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SOURCE

Source: Kirkwood CK, Melton ST, Well BG. Posttraumatic Stress Disorder and Obsessive-Compulsive Disorder. In: DiPiro JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Posey LM, eds. Pharmacotherapy: A Pathophysiologic Approach. 10th ed. New York, NY: McGraw-Hill; 2017. https://accesspharmacy.mhmedical.com/content.aspx?bookid=1861&sectionid=146065465

KEY CONCEPTS

  • Short-term goal for posttraumatic stress disorder (PTSD)—reduction in core symptoms

  • Long-term goal for PTSD—remission

  • Cognitive behavioral therapy (CBT) and eye movement desensitization and reprocessing—most effective nonpharmacologic methods to reduce PTSD symptoms

  • First line for PTSD → selective serotonin reuptake inhibitors (SSRIs) or venlafaxine

    • Adequate trial of SSRI includes appropriate dosing and duration

    • If respond to pharmacotherapy—continue treatment for at least 12 months

  • First line for obsessive-compulsive disorder (OCD) → SSRI

    • Augmentation with low doses of antipsychotics may be helpful

    • If inadequate response to SSRI after 4–6 weeks at maximum dose—switch to another SSRI

    • Medication taper can be considered after 1–2 years of treatment

POSTTRAUMATIC STRESS DISORDER

  • Can develop from traumatic or stressful events (wars, terrorist attacks, torture, robbery, natural disasters, etc.)

  • Significant psychiatric illness in civilian and deployed service personnel

    • Increase in suicide rates

  • Co-occurrence with anxiety, depression, substance abuse, and traumatic brain injury make it hard to diagnose

EPIDEMIOLOGY

  • Lifetime prevalence is 8.7% in the United States.

  • 60% of men and 50% of women are exposed to a life-threatening traumatic event—8.2% (men) and 20% (women) will develop PTSD.

    • Previous exposure and intensity of response to trauma/event increases risk of PTSD.

    • Men—assaulted more frequently; women—rape/sexual abuse

ETIOLOGY

  • Exact etiology unknown

PATHOPHYSIOLOGY

  • Neuroendocrine theories

    • Abnormalities occurring pretrauma, during trauma, and posttrauma contribute to PTSD

    • Normally corticotropin releasing factor (CRF) stimulates release of cortisol from adrenal glands. Catecholamines and cortisol levels rise in tandem, which reduces stress response by tempering the sympathetic reaction through negative feedback on pituitary and hypothalamus.

    • Hypersecretion of CRF but subnormal levels of cortisol leads to greater severity of PTSD symptoms, particularly in nonmilitary patients.

  • Neurochemical theories

    • Neurotransmitters potentially involved: 5-HT (serotonin), NE (norepinephrine), glutamate

    • Dysregulation of processing of sensory input and memories may contribute to dissociative and hypervigilant symptoms.

    • Abnormalities of GABA inhibition may lead to increased awareness or response to stress.

  • Neuroimaging studies

    • Studies suggest certain areas of brain are altered by psychological trauma: amygdala, ventromedial prefrontal cortex, dorsal anterior cingulate cortex, and hippocampus.

      • Decreased amygdala activation correlated with resilience to PTSD and response to cognitive behavioral therapy (CBT)

      • Most consistent findings are decreased hippocampus volumes and N-acetylaspartate levels.

Diagnosis

  • Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5)

  • Exposure to traumatic event

  • Must have at least one intrusion symptom, at least one symptom of avoidance of stimuli associated with trauma, and at least two symptoms of increased arousal—symptoms must be present for >1 month and cause significant distress/impairment in functioning

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