Abnormal Psychology Study Guide

Lesson 6 – Trauma and Stressor-Related Disorders

Posttraumatic Stress Disorder (PTSD)

• DSM-5 Symptom Clusters: PTSD symptoms are grouped into four clusters: intrusion (re-experiencing trauma via intrusive memories, nightmares, flashbacks)​pmc.ncbi.nlm.nih.gov, avoidance (efforts to avoid trauma-related thoughts, feelings, or reminders)​pmc.ncbi.nlm.nih.gov, negative alterations in cognition and mood (e.g. persistent negative beliefs, blame, estrangement, inability to feel positive)​ncbi.nlm.nih.gov​ncbi.nlm.nih.gov, and alterations in arousal and reactivity (e.g. irritability/anger, hypervigilance, exaggerated startle, sleep disturbance)​ncbi.nlm.nih.gov​ncbi.nlm.nih.gov. For a PTSD diagnosis, symptoms in all four clusters must persist for over 1 month and cause significant distress or impairment​ncbi.nlm.nih.gov​opentext.wsu.edu. (If symptoms resolve sooner, see Acute Stress Disorder below.)
• Etiological Factors: PTSD risk increases with severe or prolonged trauma and lack of social support. Prior trauma or adverse childhood experiences, being female, and belonging to marginalized groups also heighten risk​psychiatry.org​psychiatry.org. Biological factors (e.g. hyperreactive HPA stress response, or smaller hippocampal volume) and psychological factors (e.g. tendency to catastrophize or feeling helpless) can contribute to vulnerability. Nonetheless, most trauma survivors do not develop PTSD​psychiatry.org, indicating resilience and post-trauma support are protective.
• Gender and Trauma (Table 6.1 insight): Women are twice as likely as men to develop PTSD after trauma​nami.org. Around 10–12% of women and ~4–6% of men will have PTSD in their lifetime​nami.org. This disparity arises partly because women more often experience high-impact traumas like rape or childhood sexual abuse, which carry a higher “conditional” risk of PTSD​nami.org. Men experience trauma more frequently overall (e.g. accidents, combat) but have lower rates of PTSD per trauma. In sum, trauma type and social factors (e.g. stigma, support) influence the gender differences in PTSD prevalence.
• PTSD vs. Acute Stress Disorder vs. Adjustment Disorder: All are trauma/stress-related disorders, but they differ in timing and severity:
  • Acute Stress Disorder (ASD): Similar symptoms to PTSD but occurs immediately after trauma. Duration is 3 days up to 1 month post-trauma; if it lasts longer, the diagnosis may transition to PTSD​opentext.wsu.edu​opentext.wsu.edu. ASD requires ≥9 symptoms across categories of intrusion, negative mood, dissociation, avoidance, and arousal (these symptoms overlap with PTSD’s clusters, but ASD does not require one of each category)​opentext.wsu.edu. ASD by definition occurs within 1 month of the event.
  • PTSD: Requires symptoms from each of the four clusters for >1 month after trauma​opentext.wsu.edu​opentext.wsu.edu. Onset may be delayed, but full criteria must occur at least one month post-trauma. PTSD often involves more enduring or severe symptoms than ASD, potentially including persistent cognitive/mood changes and aggressive or self-destructive behavior in the arousal domain.
  • Adjustment Disorder: Involves emotional or behavioral symptoms (e.g. anxiety, depression, or conduct disturbances) in response to an identifiable stressor (not necessarily a life-threatening trauma)​opentext.wsu.edu​opentext.wsu.edu. Symptoms begin within 3 months of the stressor and cause disproportionate distress or impairment in functioning​opentext.wsu.edu​opentext.wsu.edu. Unlike PTSD/ASD, there are no specific symptom clusters required – any symptoms (depressive, anxious, etc.) can manifest, as long as they are excessive relative to the stressor. Adjustment disorders are typically short-term (symptoms usually resolve within 6 months after the stressor or its consequences end) and do not involve the severe intrusive or dissociative symptoms seen in PTSD/ASD.
• Prolonged Exposure Therapy (for PTSD): A highly effective trauma-focused psychotherapy for PTSD. Key components include: (1) Psychoeducation – teaching about common trauma reactions and how avoidance maintains PTSD, instilling hope that confronting memories can help​ptsd.va.gov. (2) In vivo exposure – gradual, repeated confrontation with safe situations or cues the patient has been avoiding (e.g. driving if the trauma was a car accident) to extinguish fear responses​ptsd.va.gov. (3) Imaginal exposure – repeated, prolonged recounting of the traumatic memory in detail (typically in therapy sessions, often audio-recorded) to process the trauma. After each imaginal exposure, the therapist and patient process the experience, discussing emotions and new insights (correcting distorted beliefs like self-blame)​ptsd.va.gov. Through these steps, avoidance is reduced and the trauma memory becomes less distressing over time. Prolonged Exposure has the strongest evidence base and often leads to significant PTSD symptom reduction and even loss of diagnosis for many patients​ptsd.va.gov​ptsd.va.gov.

Enhanced PTSD Diagnostic Criteria & Features:

• Exposure Criteria explicitly include:
  • Direct experience, witnessing, learning the event occurred to someone close, or repeated exposure to aversive details (first responders).
• Additional Diagnostic Features clearly stated:
  • Persistent re-experiencing through images, thoughts, dreams.
  • Avoidance of trauma-related stimuli.
  • Negative changes in cognitions and mood.
  • Increased arousal/reactivity (insomnia, hypervigilance).
  • Duration requirement: symptoms must persist for 1+ month and impair functioning.

Lesson 7 – Somatic and Factitious Disorders

Somatic Symptom Disorder (SSD) and Illness Anxiety Disorder

• Somatic Symptom Disorder: Characterized by one or more physical symptoms that are distressing or disrupt daily life, coupled with excessive thoughts, feelings, or behaviors related to those symptoms​opentext.wsu.edu. The person’s suffering is authentic, whether or not a medical explanation is found. Common features include persistent high anxiety about health and frequent healthcare use. The individual often spends a lot of time and energy on the symptoms or health concerns, and has a tendency to catastrophize normal bodily sensations (e.g. interpreting a mild headache as a brain tumor)​opentext.wsu.edu​opentext.wsu.edu. Importantly, a diagnosed medical condition does not rule out SSD – it can be comorbid if the reaction is excessive​opentext.wsu.edu. In sum, SSD is defined by disproportionate worry and behavioral involvement in health issues, rather than by the somatic symptoms alone.
• Illness Anxiety Disorder (IAD): Formerly called hypochondriasis. The hallmark is preoccupation with having or acquiring a serious illness without significant somatic symptoms​opentext.wsu.edu. The individual typically has minimal or no physical complaints; instead, it is the idea of being ill that causes anxiety. They might misinterpret normal sensations (like mild fatigue or a minor rash) as signs of severe disease. Despite medical evaluation and reassurance, the high health anxiety persists​opentext.wsu.edu. People with IAD often excessively check their body for signs of illness or, conversely, avoid doctors and hospitals due to fear of bad news. DSM-5 recognizes two subtypes: care-seeking type – frequent doctor visits, tests, and seeking reassurance; and care-avoidant type – avoiding medical care due to distrust or fear​my.clevelandclinic.org​my.clevelandclinic.org. Unlike SSD, in illness anxiety disorder actual somatic symptoms are absent or very mild – it’s the health anxiety that is prominent.

Conversion Disorder (Functional Neurological Symptom Disorder)

• Conversion Disorder: Involves neurological-like symptoms (alterations in motor or sensory function) that are incompatible with recognized medical conditions​opentext.wsu.edu. Examples include paralysis or weakness of a limb, non-epileptic seizures, loss of sensation or vision, tremors, or aphonia (loss of voice) with no neurological cause found​opentext.wsu.edu. The term “conversion” originates from Freud’s idea of psychological stress being converted into physical symptoms. While patients are not faking symptoms, the symptoms are thought to arise from psychological factors (often acute stress or trauma). A key diagnostic criterion is evidence of internal inconsistency or incompatibility with neurological disease (for instance, normal EEG during psychogenic “seizures”)​opentext.wsu.edu. Prognosis: Conversion symptoms are often short-lived – studies indicate as many as 90% of acute conversion episodes resolve within days to a month​journalofethics.ama-assn.org. Many patients never have another episode after the first resolves. However, up to 25% may experience recurrent episodes during times of stress​journalofethics.ama-assn.org. Conversion disorder can become chronic in some cases (especially if precipitating conflicts aren’t addressed), but generally a sudden onset, clearly identifiable stressor, and good premorbid functioning predict better recovery​journalofethics.ama-assn.org. Treatment involves psychotherapy (e.g. stress management, trauma-focused therapy) and rehabilitation approaches; importantly, a compassionate doctor-patient relationship (acknowledging the symptoms are real and distressing, even without a medical cause) helps prevent iatrogenic harm.

Factitious Disorders (Including Munchausen Syndromes)

• Factitious Disorder: Unlike the above somatic disorders, factitious disorder is defined by deliberate falsification or induction of symptomswith the intent to assume the sick role, without obvious external incentives​opentext.wsu.edu. In other words, the person wants to be seen as ill or injured and will fabricate symptoms, manipulate diagnostic tests, or even physically harm themselves to produce symptoms. Examples include injecting oneself with bacteria to cause infection, adding blood to a urine sample, or pretending to have seizures​opentext.wsu.edu. Two forms are recognized:
  • Factitious Disorder Imposed on Self: (Munchausen syndrome) – The individual feigns, exaggerates, or induces illness in themselves. They might peregrinate between hospitals, eagerly undergo invasive procedures, and invent dramatic medical histories.
  • Factitious Disorder Imposed on Another: (Munchausen by proxy) – The perpetrator (often a caregiver, like a parent) intentionally causes or fabricates illness in someone else (the victim) under their care, in order to gain attention or sympathy by proxy. For example, a mother might secretly poison a child to make the child appear chronically ill, then devote herself to the child’s care and engage with medical providers. Note: This is also considered a form of abuse.
• In factitious disorders, the motivation is internal (psychological need to be seen as ill), distinguishing it from malingering, where deception is for external gain (money, avoiding legal trouble, etc.). Factitious disorder can be dangerous (due to unnecessary treatments or injury to self/others) and is often challenging to treat, as patients typically deny the deception and may leave treatment if confronted. Psychological factors like history of childhood illness or trauma, or a need for attention, may underlie the behavior​opentext.wsu.edu.

Difference Summary: In SSD and IAD, the patient truly believes they are ill (no intentional deception). In Conversion, symptoms are not consciously produced and stem from psychological distress. In Factitious Disorder, symptoms are consciously faked/induced, but for psychological reasons (to occupy the sick role), not for material gain. The presence of intentional deception and lack of external reward is what sets factitious disorders apart​

opentext.wsu.edu.

Somatic and Factitious Disorders

Enhanced Understanding:

• Body Dysmorphic Disorder:
  • Marked by persistent preoccupation with imagined or slight physical defects.
  • Characteristic repetitive behaviors (e.g., checking mirrors, grooming).
• Hoarding Disorder (distinct from OCD):
  • Excessive collection, inability to discard, extreme clutter, early onset, and progressive worsening.
• Trichotillomania & Excoriation Disorder:
  • Hair-pulling and skin-picking compulsions, respectively, causing noticeable damage and impairment.

Lesson 8 – Dissociative Disorders

Dissociative Amnesia (with or without Fugue)

• Definition: Dissociative Amnesia involves an inability to recall important autobiographical information, usually of a traumatic or stressful nature, that is too extensive to be explained by ordinary forgetfulness​psychiatry.org. The memory loss can be localized (unable to recall a specific event or period, e.g. the hours during a disaster), selective (forgetting some but not all events during a period, or only aspects of a traumatic event), generalized (complete loss of memory for one’s life history/identity – very rare), continuous (ongoing amnesia from a point in the past up to the present, including inability to form new memories), or systematized (loss of memory for a specific category of information, such as all memories related to one’s family)​my.clevelandclinic.org​my.clevelandclinic.org. Despite the memory gaps, other cognitive functions remain intact.
• Dissociative Fugue (specifier): A dissociative fugue is a specifier for dissociative amnesia. It refers to purposeful travel or bewildered wandering away from home or one’s customary environment, accompanied by amnesia for identity or other important autobiographical information​my.clevelandclinic.org. In a fugue state, a person might suddenly travel to another city and forget who they are or assume a new identity for a time. Fugue states are typically brief (hours to days) and recovery can be abrupt – the person may suddenly recall their identity, with amnesia for the fugue period. Fugue is rare, usually precipitated by severe stress or conflict. (In DSM-IV, fugue was a separate diagnosis; in DSM-5 it’s a subtype of dissociative amnesia​psychcentral.com.)
• Key Point: In dissociative amnesia, the memory loss is psychological in origin (not due to brain injury, substance, or medical condition) and often centers on traumatic experiences. The person is typically aware of their memory gaps (except in fugue, where they might not realize anything is missing until they “come to”). There is often minimal concern about the missing memories (especially in localized amnesia), which is termed “la belle indifférence” in some cases – though this is not always present​journalofethics.ama-assn.org.

Depersonalization/Derealization Disorder

• This disorder is characterized by persistent or recurrent episodes of depersonalization, derealization, or both. During episodes, reality testing remains intact (the person knows these experiences are not literally real)​psychiatry.org, but the symptoms cause significant distress.
  • Depersonalization – a feeling of detachment from one’s self, as if observing one’s thoughts, feelings, body, or actions from outside. Individuals describe feeling like they are in a dream or not in control of their speech or movements, or that their body isn’t their own. They may feel emotionally numb or as if they have no identity​psychiatry.org.
  • Derealization – a sensation of unreality or detachment from one’s surroundings. The world feels strange, dreamlike, or foggy; people or objects may seem unreal, visually distorted, or lifeless​psychiatry.org. For example, a person might sense that the environment “isn’t real” or is muted and distant, as if a veil separates them from the world.
• Episodes can vary in length from brief moments to years. A common onset is in adolescence, and triggers can include stress, trauma, or substance use. While depersonalization/derealization can occur transiently in other disorders (like panic attacks or PTSD), in this disorder they are the primary problem. Treatment often involves therapy to address underlying anxiety or trauma and techniques to ground the person in reality.

Dissociative Identity Disorder (DID)

• Definition: DID (formerly multiple personality disorder) is characterized by the presence of two or more distinct identities or personality states (“alters”) that recurrently take control of the person’s behavior, along with gaps in memory for everyday events, personal information, or traumatic events that are too extensive to be ordinary forgetting​psychiatry.org. Individuals with DID experience themselves as having different identities or selves, each with its own relatively enduring pattern of perceiving and interacting with the world. These identity states may have unique names, mannerisms, voices, and even physical postures or allergies. Switching between alters is often triggered by stress or reminders of trauma and can be sudden.
• Distinguishing Features: DID typically involves severe childhood trauma (often chronic abuse) as an antecedent; it’s understood as an extreme form of dissociation where different aspects of identity and memory segregate. Unlike dissociative amnesia alone, DID’s memory gaps encompass more than traumatic events – individuals may “lose time” during which an alternate identity was in control (finding objects they don’t remember buying, or being called by an unfamiliar name). Unlike depersonalization disorder, in DID the person may actually act out different roles (alters), not just feel detached. When a different identity is dominant, the person may speak differently, have different preferences or skills, and be unable to recall information encoded by other alters. These features help distinguish DID from other dissociative disorders. Importantly, culturally normative experiences of possession or trance (e.g. in religious rituals) are not DID; DSM-5 excludes those accepted practices​psychiatry.org.
• Treatment (3-Phase Approach): Treating DID is typically a long-term process with a phase-oriented approach​did-research.org:
  • Phase 1: Safety & Stabilization. The therapist first focuses on ensuring the individual is safe (protecting them from self-harm or ongoing abuse) and building a trusting therapeutic alliance with all facets of the personality​cf.healthyplace.com. This phase involves educating the person about DID, establishing communication and cooperation among alters, and improving coping skills. For example, the therapist may contact various alters (sometimes via hypnosis or journaling) to understand their roles and to negotiate safety contracts (e.g. no self-harm pacts)​cf.healthyplace.com​cf.healthyplace.com. Comorbid issues (like depression, PTSD, or substance use) are addressed, and grounding techniques are taught to manage dissociative episodes​did-research.org​did-research.org. The goal is to stabilize mood, reduce dissociative switching, and prepare for trauma processing.
  • Phase 2: Processing Trauma. Once stable, therapy carefully works through the traumatic memories that underlie the disorder. This might involve gradual exposure to traumatic recollections, with each alter that holds trauma memories sharing their experiences in therapy. The therapist helps the individual (and their alters) emotionally process and make sense of the trauma, correcting any distorted beliefs (e.g. self-blame) and integrating memory fragments. This often has to be done very cautiously and interspersed with stabilization sessions to avoid overwhelming the patient​did-research.org.
  • Phase 3: Integration and Rehabilitation. The final phase focuses on integrating the identities into one cohesive self or, at least, achieving a harmonious collaboration between alters. Integration (sometimes called fusion) means that the alter identities come to function as a single identity state. Techniques include encouraging alters to share memories and merge, and resolving internal conflicts between parts. For many, full fusion of all identities may be the goal; for others, improving cooperation may suffice. In this phase, the patient works on developing a unified sense of identity and coping as one whole person. They also address any practical life re-adjustments and skills needed after integration (e.g. interpersonal skills, managing feelings without “escaping” into an alter). Therapy at this stage might involve grieving the loss of perceived separate selves and solidifying adaptive coping strategies for the future​cf.healthyplace.com. Even after formal integration, ongoing therapy or support is often recommended to reinforce skills and prevent relapse.
• Therapeutic Steps: (Summary of key steps from Sue, 2021): The clinician will (1) establish trust and safety, (2) gently confirm the DID diagnosis and educate the person about the condition, (3) facilitate communication with and between alters (perhaps via writing or inner dialogue), (4) negotiate agreements among alters for safety (no self-harm, participation in therapy)​cf.healthyplace.com, (5) gather each alter’s history and functions (identifying trauma memories held by each)​cf.healthyplace.com, (6) process and treat the traumas and problems of each alter, and (7) work toward integration of the personality structure (blending alters into one)​cf.healthyplace.com. Throughout, the therapist reinforces that all alters are part of one person and seeks to foster cooperation rather than internal conflict. With consistent treatment, many DID patients show improvements – reduced dissociation, better overall functioning, and fewer comorbid symptoms​did-research.org​did-research.org. DID therapy is often intense and lengthy, but the evidence shows that proper treatment can significantly improve quality of life​did-research.org.

Lesson 9 – Depressive Disorders

Major Depressive Episode (MDE) and Major Depressive Disorder (MDD)

• DSM-5 Criteria for MDE: A major depressive episode is defined by ≥5 of the following symptoms present most of the day, nearly every day for at least 2 weeks (representing a change from previous functioning)​ncbi.nlm.nih.gov​ncbi.nlm.nih.gov. At least one of the symptoms must be (1) depressed mood or (2) loss of interest/pleasure. The full symptom list (“SIGECAPS”) includes:
  1. Depressed mood – feeling sad, empty, hopeless, or irritable (in children/teens)​ncbi.nlm.nih.gov.
  2. Markedly diminished interest or pleasure in almost all activities (anhedonia)​ncbi.nlm.nih.gov.
  3. Significant weight loss or gain (e.g. ±5% body weight in a month) or change in appetite (up or down)​ncbi.nlm.nih.gov.
  4. Insomnia or hypersomnia (difficulty sleeping or sleeping excessively)​ncbi.nlm.nih.gov.
  5. Psychomotor agitation or retardation (observable restlessness or slowed movements/speech)​ncbi.nlm.nih.gov.
  6. Fatigue or loss of energy nearly every day​ncbi.nlm.nih.gov.
  7. Feelings of worthlessness or excessive/inappropriate guilt (which may be delusional)​ncbi.nlm.nih.gov.
  8. Diminished ability to think or concentrate, or indecisiveness (either subjective or observed by others)​ncbi.nlm.nih.gov.
  9. Recurrent thoughts of death, suicidal ideation, or suicide attempt/plan​ncbi.nlm.nih.gov.
  These symptoms must cause clinically significant distress or impairment and not be attributable to substance use or another medical condition​ncbi.nlm.nih.gov. Also, to distinguish an MDD diagnosis, the episode cannot be better explained by a psychotic disorder and there must never have been a manic or hypomanic episode (otherwise it would be bipolar disorder)​ncbi.nlm.nih.gov.
• Major Depressive Disorder: MDD is diagnosed when a person has had one or more major depressive episodes. It can be specified as single episode (only one lifetime MDE) or recurrent (≥2 episodes). Recurrent depression is common – after one episode, the risk of another is about 50%, and it increases to 70% after two and 90% after three episodes​ncbi.nlm.nih.gov. Each episode can last months if untreated, and over a lifetime, MDD may be a chronic, relapsing illness for some.

Single vs. Recurrent Episodes: In single-episode MDD, the individual experiences one discrete period of depression and then recovers. In recurrent MDD, depressive episodes come back periodically, with at least 2 consecutive months in between episodes where the person is mostly symptom-free (this gap is required to consider them separate episodes). Recurrent MDD tends to be more severe in terms of long-term impact and often necessitates maintenance treatment to prevent future episodes​

ncbi.nlm.nih.gov. Clinically, noting if MDD is recurrent is important because it may prompt preventive strategies (e.g. ongoing therapy or medication even between episodes).

Persistent Depressive Disorder (PDD/Dysthymia)

• DSM-5 Criteria: Persistent depressive disorder is a chronic, long-lasting depression. The core feature is a depressed mood for most of the day, more days than not, for at least 2 years (1 year in children/adolescents)​ncbi.nlm.nih.gov. During this period, the person has never been without depressive symptoms for more than 2 months at a time​ncbi.nlm.nih.gov. In addition to depressed mood, at least two of the following must be present: poor appetite or overeating, insomnia or hypersomnia, low energy or fatigue, low self-esteem, poor concentration or difficulty making decisions, and feelings of hopelessness​ncbi.nlm.nih.gov​ncbi.nlm.nih.gov. These chronic symptoms may be milder than those of MDD (e.g. suicidal ideation might be absent), but the enduring nature causes significant distress or impairment. Notably, if a person meets full criteria for a major depressive episode during the 2-year period, they can be given both diagnoses (MDD and PDD) – often referred to as “double depression” when a major depressive episode occurs on top of dysthymia​ncbi.nlm.nih.gov​ncbi.nlm.nih.gov. PDD encapsulates what was historically called dysthymic disorder. In summary, think of PDD as a “low-grade” depression that is continuously present for years – the person may report “I’ve always been this way.” Though less acute than MDD, PDD’s chronicity can be debilitating (e.g. persistent pessimism, low drive, and low self-worth).

Depressive Symptom Domains

Depressive symptoms can be understood across four domains – affective, cognitive, behavioral, and physiological:

• Affective (Mood) Symptoms: This includes the core feelings of depression. People often feel sad, empty, hopeless, or tearful. They may report pervasive irritability or an inability to experience pleasure (anhedonia) – things that once made them happy no longer do​psychiatry.org. Anxiety can also be present. These mood symptoms are often accompanied by feelings of worthlessness or excessive guilt. In PDD, the affective state is a persistent gloominess or low mood.
• Cognitive Symptoms: Depression markedly affects how a person thinks. Common cognitive distortions include negative beliefs about oneself, the world, and the future (Beck’s cognitive triad). Depressed individuals often have difficulty concentrating or making decisions​psychiatry.org. Memory may feel impaired (often due to poor focus). They frequently harbor self-critical or defeatist thoughts – e.g. “I’m a failure,” “Nothing good ever happens.” There may be pervasive guilt over minor things. In more severe cases, suicidal ideation can occur, ranging from passive wishes not to wake up to active planning of suicide​psychiatry.org. Six common cognitive distortions associated with depression are:
  • Arbitrary inference: drawing negative conclusions with no or insufficient evidence (e.g. assuming a friend is mad at you because they briefly frowned)​en.wikipedia.org.
  • Selective abstraction: focusing on one negative detail in a situation while ignoring the broader context (e.g. dwelling on a single criticism amid lots of praise)​en.wikipedia.org.
  • Overgeneralization: applying the outcome of one event to all others (“I failed this exam, so I’ll fail all exams”)​en.wikipedia.org.
  • Magnification (catastrophizing) and Minimization: exaggerating the importance of problems or flaws (making mountains out of molehills)​en.wikipedia.org, while downplaying positives or strengths (“Sure I got an A this time, but it was just luck”). This distortion fuels a sense that problems are huge and victories are trivial.
  • Personalization: blaming oneself for events outside one’s control (e.g. “My team lost; it must be because I’m bad luck”)​en.wikipedia.org.
  • Polarized (Black-and-White) Thinking: seeing things in all-or-nothing terms with no middle ground (“If I’m not perfect, I’m a complete failure”)​psychcentral.com. This rigidity can lead to frequent self-judgment and giving up after minor setbacks.
  Learning to identify and challenge these distorted thoughts is a key component of cognitive-behavioral therapy for depression.
• Behavioral Symptoms: Depression often produces visible changes in behavior. Social withdrawal is common – depressed individuals may pull away from friends and activities, retreating due to lack of interest or energy. There may be a drop in productivity at work or school. Psychomotor retardation can occur: the person moves or talks more slowly, with diminished facial expressions and long pauses. In contrast, some experience psychomotor agitation like pacing, hand-wringing, or fidgeting​psychiatry.org​my.clevelandclinic.org. Depressed people may neglect responsibilities or personal care (e.g. not showering, staying in bed for hours). They often stop pursuing hobbies they used to enjoy. This behavioral inertia feeds the depression (loss of rewarding activities). In severe cases, behavior can include suicide attempts. On the flip side, milder depression might manifest in behavior as increased reassurance-seeking or repeated crying spells. Overall, a loss of motivation and reduced activity level are hallmark behavioral signs.
• Physiological (Somatic) Symptoms: Depression is a whole-body disorder, so physical functions commonly change. Sleep disturbances are classic – many depressed patients suffer from insomnia (especially early morning awakening or trouble falling asleep) or sometimes hypersomnia (sleeping a lot but still feeling fatigued)​psychiatry.org. Appetite and weight changes are also frequent: some lose appetite and weight, while others overeat “comfort foods” and gain weight​psychiatry.org. Low energy or fatigue is nearly universal – the person feels exhausted doing minor tasks​psychiatry.org. They may have various unexplained aches or pains, headaches, or digestive problems (mind-body connections). Libido often decreases as well. Physically, depression can weaken the immune system and is associated with conditions like chronic pain. Patients often say they feel “slowed down” or physically “heavy.” These somatic symptoms reinforce the other domains; e.g. poor sleep and low energy worsen concentration and mood, creating a vicious cycle.

Specifiers for Depressive Disorders

Depressive disorders can be described with specifiers to indicate particular features:

• With Psychotic Features: The depression is accompanied by delusions or hallucinations. For example, a severely depressed person might have mood-congruent delusions (such as believing they have committed an unforgivable sin, or that their body is rotting) or hear accusatory voices. Psychotic features signal a very severe depression; by definition, if psychosis occurs exclusively during a depressive episode, it’s still MDD, but labeled MDD with psychotic features. These cases often require antipsychotic medication in addition to antidepressants, and the presence of psychosis is a poor prognostic indicator.
• With Catatonic Features: Involves catatonia – a syndrome of motoric immobility or excessive, purposeless motor activity, extreme negativism (resistance to movement or instructions), mutism, peculiar posturing, echolalia (mimicking speech) or echopraxia (mimicking movements). In depression with catatonic features, the person may, for example, sit mute and unresponsive for hours or exhibit waxy flexibility (remaining in positions they are placed). Catatonic depression is relatively uncommon and often requires treatments like benzodiazepines or ECT.
• With Seasonal Pattern: (formerly Seasonal Affective Disorder, SAD) – Depressive episodes that regularly occur at a particular time of year, most often beginning in fall or winter and remitting in spring. Seasonal pattern is identified when at least two consecutive years of episodes follow this timing. Winter depression is thought to be related to reduced sunlight; symptoms often include low energy, oversleeping, overeating (carbohydrate craving), and weight gain. Light therapy is a well-known treatment. Specifying “with seasonal pattern” helps differentiate it from non-seasonal depression; importantly, between seasonal episodes the person’s mood is normal.
• With Peripartum Onset: Depression that begins during pregnancy or within 4 weeks of childbirth. (Clinicians often consider the postpartum period up to 3-6 months after delivery as relevant.) Commonly known as postpartum depression, it affects roughly 1 in 7 women after birth​postpartumdepression.org. Symptoms are the same as major depression (sadness, hopelessness, low energy, changes in sleep/appetite, etc.), but also often include excessive worry about the baby, feelings of being an inadequate mother, or, in severe cases, thoughts of harming the baby or oneself (in postpartum psychosis, which is a rarer, extreme variant, there can be psychotic beliefs about the infant). Prevalence: Estimates vary, but about 10–20% of new mothers experience clinical postpartum depression​postpartumdepression.org. If including those with less severe symptoms, the rates could be higher. Recurrence risk: Women who have had one peripartum depression have a high risk of recurrence with future pregnancies. Studies indicate a past postpartum depression makes a subsequent episode much more likely (some research cites ~25–50% risk of recurrence)​emedicine.medscape.com. And if a woman has had a postpartum depression with psychotic features, the risk of psychosis with each future delivery may be as high as 30–50%​ncbi.nlm.nih.gov. Thus, clinicians closely monitor women with a history of peripartum depression in later pregnancies. Early intervention (therapy, support, possibly medication) can mitigate these episodes.

Cognitive Distortions in Depression (Beck’s Theory)

Depression is strongly linked with negative thinking patterns. Aaron Beck outlined several cognitive distortions that depressed individuals commonly exhibit (six were emphasized in our lesson):

• Arbitrary Inference: Drawing negative conclusions without sufficient evidence. Example: Your boss frowns one day, so you immediately think “I’m about to be fired,” even though there’s no actual indication of that​en.wikipedia.org.
• Selective Abstraction: Focusing on one negative detail while ignoring everything else. Example: In a presentation that was well-received overall, you focus only on a minor point you stumbled on, convincing yourself it was a disaster​en.wikipedia.org.
• Overgeneralization: Applying one bad experience to all contexts. Example: You get one rejection from a job application and conclude “I’ll never get a job anywhere”​en.wikipedia.org.
• Magnification and Minimization: Also known as catastrophizing (blowing problems way out of proportion) and downplaying positives. Example: You make a small mistake and regard it as a catastrophe (“Now everything is ruined!”)​en.wikipedia.org. Conversely, you achieve something good but dismiss it (“It’s not a big deal, anyone could have done that”). This distortion amplifies perceived failures and shrinks successes, fueling low self-worth.
• Personalization: Taking things too personally – assuming responsibility for negative events that are not actually your fault. Example: Your child’s poor grades make you think “I’m a terrible parent” (attributing the child’s actions entirely to your shortcomings)​en.wikipedia.org. Or if two co-workers aren’t talking to each other, you irrationally believe it’s because you did something wrong.
• Polarized Thinking: Also called all-or-nothing thinking. Viewing situations in black-and-white terms, with no middle ground​psychcentral.com. If something isn’t perfect, it’s deemed a total failure. Example: A student gets a B+ and considers themselves an utter failure because it’s not an A. This kind of dichotomous thinking leaves no room for moderate success and can lead to extreme emotional swings (e.g. one mistake ruins an entire day because it’s “all bad” now).

Recognizing these distortions is the first step in cognitive-behavioral therapy; patients learn to challenge and reframe such thoughts into more balanced, realistic thoughts (e.g. “One rejection doesn’t mean I’ll never get a job; many people face a few rejections before finding the right position”).

Beck Depression Inventory-II (BDI-II) – Score Cutoffs

The BDI-II is a 21-item self-report inventory widely used to assess the severity of depressive symptoms. Each item is rated 0–3, so the total score ranges from 0 to 63. Standard score cutoffs for BDI-II:

• 0–13: Minimal or no depression​pmc.ncbi.nlm.nih.gov. (This is within normal range or transient, subclinical sadness.)
• 14–19: Mild depression​pmc.ncbi.nlm.nih.gov. (Suggests mild mood disturbance – perhaps dysthymia or mild MDD.)
• 20–28: Moderate depression​pmc.ncbi.nlm.nih.gov. (Symptoms are clearly present and impactful – typical of an MDE of moderate severity.)
• 29–63: Severe depression​pmc.ncbi.nlm.nih.gov. (Indicates a significant clinical depression; scores in the 30s or above often coincide with suicidal thoughts and functional impairment requiring active treatment.)

Clinicians use these cutoffs to gauge improvement (e.g. a drop from 30 to 15 would indicate improvement from severe to mild depression) and to make decisions about the level of care needed. The BDI-II is not a diagnostic tool by itself but a helpful indicator of symptom severity and change over time.

Prevalence of Peripartum (Postpartum) Depression & Recurrence Risk

As noted, peripartum depression is fairly common. Approximately 10% of new mothers experience postpartum depression, though some studies show it may be up to 15–20% (around 1 in 7) when including minor cases​

postpartumdepression.org. It can often go undiagnosed, so actual prevalence might be higher. Risk factors include a history of depression, stressful life events, lack of social support, and hormonal changes. Regarding recurrence, women who have had postpartum depression previously have a significantly elevated risk in subsequent pregnancies. Sources indicate about 25–50% will have another postpartum depressive episode after a prior one​

emedicine.medscape.com. If the prior episode included psychotic features (postpartum psychosis), the recurrence risk is even greater – on the order of 30–50% for psychosis with each later delivery​

ncbi.nlm.nih.gov. Therefore, obstetricians and psychiatrists closely monitor and sometimes prophylactically treat high-risk women (with therapy, support groups, or medication immediately postpartum). The good news is that 80% of women with postpartum depression recover fully with proper treatment and support​

postpartumdepression.org. Early intervention is key, both for the mother’s well-being and the infant’s development.

Treatments for Depression (Briefly)

Managing depression usually involves a combination of:

• Therapy: Especially Cognitive Behavioral Therapy (CBT), which addresses negative thought patterns and encourages activation (scheduling activities to counter avoidance) – it’s highly effective for mild to moderate depression. Other therapies include Interpersonal Therapy (IPT) (focusing on relationship issues and role transitions), Psychodynamic therapy (exploring underlying conflicts), and newer approaches like mindfulness-based therapies.
• Antidepressant Medications: Such as SSRIs (e.g. sertraline, fluoxetine), SNRIs, bupropion, mirtazapine, or TCAs/MAOIs in some cases. Medications can help correct neurotransmitter imbalances and are often indicated for moderate to severe depression, particularly if there are neurovegetative symptoms (sleep/appetite change) or recurrent episodes. They typically take a few weeks to work and might be continued for 6–12 months or longer to prevent relapse.
• Combined Treatment: The combination of therapy + medication tends to be more effective than either alone, especially in chronic or severe depression, by addressing both biological and psychosocial aspects.
• Electroconvulsive Therapy (ECT): A treatment reserved for severe depression that has not responded to other treatments, or when rapid response is needed (e.g. severe suicidal risk or psychotic depression). ECT involves brief controlled seizures under anesthesia and can be highly effective in refractory cases​psychiatry.org​psychiatry.org.
• Other Biological Treatments: These include Transcranial Magnetic Stimulation (TMS) for medication-resistant depression, light therapy for seasonal depression, and emerging options like ketamine infusions or esketamine nasal spray for treatment-resistant depression (which can have rapid antidepressant effects).
• Lifestyle and Support: Regular exercise, adequate sleep, and nutrition have mood benefits. Psychoeducation for patients and families, support groups, and reducing stress can all augment primary treatments. In peripartum depression, ensuring mother-baby bonding and practical support at home is crucial as part of recovery.
• Note: If depression is accompanied by psychotic features, an antipsychotic is usually added to the regimen until the psychosis resolves​psychiatry.org.

Overall, depressive disorders are treatable, and the prognosis is good with appropriate intervention – most people will experience improvement, and many will recover fully. The challenge is to identify depression early and engage the person in treatment, while addressing any co-occurring problems (anxiety, substance use, etc.) that can complicate recovery.

Detailed Prevalence & Causes Expanded:

• Major Depressive Disorder (MDD):
  • Lifetime prevalence: 16%, 12-month: 6%.
  • Gender differences: Women 1.5–3 times more likely than men.
  • Median lifetime number of episodes: 4-7 episodes.
  • Typical untreated episode duration: 2-9 months.
  • Genetic contribution: Moderate (30–40% heritability).
  • Neurotransmitter theory (“Permissive Hypothesis”): Low serotonin allows mood fluctuations via other neurotransmitters.
  • Psychological models:
    • Learned Helplessness (Seligman): Loss of perceived control.
    • Negative Cognitive Triad (Beck): Pessimistic view of self, world, and future.
• Double Depression:
  • Co-occurrence of mild depressive symptoms (Persistent Depressive Disorder) with intermittent major depressive episodes.
• Persistent Depressive Disorder (Dysthymia):
  • Chronic depression lasting at least 2 years, symptom-free periods <2 months.
  • Symptoms less intense but persistent, affecting mood and self-esteem.
• Treatment Clarifications:
  • SSRIs effectiveness (~50%), normal functioning achieved in only 25%.
  • CBT equivalent in effectiveness to medication initially but provides longer-lasting benefits.

Lesson 10 – Bipolar Disorders

Manic Episode (DSM-5 Criteria)

A manic episode is a distinct period of abnormally and persistently elevated, expansive, or irritable mood, AND abnormally and persistently increased goal-directed activity or energy, lasting at least 1 week (or any duration if hospitalization is required)​

medcentral.com​

psychiatryonline.org. It is often described as feeling “on top of the world” or extremely agitated. During this period, the person experiences ≥3 of the following symptoms (4 if mood is only irritable) to a significant degree​

psychiatry.org​

psychiatry.org:

• Inflated self-esteem or grandiosity – ranging from uncritical self-confidence to delusional grandiosity. (They may believe they have special powers, fame, or exceptional talents.)
• Decreased need for sleep – for example, feeling rested after only 3 hours of sleep, or going days with very little sleep​my.clevelandclinic.org.
• More talkative than usual or pressure to keep talking – rapid, loud speech that may be difficult to interrupt​my.clevelandclinic.org.
• Flight of ideas or racing thoughts – thoughts jump quickly from one topic to another, often so rapidly that it’s hard for others to follow​my.clevelandclinic.org.
• Distractibility – attention is easily pulled to irrelevant or unimportant stimuli (e.g. can’t finish a task because any new stimulus grabs their focus)​my.clevelandclinic.org.
• Increase in goal-directed activity (socially, at work or school, sexually) or psychomotor agitation – e.g. starting multiple new projects or hobbies, pacing, excessive planning of events​my.clevelandclinic.org.
• Excessive involvement in risky activities that have high potential for painful consequences – e.g. unrestrained buying sprees, reckless driving, gambling, inappropriate sexual encounters, foolish business investments​my.clevelandclinic.org.

These symptoms represent a marked change from the person’s usual behavior and are typically visible to others (friends/family clearly notice the person is “not themselves”)​

psychiatry.org. The episode is severe enough to cause impairment in social or occupational functioning; often, judgment is impaired and hospitalization is needed to prevent harm (e.g. to contain wild spending or protect from risky behaviors)​

psychiatry.org. If psychotic features (hallucinations or delusions) are present, the episode is by definition manic (not hypomanic)​

floridabhcenter.org.

Hypomanic Episode: By contrast, a hypomanic episode meets similar symptom criteria but is less severe and shorter: lasting at least 4 days, and without psychotic symptoms​

psychiatry.org​

psychiatry.org. In hypomania, mood and functioning are changed, but not so extreme as to cause marked impairment – the person might even be quite productive during hypomania, and hospitalization is not required. Hypomania can escalate to full mania, but by itself it’s a milder elevation of mood.

Bipolar I vs Bipolar II vs Cyclothymic Disorder

• Bipolar I Disorder: This diagnosis is defined by the occurrence of at least one manic episode in a lifetime​mind.org.uk. Most individuals with Bipolar I also experience major depressive episodes, but a depressive episode is not required for the diagnosis (some people have mania with only mild or no depression, though that’s less common). In Bipolar I, the manic episodes tend to be more severe, often with psychotic features or requiring hospitalization. Essentially, Bipolar I = Mania (with or without depression). For example, someone might have manic episodes and also depressive episodes – that is classic Bipolar I. Even if they’ve had just one manic episode ever (and many depressions), it’s still Bipolar I.
• Bipolar II Disorder: This disorder involves at least one hypomanic episode and at least one major depressive episode​psychiatry.org. Crucially, full manic episodes have never occurred – if a mania happens, the diagnosis would shift to Bipolar I. Bipolar II can be thought of as “softer” bipolar: hypomania + severe depression. The hypomanic episodes in Bipolar II are noticeable but not devastating – often the person might feel very productive or energized, and sometimes they may not recognize anything is wrong (loved ones might perceive them as simply “peppier” or more irritable than usual for a few days). However, the depressive episodes in Bipolar II can be just as severe and disabling as in Bipolar I. In fact, Bipolar II patients often seek help during depression and may not report their hypomanias unless specifically asked. Bipolar II is sometimes misdiagnosed as unipolar depression until a hypomanic episode is observed or identified in history. In summary, Bipolar II = Major Depression + Hypomania, with no mania.
• Cyclothymic Disorder: Cyclothymia is a chronic, fluctuating mood disturbance for ≥2 years (≥1 year in youth) where the person experiences numerous periods of hypomanic symptoms (that do not meet full criteria for hypomanic episodes) and numerous periods of depressive symptoms (not meeting full criteria for major depression)​psychiatry.org. Essentially, it’s like a milder, persistent form of bipolarity. During the 2-year span, the person isn’t symptom-free for longer than 2 months at a time. The highs of cyclothymia are less intense than hypomania (e.g. elevated mood but perhaps not quite enough to cause serious trouble), and the lows are milder than major depression (dysthymia-like). However, mood swings happen relatively often, and the person is never fully stable for long​healthline.com​psychiatry.org. Cyclothymic individuals may be seen as “moody” or inconsistent, with ups and downs that, while subclinical, can still affect their life (e.g. unpredictable energy and optimism followed by periods of gloom or apathy). If a full manic or depressive episode develops, the diagnosis would shift to bipolar I or II. Think of cyclothymia as the bipolar spectrum’s chronic, subthreshold condition – symptoms are less severe but more persistent than in bipolar I/II​psychiatry.org. It can precede Bipolar I or II in some cases, or remain cyclothymic lifelong.

In short: Bipolar I = mania (full send highs, big highs) ± depression; Bipolar II = hypomania (milder highs) + definite major depression; Cyclothymia = numerous mild highs and mild lows over years, never hitting full mania or full depression but never stable for long​

psychiatry.org. The severity of mood swings increases as you go from cyclothymia (least severe) → bipolar II → bipolar I (most severe highs).

Rapid Cycling Specifier in Bipolar Disorder

• Definition: Rapid cycling is a specifier indicating a high frequency of mood episodes. Specifically, it means four or more mood episodes (depressive, manic, or hypomanic) in a 12-month period​dbsalliance.org​dbsalliance.org. These episodes must meet full criteria for mania, hypomania, or depression (so brief mood swings that don’t last long enough don’t count towards the four, except in terms of “ultra-rapid” patterns). Rapid cycling can occur in Bipolar I or II.
• Clinical Implications: Rapid cycling is associated with a more difficult course of illness. Patients with rapid cycling tend to have greater morbidity – mood shifts are quick and often unpredictable (episodes can even cycle within weeks or months, and if mood shifts occur within a single month, it may be called “ultra-rapid” cycling​dbsalliance.org). Rapid cycling bipolar disorder often responds less well to standard treatments (like lithium), and may require combination therapies (mood stabilizers + anticonvulsants, etc.). It is seen more frequently in women (some studies suggest) and may be precipitated by certain factors like antidepressant use or thyroid dysfunction. Importantly, rapid cycling is sometimes a transient pattern – up to half of bipolar patients might experience rapid cycling at some point, but for many it is temporary, resolving within a few years​dbsalliance.org​dbsalliance.org. For a subset, though, rapid cycling can persist and become part of their long-term illness pattern. The presence of rapid cycling often means clinicians need to be vigilant about treatment adherence and possibly avoid antidepressants (which might trigger switches), optimize thyroid levels, and use agents like valproate or atypical antipsychotics which have shown some efficacy in rapid cyclers​sciencedirect.com. Psychologically, rapid cycling can be very distressing – patients feel they barely get relief from one episode before swinging into another mood state. Emphasizing routine (sleep/wake cycles, consistent daily structure) is often advised, as chaotic lifestyle can exacerbate mood instability. In summary, the rapid cycling specifier signifies a more refractory bipolar course with frequent mood episode recurrence, guiding clinicians to a more aggressive or nuanced management strategy.

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Note: Bipolar disorder management typically involves mood stabilizers (like lithium, anticonvulsants such as valproate or lamotrigine, and atypical antipsychotics). Psychoeducation for bipolar is crucial – patients learn to identify early warning signs of mood swings, adhere to medications, regulate sleep, and avoid triggers (e.g. substance use). Therapy (like CBT or interpersonal and social rhythm therapy) can help with coping and medication adherence​

psychiatry.org​

psychiatry.org. Bipolar depression often requires careful treatment to avoid pushing the person into mania (e.g. using mood stabilizer or antipsychotic adjuncts rather than antidepressant monotherapy). Rapid cyclers in particular benefit from strict routine and often combination pharmacotherapy. With proper treatment, many people with bipolar I or II can lead productive lives, though it’s typically a lifelong condition that requires ongoing management.

Clarifications on Bipolar Disorders & Rapid Cycling:

• Bipolar I:
  • Lifetime prevalence ~1%, onset typically 15-18 years old.
  • Equally common across genders.
• Rapid Cycling Specifier:
  • Defined explicitly as 4+ mood episodes per year.
  • Occurs in 20–50% of bipolar cases.
  • More prevalent in females, potentially induced by antidepressants.
  • Generally, a temporary rather than permanent pattern.
• Causes and Treatments Expanded:
  • Biological explanations include strong genetic link (up to 24% prevalence in first-degree relatives) and neurotransmitter disruptions (especially dopamine).
  • Psychological triggers often involve significant stressful life events, especially positive stressors.
  • Lithium Carbonate remains primary treatment (effective for about 50%), mood-stabilizing, significantly reduces suicide risk.

Uncategorized

Anxiety Disorders (Critical additions relevant for comprehensive understanding):

• Generalized Anxiety Disorder (GAD):
  • Persistent, generalized worry and tension without specific triggers.
  • Lifetime prevalence 5.7%; 2:1 female-to-male ratio.
• Panic Disorder & Agoraphobia:
  • Recurrent unexpected panic attacks followed by ≥1 month of anticipatory anxiety or behavioral change.
  • Panic Control Treatment (PCT): exposure to panic sensations, cognitive therapy, relaxation strategies.
  • Agoraphobia: Avoidance of situations where escape/help would be difficult in the event of panic symptoms.
• Specific Phobias:
  • Animal, Natural Environment, Blood-Injection-Injury, Situational, and Other types.
  • Gradual exposure treatments highly effective.
• Social Anxiety Disorder:
  • Fear of social scrutiny, lasting ≥6 months.
  • Biological and cognitive-behavioral treatments emphasized, including exposure therapy and cognitive restructuring.
• Obsessive-Compulsive Disorder (OCD):
  • Obsessions (persistent, distressing thoughts) and compulsions (ritualistic behaviors).
  • Strong biological (basal ganglia, frontal-thalamic circuitry) and psychological explanations.
  • Primary treatment: Exposure and Response Prevention (ERP).
• Intellectual Disability & Learning Disorders:
  • Intellectual disability includes deficits in adaptive functioning and IQ below developmental standards.
  • Specific Learning Disorder includes impairments in reading, writing, mathematics.

Comprehensive Summary of Suicide (Critical Addition):

• Terms clarified: suicidal ideation, plans, attempts.
• Prevalence highest among Non-Hispanic Whites, Native Americans; males more likely to complete suicide; females attempt more frequently.
• Key risk factors include previous suicide attempts, low serotonin, mental disorders (especially mood disorders), substance abuse, stressful life events, and familial suicide history.
• CBT significantly reduces future suicide risk.

Developmental Psychopathology (Critical Context):

• Focuses on how disorders emerge and evolve across development.
• Cautions against pathologizing normal childhood behaviors.
• Emphasizes early intervention.
• ADHD:
  • Symptoms: inattention, hyperactivity-impulsivity; more common in boys (3:1).
  • Biological (dopamine transporter gene), psychosocial impacts discussed.
  • Treatments include stimulants (e.g., Ritalin), parent training, behavioral reinforcement.
• Autism Spectrum Disorder (ASD):
  • Social communication deficits, restricted repetitive behaviors.
  • Biological theories: amygdala dysfunction, lower oxytocin levels, strong genetic basis.
  • Early, structured intervention essential; parental involvement critical.