Medical School · Year 2 · Psychiatry · includes a quiz and discussion video

Lecture 4: Trauma-Related and Obsessive-Compulsive Disorders

Unit 2.6: Psychiatry

Learning Objectives

By the end of this lecture, students will be able to:

1. Describe the diagnostic criteria and neurobiology of PTSD
2. Explain the treatment approaches for trauma-related disorders
3. Describe the phenomenology and diagnosis of OCD
4. Explain the neurobiological basis of OCD
5. Describe evidence-based treatments for OCD
6. Explain related disorders in the OCD spectrum

Lecture Outline

I. Post-Traumatic Stress Disorder Overview

Post-traumatic stress disorder develops following exposure to traumatic events and is characterized by a distinctive constellation of symptoms organized into four clusters. While trauma exposure is unfortunately common, affecting sixty to seventy percent of the population at some point, only a minority of exposed individuals develop PTSD, with lifetime prevalence estimated at approximately seven percent. Women develop PTSD at roughly twice the rate of men despite experiencing fewer traumatic events overall, suggesting sex-related differences in vulnerability. Risk factors for developing PTSD following trauma include greater severity and duration of the traumatic event, interpersonal nature of the trauma such as assault or abuse, prior trauma history, and lack of social support in the aftermath.

The DSM-5 criteria for PTSD require exposure to actual or threatened death, serious injury, or sexual violence. Exposure can occur through direct experience of the traumatic event, witnessing the event as it occurs to others, learning that a close family member or close friend experienced the event, or experiencing repeated or extreme exposure to aversive details of traumatic events as occurs with first responders or professionals. Importantly, exposure through electronic media, television, movies, or pictures does not qualify unless it is work-related.

The four symptom clusters of PTSD include intrusion symptoms, avoidance symptoms, negative alterations in cognitions and mood, and alterations in arousal and reactivity. Diagnosis requires at least one intrusion symptom, at least one avoidance symptom, at least two symptoms from the cognition and mood cluster, and at least two symptoms from the arousal and reactivity cluster. All symptoms must be present for more than one month following the trauma, must cause clinically significant distress or impairment in functioning, and must not be attributable to the physiological effects of a substance or another medical condition.

The qualifying traumatic events for PTSD are specifically defined and include actual or threatened death, serious injury, or sexual violence. Common precipitating events include combat exposure, physical assault, sexual assault or abuse, motor vehicle accidents, natural disasters, and life-threatening medical events. The nature of the trauma influences both the likelihood of developing PTSD and the specific symptom profile, with interpersonal trauma such as assault or abuse carrying higher risk than natural disasters or accidents.

<image>Panel A displays a flowchart of trauma exposure to PTSD development, showing that 60-70% experience trauma but only 7% develop PTSD, with risk factors (severity, interpersonal nature, prior trauma, lack of support) moderating the pathway. Panel B illustrates the four types of qualifying exposure: direct experience (person in traumatic event), witnessing (person observing trauma), learning about (news of close family/friend trauma), and repeated professional exposure (first responder imagery). Panel C shows the PTSD symptom cluster requirements: at least one from intrusion, at least one from avoidance, at least two from cognitions/mood, at least two from arousal, all for more than one month. Panel D presents a bar graph of PTSD prevalence by trauma type, showing highest rates for interpersonal violence (combat, sexual assault) and lower rates for accidents and natural disasters.</image>

II. PTSD Symptom Clusters in Detail

The intrusion symptom cluster represents the re-experiencing phenomena that are hallmarks of PTSD. Intrusive memories are recurrent, involuntary, and distressing recollections of the traumatic event that intrude into consciousness uninvited. Nightmares involve distressing dreams with content related to the trauma that may replay the event or contain emotionally similar themes. Flashbacks are dissociative reactions in which the individual feels or acts as if the traumatic event were recurring, ranging from brief sensory intrusions to complete loss of awareness of present surroundings. Psychological distress and physiological reactivity occur upon exposure to internal or external cues that symbolize or resemble an aspect of the traumatic event.

The avoidance symptom cluster involves persistent effortful avoidance of trauma-related stimuli. Internal avoidance refers to avoiding distressing memories, thoughts, or feelings about or closely associated with the traumatic event. External avoidance involves avoiding reminders such as people, places, conversations, activities, objects, or situations that arouse distressing memories, thoughts, or feelings about the trauma. This avoidance is a key maintaining factor of PTSD, as it prevents the natural processing and extinction of the trauma memory.

The negative cognitions and mood cluster represents persistent and distorted negative changes in cognition and mood following the trauma. Symptoms include inability to remember important aspects of the traumatic event due to dissociative amnesia rather than head injury or substances, persistent and exaggerated negative beliefs about oneself, others, or the world such as believing oneself is permanently damaged or the world is completely dangerous, persistent distorted cognitions about the cause or consequences of the trauma leading to self-blame or blaming others, persistent negative emotional states including fear, horror, anger, guilt, or shame, markedly diminished interest in significant activities, feelings of detachment or estrangement from others, and persistent inability to experience positive emotions.

The arousal and reactivity cluster involves marked alterations in arousal and reactivity associated with the trauma. Symptoms include irritable behavior and angry outbursts with little or no provocation typically expressed as verbal or physical aggression, reckless or self-destructive behavior, hypervigilance involving a heightened state of alertness to potential threats, exaggerated startle response to unexpected stimuli, problems with concentration, and sleep disturbance including difficulty falling or staying asleep or restless sleep.

<image>Panel A displays the intrusion symptom cluster with icons: intrusive memories (brain with flashback), nightmares (sleeping figure with disturbed dreams), flashbacks (double-image showing past and present overlapping), psychological distress to cues (distress response to reminder), and physiological reactivity (body with autonomic activation). Panel B shows avoidance symptoms divided into internal avoidance (thought bubble being blocked) and external avoidance (person avoiding locations, people, and situations related to trauma). Panel C illustrates negative cognitions and mood with examples: negative beliefs about self ("I am damaged"), world ("Nowhere is safe"), distorted blame, negative emotions (fear, guilt, shame icons), diminished interest, detachment, and inability to feel positive emotions. Panel D depicts arousal and reactivity symptoms: anger outbursts (irritated figure), reckless behavior, hypervigilance (scanning figure), exaggerated startle (startled figure), concentration problems, and sleep disturbance.</image>

III. PTSD Specifiers and Related Conditions

PTSD specifiers in DSM-5 include the dissociative subtype and delayed expression. The dissociative subtype applies when the individual experiences persistent or recurrent symptoms of depersonalization, feeling detached from one's own mind or body as if one were an outside observer, or derealization, experiencing the world as unreal, dreamlike, distant, or distorted. The delayed expression specifier indicates that full diagnostic criteria are not met until at least six months after the trauma, although some symptoms may begin immediately.

Acute stress disorder shares many features with PTSD but differs primarily in temporal relationship to the trauma. The diagnosis applies when symptoms occur from three days to one month after traumatic exposure and requires at least nine symptoms from any of the five categories of intrusion, negative mood, dissociation, avoidance, and arousal. If symptoms persist beyond one month, the diagnosis transitions to PTSD. Acute stress disorder has predictive value for identifying individuals at risk for developing PTSD, though many individuals develop PTSD without preceding acute stress disorder.

Complex PTSD, included in the ICD-11 but not DSM-5, extends beyond standard PTSD criteria to capture the effects of prolonged, repeated trauma, particularly trauma occurring in childhood or involving interpersonal victimization. In addition to the core PTSD symptom clusters, complex PTSD includes severe and persistent problems with affect regulation, persistent negative beliefs about oneself as diminished, defeated, or worthless accompanied by feelings of shame or guilt, and persistent difficulties sustaining relationships and feeling close to others. This presentation is often seen in survivors of childhood abuse, domestic violence, or prolonged captivity.

Adjustment disorder represents a less severe stress-related condition occurring in response to an identifiable stressor that does not meet the threshold for trauma. Symptoms must develop within three months of the stressor and are characterized by marked distress out of proportion to the severity of the stressor or significant impairment in functioning. The symptoms do not meet criteria for another mental disorder and do not represent normal bereavement. Once the stressor or its consequences have terminated, symptoms should not persist for more than an additional six months.

<image>Panel A illustrates the dissociative subtype with depersonalization shown as a person observing themselves from outside their body and derealization shown as a dreamlike, distorted environment surrounding the person. Panel B displays a timeline comparing acute stress disorder (3 days to 1 month) with PTSD (greater than 1 month), showing transition when symptoms persist, with delayed expression PTSD noted as full criteria not met until 6 or more months post-trauma. Panel C presents complex PTSD as standard PTSD criteria plus three additional domains: affect dysregulation (emotional instability graph), negative self-concept (diminished self-image), and relationship difficulties (broken connection between figures). Panel D shows adjustment disorder criteria as a flowchart: identifiable stressor (not trauma) → symptoms within 3 months → marked distress or impairment → resolution within 6 months of stressor ending.</image>

IV. PTSD Neurobiology and Treatment

The neurobiology of PTSD involves alterations in multiple brain circuits and neurotransmitter systems. The amygdala, central to threat detection and fear conditioning, shows hyperactivity in PTSD, leading to enhanced fear responses and difficulty distinguishing safe from dangerous stimuli. The prefrontal cortex, responsible for top-down regulation of the amygdala and for extinction learning, is hypoactive, resulting in impaired ability to modulate fear responses. The hippocampus, involved in contextual memory and distinguishing between past and present, shows reduced volume and function, contributing to the context-independent triggering of trauma memories. Paradoxically, the hypothalamic-pituitary-adrenal axis often shows low cortisol levels in PTSD, contrary to what might be expected in a stress-related disorder. The noradrenergic system is hyperactive, contributing to hyperarousal, exaggerated startle, and the intense physiological reactions to trauma reminders.

Trauma-focused psychotherapy represents first-line treatment for PTSD with the strongest evidence base. Prolonged Exposure involves repeated imaginal exposure to the trauma memory and in vivo exposure to avoided situations, with the goal of promoting emotional processing and extinction of fear responses. Cognitive Processing Therapy focuses on identifying and challenging maladaptive trauma-related beliefs, particularly regarding safety, trust, power and control, esteem, and intimacy. Eye Movement Desensitization and Reprocessing combines exposure to trauma memories with bilateral stimulation, typically through guided eye movements, with proposed mechanisms involving working memory taxation and reconsolidation. Trauma-focused cognitive-behavioral therapy integrates cognitive restructuring with exposure elements.

Pharmacotherapy for PTSD is generally considered second-line after psychotherapy or is used when evidence-based psychotherapy is unavailable or refused. Sertraline and paroxetine are the only FDA-approved medications for PTSD. Venlafaxine has demonstrated efficacy but is not FDA-approved for this indication. Prazosin, an alpha-1 adrenergic blocker, has shown efficacy specifically for trauma-related nightmares and sleep disturbance. Notably, benzodiazepines are not recommended for PTSD and may actually worsen outcomes by interfering with extinction learning and processing.

Treatment of PTSD proceeds through phases designed to ensure safety and build skills before confronting trauma material. The first phase focuses on safety and stabilization, addressing any ongoing danger, reducing acute symptoms, and establishing a therapeutic alliance. The second phase involves psychoeducation about PTSD and trauma responses, normalizing symptoms and building hope for recovery. The third phase, when the patient is stable enough to tolerate distress, involves trauma-focused therapy with active processing of the trauma memory. Medication may serve as adjunctive treatment throughout or as primary treatment when trauma-focused therapy is not available or tolerated.

<image>Panel A shows a brain diagram highlighting PTSD neurobiology: hyperactive amygdala (enhanced fear response), hypoactive prefrontal cortex (impaired regulation and extinction), reduced hippocampal volume (context-independent triggering), and hyperactive noradrenergic system (hyperarousal). Panel B displays the three main evidence-based psychotherapies: Prolonged Exposure (imaginal and in vivo exposure leading to extinction), CPT (identifying and challenging maladaptive beliefs), and EMDR (trauma memory processing with bilateral stimulation). Panel C presents pharmacotherapy options with FDA-approved medications (sertraline, paroxetine) highlighted and prazosin noted for nightmares, with a warning symbol over benzodiazepines marked "not recommended." Panel D illustrates treatment phases as a stepped diagram: Phase 1 (safety, stabilization), Phase 2 (psychoeducation), Phase 3 (trauma-focused therapy when stable), with medication as parallel adjunctive option.</image>

V. Obsessive-Compulsive Disorder Overview

Obsessive-compulsive disorder is characterized by the presence of obsessions, compulsions, or both that are time-consuming or cause clinically significant distress or impairment. The lifetime prevalence is approximately two to three percent, with equal rates in males and females in adulthood though boys predominate in childhood-onset cases. Onset typically occurs in childhood or adolescence with a bimodal distribution, and the course is generally chronic with symptoms waxing and waning over time. OCD was reclassified in DSM-5 from the anxiety disorders to a separate category of obsessive-compulsive and related disorders, recognizing its distinctive phenomenology and neurobiology.

The diagnostic criteria require the presence of obsessions, compulsions, or both. Obsessions are defined as recurrent and persistent thoughts, urges, or images that are experienced as intrusive and unwanted and that in most individuals cause marked anxiety or distress. The individual attempts to ignore or suppress these thoughts, urges, or images, or to neutralize them with some other thought or action. Compulsions are repetitive behaviors or mental acts that the individual feels driven to perform in response to an obsession or according to rules that must be applied rigidly, aimed at preventing or reducing anxiety or distress or preventing some dreaded event, though not connected in a realistic way or clearly excessive.

Obsessions have distinctive characteristics that distinguish them from other types of repetitive thinking. They are intrusive, meaning they enter consciousness uninvited and are not simply excessive worries about real-life problems. They are unwanted and ego-dystonic, meaning they are experienced as distressing and inconsistent with the individual's values or sense of self. They cause anxiety or distress, motivating attempts to suppress or neutralize them. The individual recognizes, at least at some point, that the obsessional thoughts are a product of their own mind rather than imposed from outside.

Compulsions are performed in response to obsessions or according to rigid rules and are aimed at reducing distress or preventing feared outcomes. They may be overt behaviors such as handwashing, checking, or arranging, or they may be covert mental acts such as counting, praying, or silently repeating words. The compulsions are either not connected in a realistic way with what they are designed to neutralize or are clearly excessive. The individual may recognize that the compulsions are irrational but still feels compelled to perform them to reduce anxiety, creating a cycle in which temporary relief reinforces the compulsive behavior.

<image>Panel A displays the obsession-compulsion cycle as a circular diagram: obsessive thought (intrusive, unwanted) → anxiety and distress → compulsion performed (to reduce anxiety) → temporary relief → obsessive thought returns (cycle continues). Panel B shows the defining features of obsessions: intrusive (entering mind uninvited), unwanted and ego-dystonic (inconsistent with values), distressing (causing anxiety), recognized as own thoughts. Panel C illustrates the defining features of compulsions: performed in response to obsessions or rigid rules, aimed at reducing distress or preventing feared outcome, not realistically connected or clearly excessive, recognized as irrational but compelling. Panel D presents epidemiological data: 2-3% lifetime prevalence, equal sex ratio (with boys predominating in childhood), bimodal age of onset (childhood/adolescence peaks), chronic waxing-waning course.</image>

VI. OCD Symptom Dimensions

Contamination obsessions and washing compulsions represent one of the most common OCD presentations. Obsessions typically involve fear of contamination by germs, dirt, chemicals, bodily fluids, or environmental contaminants, with associated fears of becoming ill, spreading illness to others, or causing harm. Compulsions include excessive handwashing, showering, cleaning of objects or surfaces, and avoidance of perceived contaminants. Patients may spend hours washing or develop ritualized cleaning routines that must be performed in precise sequences.

Harm obsessions and checking compulsions center on intrusive thoughts about potential harm to oneself or others and the felt responsibility to prevent such harm. Obsessions may involve fears of causing accidents, fires, break-ins, or violence, or fears that one has inadvertently caused harm. Compulsions include repeated checking of locks, appliances, and switches, seeking reassurance from others that harm has not occurred, and mental reviewing of actions to confirm safety. The checking typically provides only brief relief before doubt returns.

Symmetry obsessions and ordering or repeating compulsions involve a need for things to be just right, symmetrical, or exact. Obsessions include uncomfortable feelings when things are not perfectly aligned or arranged, a sense that something is incomplete or not right until actions are performed a certain way, and sometimes magical thinking connecting disorder with harm. Compulsions include arranging objects until they feel right, repeating actions until performed perfectly, counting, and evening-up behaviors.

Forbidden thought obsessions represent particularly distressing intrusive thoughts that are aggressive, sexual, or religious in nature. These thoughts are ego-dystonic and deeply disturbing precisely because they contradict the individual's values and self-concept. Aggressive obsessions may involve intrusive images of harming loved ones. Sexual obsessions may involve unwanted thoughts about inappropriate sexual acts. Religious obsessions, or scrupulosity, involve excessive concerns about sin, blasphemy, or religious observance. Compulsions are often mental rituals including praying, mental neutralization, and avoidance of situations that trigger the thoughts.

<image>Panel A illustrates contamination and washing: obsession (fear of germs, illness, spreading contamination shown as contaminating particles), compulsion (excessive handwashing with water and soap imagery, cleaning rituals). Panel B shows harm and checking: obsession (thoughts of responsibility for preventing harm, doubt about safety), compulsion (repeated checking of locks, appliances, seeking reassurance). Panel C depicts symmetry and ordering: obsession (need for things to be just right, uncomfortable when asymmetrical), compulsion (arranging objects, repeating actions until perfect, counting). Panel D presents forbidden thoughts: ego-dystonic aggressive, sexual, or religious intrusive thoughts (shown as unwanted thought bubbles), with mental compulsions (prayer, neutralization, avoidance) attempting to suppress or counteract.</image>

VII. OCD Neurobiology

The cortico-striato-thalamo-cortical circuit is centrally implicated in OCD pathophysiology. This circuit involves projections from the orbitofrontal cortex, which is involved in error detection and the feeling that something is wrong, and the anterior cingulate cortex, which monitors conflict, to the striatum, particularly the caudate nucleus, which is involved in habit formation and action selection. The striatum projects to the thalamus, which then projects back to the cortex, completing the loop. In OCD, this circuit is hyperactive, creating a sense that something is wrong that cannot be resolved, driving repetitive checking and ritualistic behavior.

Neuroimaging studies consistently demonstrate increased activity in the orbitofrontal cortex, caudate nucleus, and anterior cingulate cortex in individuals with OCD both at rest and when symptoms are provoked. Symptom provocation paradigms, in which individuals are exposed to their specific trigger stimuli, reliably activate these regions. Importantly, successful treatment, whether with medication or cognitive-behavioral therapy, leads to normalization of activity in these regions, suggesting that the hyperactivity is a state marker of active OCD rather than a fixed trait.

Neurotransmitter systems implicated in OCD include serotonin, glutamate, and dopamine. The serotonin hypothesis is supported by the efficacy of serotonergic medications, with SSRIs and clomipramine as first-line treatments. Higher doses and longer treatment durations are required than for depression, suggesting a different mechanism than simple serotonin deficiency. Glutamate, the brain's primary excitatory neurotransmitter, shows emerging evidence of involvement, with glutamatergic agents such as memantine and N-acetylcysteine under investigation as augmentation strategies. Dopamine appears particularly relevant in OCD with comorbid tics, with antipsychotic augmentation showing efficacy in this subgroup.

Genetic factors contribute substantially to OCD risk, with heritability estimated at forty to fifty percent. First-degree relatives of individuals with OCD have a ten-fold increased risk of developing the disorder. PANDAS (Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcal Infections) represents a distinct etiology in which OCD symptoms arise acutely following streptococcal infection, presumably through autoimmune mechanisms affecting the basal ganglia. This subgroup may benefit from immune-modulating treatments in addition to standard OCD therapies.

<image>Panel A displays the CSTC circuit as a diagram showing the orbitofrontal cortex (error detection) and anterior cingulate cortex (conflict monitoring) projecting to the caudate nucleus (habit formation), then to the thalamus (relay), and back to the cortex, with the loop labeled as hyperactive in OCD. Panel B shows neuroimaging findings with a brain image highlighting increased activation in OFC, caudate, and ACC, noting that treatment normalizes activity. Panel C illustrates neurotransmitter involvement: serotonin (SSRIs effective, higher doses needed), glutamate (emerging target, augmentation strategies), dopamine (relevant in tic-related OCD). Panel D presents genetic and autoimmune factors: 40-50% heritability, 10x risk in first-degree relatives, PANDAS mechanism showing streptococcal infection → autoimmune response → basal ganglia effects → acute OCD onset.</image>

VIII. OCD Treatment

First-line pharmacotherapy for OCD consists of SSRIs, but with important differences from their use in depression. Higher doses are typically required, often at maximum approved doses or above. Longer treatment trials are necessary, with eight to twelve weeks needed for full effect compared to four to six weeks for depression. Treatment must be long-term given the high relapse rate when medications are discontinued. All SSRIs appear similarly effective, with fluoxetine, fluvoxamine, sertraline, and paroxetine having FDA approval for OCD. Clomipramine, a tricyclic antidepressant with strong serotonergic activity, is perhaps the most efficacious medication but is limited by side effects including anticholinergic effects, sedation, and cardiac conduction effects requiring ECG monitoring.

Augmentation strategies are employed when SSRI monotherapy is insufficient. Antipsychotic augmentation, particularly with risperidone or aripiprazole, has the strongest evidence and is especially effective in patients with comorbid tics. Combining an SSRI with clomipramine requires caution due to drug interactions and the need to monitor clomipramine levels. Glutamatergic agents including memantine and N-acetylcysteine show preliminary evidence as augmentation strategies. For treatment-resistant cases, clomipramine monotherapy may be tried if not already used.

Exposure and Response Prevention is the gold-standard psychotherapy for OCD, with efficacy equivalent to medication and durability advantages. The exposure component involves systematically confronting situations, objects, or thoughts that trigger obsessions, typically following a hierarchy from less to more anxiety-provoking. The response prevention component involves refraining from performing the compulsion that would normally follow the obsession. This combination allows anxiety to habituate and teaches the individual that the feared consequences do not occur, leading to extinction of the obsessional fears.

The ERP hierarchy is constructed collaboratively with the patient, identifying specific triggers and rating their associated distress. Treatment typically begins with moderately distressing exposures and progresses to more challenging ones as confidence builds. For example, a patient with contamination obsessions might begin by touching a doorknob and waiting before washing, progressing to touching increasingly contaminated surfaces with longer delays before washing. The exposure must be done without the compulsion for habituation and learning to occur; merely touching the contaminated object and then washing provides no benefit.

<image>Panel A presents SSRI treatment for OCD with key differences from depression: higher doses (showing dose escalation graph), longer trials (8-12 weeks vs 4-6 weeks timeline), and long-term duration. Panel B displays augmentation strategies in a flowchart: SSRI inadequate → add antipsychotic (especially with tics) → consider glutamatergic agents → consider clomipramine combination with monitoring. Panel C illustrates Exposure and Response Prevention with exposure component (systematic confrontation with triggers following hierarchy) and response prevention component (refraining from compulsion), leading to habituation and extinction. Panel D shows an example ERP hierarchy for contamination OCD as a ladder, with lower rungs showing touching clean surfaces, middle rungs showing touching doorknobs and waiting, and upper rungs showing touching "contaminated" items without washing, with anxiety levels decreasing across repeated exposures.</image>

IX. OCD-Related Disorders

Body dysmorphic disorder involves preoccupation with one or more perceived defects or flaws in physical appearance that are not observable or appear only slight to others. The individual performs repetitive behaviors in response to the appearance concerns, such as mirror checking, excessive grooming, seeking reassurance, or comparing their appearance with others. These mental acts may also include comparing specific body parts with those of others. Insight is often poor, with individuals genuinely believing their appearance is abnormal despite reassurance. Treatment parallels OCD with high-dose SSRIs and CBT focusing on exposure to appearance triggers and prevention of ritualistic behaviors.

Hoarding disorder, now a separate diagnosis in DSM-5, is characterized by persistent difficulty discarding possessions regardless of their actual value, due to a perceived need to save items and distress associated with discarding them. The difficulty results in accumulation of possessions that clutter living areas and substantially compromise their intended use. The clutter must cause clinically significant distress or impairment in functioning. Unlike OCD where hoarding stems from obsessions about discarding, primary hoarding involves excessive emotional attachment to possessions and is more resistant to standard OCD treatments including SSRIs.

Trichotillomania, or hair-pulling disorder, involves recurrent pulling out of one's hair resulting in hair loss, despite repeated attempts to decrease or stop the behavior. The pulling causes clinically significant distress or impairment. Common sites include the scalp, eyebrows, and eyelashes. The behavior may be automatic, occurring without full awareness, or focused, occurring in response to tension or urge. Treatment approaches include habit reversal training, in which patients learn to recognize pulling urges and substitute alternative behaviors, and N-acetylcysteine has shown some efficacy.

Excoriation disorder, or skin-picking disorder, involves recurrent picking at one's skin resulting in skin lesions, despite repeated attempts to decrease or stop the behavior. As with hair-pulling, the behavior causes clinically significant distress or impairment. Patients typically pick at perceived imperfections, scabs, or normal skin. The behavior often results in noticeable skin damage requiring concealment. Treatment approaches are similar to trichotillomania, with habit reversal training as the primary psychotherapy and SSRIs sometimes helpful.

<image>Panel A illustrates body dysmorphic disorder: perceived flaw (magnified minor imperfection that others don't notice), repetitive behaviors (mirror checking, grooming, reassurance-seeking), poor insight. Panel B shows hoarding disorder: difficulty discarding (emotional attachment to possessions), accumulation (cluttered living space), and impaired functioning (inability to use rooms for intended purpose), noting resistance to standard OCD treatments. Panel C depicts trichotillomania: hair pulling behavior, resulting hair loss (scalp, eyebrows, eyelashes shown), urge-pull-relief cycle, and habit reversal training intervention. Panel D presents excoriation disorder: skin picking at perceived imperfections, resulting lesions requiring concealment, similar urge-pick-relief cycle, and treatment with habit reversal training and SSRIs.</image>

X. Special Considerations in OCD and Trauma Disorders

Distinguishing OCD from related conditions is essential for appropriate treatment. Generalized anxiety disorder involves worries about real-life concerns rather than intrusive irrational thoughts and does not feature ritualistic compulsions. Specific phobias involve fear of specific objects or situations but lack the obsessional thinking and compulsive rituals of OCD. Obsessive-compulsive personality disorder is characterized by ego-syntonic perfectionism and rigidity that the individual considers reasonable, in contrast to the ego-dystonic obsessions of OCD. Psychosis may involve bizarre delusions, but OCD patients typically maintain insight that their thoughts are irrational even when engaging in compulsions. Autism spectrum disorder may include stereotyped behaviors, but these are typically pleasurable rather than anxiety-reducing.

Children and adolescents with OCD present with age-appropriate manifestations. Younger children may not recognize their symptoms as excessive or irrational, affecting insight assessment. PANDAS and PANS represent acute-onset OCD following streptococcal or other infections, requiring evaluation for autoimmune etiology. Treatment approaches include family involvement in CBT and careful consideration of medication in youth. Family accommodation, in which family members participate in rituals or modify behavior to reduce patient distress, is common and maintaining of symptoms, making family intervention essential.

Treatment-resistant OCD is defined as failure to respond to adequate trials of at least two SSRIs plus ERP. Management options include clomipramine if not already tried, augmentation with antipsychotics, intensive residential or partial hospitalization programs with specialized OCD treatment, and in severe refractory cases, neurosurgical interventions including deep brain stimulation on an experimental basis. Quality ERP delivery is essential, as inadequate psychotherapy trials should not be counted as treatment failures.

Common comorbidities significantly impact OCD assessment and treatment. Major depression frequently co-occurs and is effectively treated with the same SSRIs used for OCD. Tic disorders, including Tourette syndrome, often co-occur with OCD and may warrant antipsychotic augmentation. Other anxiety disorders are common and can be addressed with SSRIs and exposure-based treatment. ADHD co-occurrence requires careful consideration, as stimulants have mixed evidence regarding effects on OCD symptoms.

<image>Panel A presents a differential diagnosis comparison chart with columns for OCD, GAD, OCPD, and phobias, comparing thought quality, ritualistic behavior, insight, and ego-syntonicity. Panel B shows pediatric considerations: age-appropriate assessment of insight, PANDAS/PANS evaluation flowchart (acute onset → infection screening → consider autoimmune treatment), family involvement and accommodation patterns. Panel C illustrates treatment-resistant OCD as a stepped care model: first-line SSRI + ERP → switch SSRI, ensure adequate ERP → clomipramine → antipsychotic augmentation → intensive programs → experimental neurosurgical options. Panel D displays common comorbidities with treatment implications: depression (same SSRIs), tic disorders (consider antipsychotic augmentation), anxiety disorders (integrated exposure treatment), ADHD (careful monitoring of stimulant effects).</image>

Summary

• PTSD develops following trauma exposure (actual or threatened death, serious injury, or sexual violence) with four symptom clusters: intrusion, avoidance, negative cognitions and mood, and alterations in arousal and reactivity
• PTSD diagnosis requires at least one intrusion symptom, one avoidance symptom, two cognition/mood symptoms, and two arousal symptoms, all persisting more than one month
• Trauma-focused psychotherapies (Prolonged Exposure, CPT, EMDR) are first-line PTSD treatments; sertraline and paroxetine are FDA-approved medications
• Acute stress disorder has similar symptoms to PTSD but lasts three days to one month; complex PTSD includes affect dysregulation, negative self-concept, and relationship difficulties
• OCD features intrusive, unwanted obsessions and/or compulsions performed to reduce anxiety, requiring more than one hour daily or significant distress
• Common OCD dimensions include contamination and washing, harm and checking, symmetry and ordering, and forbidden thoughts
• The cortico-striato-thalamo-cortical circuit shows hyperactivity in OCD, with serotonergic medications and ERP both normalizing circuit function
• OCD treatment requires high-dose SSRIs with extended trials; Exposure and Response Prevention is the gold-standard psychotherapy
• Related disorders include body dysmorphic disorder, hoarding disorder, trichotillomania, and excoriation disorder
• ERP involves systematic exposure to obsessional triggers while preventing the compulsive response, allowing habituation and extinction

Key Terms

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