourself and others and seek out someone you trust to debrief if needed Suicide Call Back Service 1300 659 456 Emergency call 000 Student services between 8:45-5:00 business days 1800 817 675 Out of hours counselling between 5:00pm-9:00am weekdays and 24 hours on weekends/public holidays 1300 511 709  A diagram of a group of people Description automatically generated Psychological treatment for depression ============================================================ Psychological treatments for depression can be very effective, and relatively brief (approximately 3-4 months of weekly sessions) *Interpersonal psychotherapy(above)* *Cognitive-behavioural therapy* \^ inline with Beck's theory of depression that depression is caused by negative schema and negative bias. - \^ maladaptive behaviours and thoughts - Client given homework to record their neg thoughts and behaviours - In the next session they go through the neg schemas and see if there is any evidence - Client given more homework to correct or reframe thoughts - See example below  Example of thought and behaviour monitoring How effective is CBT for kids with depression - Very effective for short term and EVEN LONG TERM! Which is great has depression has a high rate of relapse More below  CBT is not a finished product, got to keep working on thought monitoring etc - Can be improved by involving other people (if childs caregiver (parent) envolved results improved especially if kid under 12). Helps parents parent - Interpersonal therapies can be just as effective for kids as CBT  Mindfulness based interventions - Can be effective, but very versatile (depends heavily on client) - Works well with CBT - Works better than non-evidence based therapies (PSYCHS SHOULD NOT BE USING NONE EVIDENCE BASED TECHNIQUES) - \^a should be the case thing - Easy intervention to develop and use (can be on a watch or phone) Medication is often necessary for bipolar disorders (but therapy is also good) - Psychoeducation: informing client of their condition, what to expect, relapse, signs to be mindful of. Normalises the condition. Lets them know about the dangers of manic and depressive symptoms (importance of preventing with medications, mood stabilisers)  - Mood stabilisers / anti-depressants recommended for treatment of moderately severe depression. No superior anti-depressant (individual difference). However SSRIs seem to be a favourite - \^continue taking meds at same dosage used while having symptoms recommended for up to a year, as reduced chance of a relapse from 40% to 20% (for major depressive disorder). - Argued over prescribed as also given to mild and moderate depression - Found there was little diff between anti-dep and placebo for mild to mod dep - \^clear evidence they are more effective than placebos for major and severe depression - Mood stabilisers are required/recommended for the entirety of someone's life if they have BPD (bipolar). Controls both depressive and manic - Lithium is the most common mood stabiliser. Can have nasty side effects, needs careful monitoring - Works much better than a placebo - Bipolar often managed multidisciplinary with a psych, GP, and psychiatrist - Focus with bipolar is managing symptoms not getting rid of disorder (as you can't get rid of it) Electroconvulsive therapy (ECT) ===============================  - Controversial as given someone a seizure by electrocuting the sides of the skull - Used when other methods aren't working (for depression) - Bilateral ECT is when current isa applied to both sides of the head simultaneously WHILE AWAKE. We now give them a muscle relaxant (waking with no memory of event) - Unilateral also used (current one side of the head) - It is a last resort as side effects include memory issues, cognitive difficulties (for up to 6 months) - BUT seen as a valid last resort as giving the high risk of suicide, ECT holds a possibility of reducing it Fear & Anxiety Differ in psych and Phys response Fear= reaction to immediate danger, source of danger is right there, prepared for fight or flight Anxiety= neg future oriented mood state, subjective, sympathetic arousal (increased arousal and muscle attention) Fear & Anxiety & Panic Panic= suddenly feel intense fear and discomfort, racing heartbeat, shortened breath. However the danger is not right there. Panic attacks not a psych disorder But the fear of having a panic attack is a psychological disorder Six fundamental processes that are altered in anxiety disorders: 1. Increased attention to threats 2. Impaired ability to discriminate threat from safety 3. Increased avoidance behaviours 4. Heightened reactivity to threat uncertainty (ambig stimuli) 5. Overvaluation of threat significance and likelihood 6. Maladaptive behavioural and cognitive control in the presence of threats Common brain areas seen in these 6 altered processes: Amyg: structure size of pea in limbic system, receives input from brain and sends that info down the sympathetic nervous system for fight or flight Prefron cort or anterior cingulate: info retrieved from sensory relay (thalamus) compares stim to past experience, and guide conscious decision making. Executive, goal directed behaviours \^ Hippo campus: either inhibit or excited in each phase. Mem storage, have you seen something like this before are you safe (does not work as well in those with anxiety) The Current Theoretical standpoint on fear, anxiety and threat Amygdala is central point of fear in the brain (but he has changed his mind). Now believes the fear response is the cog/emotional response. The threat response is the physiological response. i.e there is a fear response and a threat response, they are separate but can work together. We are wired to respond to threat real or imagined, our body sends this to our brain making us feel fear. Understanding anxiety ===================== Common themes in anxiety disorders (turning 6 from before to 3): - - - - - - Anxiety disorders in the DSM-5-TR ================================= Separation Anxiety Disorder Selective Mutism Specific Phobia Social Anxiety Disorder Panic Disorder Panic Attack Specifier Agoraphobia Generalized Anxiety Disorder Substance/Medication-Induced Anxiety Disorder Anxiety Disorder Due to Another Medical Condition \^ organised in order of likeliness of being diagnosed from youngest age to oldest Anxiety disorders in the DSM-5-TR ================================= Separation Anxiety Disorder Selective Mutism Specific Phobia Social Anxiety Disorder Panic Disorder Panic Attack Specifier Agoraphobia Generalized Anxiety Disorder Highlighted above ones discussed in this lecture Separation anxiety disorder =========================== [Cognitive behavioural case formulation] A A.Developmentally inappropriate and excessive fear or anxiety concerning separation from those to whom the individual is attached. B. The fear, anxiety, or avoidance is persistent, lasting at least 4 weeks in children and adolescents and typically 6 months or more in adults C. The disturbance causes clinically significant distress or impairment in social, academic, occupational, or other important areas of functioning.  [Trigger] \[caregiver\] leaving leaving Leaving \[caregiver\] \[caregiver\] might not come back \[caregiver\] might get hurt \[caregiver\] might die Anxiety Refusing to leave (caregiver) Shadowing (caregiver) Sleeping in (caregivers) bed  Selective mutism: able to speak, but become mute in certain situations often social, appears when they are around school aged. Kids communicate anxiety or fear as headaches, tummy ache (Physical complaints). Term: situational mutism better choice, as the kids do not have a choice in their mutism (part of the fear response) Specific phobia A. Marked fear or anxiety about a specific object or situation (e.g., flying heights, animals, receiving an injection, seeing blood). C. The phobic object or situation is actively avoided or endured with intense fear or anxiety. D. The fear or anxiety is out of proportion to the actual danger posed by the specific object or situation and to the sociocultural context. A clear trigger causes the anxiety Social anxiety disorder A. Marked fear or anxiety about one or more social situations in which the individual is exposed to possible scrutiny by others B. The individual fears that they will act in a way or show anxiety symptoms that will be negatively evaluated C. The social situations almost always provoke fear or anxiety D. The social situations are avoided or endured with intense fear or anxiety E. The fear/anxiety is out of proportion to the actual threat posed by the social situation/sociocultural context [Cognitive behavioural case formulation] Avoiding eye contact won't stop people from talking to you Panic disorder A. Recurrent unexpected panic attacks. A panic attack is an abrupt surge of intense fear or intense discomfort and during which time four (or more) of the following symptoms happen B. At least one of the attacks has been followed by 1 month (or more) of one or both of the following: 1. Persistent concern or worry about additional panic attacks or their consequences 2. A significant maladaptive change in behaviour related to the attacks The fear of having panic attacks is the disorder, not the panic attack itself. Panic attacks can be a symptom of other disorders though Symptoms: shortness of breath, heart palpitations, dissociation, fear they are gonna die while having these symptoms **Agoraphobia** A. Marked fear or anxiety about two (or more) of the following five situations: B. The individual fears or avoids these situations because of thoughts that escape might be difficult or help might not be available. C. The situations almost always provoke fear or anxiety. D. The situations are actively avoided. E. The fear or anxiety is out of proportion to the actual danger posed by the situation. F. The fear, anxiety, or avoidance is persistent.  Has very specific fears: tight spaces, being on a bus, losing control in public space. \^ all are hard to escape if in them Generalized anxiety disorder A. Excessive anxiety and worry, occurring more days than not for at least 6 months, about a number of events or activities. B. The individual finds it difficult to control the worry. C. The anxiety and worry are associated with three (or more) of the following six symptoms D. The anxiety, worry, or physical symptoms cause clinically significant distress or impairment in social, occupational, or other important areas of functioning. Consistent worry about something that normally would not warrant such anxiety Intolerance of uncertainty: the ambiguity causes them to stress, any possible gap for uncertainty is filled with worry A few things to draw your attention to... ========================================= The fear or anxiety is pervasive in a number of different areas of functioning ============================================================================== The fear or anxiety is actively avoided The fear of anxiety (typically) has a trigger Focus on the trigger in therapy Remember worry is normal   GWAS (is the gold standard) Genome wide association studies Collect the genetic data of people with a without a disorder (huge numbers of people) Aim is to find what the genetic differences in the single nucleotide polymorphisms Study above on major depressive disorder This study is a meta analysis of GWAS on major depression studied - Found 40 differing single nucleotide polymorphisms (SNP) - \^ snp's hold little sway or influence on their own - Many of the 40 differences/variations are common - What differs is the stress, trauma, attachment style which can trigger these snps and increase chance of anxiety disorders - Also identified difference as prefrontal cortex, and anterior cingulate cortex which confirms beliefs that major depression is a disorder of neurotransmitting problems - \^ context: neurons send messages across nervous system, microglia maintain health of the neuron, astrocytes supply nutrition - Knowing that major depression is an issue of the neuron (transmission) not neuron health through microglia and astrocytes. meaning research can focus on understanding which neurotransmitters are the problem. Neurobiology of anxiety (Grupe & Nitschke (2013))  Three main structures for depression: Amygdala Hippocampus Prefrontal cortex Look on the right for processes and parts of the brain Prefrontal cortex \^notice a lot of decision making is required (using prefrontal cortex, which is where we have learnt the communication problems are occurring. \^prefrontal not active in reactions hippocampus \^ hippocampus great for when you have context, or a memory of a stimulus to determine its threat Amygdala: projects to sympathetic structures to respond to fear Pitman et al. (2012). *Nature Reviews Neuroscience* *Mild stress \^see the loop in graph above* *In terms of neurotransmitter we have a peak stress we can deal with* *Mild stress prefrontal cortex (pfc) inhibits amygdala (the basolateral nucleus of the amygdala). Amyg sends info through subcortical structures like the locus ceruleus, and the RAF nucleus, ultimately sends the right amount of dopamine, adrenaline, and serotonin to the prefrontal cortex to activate it the right amount.* *Extreme stress (see above)* - *RAF nucleus and locus coeruleus dumps dop, adre, sero back into the amyg to continue its activation* - *At the same time inhib signal (excessive dopa and sero) going to prefrontal cortex to shut it down, so it can't make effective decisions* - *Amygdala during extreme stress will also be releasing cortisol from the endocrine system* -  *\^ going back to genetics, this study (highlighted yellow) looked at chance of kid developing disorder if both parents had it (specifically depression)* *\^ result, twice (2.5) as likely if one parent had a major depressive disorder and 2.8 times if both parents did.* *Graph on the left:* - *When depression arises between those with 0 depressed parents, 1 depressed parent, two depressed parents* - Adverse Childhood Experiences (ACEs) Bomysoad & Francis (2020). *Journal of Adolescent Health.* Looked at what happened to the child, as well as their environment (how far removed from traumas Cumulative ACEs have a huge impact on future behaviours and depressions  *People with depression have a negative cog bias* *e.g. people with depression over generalise from isolated events* *\* personalisation, blaming themselves for things that aren't their fault* *\* black and white thinking, either good or bad* *\^ these thinking traps, cog distortions cause further rumination* *Remember bad situations to happen, and CBT can not always get people out of valid bad situations, other forms of therapy are needed.* *CBT more or less claims it is not the situation that is the problem, but how we think about it and respond to it.* *\^problem when the thought exceeding reality negatively* *In really bad situations need to problem solve not reframe*  Different theories view anxiety differently. This does not change approach but how the psych looks at the predisposing and precipitating factors. The lens to view the case. No correct lens as ALL have sufficient evidence. Psych the expert in broad ideas of psychology and conditions, but client expert in their own existence. WHAT LENS DO I HAVE? What are my biases, how do I reduce them in therapy Behaviourist: - See anxiety as a learned response through operant and classical conditioning - \^ develops in response to stimuli which triggers the learnt anxiety response - People with Anxiety engage in lots of negative self-talk, irrational beliefs (CBT vibes) - Anxiety learnt by watching our peers behave to stimuli 1. Avoidance behaviours and 2. Safety behaviours In the maintenance of anxiety Avoidance behaviours: anything that preserves anxious associations through negative reinforcement. E.g. person experiences anxiety because dog is close by, they experience the physiological reaction of anxiety, so they avoid the dog, leaving the situation. They feel relief, positively reinforcing dogs are bad. (vicious cycle of anxiety from above). Safety behaviours: behaviours performed with intention of reducing anxiety, so they can cope, caveat is it further strengthens the anxious association. E.g. someone with general anxiety disorder may seek constant reassurance they are on the right track, or rehearse lines for social interactions to feel more secure, or attend parties but avoid eye contact to reduce meeting strangers, someone with panic disorder might try and restrict physical activity (in cartoon), so the do not have physiological symptoms similar to a panic attack. WHAT BEHAVIOURS ARE PREVENTING IMPROVEMENT *A behavioural psychologist, a cognitive psychologist, and a social learning theorist walk into a bar. The bartender asks them what they want, and the behavioural psychologist says, \"I\'ll have what he\'s having,\" pointing to the person next to him. The cognitive psychologist says, \"I\'ll have a drink that stimulates my neural pathways and enhances my cognitive function.\" The social learning theorist says, \"I\'ll have a drink that\'s popular among my peers and reinforces my desire to be part of a group.\"* *The bartender looks at them and says, \"So, three beers then?\"* **Required readings** Barlow, D. H., Durand, V. M., & Hofmann, S. G. (2022). Psychopathology: An Integrative Approach to Mental Disorders. Cengage. - Chapter 5: Anxiety, Trauma- and Stressor-Related, and Obsessive-Compulsive and Related Disorders. - **Just the anxiety disorders part.** - Chapter 7: Mood Disorders and Suicide. **Recommended reading** LeDoux, J. (2016). *Anxious: Using the Brain to Understand and Treat Fear and Anxiety*. Penguin Books. - Chapter 1: The Tangled Web of Anxiety and Fear - Available via the Reading List. **Barlow, D. H., Durand, V. M., & Hofmann, S. G. (2022). Psychopathology: An Integrative Approach to Mental Disorders. Cengage.** - **Chapter 5: Anxiety, Trauma- and Stressor-Related, and Obsessive-Compulsive and Related Disorders.** - **[Just the anxiety disorders part.]** **[= ]** - Panic attack case study - Two types of panic attacks 1= expected panic attacks/cued panic attacks= something you know causes panic causing panic e.g. known fear of heights and looking over a cliff 2= unexpected panic attacks/uncued panic attacks= no known trigger, do not know when or where it will occur Panic disorder more connected to type 2 (unexpected panic attacks/ uncued panic attacks). While phobias or fears connected to expected panic attacks/cued panic attacks Fear is an intense emotional alarm accompanied by a surge of energy in the autonomic nervous system (look at image below)  **Measures of heart rate, frontalis EMG, and temperature during a panic attack** A person with her arms crossed Description automatically generated **Emotional state anxiety and fear**  **Diagnostic Criterion of Panic attack** **Biological contributions** - Genetic predisposition to be more tense, anxious etc (or is it picked up from observing parents and family members?) - Panic disorders caused by having the right genes triggered by the environment - Depleted levels of gamma-aminobutyric acid (GABA), part of the GABA-benzodiazepine system, are associated with increased anxiety, although the relationship is not quite so direct. The noradrenergic will be turned on, because corticotropin releasing factor (CRF) activates the hypothalamic pituitary-adrenocortical (HPA) axis. Genetics determine how easily this CRF will be turned on - CRF system has wide-ranging effects on areas of the brain implicated in anxiety, including the emotional brain (the limbic system), particularly the hippocampus and the amygdala; the locus coeruleus in the brain stem; the prefrontal cortex; and the dopaminergic neurotransmitter system. - In the laboratory, panic attacks can be induced by inhaling CO2 -enriched air in healthy people and even more so in patients with panic disorder, and this response seems to be promoted by the amygdala (Taugher et al., 2020). - CRF system is also directly related to the GABA--benzodiazepine system and the serotonergic and noradrenergic neurotransmitter systems, and a specific single-nucleotide polymorphism (SNP) (see Chapter 2 for more details) coding for the corticotropin-releasing hormone receptor was an important risk allele (Weber et al., 2016). - The area of the brain most often associated with anxiety is the limbic system (Britton & Rauch, 2009; Gray & McNaughton, 2003; Hermans et al., 2011; LeDoux, 2002, 2015; Raber et al., 2019 The limbic system acts as a mediator between the brain stem and the cortex. \^brain stem monitors and senses changes in bodily functions and relays these potential danger signals to higher cortical processes through the limbic system. Jeff Gray found identified a brain circuit in the limbic system that leadsa from the septal and hippocampus area to the frontal cortex. The septal--hippocampal system is activated by CRF and serotonergic- and noradrenergic-mediated pathways originating in the brain stem.) \^The system that Gray calls the behavioral inhibition system (BIS) is activated by signals from the brain stem of unexpected events, such as major changes in body functioning that might signal danger. Danger signals in response to something we see that might be threatening descend from the cortex to the septal--hippocampal system. The BIS also receives a big boost from the amygdala (LeDoux, 1996, 2002, 2015). When the BIS is activated by signals that arise from the brain stem or descend from the cortex, our tendency is to freeze, experience anxiety, and apprehensively evaluate the situation to confirm that danger is present. **The behavioural inhibition system (BIS) circuit is distinct from the circuit involved in panic!!** **fight/flight system (FFS)=** This circuit originates in the brain stem and travels through several midbrain structures, including the amygdala, the ventromedial nucleus of the hypothalamus, and the central gray matter. When stimulated in animals, this circuit produces an immediate alarm-and-escape response that looks very much like panic in humans (Gray & McNaughton, 2003). The FFS is activated partly by deficiencies in serotonin, suggest Gray and McNaughton (2003) and Graeff (2004). anxiety disorders (such as social anxiety disorder, which we discuss later), activation of a network that involves the prefrontal cortex and the amygdala while performing certain tasks can predict response to Cognitive Behavioral Therapy (CBT) (Hahn et al., 2015). \^factors in your environment can change the sensitivity of these brain circuits, making you more or less susceptible to developing anxiety and its disorders. (Francis, Diorio, Plotsky, & Meaney, 2002; Stein, Schork, & Gelernter, 2007) **\^case study found smoking leads to increased risk of anxiety disorders** \^one important study suggested that cigarette smoking as a teenager is associated with greatly increased risk for developing anxiety disorders as an adult, particularly panic disorder and generalized anxiety disorder (Johnson et al., 2000). Nearly 700 adolescents of a community-based sample from upstate New York were followed into adulthood. Teens who smoked 20 or more cigarettes daily were 15 times more likely to develop panic disorder and 5 times more likely to develop generalized anxiety disorder than teens who smoked less or didn't smoke. **Current opinion on the link between smoking and anxiety** The current thinking about the link between smoking and anxiety is that anxiety sensitivity (the general tendency to fear bodily sensations, which we briefly discuss later), distress tolerance (the amount of distress a person can tolerate), and anhedonia (the inability to feel pleasure) all contribute to smoking. \^other factors include acculturative stress (Zvolensky et al., 2020), in people with anxiety disorders, the limbic system, including the amygdala, is overly responsive to stimulation or new information (abnormal bottom-up processing); at the same time, controlling functions of the cortex that would down-regulate the hyperexcitable amygdala are deficient (abnormal top-down processing). Despite these biological abnormalities, psychological treatments, in particular CBT, can effectively treat these disorders across the age range (Carpenter et al., 2018; Hofmann, Asnaani, Vonk, Sawyer, & Fang, 2012;; Kendall & Peterman, 2015). **Anxiety disorders could stem from our childhood at the realisation that we are not the centre of the universe and that we are not in control. This causes a deep uncertainty about ourselves and our ability to deal with upcoming events.** \^ our parent's behaviour not only influence this but feeds it. - parents who interact in a positive and predictable way with their children by responding to their needs, particularly when the child communicates needs for attention, food, relief from pain, and so on. - \^These parents teach their children that they have control over their environment and their responses have an effect on their parents and their environment. **Providing a secure home base allows children to go out and explore in the crazy world developing coping skills. Sense of control.** \^parents who are over protective and over intrusive who "clear the way" for their children, never letting them experience any adversity, create a situation in which children never learn how to cope with adversity when it comes along. these children don't learn that they can control their environment. A variety of evidence has accumulated supporting these ideas (Barlow, 2002; Chorpita & Barlow, 1998; Dan, Sagi-Schwartz, Bar-haim, & Eshel, 2011; Fulton, Kiel, Tull, & Gratz, 2014; Gallagher et al., 2014; Racine et al., 2021; White, Brown, Somers, & Barlow, 2006). **A sense of control (or lack of it) that develops from these early experiences is the psychological factor that makes us more or less vulnerable to anxiety in later life.** ***[anxiety sensitivity=]*** tendency to respond fearfully to anxiety symptoms \^important personality trait that determines who will and who will not experience problems with anxiety under certain stressful conditions (Reiss, 1991). We have conditioned stimuli that cause fear and they are not always warranted. They are an issue when something that is not dangerous causes the fear response. \^sensing your heartbeat or temperature has gone up (plus other anxiety related symptoms like sweating (physiological symptoms)) may make some people get more anxious and increase the risk of an anxiety attack. Although when seeing a feared cue, goes from eyes to the amygdala triggering fear \\/anxiety response before it gets to be processed by the cortex (Bouton et al., 2001; LeDoux, 2002, 2015; LeDoux & Brown, 2017; LeDoux & Hofmann, 2018). **[Social Contributions to Anxiety Disorders ]** - Stressful life events e.g. deaths, divorce, sickness, injury, financial difficulty - Families often have the same physiological responses to stress, if one gets headaches likely another will **[An Integrated Model]** **[triple vulnerability theory (]**Barlow, 2000, 2002; Barlow, Ellard, et al., 2014; Brown & Naragon-Gainey, 2013) 1. The first vulnerability (or diathesis) is a ***[generalized biological vulnerability]***. We can see that a tendency to be uptight or high-strung might be inherited. But a generalized biological vulnerability to develop anxiety is not sufficient to produce anxiety itself. 2. The second vulnerability is a ***[generalized psychological vulnerability]***. believing the world is dangerous and out of control, and you might not be able to cope when things go wrong based on your early experiences. If this perception is strong, you have a generalized psychological vulnerability to anxiety. 3. The third vulnerability is a ***[specific psychological vulnerability]*** in which you learn from early experience, such as being taught by your parents, that some situations or objects are fraught with danger (even if they really aren't). For example, if one of your parents is afraid of dogs or expresses anxiety about being evaluated negatively by others, you may well develop a fear of dogs or of social evaluation. Triple Vulnerability Theory \^Anxiety caused from a lot of pressure, particularly from interpersonal stressors, a given stressor could activate your biological tendencies to be anxious and your psychological tendencies to feel you might not be able to deal with the situation and control the stress. \^Once this cycle starts, it tends to feed on itself, so it might not stop even when the particular life stressor has long since passed. \^Anxiety can be general, evoked by many aspects of your life. But it is usually focused on one area, such as social evaluations or grades (Barlow, 2002). anxiety increases the likelihood of panic. This relationship makes sense from an evolutionary point of view because sensing a possible future threat or danger (anxiety) should prepare us to react instantaneously with an alarm response if the danger becomes imminent (Bouton, 2005). Anxiety and panic need not occur together, but it makes sense that they often do. Comorbidity of Anxiety and Related Disorders argument formulated in process-based therapy is that for therapy to be effective, it needs to target the underlying processes of change rather than the DSM-defined psychiatric syndromes (Hofmann & Hayes, 2019). Study on whether unified protocol (UP) a transdiagnostic treatment for all anxiety and related disorders was more effective than single disorder protocols (SDP). \^The results showed that patients were more likely to complete treatment with the UP than with SDPs and that SDPs were superior to the waitlist control condition immediately after the intervention. Most important, the results also showed that the UP and the SDPs were similarly efficacious at posttreatment and follow-up. This study is important because a unified treatment protocol facilitates dissemination of evidence-based psychological treatments since clinicians have to master the administration of only one protocol rather than six to eight individual treatments. 55% of the patients who received a principal diagnosis of an anxiety or depressive disorder had at least one additional anxiety or depressive disorder at the time of the assessment. If we consider whether patients met criteria for an additional diagnosis at any time in their lives rather than just at the time of the assessment, the rate increases to 76%. most common additional diagnosis for all anxiety disorders was major depression, which occurred in 50% of the cases over the course of the patient's life, probably due to the shared vulnerabilities between depression and anxiety disorders in addition to the disorder-specific vulnerability. \^WHY= anxiety and depression have the same underlying factor (low-self-esteem, and adverse childhood experience) and similar genetics **Comorbidity with Physical Disorders** anxiety disorder was uniquely and significantly associated with thyroid disease, respiratory disease, gastrointestinal disease, arthritis, migraine headaches, and allergic conditions (Sareen et al., 2006). Thus, people with these physical conditions are likely to have an anxiety disorder but are not any more likely to have another psychological disorder. the anxiety disorder most often begins before the physical disorder, suggesting (but not proving) that something about having an anxiety disorder might cause or contribute to the cause of the physical disorder if someone has both an anxiety disorder and one of the physical disorders mentioned earlier, that person will suffer, as studies have shown, from greater disability and a poorer quality of life from both the physical problem and the anxiety problem than if that individual had just the physical disorder alone (Belik, Sareen, & Stein, 2009; Comer et al., 2011; Sareen et al., 2006). DSM-5 now makes it explicit that panic attacks often co-occur with certain medical conditions, particularly cardio, respiratory, gastrointestinal, and vestibular (inner ear) disorders, even though the majority of these patients would not meet criteria for panic disorder (Kessler et al., 2006). **Chapter 7: Mood Disorders and Suicide.** **Keisha case study** **Keisha... Weathering Depression** Keisha was a shy 16-year-old who came to our clinic with her parents. For several years, Keisha had seldom interacted with anybody outside her family because of her considerable social anxiety. Going to school was difficult, and as her social contacts decreased, her days became empty and dull. By the time she was 16, a deep, all-encompassing depression blocked the sun from her life. Here is how she described it later: The experience of depression is like falling into a deep, dark hole that you cannot climb out of. You scream as you fall, but it seems like no one hears you. Some days you float upward without even trying; on other days, you wish that you would hit bottom so that you would never fall again. Depression affects the way you interpret events. It influences the way you see yourself and the way you see other people. I remember looking in the mirror and thinking that I was the ugliest creature in the world. Later in life, when some of these ideas would come back, I learned to remind myself that I did not have those thoughts yesterday and chances were that I would not have them tomorrow or the next day. It is a little like waiting for a change in the weather. But at 16, in the depths of her despair, Keisha had no such perspective. She often cried for hours at the end of the day. She had begun drinking alcohol the year before, with the blessing of her parents, strangely enough, because the pills prescribed by her family doctor did no good. A glass of wine at dinner had a temporary soothing effect on Keisha, and both she and her parents, in their desperation, were willing to try anything that might make her a more functional person. But one glass was not enough. She drank increasingly more often. She began drinking herself to sleep. It was a means of escaping what she felt: "I had very little hope of positive change. I do not think that anyone close to me was hopeful, either. I was angry, cynical, and in a great deal of emotional pain." Keisha's life continued to spiral downward. For several years, Keisha had thought about suicide as a solution to her unhappiness. At 13, in the presence of her parents, she reported these thoughts to a psychologist. Her parents wept, and the sight of their tears deeply affected Keisha. From that point on, she never expressed her suicidal thoughts again, but they remained with her. By the time she was 16, her preoccupation with her own death had increased: I think this was just exhaustion. I was tired of dealing with the anxiety and depression, day in and day out. Soon I found myself trying to sever the few interpersonal connections that I did have, with my closest friends, with my mother, and my oldest brother. I was almost impossible to talk to. I was angry and frustrated all the time. One day I went over the edge. My mother and I had a disagreement about some unimportant little thing. I went to my bedroom where I kept a bottle of whiskey or vodka or whatever I was drinking at the time. I drank as much as I could until I could pinch myself as hard as I could and feel nothing. Then I got out a very sharp knife that I had been saving and slashed my wrist deeply. I did not feel anything but the warmth of the blood running from my wrist. The blood poured out onto the floor next to the bed that I was lying on. The sudden thought hit me that I had failed, that this was not enough to cause my death. I got up from the bed and began to laugh. I tried to stop the bleeding with some tissues. I stayed calm and frighteningly pleasant. I walked to the kitchen and called my mother. I cannot imagine how she felt when she saw my shirt and pants covered in blood. She was amazingly calm. She asked to see the cut and said that it was not going to stop bleeding on its own and that I needed to go to the doctor immediately. I remember as the doctor shot novocaine into the cut he remarked that I must have used an anesthetic before cutting myself. I never felt the shot or the stitches. After that, thoughts of suicide became more frequent and more real. My father asked me to promise that I would never do it again, and I said I would not, but that promise meant nothing to me. I knew it was to ease his pains and fears and not mine, and my preoccupation with death continued. - The fundamental experiences of depression and mania contribute, either singly or together, to all the mood disorders - The most commonly diagnosed and most severe depression is called a major depressive episode DSM-5 criteria describe it as an extremely depressed mood state that lasts at least 2 weeks and includes cognitive symptoms (such as feelings of worthlessness and indecisiveness) and disturbed physical functions (such as altered sleeping patterns, significant changes in appetite and weight, or a notable loss of energy) to the point that even the slightest activity or movement requires an overwhelming effort. The episode is typically accompanied by a general loss of interest in things and an inability to experience any pleasure from life, including interactions with family or friends or accomplishments at work or at school. the most central indicators of a full major depressive episode are the physical changes (sometimes called somatic or vegetative symptoms) (Regier et al., 2013; Tang & Thomas, 2020), along with the behavioral and emotional "shutdown," as reflected by low behavioral activation (Dimidjian, Barrera, Martell, Muñoz, & Lewinsohn, 2011). In more sever cases= dysfunctional reward processing (Halahakoon et al., 2020) and anhedonia (loss of energy and inability to engage in pleasurable activities or have any "fun"). The duration of a major depressive episode, if untreated, is approximately 4 to 9 months (Hasin, Goodwin, Stinson, & Grant, 2005; Kessler & Wang, 2009). **DSM 5 Major Depressive Disorder Criterion** A. Five (or more) of the following symptoms have been present during the same 2-week period and represent a change from previous functioning; at least one of the symptoms is either 1. depressed mood or 2. loss of interest or pleasure. *[Note:]* Do not include symptoms that are clearly due to a general medical condition or mood-incongruent delusions or hallucinations. 1. Depressed mood most of the day, nearly every day, as indicated by either subjective report (e.g., feels sad, empty, hopeless) or observation made by others (e.g., appears tearful). (Note: In children and adolescents can be irritable mood.) 2. Markedly diminished interest or pleasure in all, or almost all, activities most of the day, nearly every day (as indicated by either subjective account or observation). 3. Significant weight loss when not dieting or weight gain (e.g., a change of more than 5% of body weight in a month), or decrease or increase in appetite nearly every day. (Note: In children, consider failure to make expected weight gains.) 4. Insomnia or hypersomnia nearly every day. 5. Psychomotor agitation or retardation nearly every day (observable by others, not merely subjective feelings of restlessness or being slowed down). 6. Fatigue or loss of energy nearly every day. 7. Feelings of worthlessness or excessive or inappropriate guilt (which may be delusional) nearly every day (not merely self-reproach or guilt about being sick). 8. Diminished ability to think or concentrate, or indecisiveness, nearly every day (either by subjective account or as observed by others). 9. Recurrent thoughts of death (not just fear of dying), recurrent suicidal ideation without a specific plan, or a suicide attempt or a specific plan for suicide. B. The symptoms cause clinically significant distress or impairment in social, occupational, or other important areas of functioning. C. The episode is not attributable to the direct physiological effects of a substance or another medical condition. **Manic Episodes=** **DSM 5 Criteria for Manic Episode** A. A distinct period of abnormally and persistently elevated, expansive, or irritable mood and abnormally and persistently increased activity or energy, lasting at least 1 week and present most of the day, nearly every day (or any duration if hospitalization is necessary). B. During the period of mood disturbance and increased energy or activity, three (or more) of the following symptoms (four if the mood is only irritable) are present to a significant degree and represent a noticeable change from usual behavior: 1. Inflated self-esteem or grandiosity 2. Decreased need for sleep (e.g., feels rested after only 3 hours of sleep) 3. More talkative than usual or pressure to keep talking 4. Flight of ideas or subjective experience that thoughts are racing 5. Distractibility (i.e., attention too easily drawn to unimportant or irrelevant external stimuli), as reported or observed 6. Increase in goal-directed activity (either socially, at work or school, or sexually) or psychomotor agitation (i.e., purposeless non-goal-directed activity) 7. Excessive involvement in activities that have a high potential for painful consequences (e.g., engaging in unrestrained buying sprees, sexual indiscretions, or foolish business investments) C. The mood disturbance is sufficiently severe to cause marked impairment in social or occupational functioning or to necessitate hospitalization to prevent harm to self or others, or there are psychotic features. D. The episode is not attributable to the physiological effects of a substance (e.g., a drug of abuse, a medication, other treatment) or to another general medical condition. ***[\^Note:]** A full manic episode that emerges during antidepressant treatment (e.g., medication, electroconvulsive therapy) but persists at a fully syndromal level beyond the physiological effect of that treatment is sufficient evidence of a manic episode and, therefore, a bipolar I diagnosis.* The second fundamental state in mood disorders is abnormally exaggerated elation, joy, or euphoria. In mania, individuals find extreme pleasure in every activity; some patients compare their daily experience of mania with a continuous sexual orgasm. They become extraordinarily active (hyperactive), require little sleep, and may develop grandiose plans, believing they can accomplish anything they desire. DSM-5 highlights this feature by adding "persistently increased goal-directed activity or energy" to the "A" criteria (see DSM-5 Table 7.2) (American Psychiatric Association, 2013). Speech is typically rapid and may become incoherent, because the individual is attempting to express so many exciting ideas at once; this feature is typically referred to as flight of ideas. DSM-5 also defines a hypomanic episode, a less severe version of a manic episode that does not cause marked impairment in social or occupational functioning and need last only 4 days rather than a full week. (Hypo means "below"; thus the episode is below the level of a manic episode.) A hypomanic episode is not in itself necessarily problematic, but its presence does contribute to the definition of several mood disorders. Despite the term bipolar referring to both manic and depressive episodes they are not opposites. An individual can experience manic symptoms but feel somewhat depressed or anxious at the same time or be depressed with a few symptoms of mania. This episode is characterized as having "mixed features" (Baldessarini, Vazques, & Tondo, 2020; Na, Kang, & Cho, 2021). An individual can experience manic symptoms but feel somewhat depressed or anxious at the same time or be depressed with a few symptoms of mania. This episode is characterized as having "mixed features" (Baldessarini, Vazques, & Tondo, 2020; Na, Kang, & Cho, 2021). In one study, 30% of 1,090 patients hospitalized for acute mania had mixed episodes (Hantouche et al., 2006), In another study as many as two-thirds of patients with bipolar depressed episodes also had manic symptoms, most often racing thoughts (flight of ideas), distractibility, and agitation. These patients were also more severely impaired than those without concurrent depression and manic symptoms (Goldberg et al., 2009; Swann et al., 2013). In DSM-5, the term mixed features requires specifying whether a predominantly manic or predominantly depressive episode is present and then noting if enough symptoms of the opposite polarity are present to meet the mixed features criteria. one study, out of 356 patients with bipolar disorder, 62 (17.4%) were predominantly depressed, 41 (11.5%) were predominantly manic, and 253 (71.1%) were neither predominantly depressed nor manic (Sentissi et al., 2019). Clinicians want to do everything possible to relieve people like Keisha from their current depressive episode, but an equally important goal is to prevent future episodes---in other words, to help people like Keisha stay well for a longer period. Studies have been conducted that evaluate the effectiveness of treatment in terms of this second goal (Cuijpers, 2015; Fava et al., 2004; Hollon, Stewart, & Strunk, 2006; Otto & Applebaum, 2011; Teasdale et al., 2001). **Depressive Disorders** **Several types of Mood disorder which only differ in frequency and severity** with which depressive symptoms occur and the course of the symptoms (chronic---meaning almost continuous---or nonchronic) - two most important factors that describe mood disorders are severity and chronicity (Klein, 2010 **Clinical Descriptions** The most easily recognized mood disorder is major depressive disorder, defined by the presence of depression and the absence of manic, or hypomanic episodes, before or during the disorder**.** **Recurrent=** two or more major depressive episodes occurred and were separated by at least 2 months during which the individual was not depressed, the major depressive disorder is noted as being recurrent Recurrence is important in predicting the future course of the disorder, as well as in choosing appropriate treatments. 35% to 85% of people with single-episode occurrences of major depressive disorder later experience a second episode (Angst, 2009; Eaton et al., 2008; Judd, 2000; Souery, et al., 2012)... based on follow-ups as long as 23 years (Eaton et al., 2008) Depressive episode recurrence+ - 1^st^ year following depressive episode 20% - 2^nd^ year following depressive episodes 40% Unipolar depression is often a chronic condition that waxes and wanes over time but seldom disappears (Judd, 2012). The median lifetime number of major depressive episodes is four to seven; in one large sample, 25% experienced six or more episodes (Angst, 2009; Kessler & Wang, 2009). The median duration of recurrent major depressive episodes is 4 to 5 months (Boland & Keller, 2009; Kessler et al., 2003), somewhat shorter than the average length of the first episode. **DSM 5 Diagnostic Criteria for Major Depressive Disorder** D. At least one major depressive episode (DSM-5 Table 7.1, criteria A--C). E. At least one major depressive episode is not better explained by schizoaffective disorder and is not superimposed on schizophrenia, schizophreniform disorder, delusional disorder, or other specified and unspecified schizophrenia spectrum and other psychotic disorders. F. There has never been a manic episode or hypomanic episode. Note: This exclusion does not apply if all of the manic-like or hypomanic-like episodes are substance-induced or are attributable to the direct physiological effects of another medical condition. **Specify if:** - Single episode or recurrent episode - Mild, moderate, severe - With psychotic features - With anxious distress - With mixed features - With melancholic features - With atypical features - With mood-congruent psychotic features - With mood-incongruent psychotic features - With catatonia - With peripartum onset - With seasonal pattern (recurrent episode only) In partial remission, in full remission **Persistent Depressive Disorder** **Persistent depressive disorder** shares many of the symptoms of major depressive disorder but differs in its course. There may be fewer symptoms (as few as two; see DSM-5 Table 7.4), but depression remains relatively unchanged over long periods, sometimes 20 or 30 years or more (Angst, 2009; Cristancho, Kocsis, & Thase, 2012; Klein, 2008; Klein, Shankman, & Rose, 2006; Murphy & Byrne, 2012). **DSM 5 Table 7.4 Diagnostic Criteria for Persistent Depressive Disorder** G. Depressed mood for most of the day, for more days than not, as indicated by either subjective account or observation by others, for at least 2 years. Note: In children and adolescents, mood can be irritable and duration must be at least 1 year H. Presence, while depressed, of two (or more) of the following: 1. Poor appetite or overeating 2. Insomnia or hypersomnia 3. Low energy or fatigue 4.Low self-esteem 5.Poor concentration or difficulty making decisions 6. Feelings of hopelessness I. During the 2-year period (1 year for children or adolescents) of the disturbance, the individual has never been without the symptoms in criteria A and B for more than 2 months at a time. J. Criteria for major depressive disorder may be continuously present for 2 years. **E**.There has never been a manic episode or a hypomanic episode. **F.** The disturbance is not better explained by a persistent schizoaffective disorder, schizophrenia, delusional disorder, or other specified or unspecified schizophrenia spectrum and other psychotic disorder. **G.** The symptoms are not attributable to the physiological effects of a substance (e.g., a drug of abuse, a medication) or another medical condition (e.g., hypothyroidism). **H.** The symptoms cause clinically significant distress or impairment in social, occupational, or other important areas of functioning. **Specify if:** With anxious distress With atypical features Specify if: In partial remission In full remission Specify if: **Early onset:** If onset is before age 21 years **Late onset:** If onset is at age 21 years or older **Specify if** (for most recent 2 years of persistent depressive disorder): **With pure dysthymic syndrome:** Full criteria for a major depressive episode have not been met in at least the preceding 2 years. **With persistent major depressive episode:** Full criteria for a major depressive episode have been met throughout the preceding 2-year period **With intermittent major depressive episodes, with current episode:** Full criteria for a major depressive episode are currently met, but there have been periods of at least 8 weeks in at least the preceding 2 years with symptoms below the threshold for a full major depressive episode **With intermittent major depressive episodes, without current episode:** Full criteria for a major depressive episode are not currently met, but there has been one or more major depressive episodes in at least the preceding 2 years. **Specify current severity:** Mild Moderate Severe **Persistent depressive disorder**= depressed mood that continues at least 2 years, during which the patient cannot be symptom free for more than 2 months at a time even though they may not experience all of the symptoms of a major depressive episode. - Persistent depressive disorder differs from a major depressive disorder in the number of symptoms required, but mostly it is in the chronicity (Schramm, Klein, Elsaesser, Furukawa, & Domschke, 2020). - It is considered more severe, since patients with persistent depression present with higher rates of comorbidity with other mental disorders, are less responsive to treatment, and show a slower rate of improvement over time. Klein and colleagues - in a 10-year prospective follow-up study, suggest that chronicity (versus nonchronicity) is the most important distinction in diagnosing depression independent of whether the symptom presentation meets criteria for a major depressive disorder (as noted above) because these two groups (chronic and nonchronic) seem different, not only in course over time but also in family history and cognitive style. About 20% of patients with a major depressive episode report chronicity of this episode for at least 2 years, thereby meeting criteria for persistent depressive disorder (Klein, 2010). **Double Depression** - Individuals who have major depressive episodes and persistent depression with fewer symptoms are said to have double depression - Klein et al. (2006) found that the relapse rate of depression among people meeting criteria for DSM-IV dysthymia was 71.4%. Also, double depression is more difficult to treat than either the major depression or the dysthymia alone (May, Shaffer, & Yoon, 2020). Consider the case of Jack. Jack Case Study Jack A Life Kept Down Jack was a 49-year-old divorced white man who lived at his mother's home with his 10-year-old son. He complained of chronic depression, saying he finally realized he needed help. Jack reported that he had been a pessimist and a worrier for much of his adult life. He consistently felt kind of down and depressed and did not have much fun. He had difficulty making decisions, was generally pessimistic about the future, and thought little of himself. During the past 20 years, the longest period he could remember in which his mood was "normal" or less depressed lasted only 4 or 5 days. Despite his difficulties, Jack had finished college and obtained a master's degree in public administration. People told him his future was bright and he would be highly valued in state government. Jack did not think so. He took a job as a low-level clerk in a state agency, thinking he could always work his way up. He never did, remaining at the same desk for 20 years. Jack's wife, fed up with his continued pessimism, lack of self-confidence, and relative inability to enjoy day-to-day events, became discouraged and divorced him. Jack moved in with his mother so that she could help care for his son and share expenses. About 5 years before coming to the clinic, Jack had experienced a bout of depression worse than anything he had previously known. His self-esteem went from low to nonexistent. From indecisiveness, he became unable to decide anything. He was exhausted all the time and felt as if lead had filled his arms and legs, making it difficult even to move. He became unable to complete projects or to meet deadlines. Seeing no hope, he began to consider suicide. After tolerating a listless performance for years from someone they had expected to rise through the ranks, Jack's employers finally fired him. After about 6 months, the major depressive episode resolved and Jack returned to his chronic but milder state of depression. He could get out of bed and accomplish some things, although he still doubted his own abilities. He was unable to obtain another job, however. After several years of waiting for something to turn up, he realized he was unable to solve his own problems and that without help his depression would continue. After a thorough assessment, we determined that Jack suffered from a classic case of double depression.  \^Six graphs labelled a through f show various course configurations of nonbipolar depression. Time is represented on the horizontal axis and mood is represented on the vertical axis. Each panel shows two vertical lines connected by a horizontal line. Blue shaded regions are present on the bottom-side of the horizontal line. Graph a shows two blue square-shaped regions, one toward left and one toward right. Graph b shows a small blue plateau-shaped region starting slightly left of the left vertical axis and ending at the right vertical axis. The graph c is similar to graph b except there is a raised region in the center. Graph d shows a broad blue rectangular-shaped region starting slightly left of the left vertical axis and ending at the right vertical axis. Graph e is similar to graph c except the raised region is toward left. The graph f is similar to graph f except there are two raised regions, one toward left and one toward right. Pictorial representation of various course configurations of nonbipolar depression. The horizontal axis represents time, and the vertical axis represents mood, with the horizontal black line representing euthymic, or normal, mood, and the magnitude of downward deflection (the blue area) reflecting severity of depressive symptoms. Panel a. is nonchronic major depressive disorder (in this case, recurrent, as two depressive episodes are depicted). b. Panel (b) is persistent depressive disorder with pure dysthymic syndrome. c. Panel (c) is double depression (major depressive episode occurring within the course of persistent depressive disorder). d. Panel (d) is chronic major depressive episode. e. Panel (e) is major depressive episode in partial remission. f. Panel (f) is recurrent major depression without full inter episode recovery. Based on D. N. Klein, 2010, Chronic depression: Diagnosis and classification, Current Directions in Psychological Science, 19(2), 96--100. **Additional Defining Criteria for Depressive Disorders** In addition to rating severity of the episode as mild, moderate, or severe, clinicians use eight basic specifiers to describe depressive disorders. These are 1. with psychotic features (mood-congruent or mood-incongruent), 2. with anxious distress (mild to severe), 3. with mixed features, 4. with melancholic features, 5. with atypical features, 6. with catatonic features, 7. with peripartum onset, and 8. with seasonal pattern. Some of these specifiers apply only to major depressive disorder. Others apply to both major depressive disorder and persistent depressive disorder. Each is described briefly below. 1. *Psychotic features specifiers.* Some individuals in the midst of a major depressive (or manic) episode may experience psychotic symptoms, specifically **hallucinations** (seeing or hearing things that aren't there) and **delusions** (strongly held but inaccurate beliefs) (Rothschild, 2013). *Somatic (physical) delusions*, believing, for example, that their bodies are rotting internally and deteriorating into nothingness *(auditory hallucinations)* Some may hear voices telling them how evil and sinful they are *Delusions of grandeur* (believing, for example, they are supernatural or supremely gifted) that do not seem consistent with the depressed mood. This is a mood-incongruent hallucination or delusion. Although quite rare, this condition signifies a serious type of depressive episode that may progress to schizophrenia (or may be a symptom of schizophrenia to begin with). Delusions of grandeur accompanying a manic episode are mood congruent. psychotic symptoms accompany depressive episodes are relatively rare, occurring in 5% to 20% of identified cases of depression (Flores & Schatzberg, 2006; Ohayon & Schatzberg, 2002). Psychotic features in general are associated with a poor response to treatment, greater impairment, and fewer weeks with minimal symptoms, compared with nonpsychotic depressed patients over a 10-year period (Busatto, 2013; Flint, Schaffer, Meyers, Rothschild, & Mulsant, 2006). 2. *Anxious Distress Specifier=* - Anxiety symptoms can meet an anxiety diagnosis (comorbidity with a mood disorder) or meet a diag - presence of anxiety indicates a more severe condition, makes suicidal thoughts and fatal suicide attempts more likely, and predicts a less effective outcome from treatment. 3. *Mixed features specifier* - Predominantly depressive episodes that have several (at least three) symptoms of mania as described above would meet this specifier, which applies to major depressive episodes both within major depressive disorder and persistent depressive disorder. 4. *Melancholic features specifier=* This specifier applies only if the full criteria for a major depressive episode have been met, whether in the context of a persistent depressive disorder or not. Melancholic specifiers include some of the more severe somatic (physical) symptoms, such as early-morning awakenings, weight loss, loss of libido (sex drive), excessive or inappropriate guilt, and anhedonia (diminished interest or pleasure in activities). "melancholic" does seem to signify a severe type of depressive episode. Whether this type is anything more than a different point on a continuum of severity remains to be seen (Johnson, Cueller, & Miller, 2009; Klein, 2008; Parker, McCraw, et al., 2013; Sun et al., 2012). 5. *Catatonic features specifier*= an absence of movement (a stuporous state) or catalepsy, in which the muscles are waxy and semirigid, so a patient's arms or legs remain in any position in which they are placed. Catatonic symptoms may also involve excessive but random or purposeless movement. Catalepsy was thought to be more commonly associated with schizophrenia, but some studies have suggested it may be more common in depression than in schizophrenia (Huang, Lin, Hung, & Huang, 2013). This response may be a common "end state" reaction to feelings of imminent doom and is found in many animals about to be attacked by a predator (Moskowitz, 2004). 6. *Atypical features specifier* = consistently oversleep and overeat during their depression and therefore gain weight, leading to a higher incidence of diabetes (Glaus et al., 2012; Kessler & Wang, 2009). Although they also have considerable anxiety, they can react with interest or pleasure to some things, unlike most depressed individuals. The atypical group also has more symptoms, more severe symptoms, more suicide attempts, and higher rates of comorbid disorders including alcohol use disorder (Bech, 2009; Blanco et al., 2012; Glaus et al., 2012; Matza, Revicki, Davidson, & Stewart, 2003). 7. *Peripartum onset specifier* = Peri means "surrounding"---in this case, the period of time just before and just after the birth. This specifier can apply to both major depressive and manic episodes. Between 13% and 19% of all women giving birth (one in eight) meet criteria for a diagnosis of depression, referred to as peripartum depression. In one study, 7.2% met criteria for a full major depressive episode (Gavin et al., 2005). Typically, a somewhat higher incidence of depression is found postpartum (after the birth) than during the period of pregnancy itself (Viguera et al., 2011). In another important study, 14% of 10,000 women who gave birth screened positively for depression, and fully 19.3% of those depressed new mothers had serious thoughts of harming themselves (Wisner et al., 2013). During the peripartum period (pregnancy and the 6-month period immediately following childbirth), early recognition of possible psychotic depressive (or manic) episodes is important because in a few tragic cases a mother in the midst of an episode has killed her newborn child (Purdy & Frank, 1993; Sit, Rothschild, & Wisner, 2006). Fathers don't entirely escape the emotional consequences of birth. Ramchandani and colleagues (Ramchandani, Stein, Evans, O'Connor, & the ALSPAC Study Team, 2005) followed 11,833 mothers and 8,431 fathers for 8 weeks after the birth of their children. Of the mothers, 10% showed a marked increase in depressive symptoms on a rating scale, but so did 4% of the fathers. If you extend the period from the 1st trimester to 1 year after birth, the rate of depression is approximately 10% for fathers and as high as 40% for mothers. And depression in fathers was associated with adverse emotional and behavioral outcomes in children 3.5 years later (Paulson & Bazemore, 2010). A review of the literature shows that psychological interventions for paternal peripartum depression has a positive impact on the father and also on the father-child and the marital relationship (Goldstein, Rosen, Howlett, Anderson, & Herman, 2020). In general, guidelines for treating and preventing peripartum depression include cognitive behavioral therapy and interpersonal therapy (Curry et al., 2020). 8. *Seasonal pattern specifier* This temporal specifier applies to recurrent major depressive disorder (and also to bipolar disorders). It accompanies episodes that occur during certain seasons (e.g., winter depression). The most usual pattern is a depressive episode that begins in the late fall and ends with the beginning of spring. (In bipolar disorder, individuals may become depressed during the winter and manic during the summer.) These episodes must have occurred for at least 2 years with no evidence of nonseasonal major depressive episodes occurring during that period of time. This condition is called seasonal affective disorder (SAD). 2.7% of North Americans (Lam et al., 2006; Levitt & Boyle, 2002). But fully 15% to 25% of the population might have some vulnerability to seasonal cycling of mood that does not reach criteria for a disorder (Kessler & Wang, 2009; Sohn & Lam, 2005). Although SAD seems a bit different from other major depressive episodes, family studies have not yet revealed any significant differences that would suggest winter depressions are a separate type (Lam & Lavitan, 2000). Emerging evidence suggests that SAD may be related to daily and seasonal changes in the production of melatonin, a hormone secreted by the pineal gland. Because exposure to light suppresses melatonin production, it is produced only at night. Melatonin production also tends to increase in winter, when there is less sunlight. One theory is that increased production of melatonin might trigger depression in vulnerable people (Goodwin & Jamison, 2007; Lee et al., 1998). (MORE DISCUSSED) As you might expect, the prevalence of SAD is higher in extreme northern and southern latitudes because there is less winter sunlight. However, there is a big variation in the degree to which people are affected by seasonal changes and daylight exposure. We discuss some of the reasons, which are also linked to sleep--wake cycles, in Chapter 8. Table 7.1 Summary of Remission Rates   Remission Rate % (Number of Patients)   Morning Light Evening Light Placebo (Negative-Ion Generator) Terman et al., 1998       First treatment 54% (25 of 46) 33% (13 of 39) 11% (2 of 19) Crossover 60% (28 of 47) 30% (14 of 47) Not done Eastman et al., 1998       First treatment 55% (18 of 33) 28% (9 of 32) 16% (5 of 31) Lewy et al., 1998       First treatment 22% (6 of 27) 4% (1 of 24) Not done Crossover 27% (14 of 51) 4% (2 of 51) Not done A screenshot of a medical report Description automatically generated  **Onset and Duration of Mood disorders (Depression and Mania)** - risk for developing major depression is fairly low until the early teens, when it begins to rise in a steady (linear) fashion (Rohde, Lewinsohn, Klein, Seeley, & Gau, 2013). - symptoms of depression were highest in young adults, decreased across middle adulthood, and then increased again in older age, with older people also experiencing an increase in distress associated with these symptoms (Sutin et al., 2013). -. Kessler and colleagues (2003) 25% of people 18 to 29 years had already experienced major depression, a rate far higher than the rate for older groups when they were that age. - Rohde and colleagues (2013) children ages 5 to 12, 5% had experienced major depressive disorder. The corresponding figures in adolescence (ages 13 to 17) was 19%; in emerging adulthood (ages 18 to 23), 24%; and in young adulthood (ages 24 to 30), 16%. - the probability of remission of the episode within 1 year approaches 90% (Kessler & Wang, 2009). In those severe cases in which the episode lasts 5 years or longer, 38% can be expected to eventually recover (Mueller et al., 1996). - Investigators have found a lower (0.07%) prevalence of persistent mild depressive symptoms in children compared with adults (3% to 6%) (Klein, Schwartz, Rose, & Leader, 2000) - symptoms tend to be stable throughout childhood (Garber, Gallerani, & Frankel, 2009). Kovacs, Akiskal, Gatsonis, and Parrone (1994) found that 76% of a sample of children with persistent mild depressive symptoms later developed major depressive disorder. - Persistent depressive disorder may last 20 to 30 years or more, although studies have reported a median duration of approximately 5 years in adults (Klein et al., 2006) and 4 years in children (Kovacs et al., 1994). - Klein and colleagues (2006), in the study mentioned earlier, conducted a 10-year follow-up of 97 adults with DSM-IV dysthymia (now known as persistent depressive disorder, which is characterized by fewer or more mild symptoms of depression) and found that 74% had recovered at some point but 71% of those had relapsed. A graph of depression and depression Description automatically generated with medium confidence Dysthymic Pure dysthymic disorder Nonchronic major depressive disorder **From Grief to Depression** A new diagnosis of prolonged grief disorder where individuals experience intense grief that lasts a year or more. The natural grieving process called ***acute grief*** can also be closely related to depression. After the loss of someone you love you may experience= depressive symptoms as well as anxiety, emotional numbness, and denial, full major depressive episode, perhaps with psychotic features, suicidal ideation, or severe weight loss and so little energy that the individual cannot function (Maciejewski, Zhang, Block, & Prigerson, 2007). The natural grieving process has peaked within the first 6 months, although some people grieve for a year or longer (Currier, Neimeyer, & Berman, 2008; Maciejewski et al., 2007). **Acute Grief** lasts between 6 months-1 year. **Integrated Grief**, after acute grief people enter integrated grief, in which the finality of death and its consequences are acknowledged and the individual adjusts to the loss. New, bittersweet, but mostly positive memories of the deceased person that are no longer dominating or interfering with functioning are then incorporated into memory (Shear et al., 2011). Integrated grief often recurs at significant anniversaries, such as the birthday of the loved one, holidays, and other meaningful occasions, including the anniversary of the death. This is all a very normal and positive reaction. In fact, mental health professionals are concerned when someone does not grieve after a death because grieving is our natural way of confronting and handling loss. After 6 months to a year or so, the chance of recovering from severe grief without treatment is considerably reduced. At this stage, suicidal thoughts increase substantially and focus mostly on joining the beloved deceased (Stroebe, Stroebe, & Abakoumkin, 2005). The ability to imagine events in the future is generally impaired, since it is difficult to think of a future without the deceased (MacCallum & Bryant, 2011; Robinaugh & McNally, 2013). Individuals also have difficulty regulating their own emotions, which tend to become rigid and inflexible (Gupta & Bonanno, 2011). Many of the psychological and social factors related to mood disorders in general, including a history of past depressive episodes, also predict the development of the new disorder. In children and young adults, the sudden loss of a parent makes them particularly vulnerable to severe depression beyond the normal time for grieving, suggesting the need for immediate intervention for some (Brent, Melhem, Donohoe, & Walker, 2009; Melhem, Porta, Shamseddeen, Payne, & Brent, 2011). the very strong yearning in complicated grief seems to be associated with the activation of the dopamine neurotransmitter system. This is in contrast to major depressive disorder, in which activation is reduced in this system (O'Connor et al., 2008). Also, brain-imaging studies indicate that areas of the brain associated with close relationships and attachment are active in grieving people, in addition to areas of the brain associated with more general emotional responding (Gündel, O'Connor, Littrell, Fort, & Lane, 2003). Prolonged grief disorder is now included as a new diagnostic category in the DSM-5.  Queen Victoria remained in such deep mourning for her husband, Prince Albert, that she was unable to perform as monarch for several years after his death. Table 7.2 Acute and Integrated Grief Common symptoms of acute grief that are within normal limits within the first 6--12 months after: Recurrent, strong feelings of yearning, wanting very much to be reunited with the person who died; possibly even a wish to die in order to be with deceased loved one - Pangs of deep sadness or remorse, episodes of crying or sobbing, typically interspersed with periods of respite and even positive emotions - Steady stream of thoughts or images of deceased, may be vivid or even entail hallucinatory experiences of seeing or hearing deceased person - Struggle to accept the reality of the death, wishing to protest against it; there may be some feelings of bitterness or anger about the death Somatic distress, for example, uncontrollable sighing, digestive symptoms, loss of appetite, dry mouth, feelings of hollowness, sleep disturbance, fatigue, exhaustion or weakness, restlessness, aimless activity, difficulty initiating or maintaining organized activities, and altered sensorium - Feeling disconnected from the world or other people, indifferent, not interested, or irritable with others - Symptoms of integrated grief that are within normal limits: - Sense of having adjusted to the loss - Interest and sense of purpose, ability to function, and capacity for joy and satisfaction are restored - Feelings of emotional loneliness may persist - Feelings of sadness and longing tend to be in the background but still present - Thoughts and memories of the deceased person accessible and bittersweet but no longer dominate the mind - Occasional hallucinatory experiences of the deceased may occur - Surges of grief in response to calendar days or other periodic reminders of the loss may occur Source: M. K. Shear, N. Simon, M. Wall, S. Zisook, R. Neimeyer, N. Duan, & A. Keshaviah, (2011), Complicated grief and related bereavement issues for DSM-5, Depression and Anxiety, 28, 103--117. As with those diagnosed with posttraumatic stress, one therapeutic approach is to help grieving individuals reexperience the trauma under close supervision (Shear et al., 2014). Usually, the grieving person is encouraged to talk about the loved one, the death, and the meaning of the loss while experiencing all the associated emotions until that person can come to terms with reality. This would include incorporating positive emotions associated with memories of the relationship into the intense negative emotions connected with the loss, and arriving at the position that it is possible to cope with the pain and life will go on, thereby achieving a state of integrated grief (Currier et al., 2008). Several studies have demonstrated that this approach is successful compared to alternative psychological treatments that also focus on grief and loss (Bryant et al., 2014; Shear et al., 2014; Simon, 2013).