Stress-related Disorders

Stress-related disorders are a group of conditions in which identifiable psychosocial stressors or traumatic events lead to clinically significant emotional, behavioral, or physiological symptoms, including acute stress disorder, post-traumatic stress disorder, and adjustment disorders.

Epidemiology

Risk factors for stress-related disorders are best understood through the biopsychosocial model, and many are shared across ASD, PTSD, and adjustment disorder ^[1]^[2]:

Domain	Risk Factors
Pre-trauma / Predisposing	Pre-existing psychiatric disorder (depression, anxiety) ^[1]^[2]; Prior traumatic exposure ("sensitisation") ^[2]; Female gender ^[1]^[2]; Neuroticism ^[1]^[2]; Lower intelligence ^[2]; Genetic/familial vulnerability ^[1]; Early life adversity (abuse, neglect)
Peri-trauma	Trauma severity / "dose" ^[1]; Intentional interpersonal violence > accidents/disasters ^[2]; Autonomic arousal immediately after trauma predicts PTSD ^[1]; Perceived life threat; Dissociation at time of trauma
Post-trauma / Perpetuating	Lack of social support ^[1]^[2]; Avoidant coping ^[2]; Ongoing life stressors; Substance use; Lack of early intervention

High Yield

Autonomic arousal immediately after trauma predicts PTSD ^[1]. This is clinically important because it provides a biological marker that can identify individuals at risk early — those with tachycardia, hyperventilation, and heightened startle in the acute phase are more likely to develop chronic PTSD.

Anatomy and Neurocircuitry of the Stress Response

Understanding the neurobiology helps you understand why these patients have the symptoms they do.

The brain's response to threat is mediated by a network centred on the amygdala:

Structure	Normal Function	Abnormality in PTSD
Amygdala	Detects threat, initiates fear response	Hyperactive — exaggerated fear responses, hypervigilance
Hippocampus	Contextualises memories (where, when, safe vs. unsafe)	Reduced volume ^[1]^[2] — failure to contextualise trauma memories → memories "float" without time/place context → re-experiencing symptoms feel like they are happening now
Prefrontal cortex (vmPFC, ACC)	Top-down inhibition of amygdala; extinction of conditioned fear	Hypoactive — failure to extinguish fear responses, poor emotional regulation
Locus coeruleus	Source of central noradrenaline	Overactive — elevated central NA → hyperarousal, exaggerated startle

Neurotransmitter	Change in PTSD	Clinical Correlate
Noradrenaline (norepinephrine)	↑central NA levels with down-regulated central adrenergic receptors ^[1]^[2]	Hyperarousal, hypervigilance, exaggerated startle, insomnia — explains why prazosin (α1-blocker) helps nightmares
CRF (corticotropin-releasing factor)	↑CRH in CSF ^[1]	Central stress drive, anxiety
Cortisol	↓plasma cortisol ^[1]	Supersensitive negative feedback (see above)
Serotonin (5-HT)	Dysregulated	Mood, irritability, impulsivity — explains why SSRIs help
GABA	↓	Loss of inhibitory tone → anxiety, hyperarousal

Aetiology

The aetiology of stress-related disorders is best organized using the biopsychosocial framework ^[1]^[2].

Factor	Detail
Genetic/familial vulnerability ^[1]	Genetics account for ~1/3 of variance in susceptibility to PTSD ^[2]; effect partly but not completely mediated through personality (i.e., neuroticism); familial aggregation present
Neurobiological	↑central NA with down-regulated adrenergic receptors; ↓plasma cortisol with upregulated glucocorticoid receptors; ↑CRH in CSF; ↓hippocampus, left amygdala, ACC volume ^[1]^[2]
Stress-induced release	Norepinephrine, CRF, Cortisol — the triad of the acute stress neurochemical cascade ^[1]
Autonomic arousal immediately after trauma predicts PTSD ^[1]	Peri-traumatic sympathetic activation (HR, BP) is a biological predictor

Factor	Detail
Conditioned fear ^[1]	Classical conditioning: the traumatic event (UCS) becomes associated with contextual cues (CS). Later, the CS alone triggers a fear response (CR). In PTSD, there is failure to extinguish this conditioned response — the brain keeps responding as though the trauma is recurring. This is the basis for exposure therapy (systematic extinction of the conditioned fear response) ^[2]
Cognitive theories	Overwhelming of normal cognitive processing of emotionally charged information → memories persist in an unprocessed form → can intrude into conscious awareness (flashbacks, nightmares) ^[2]. This is the basis for cognitive restructuring in trauma-focused CBT
Psychodynamic theories	Early developmental difficulties → incomplete emotional development → ↑susceptibility to traumatic stressors ^[2]
Personality factors	Neuroticism is consistently associated ^[1]^[2]. Neuroticism reflects a tendency toward negative affect, emotional instability, and heightened threat sensitivity
Avoidant coping	Avoidance prevents emotional processing of trauma → perpetuates unprocessed memories → maintains re-experiencing and hyperarousal ^[2]

Factor	Detail
Lack of social support ^[1]^[2]	The single strongest modifiable post-trauma risk factor. Social support buffers stress by providing emotional processing, practical help, and meaning-making
Female gender ^[1]^[2]	~2× risk of PTSD compared to males (despite lower trauma exposure). Hypothesised mechanisms: hormonal (oestrogen modulates fear conditioning), higher rates of sexual trauma, social/cultural factors
Lower intelligence ^[2]	May impair cognitive processing of trauma and problem-solving coping
Prior trauma / psychiatric Hx ("sensitisation") ^[2]	Each trauma lowers the threshold for subsequent PTSD — the brain becomes "sensitised"
Trauma type	PTSD more commonly follows intentional acts of interpersonal violence (especially combat, sexual assaults) than accidents or disasters ^[2]. Why? Interpersonal violence shatters trust in other humans and creates a sense of betrayal, which is harder to process than impersonal events

The Stress-Vulnerability Model

Psychiatric disorders or maladaptive stress reactions occur when stress overwhelms vulnerability ^[2]. Two people exposed to the same trauma may have different outcomes depending on their biological vulnerability (genetics, brain structure), psychological resilience (coping style, personality), and social buffers (support network). This model is the foundation for understanding all stress-related disorders and guides a multi-modal treatment approach targeting all three domains.

Trauma- and Stressor-Related Disorders include ^[1]:

Acute Stress Reaction
Post-traumatic Stress Disorder
Adjustment Disorders

The key distinction is based on (a) the nature of the stressor and (b) the time course:

	Traumatic Stress	Psychosocial Stress
Definition	Occurs outside range of normal human experience — would be experienced as traumatic by most people ^[2]	Any life event/condition that places strain on coping — subjective ^[2]
Examples	Combat, sexual assault, natural disaster, serious accident, witnessing death	Relationship breakdown, job loss, illness, financial difficulty, bereavement
Physical/psychological integrity	Often involves circumstances where a person feels their own or a loved one's physical or psychological integrity is threatened ^[2]	Not necessarily life-threatening
Associated Dx	ASD, PTSD	Normal reaction, adjustment disorder, precipitation of other psychiatric conditions (mood, anxiety, psychotic) ^[2]

Time Frame	Immediate to 2–3 days	2–3 days to 1 month	> 1 month
Traumatic stressor with trauma-related symptoms (re-experiencing, dissociation, avoidance)
DSM-5	/	Acute Stress Disorder	PTSD
ICD-10	Acute Stress Reaction	Acute Stress Disorder	PTSD

Time Frame	Immediate to 6 months after resolution	> 6 months after resolution
Any stressor with non-trauma-related symptoms (anxiety, depression, mixed)
DSM-5	Adjustment Disorder or depressive/anxiety disorder	Depressive/anxiety disorder
ICD-10	Adjustment Disorder or depressive/anxiety disorder	Depressive/anxiety disorder

ICD-10 vs DSM-5: Acute Stress

Acute stress reaction (ICD-10) refers to the acute, short-lived, normal reaction (resolves in hours to days) after traumatic stressor. Acute stress disorder (DSM-5) refers to the more prolonged abnormal response (3 days to 4 weeks) which is less common and may predict later onset of PTSD ^[2]. Don't confuse these — they capture different temporal phases of the same spectrum.

Clinical Features

Clinical features are organised by disorder, with symptoms and signs separated and pathophysiological basis explained inline.

1. Acute Stress Reaction (ICD-10) / Acute Stress Response

Time course: Starts ≤1 hour from stressor, diminishes after ≤48 hours, disappears within a few days ^[2]

This is essentially the normal acute response to extreme trauma. Think of it as the "fight-or-flight" response that hasn't yet turned pathological.

Symptom	Pathophysiological Basis
Dazed, bewildered state	Overwhelming of cortical processing capacity; prefrontal cortex "shuts down" under extreme amygdala activation
Narrowing of attention / difficulty processing stimuli	Thalamic gating redirects processing to survival-relevant stimuli; non-essential cortical processing is suppressed
Disorientation	Hippocampal function impaired by acute cortisol surge → difficulty with spatial and temporal orientation
Anxiety, fear, anger	Amygdala-driven emotional activation; noradrenaline surge from locus coeruleus
Autonomic symptoms: tachycardia, sweating, flushing	Sympathetic activation via hypothalamus → sympathetic chain (fight-or-flight response)
Dissociative symptoms (depersonalisation, derealisation)	Thought to be a protective "circuit breaker" — the brain detaches from overwhelming reality to prevent further psychological damage. Mediated by endogenous opioid release and prefrontal-limbic disconnection

2. Acute Stress Disorder (DSM-5)

Time course: Starts during or shortly after stressor; lasts ≥3 days but ≤4 weeks ^[2]

This represents the more prolonged abnormal response that is a risk factor for PTSD. If symptoms persist beyond 1 month, you reclassify as PTSD.

The DSM-5 requires 9 or more symptoms from any of 5 categories (intrusion, negative mood, dissociation, avoidance, arousal):

A. Intrusion / Re-experiencing symptoms

Symptom	Pathophysiological Basis
Flashbacks (involuntary, vivid reliving of the event)	Trauma memories are encoded by the amygdala in a sensory-rich, emotionally charged, but contextually poor form (due to hippocampal impairment). When triggered, these memories replay as though the event is happening now because they lack the hippocampal "time stamp"
Nightmares	During REM sleep, the amygdala is highly active while prefrontal inhibition is reduced → trauma memories replay without cortical regulation. The locus coeruleus normally goes silent during REM; in PTSD, it remains active → disrupted sleep architecture
Intrusive distressing memories	Unprocessed trauma memories stored in amygdala "leak" into consciousness when triggered by internal or external cues
Intense psychological distress or physiological reactivity to trauma reminders	Classical conditioning: environmental cues (CS) associated with the trauma (UCS) trigger the conditioned fear response

B. Negative Mood

Symptom	Pathophysiological Basis
Inability to experience positive emotions (emotional numbing, anhedonia)	Chronic amygdala activation leads to depletion of reward circuitry (ventral tegmental area → nucleus accumbens dopamine pathway). Also, persistent stress hormones blunt mesolimbic dopamine signalling

C. Dissociative Symptoms

Symptom	Pathophysiological Basis
Altered sense of reality (derealisation — "the world feels unreal")	Dissociation as a neurobiological protective mechanism: medial prefrontal cortex over-inhibits the amygdala to dampen emotional response, but at the cost of disconnection from reality
Inability to remember important aspect of trauma (dissociative amnesia)	State-dependent encoding: memories formed under extreme stress are encoded in a way that is inaccessible to normal conscious recall (hippocampal encoding impaired by cortisol/NA surge)
Depersonalisation ("I feel detached from my body")	Parietal-temporal cortex disconnection from the body map; endogenous opioid system activation

D. Avoidance Symptoms

Symptom	Pathophysiological Basis
Avoidance of trauma-related stimuli (memories, thoughts, feelings, people, places)	Operant conditioning: avoidance reduces the distressing conditioned fear response → negatively reinforced → avoidance becomes habitual. This is exactly why avoidance perpetuates the disorder — it prevents the extinction of conditioned fear

E. Arousal Symptoms

Symptom	Pathophysiological Basis
Sleep disturbance	Elevated NA from locus coeruleus disrupts sleep architecture; hyperarousal state prevents transition to deep sleep
Irritability / angry outbursts	Amygdala hyperactivation with inadequate prefrontal regulation → lowered threshold for emotional reactivity
Hypervigilance	Locus coeruleus–noradrenaline system on "high alert" → scanning environment for threats constantly
Exaggerated startle response	Sensitised amygdala–brainstem circuits (specifically the pontine reticular formation) → enhanced acoustic startle reflex
Poor concentration	Attentional resources hijacked by threat-monitoring systems; prefrontal cognitive resources diverted

3. Post-Traumatic Stress Disorder (PTSD)

Time course: Symptoms persist > 1 month after traumatic event. Should have onset within 6 months after stressor (ICD-10) ^[2]. DSM-5 includes a "delayed expression" specifier for those with onset > 6 months.

The symptom clusters are the same as ASD but are organized into 4 clusters (DSM-5) rather than 5:

Characterised by re-experiencing (flashbacks, nightmares, intrusive images), avoidance (of cues, poor memory of event, detachment/numbing) and hyperarousal (anxiety, irritability, insomnia, poor concentration) ^[2]

Cluster	Key Symptoms	Pathophysiology
B. Intrusion	Flashbacks, nightmares, intrusive memories, distress/physiological reactivity to cues	Amygdala-driven, context-poor trauma memories (hippocampal encoding failure) + conditioned fear responses
C. Avoidance	Avoidance of trauma-related thoughts, feelings, external reminders	Operant conditioning (negative reinforcement); prevents extinction
D. Negative alterations in cognition and mood	Distorted blame (self/others), persistent negative emotional state (fear, horror, anger, guilt, shame), diminished interest, feeling detached/estranged, inability to experience positive emotions	Prefrontal-limbic dysfunction, serotonin/dopamine depletion, cognitive distortions (overgeneralisation, personalisation)
E. Arousal and reactivity	Irritability, reckless/self-destructive behaviour, hypervigilance, exaggerated startle, concentration problems, sleep disturbance	Noradrenergic hyperactivation, amygdala sensitisation, impaired prefrontal regulation

Feature	ASD	PTSD
Time	3 days–4 weeks	> 1 month
Dissociation	Prominent (one of 5 categories)	May or may not be present (specifier)
Predictive value	ASD may predict later PTSD but many PTSD patients never had ASD ^[2]
Minimum symptom count	9 from any 5 categories	At least 1 intrusion + 1 avoidance + 2 cognition/mood + 2 arousal

4. Adjustment Disorder

Time course: Develops ≤3 months of stressor (DSM-5) ^[2]. Resolves within 6 months of resolution of stressor (or its consequences).

This is the "catch-all" diagnosis for clinically significant distress in response to an identifiable stressor that does not meet criteria for another specific mental disorder (e.g., MDD, GAD).

Stressor: usually adaptation to new circumstances or stressful life event (not necessarily traumatic) ^[2]
Symptoms: usually anxiety/depressive symptoms that are clearly arising from stressor and out of proportion to original stressor ("disorder" vs "normal reaction") but does not meet criteria of a specific mood/anxiety disorder ^[2]

Subtype	Features
With depressed mood	Low mood, tearfulness, hopelessness
With anxiety	Nervousness, worry, jitteriness, separation anxiety (in children)
With mixed anxiety and depressed mood	Combination of above
With disturbance of conduct	Behavioural disturbance (truancy, vandalism, reckless driving, fighting)
With mixed disturbance of emotions and conduct	Both emotional and behavioural symptoms
Unspecified	Maladaptive reactions not classifiable above

Symptom	Pathophysiological Basis
Depressed mood, tearfulness	HPA axis activation by chronic stress → serotonin/noradrenaline depletion → mood dysregulation. The stressor disrupts psychological equilibrium without reaching the severity of a major depressive episode
Anxiety, worry, nervousness	Amygdala sensitisation by ongoing stressor; lower threshold for threat detection
Impaired social/occupational functioning	Cognitive resources consumed by rumination and emotional distress → reduced executive function
Behavioural symptoms (conduct disturbance)	Impaired prefrontal regulation of impulse control under stress, particularly in adolescents

Feature	Normal Reaction	Adjustment Disorder	MDD / GAD
Distress proportionate to stressor	Yes	No — out of proportion ^[2]	May be independent of stressor
Functional impairment	Mild, transient	Significant	Significant
Meets criteria for specific disorder	No	No	Yes
Time relationship to stressor	Clear	Clear (≤3mo)	May or may not be

Mechanism	Manifestation
Amygdala hyperactivation	Fear, hypervigilance, exaggerated startle, flashbacks
Hippocampal dysfunction (↓volume)	Context-poor memories, dissociative amnesia, difficulty distinguishing safe vs. unsafe
Prefrontal hypoactivation	Poor fear extinction, emotional dysregulation, impaired concentration
↑Noradrenaline (locus coeruleus)	Hyperarousal, insomnia, startle, nightmares
↑CRH (central) / ↓cortisol (peripheral)	Chronic central stress signalling despite low baseline cortisol (PTSD-specific)
Classical conditioning (fear)	Re-experiencing triggered by cues; avoidance behaviour
Operant conditioning (avoidance)	Negative reinforcement perpetuates avoidance → prevents extinction → maintains disorder

High Yield Summary

Stress-related disorders include Acute Stress Reaction, Acute Stress Disorder, PTSD, and Adjustment Disorder ^[1]
The stress-vulnerability model explains individual susceptibility: disorder occurs when stress overwhelms vulnerability threshold ^[2]
Traumatic stress occurs outside range of normal human experience → ASD/PTSD. Psychosocial stress is subjective → adjustment disorder ^[2]
Time course is critical: ASD = 3 days–4 weeks; PTSD = > 1 month; Adjustment disorder = ≤3 months of stressor, resolves within 6 months
PTSD neurobiology: ↑amygdala, ↓hippocampus, ↓PFC, ↑NA, ↑CRH, ↓cortisol ^[1]^[2]
PTSD has LOW cortisol (unlike depression) due to upregulated glucocorticoid receptors and enhanced negative feedback ^[2]
Autonomic arousal immediately after trauma predicts PTSD ^[1]
Risk factors: female gender, neuroticism, prior trauma, pre-existing psychiatric disorder, lack of social support, trauma severity ^[1]^[2]
PTSD clusters: Intrusion + Avoidance + Negative cognition/mood + Arousal (mnemonic: I-A-N-A or think "I Avoid Negative Arousal")
Conditioned fear (classical conditioning) drives re-experiencing; avoidance (operant conditioning, negative reinforcement) maintains the disorder ^[1]^[2]
Mild TBI mimics PTSD (irritability, startle, poor concentration) but lacks re-experiencing and avoidance ^[2]
Adjustment disorder = distress out of proportion to stressor + does NOT meet criteria for another specific disorder ^[2]

Active Recall - Stress-Related Disorders: Definition, Epidemiology, Aetiology, Classification, Clinical Features

The differential diagnosis of stress-related disorders is one of the trickiest areas in psychiatry because anxiety, low mood, dissociation, and avoidance are transdiagnostic symptoms — they appear across dozens of conditions. The key clinical task is to determine whether the symptoms are best explained by a stress-related disorder (ASD, PTSD, adjustment disorder) or by another condition that shares overlapping features.

The approach rests on three fundamental questions:

Is there an identifiable stressor, and is it temporally linked to symptom onset?
Is the stressor traumatic (outside normal human experience) or psychosocial (subjective)?
Are the specific symptom clusters present (re-experiencing, avoidance, arousal, negative cognition)? Or do the symptoms better fit another diagnostic category?

Differential Diagnosis	Key Differentiating Features	Why It Can Be Confused With PTSD
Adjustment Disorder ^[2]	Stressor can be of any severity or type, but either the stressor is non-traumatic OR the symptomatology does not meet criteria for PTSD ^[2]. Adjustment disorder carries anxiety/depressive symptoms but lacks the hallmark re-experiencing cluster (flashbacks, nightmares). Temporal frame also differs (≤3 months of stressor onset, resolves within 6 months of stressor resolution).	Both are stress-related, both can have anxiety/depressive symptoms, both have a temporal link to a stressor
Acute Stress Disorder ^[2]	Lasts for 3 days to 1 month following exposure to traumatic event ^[1]^[2]. Same symptom profile as PTSD but the duration criterion distinguishes them. ASD requires 9+ symptoms from 5 categories.	Identical symptom content — the only difference is duration
Other psychiatric disorders ^[2]	Almost all psychiatric disorders can be exacerbated by traumatic stressors. If the symptom response pattern fits another disorder more than PTSD, that diagnosis should be given ^[2]. For example, if a patient develops a full major depressive episode after trauma without prominent re-experiencing/avoidance, diagnose MDD, not PTSD.	Trauma can precipitate depression, psychosis, anxiety disorders — the trauma is a risk factor, not a diagnostic criterion for these other disorders
Anxiety disorders and OCD ^[2]	OCD: recurrent intrusive thoughts are present, but they are unrelated to a traumatic event ^[2]. The intrusive thoughts in OCD concern contamination, symmetry, harm, etc. — not a specific trauma. Anxiety disorders: anxiety symptoms (worries, avoidance, arousal) are not related to traumatic events ^[2]. GAD worries are future-oriented and wide-ranging; PTSD hyperarousal is tied to the trauma.	Both OCD and PTSD have intrusive thoughts. Both GAD and PTSD have hyperarousal and worry. Both phobias and PTSD have avoidance.
Traumatic Brain Injury (TBI) ^[2]	TBI-related neurocognitive symptoms may mimic PTSD symptoms (e.g., irritability, startle response, poor concentration), but usually there are no re-experiencing and avoidance symptoms. There may be persistent disorientation and confusion ^[2].	TBI and PTSD often co-occur (e.g., combat, road traffic accidents). The overlapping symptoms are arousal-related; the distinguishing ones are re-experiencing and avoidance (present in PTSD, absent in TBI). Also look for focal neurological signs, amnesia for the event itself (retrograde, not dissociative), and cognitive deficits out of proportion.
Major Depressive Disorder	MDD has sustained low mood, anhedonia, guilt, worthlessness, suicidal ideation, vegetative symptoms (sleep, appetite, psychomotor changes). While PTSD Cluster D ("negative alterations in cognition and mood") overlaps, MDD lacks the hallmark re-experiencing (flashbacks, nightmares) and avoidance of trauma reminders. Content of rumination differs: depressive patients brood on past failures/guilt; PTSD patients re-experience the specific traumatic event.	Both have anhedonia, sleep disturbance, poor concentration, guilt. PTSD frequently co-occurs with depression ^[1] — comorbidity is the rule, not the exception
Dissociative Disorders	Dissociative identity disorder, dissociative amnesia, depersonalisation/derealisation disorder can present with amnesia, emotional numbing, and detachment. However, dissociative disorders are not necessarily linked to a single identifiable traumatic event (though often linked to childhood trauma), and they lack the re-experiencing and hyperarousal clusters of PTSD.	Both can have dissociative symptoms. DSM-5 recognises a "dissociative subtype" of PTSD, blurring the boundary further
Psychotic Disorders	Schizophrenia and brief psychotic disorder can present with paranoia, agitation, and hallucinations. However, PTSD flashbacks are reliving a real event (not a false perception), and PTSD "paranoia" is hypervigilance to real threats (not systematised delusional beliefs). Psychotic features (command hallucinations, thought disorder, bizarre delusions) are absent in PTSD.	Both can present with hypervigilance, suspiciousness, sleep disturbance, agitation. Flashbacks can superficially resemble hallucinations
Personality Disorders	Borderline personality disorder (BPD) has emotional instability, self-harm, dissociation, and interpersonal difficulties. These can look like PTSD, especially since many BPD patients have trauma histories. Key differences: BPD is a lifelong pattern (not linked to a single event), features identity disturbance and abandonment fears, and the emotional instability is more pervasive. Some personality features may be associated with vulnerability to situational distress that may resemble an adjustment disorder ^[2].	Trauma is common in BPD history; dissociation, emotional dysregulation, self-harm overlap

Differential Diagnosis	Key Differentiating Features
Depression ^[2]	If an individual meets criteria for depression, the diagnosis of adjustment disorder is not applicable ^[2]. The symptoms in adjustment disorder are subthreshold — if full MDD criteria are met, diagnose MDD. Content: depressive patients have pervasive hopelessness and vegetative symptoms; adjustment disorder symptoms are more situation-specific.
ASD / PTSD ^[2]	Temporally, adjustment disorder is diagnosed from immediate to 6 months after stressor, whereas ASD/PTSD are diagnosed based on different temporal frames. Symptomatically, adjustment disorder is diagnosed when an individual does not meet full criteria of ASD/PTSD. In terms of precipitating stressor, adjustment disorder is diagnosed when the stressor is not deemed traumatic in nature ^[2].
Personality Disorder ^[2]	It is important to understand the lifetime history of personality functioning to decide whether a stress-related disturbance exceeds what may be attributable to maladaptive personality disorder symptoms ^[2]. Personality disorders are chronic and pervasive, not reactive to a single stressor. However, patients with personality disorders are more vulnerable to developing adjustment disorders.
Normal stress reactions ^[2]	Diagnosis of adjustment disorder should only be made when the magnitude of distress and the impact on functioning exceeds what is normally expected ^[2]. If the reaction is proportionate and functional impairment is minimal and transient, it is a normal reaction to stress, not a disorder.
Other psychiatric disorders ^[2]	Almost all psychiatric disorders may be exacerbated by stressors, therefore it is essential to distinguish whether more specific disorders can be diagnosed and whether such psychiatric symptoms are present before the stressor ^[2]. If GAD, panic disorder, or substance use disorder was present before the stressor, the stressor may have exacerbated a pre-existing condition rather than caused an adjustment disorder.

This is the most commonly tested scenario: you are given a clinical vignette and must decide which stress-related disorder fits.

Feature	Acute Stress Reaction	Acute Stress Disorder	PTSD	Adjustment Disorder
Stressor type	Traumatic	Traumatic	Traumatic	Any (not necessarily traumatic) ^[2]
Onset	≤1 hour	During or shortly after trauma	Usually within 6 months	≤3 months ^[2]
Duration	Hours to days	3 days to 1 month ^[1]^[2]	> 1 month ^[2]	Resolves within 6 months of stressor resolution
Re-experiencing	Absent or minimal	Present	Present (hallmark)	Absent
Dissociation	May be present	Prominent (one of 5 categories) ^[1]	May be present (specifier)	Absent
Avoidance	Minimal	Present	Present (hallmark)	May have behavioural avoidance but not trauma-specific
Hyperarousal	Prominent (autonomic)	Present	Present (hallmark)	May have anxiety symptoms
Meets criteria for specific disorder?	N/A	No (it IS the specific disorder)	No (it IS the specific disorder)	No — residual category ^[2]

These are critical "rule-outs" before diagnosing any stress-related disorder. The principle is the hierarchy of diagnosis: organic causes take precedence ^[2].

Medical Condition	Mechanism of Mimicry	Key Differentiating Clue
Thyroid disease (especially hyperthyroidism) ^[3]	↑thyroid hormones → ↑metabolic rate, ↑sympathetic tone → anxiety, tremor, tachycardia, insomnia, irritability	Weight loss, heat intolerance, goitre, lid lag, abnormal TFTs
Epilepsy (especially temporal lobe epilepsy) ^[3]	Ictal fear, déjà vu, dissociative-like experiences, post-ictal confusion	Stereotyped episodes, aura, EEG abnormalities, brief duration
Cardiac disease ^[3] (arrhythmias, MVP)	Palpitations, chest tightness, dyspnoea → panic-like symptoms	ECG abnormalities, relationship to exertion
Phaeochromocytoma ^[3]	Episodic catecholamine surges → paroxysmal hypertension, tachycardia, diaphoresis, anxiety	Episodic hypertension, 24-hour urinary catecholamines
Vestibular dysfunction ^[3]	Dizziness, unsteadiness → anxiety, avoidance of triggers	Nystagmus, positive Dix-Hallpike, audiometry
Hypoglycaemia	Catecholamine counter-regulatory response → tremor, sweating, anxiety, confusion	Relationship to fasting/insulin, BGL confirms
Traumatic brain injury ^[2]	Direct neuronal injury → irritability, poor concentration, startle. No re-experiencing or avoidance but may have persistent disorientation and confusion ^[2]	Focal neurology, GCS history, neuroimaging, neuropsychological testing
Cushing's disease	Chronic hypercortisolism → anxiety, depression, cognitive impairment	Cushingoid features, elevated 24-hr urinary free cortisol

Substance	Mechanism	Notes
Intoxication: alcohol, stimulants (amphetamines, cocaine, caffeine), cannabis, hallucinogens	Direct psychoactive effects → anxiety, paranoia, dissociation, agitation	Temporal relationship to substance use; urine drug screen
Withdrawal: alcohol, benzodiazepines, opiates, caffeine, nicotine	Rebound sympathetic activation → anxiety, tremor, insomnia, irritability, hyperarousal	Symptoms worst in the morning (when withdrawal peaks); history of regular use and recent cessation
Side effects of medications: antidepressants (first 2 weeks), corticosteroids, sympathomimetics, anticholinergics, antipsychotics (akathisia)	Various mechanisms depending on drug	Temporal relationship to medication initiation/change

Must-Know: Akathisia vs. PTSD Hyperarousal

Akathisia (inner restlessness from antipsychotics/SSRIs) can look like PTSD hyperarousal or anxiety. The key difference: akathisia is a motor restlessness (inability to sit still, pacing) that improves with movement, whereas PTSD hyperarousal is a sensory hypervigilance (scanning for threats, exaggerated startle). Always check the medication list.

A clinically useful approach from the senior notes ^[2]: when anxiety is present, what is the patient anxious about? The content of the anxiety points to the diagnosis.

Focus of Anxiety/Fear	Most Likely Diagnosis
Fear of traumatic memory ^[3]	ASD / PTSD
Fear of imminent death ^[3]	Panic Disorder
Free-floating anxiety (multiple topics) ^[3]	GAD
Fear of specific object/situation ^[3]	Specific Phobia
Fear of embarrassment / scrutiny ^[3]	Social Anxiety Disorder
Fear of crowds / cannot escape ^[3]	Agoraphobia
Fear of intrusive, obsessive ideas ^[3]	OCD
Worry about gaining weight	Eating disorder
Worry about having serious illness	Illness anxiety disorder
Fear of being poisoned/killed	Paranoid schizophrenia
Ruminatory guilt/worthlessness	Depression
Fear of separation/abandonment	BPD / separation anxiety

This is a commonly tested comparison:

Feature	PTSD	OCD	Depression
Content	Specific to the traumatic event (the crash, the assault)	Unrelated to trauma (contamination, symmetry, harm, blasphemy)	Mood-congruent (guilt, worthlessness, hopelessness)
Nature	Involuntary replay of real past events	Ego-dystonic (unwanted, recognised as irrational) urges/images	Ego-syntonic ruminations (feel "true" to the patient)
Compulsions	Absent (avoidance is not ritualistic)	Present — ritualistic, rule-driven, often excessive and unrelated to feared outcome	Absent
Trigger	Trauma-related cues (sounds, smells, locations)	Various (contamination cues, symmetry, numbers)	Low mood, negative events
Temporal relationship	After a specific identifiable traumatic event	No temporal relationship to trauma	During depressive episodes

When approaching a patient with stress-related symptoms:

Exclude medical causes — TFTs, BGL, ECG, neuroimaging if indicated
Exclude substance causes — drug history, urine toxicology
Identify the stressor — traumatic vs. psychosocial
Match symptom profile — re-experiencing? avoidance? hyperarousal? Or just anxiety/depression?
Check duration — < 3 days (acute stress reaction), 3 days–4 weeks (ASD), > 1 month (PTSD), ≤ 3 months of stressor (adjustment disorder)
Check if criteria for another specific disorder are met — if yes, diagnose that disorder instead of adjustment disorder
Screen for comorbidities — depression, other anxiety disorders, substance use, somatization, dissociative disorders ^[1]

High Yield Summary

Adjustment disorder is a residual category — only diagnose when criteria for other specific disorders (MDD, GAD, PTSD, etc.) are NOT met ^[2]
PTSD vs. Adjustment Disorder: PTSD requires traumatic stressor + specific symptom clusters (re-experiencing, avoidance, hyperarousal). Adjustment disorder can follow any stressor and has subthreshold/non-specific symptoms ^[2]
PTSD vs. TBI: TBI mimics arousal symptoms but lacks re-experiencing and avoidance; may show persistent disorientation and confusion ^[2]
PTSD vs. OCD: Intrusive thoughts in OCD are unrelated to a traumatic event; compulsions are ritualistic and excessive ^[2]
PTSD co-morbidities: Depression, other anxiety disorders, substance use disorders, somatization, dissociative disorders ^[1]
Always exclude medical causes (thyroid, epilepsy, cardiac, phaeochromocytoma, TBI) and substance causes (intoxication, withdrawal, medication side effects) before diagnosing a stress-related disorder ^[2]^[3]
The focus/theme of anxiety helps differentiate: trauma memory = PTSD, imminent death = panic, free-floating = GAD, embarrassment = social phobia, intrusive ideas = OCD ^[3]
ASD vs. PTSD: identical symptom content; duration is the sole distinguishing feature (ASD: 3 days–4 weeks; PTSD: > 1 month) ^[1]^[2]

Active Recall - Differential Diagnosis of Stress-Related Disorders

References

^[1] Lecture slides: GC 171. Stress-related disorders and obsessive-compulsive disorder (Post-traumatic stress disorder adjustment disorder, acute stress disorder)_rev.pdf ^[2] Senior notes: ryanho-psych.md (Sections 8.3.1, 8.3.2, 8.3.3 — DDx tables for PTSD and adjustment disorder, approach to anxiety, hierarchy of diagnosis) ^[3] Lecture slides: GC 167. I feel very nervous Anxiety disorders.pdf

Diagnostic Criteria

Stress-related disorders are clinical diagnoses — there is no blood test, imaging study, or biomarker that confirms ASD, PTSD, or adjustment disorder. Diagnosis rests entirely on:

Identification of the stressor and its temporal relationship to symptoms
Pattern recognition of specific symptom clusters
Duration of symptoms
Exclusion of other medical, substance-related, and psychiatric causes
Functional impairment or clinically significant distress

This section lays out the formal criteria for each disorder, then synthesises them into a practical diagnostic algorithm.

This captures the immediate, short-lived, normal reaction to exceptional trauma. Think of it as the brain's "emergency mode" — not yet pathological ^[2].

ICD-10 Criteria ^[2]:

Criterion	Detail	Why This Criterion Exists
Temporal connection	Immediate and clear temporal connection between the impact of an exceptional stressor and symptom onset; usually within a few minutes if not immediate	Establishes causality — the stressor caused the symptoms
Symptom pattern	Mixed and usually changing picture: initial state of "daze", then depression, anxiety, anger, despair, overactivity, and withdrawal may all be seen, but no one type of symptom predominates for long	The hallmark of ASR is its fluctuating, transient nature — unlike PTSD where specific clusters persist
Resolution	Symptoms resolve rapidly — within a few hours if removed from stressful environment; if stress continues, symptoms begin to diminish after 24–48 hours and are usually minimal after about 3 days	If symptoms persist beyond this window, consider ASD or PTSD
Exclusion	Should not be used to cover sudden exacerbation of pre-existing psychiatric disorder (except personality disorders). However, prior psychiatric Hx does not invalidate the diagnosis	Prevents misattribution of pre-existing illness flare to the acute stressor, while acknowledging that prior Hx doesn't preclude a genuine acute stress reaction

Key Point

ICD-10's acute stress reaction is the normal acute response. It is transient, mixed, and self-limiting. If the patient is still significantly symptomatic after 3 days, you are moving into DSM-5's Acute Stress Disorder territory.

Similar exposure as in PTSD ^[1]. This captures the more prolonged abnormal response (3 days–1 month) that may predict later PTSD.

DSM-5 Criteria ^[1]^[2]:

Criterion	Detail
A. Exposure	Exposure to actual or threatened death, serious injury, or sexual violation in ≥1 of the following ways: (1) Directly experiencing; (2) Witnessing in person; (3) Learning that event occurred to close family member/friend (must be violent or accidental); (4) Repeated or extreme exposure to aversive details (e.g., first responders — NOT via media)
B. Symptoms	Presence of > 9 of 5 categories of: intrusion, negative mood, dissociation, avoidance, and arousal related to the trauma ^[1]
C. Duration	Duration of disturbance is 3 days to 1 month after trauma ^[1]
D. Impairment	Causes significant impairment in social, occupational, or other important functioning ^[1]
E. Exclusion	Not attributable to physiological effects of substance or another medical condition

The 5 symptom categories (need ≥9 total from any combination):

Intrusion (any of):

Recurrent, involuntary, intrusive distressing memories
Recurrent distressing dreams related to the event
Dissociative reactions (e.g., flashbacks)
Intense/prolonged distress or physiological reactivity at exposure to cues

Negative Mood:

Persistent inability to experience positive emotions

Dissociation (any of):

Altered sense of reality (derealisation, depersonalisation)
Inability to remember an important aspect of the trauma (dissociative amnesia)

Avoidance (any of):

Efforts to avoid distressing memories, thoughts, or feelings about the event
Efforts to avoid external reminders (people, places, activities)

Arousal (any of):

Sleep disturbance
Irritable behaviour/angry outbursts
Hypervigilance
Problems with concentration
Exaggerated startle response

ASD vs PTSD Criteria

The key structural difference: ASD uses a pooled 9-of-14 approach (any 9 from 5 categories), whereas PTSD uses minimum thresholds per cluster (1 intrusion + 1 avoidance + 2 cognition/mood + 2 arousal). ASD is more "flexible" because in the acute phase, symptoms may not have consolidated into the distinct PTSD clusters yet.

3. Post-Traumatic Stress Disorder (DSM-5: 309.81)

This is the most commonly tested stress-related disorder. The DSM-5 criteria are structured around Criterion A (exposure) + 4 symptom clusters (B–E) + duration + impairment + exclusion.

DSM-5 Criteria ^[1]^[2]:

Symptom	Detail
Recurrent, involuntary and intrusive memories of event ^[1]	Not just thinking about it — the memories are unwanted and break into consciousness
Recurrent trauma-related nightmares ^[1]	Content and/or affect related to the event
Dissociative reactions ^[1]	Flashbacks where the individual feels or acts as if the event is recurring (spectrum from brief episodes to complete loss of awareness of surroundings)
Intense physiologic distress at cue exposure ^[1]	Psychological distress when confronted with internal/external cues symbolising the trauma
Marked physiological reactivity at cue exposure ^[1]	Autonomic activation (tachycardia, sweating) in response to trauma reminders

Symptom	Detail
Avoidance of distressing memories, thoughts or feelings of the event(s) ^[1]	Cognitive/emotional avoidance
Avoidance of external reminders that arouse memories of event(s), e.g., people, places, activities ^[1]	Behavioural avoidance

Symptom	Detail
Inability to remember an important aspect of the traumatic event(s) ^[1]	Dissociative amnesia (not due to head injury/substance)
Persistent distorted cognitions about cause or consequence of event that lead to blame of self or others ^[1]	"It was my fault" — cognitive distortion of personalisation
Persistent negative emotional state ^[1]	Fear, horror, anger, guilt, or shame
Marked diminished interest ^[1]	In significant activities
Feeling detached from others ^[1]	Estrangement, emotional numbing
Persistent inability to experience positive emotions ^[1]	Anhedonia, constricted affect

Symptom	Detail
Irritable behavior and angry outbursts ^[1]	With little or no provocation; verbal or physical aggression
Reckless or self-destructive behavior ^[1]	New in DSM-5 (not in DSM-IV)
Hypervigilance ^[1]	Constantly scanning for threats
Exaggerated startle response ^[1]	Enhanced acoustic/tactile startle
Problems with concentration ^[1]	Attentional resources diverted to threat monitoring
Sleep disturbance ^[1]	Difficulty falling/staying asleep, restless sleep

Criterion	Requirement
F. Duration	Duration of disturbance is more than one month ^[1]
G. Impairment	Causes significant impairment in function ^[1]
H. Exclusion	Not attributable to substance or medical condition ^[2]

Specifier	Detail
With dissociative symptoms	Derealisation or depersonalisation ^[1] — the patient meets PTSD criteria AND experiences persistent/recurrent detachment from mental processes or body, or experiences of unreality of surroundings
With delayed expression	Don't meet criteria until > 6 months after event ^[1] — though some symptoms may begin immediately. Important: the full diagnostic threshold is what is delayed, not necessarily all symptoms

Minimum Symptom Count Summary for PTSD (DSM-5)

B: ≥1 intrusion + C: ≥1 avoidance + D: ≥2 cognition/mood + E: ≥2 arousal = minimum 6 symptoms across all 4 clusters, lasting > 1 month, with impairment, not substance/medical.

Mnemonic: "1-1-2-2" (B-C-D-E)

The ICD-10 criteria are simpler and narrower:

Criterion	ICD-10 Requirement
Stressor	Exposure to an exceptionally threatening/catastrophic event
Re-experiencing	Persistent remembering or "reliving" (flashbacks, vivid memories, recurring dreams) OR distress when exposed to reminders
Avoidance	Actual/preferred avoidance of circumstances resembling/associated with the stressor (not present before exposure)
Arousal	Either (a) inability to recall important aspects of exposure, OR (b) ≥2 of: difficulty falling/staying asleep, irritability/anger, difficulty concentrating, hypervigilance, exaggerated startle
Onset	Within 6 months of stressor (or the period of stress)

Key differences from DSM-5:

ICD-10 does NOT include the "negative cognitions and mood" cluster → ICD-10 PTSD is narrower
ICD-10 requires onset within 6 months (DSM-5 allows delayed expression beyond 6 months)
ICD-10 has a lower symptom threshold → captures a broader range of post-trauma presentations

5. Adjustment Disorder

Criterion	Detail	Rationale
A	Development of emotional or behavioural symptoms in response to an identifiable stressor occurring ≤3 months of onset of stressor ^[2]	Establishes temporal causation
B	These symptoms are clinically significant, as evidenced by ≥1 of: (1) Marked distress out of proportion to severity or intensity of stressor (taking into account external context and cultural factors) (2) Significant impairment in functioning ^[2]	Distinguishes from normal stress reaction
C	Does not meet criteria for another mental disorder and is not merely an exacerbation of a pre-existing mental disorder ^[2]	Residual category principle
D	Does not represent normal bereavement ^[2]	Bereavement is a normal process with its own trajectory
E	Once the stressor (or its consequences) has terminated, symptoms do not persist for > 6 months	If symptoms persist, reclassify

Criterion	Detail
Relationship	Diagnosis depends on careful evaluation of relationship between: (a) form, content, severity of symptoms; (b) previous history and personality; and (c) stressful event, situation, or life crisis ^[2]
Causation	The presence of the 3rd factor should be clearly established and there should be strong, though perhaps presumptive, evidence that the disorder would not have arisen without it ^[2]
Exclusion	If the stressor is relatively minor, or if a temporal connection (< 3 months) cannot be demonstrated, the disorder should be classified elsewhere ^[2]

Investigation Modalities

Assessment Tools

Assessment Component	What You Are Looking For	Why
Detailed psychiatric history	Nature of stressor, temporal relationship, symptom onset, premorbid personality, prior trauma Hx, substance use Hx, past psychiatric Hx	Establishes Criterion A (stressor) and temporal relationship; identifies risk factors and pre-existing conditions
Mental State Examination	Appearance (neglected? hypervigilant?), Behaviour (startle during interview?), Mood/Affect (flat? anxious? irritable?), Thought content (intrusive memories? guilt? suicidal ideation?), Perception (flashbacks? dissociation?), Cognition (orientation, concentration), Insight	Identifies the specific symptom clusters (B–E) and rules out psychosis/delirium
Functional assessment	Occupational, social, self-care functioning	Required for Criterion G (impairment) in DSM-5
Risk assessment	Suicidality, self-harm, substance misuse, reckless behaviour, violence risk	PTSD is associated with increased suicide risk, substance misuse, and interpersonal violence

Screening questions can help identify or rule out diagnoses ^[1]. These instruments do NOT replace clinical assessment but help quantify severity and monitor treatment response.

Instrument	Type	Use	Key Features
PCL-5 (PTSD Checklist for DSM-5)	Self-report, 20 items	Screening and severity monitoring for PTSD	Maps directly to DSM-5 criteria; score 0–80; provisional cutoff ~31–33; each item corresponds to a DSM-5 symptom
CAPS-5 (Clinician-Administered PTSD Scale)	Clinician-rated, structured interview	Gold standard for PTSD diagnosis and severity	Assesses each DSM-5 symptom for frequency AND intensity on 0–4 scale; yields diagnosis (yes/no) and severity score
IES-R (Impact of Event Scale – Revised)	Self-report, 22 items	Screening; measures intrusion, avoidance, hyperarousal	Widely used in research; cutoff ~33 for probable PTSD
PHQ-9	Self-report, 9 items	Screen for comorbid depression	Score 0–27; ≥10 suggests moderate depression; important given depression is a major PTSD comorbidity ^[1]
GAD-7	Self-report, 7 items	Screen for comorbid anxiety	Score 0–21; ≥10 suggests moderate anxiety
AUDIT / CAGE	Self-report	Screen for comorbid alcohol use disorder	Critical given substance use disorders are common PTSD comorbidities ^[1]
Dissociative Experiences Scale (DES)	Self-report, 28 items	Screen for dissociative symptoms	Useful for identifying the dissociative subtype of PTSD
Columbia Suicide Severity Rating Scale (C-SSRS)	Clinician or self-report	Suicide risk screening	Should be used in all PTSD patients given elevated suicide risk

CAPS-5: The Gold Standard

The CAPS-5 is the gold standard diagnostic instrument for PTSD. It is a structured clinical interview (not a self-report) that assesses each of the 20 DSM-5 PTSD symptoms for both frequency and intensity. It provides both a categorical diagnosis (PTSD present/absent) and a continuous severity score. If you see "CAPS" in an exam question, it refers to this instrument.

These are NOT diagnostic of PTSD — they are to exclude medical conditions that can present with anxiety, mood, arousal, or dissociative symptoms ^[2].

Investigation	What It Excludes	Key Findings to Look For
CBP (Complete Blood Panel)	Anaemia (fatigue, poor concentration), infection	Low Hb → fatigue/concentration problems mimicking PTSD Cluster E
Renal Function Tests / LFTs	Metabolic derangement, hepatic encephalopathy	Elevated creatinine/urea → uraemic encephalopathy causing confusion; deranged LFTs → alcoholic liver disease suggesting comorbid substance use
Thyroid Function Tests	Thyrotoxicosis (anxiety, irritability, tachycardia, tremor, insomnia)	Suppressed TSH, elevated free T4/T3 → hyperthyroidism mimicking hyperarousal symptoms. This is one of the most important organic mimics to exclude ^[2]^[4]
Blood Glucose	Hypoglycaemia (anxiety, tremor, diaphoresis, confusion)	Low BGL → catecholamine-mediated symptoms mimicking panic/anxiety
Blood alcohol level	Alcohol intoxication or withdrawal	Elevated BAL → acute intoxication; withdrawing patient may mimic hyperarousal ^[2]^[4]
Blood and urine toxicology screen	Substance intoxication/withdrawal (stimulants, cannabis, opioids)	Positive UDS for stimulants (amphetamines, cocaine) → sympathomimetic state mimicking hyperarousal; positive for cannabis → anxiety/paranoia ^[2]^[4]
Calcium / Parathyroid	Hyperparathyroidism (anxiety, depression, cognitive impairment)	Elevated Ca²⁺ → neuropsychiatric symptoms
Cortisol / ACTH stimulation	Cushing's disease or Addison's disease	Elevated cortisol → Cushing's (anxiety, depression). Note: PTSD itself has LOW cortisol — if cortisol is high, consider Cushing's as the primary diagnosis

Relevant Lecture Slide Point

From mood disorders lecture ^[4]: Assessment should include physical examination and investigation to rule out medical conditions that may cause depressive symptoms. Basic: CBP, R/LFT, thyroid function test. Others: blood alcohol level, blood and urine toxicology screen, HIV test, cosyntropin (ACTH) stimulation test (for Addison disease), EEG (for epilepsy) or CT or MRI (for organic brain syndrome or hypopituitarism) should be considered if indicated by history taking and physical examination. This applies equally to stress-related disorders.

Neuroimaging is NOT part of routine diagnostic workup for stress-related disorders. It is indicated only when:

Clinical features suggest TBI (post-accident, focal neurology, persistent confusion)
There is suspicion of intracranial pathology (tumour, stroke)
Research settings

Modality	When Indicated	Findings in PTSD (Research, Not Diagnostic)
CT Brain	Acute TBI assessment; ruling out structural lesion	Normal in PTSD; may show contusion/haemorrhage in TBI
MRI Brain	Suspected TBI with normal CT; suspected tumour/MS	Research: ↓hippocampal volume, ↓ACC volume, ↓left amygdala volume ^[2]. Clinically: used to exclude TBI, tumour
EEG	Suspected epilepsy (especially temporal lobe epilepsy)	Normal in PTSD; epileptiform discharges in TLE
fMRI (research only)	Not clinical use	Amygdala hyperactivation, PFC hypoactivation, altered connectivity

Investigation	Indication
ECG	If cardiac symptoms (palpitations, chest pain) — rule out arrhythmia, MI
24-hour urinary catecholamines/metanephrines	If episodic hypertension + anxiety → phaeochromocytoma
HIV test	If risk factors present — HIV-associated neurocognitive disorder can mimic psychiatric symptoms ^[4]
Sleep study (polysomnography)	If prominent sleep disturbance unresponsive to treatment — to exclude obstructive sleep apnoea or other primary sleep disorders

Principle	Application
Hierarchy of diagnosis ^[2]	Organic > Substance > Psychotic > Mood > Anxiety/Stress > Personality
Temporal relationship	Stressor must precede symptoms; specific time criteria for each disorder
Symptom specificity	PTSD requires trauma-specific symptoms (re-experiencing, avoidance); adjustment disorder has non-specific symptoms
Residual category ^[2]	Adjustment disorder only diagnosed when criteria for more specific disorders are NOT met
Duration	ASR: hours–days; ASD: 3 days–1 month; PTSD: > 1 month; Adjustment: onset ≤3 months, resolves ≤6 months after stressor
Functional impairment	Required for DSM-5 diagnosis of all three conditions
Comorbidity screening ^[1]	Actively screen for depression, other anxiety disorders, substance use, somatization, dissociative disorders
Screening questions can help identify or rule out diagnoses ^[1]	Use standardised instruments (PCL-5, CAPS-5, PHQ-9, AUDIT) to supplement clinical assessment

High Yield Summary

PTSD DSM-5 minimum counts: Criterion B ≥1 intrusion + C ≥1 avoidance + D ≥2 cognition/mood + E ≥2 arousal → "1-1-2-2" mnemonic. Plus: > 1 month duration, impairment, not substance/medical
ASD DSM-5: ≥9 symptoms from 5 categories (intrusion, negative mood, dissociation, avoidance, arousal) ^[1], duration 3 days–1 month
PTSD specifiers: with dissociative symptoms (derealisation/depersonalisation) and with delayed expression (criteria not met until > 6 months) ^[1]
Adjustment disorder = onset ≤3 months of stressor, distress out of proportion OR functional impairment, does NOT meet criteria for another disorder, NOT normal bereavement ^[2]
Adjustment disorder is a residual category — never diagnose it if MDD/GAD/PTSD criteria are met ^[2]
ICD-10 ASR = normal response (hours–days); DSM-5 ASD = abnormal response (3 days–4 weeks) that may predict PTSD
CAPS-5 is the gold standard diagnostic tool for PTSD
Investigations are to exclude organic mimics, NOT to diagnose PTSD: TFTs, BGL, UDS, CBP, LFT are the key baseline bloods ^[2]^[4]
Screening questions can help identify or rule out diagnoses ^[1] — use PCL-5, PHQ-9, GAD-7, AUDIT in clinical practice

Active Recall - Diagnostic Criteria, Algorithm, and Investigations for Stress-Related Disorders

Treatment Modalities by Disorder

This is the normal acute response. Your job is NOT to pathologise it but to support the person through it.

Intervention	Detail	Rationale
Ensure safety	Remove from danger, provide safe environment	Basic human need; sympathetic activation cannot subside while threat persists
Psychoeducation	Explain that the reaction is normal, expected, and self-limiting	Reduces secondary anxiety ("Am I going mad?"); normalisation prevents catastrophising about own symptoms
Social support mobilisation	Involve family, friends, community resources	Social support is the strongest modifiable protective factor against progression to PTSD
Practical support	Address immediate needs (food, shelter, communication)	Reduces ongoing stressor load; allows physiological recovery
Watchful waiting	Monitor; most resolve within hours to days	Premature intervention (e.g., forced debriefing) may be iatrogenic

Do NOT Force Debriefing

Critical Incident Stress Debriefing (CISD): although widely used, has NOT shown to be helpful in reducing psychological distress ^[2]. In fact, some evidence suggests it may be harmful by re-exposing people to trauma narratives before they are psychologically ready. Current guidelines recommend psychological first aid (practical support, safety, normalisation) rather than mandatory debriefing.

2. Acute Stress Disorder — Management

Pharmacotherapy: generally not considered helpful ^[2] for ASD. The mainstay is psychotherapy.

Trauma-focused CBT is the gold standard for ASD. It has three components, each targeting a specific pathophysiological mechanism:

Component	What It Involves	Mechanism / Why It Works
Psychoeducation ^[2]	Patients are educated on stressful reactions and their cognitive underpinnings	Normalises the experience; reduces secondary distress about symptoms; improves engagement with treatment by providing a coherent framework for understanding what is happening
Cognitive restructuring ^[2]	Address maladaptive or unrealistic appraisals by patient towards trauma, their response to the event, and fears of potential future harm	Targets Cluster D (negative cognitions): the distorted beliefs like "It was all my fault" or "Nowhere is safe" are identified, challenged, and replaced with balanced cognitions. This is based on cognitive theory — these appraisals maintain the fear response
Exposure therapy ^[2]	Assist patient in confronting feared memories and situations; allow emotional processing of emotional response following exposure to related cues	Targets Clusters B and C (intrusion and avoidance): by systematically exposing the patient to trauma-related cues in a safe, controlled setting, the conditioned fear response undergoes extinction (classical conditioning principle). The key: avoidance is negatively reinforced and prevents extinction. Exposure breaks this cycle

Intervention	Status	Evidence
Critical Incident Stress Debriefing (CISD) ^[2]	NOT recommended	Although widely used, has NOT shown to be helpful in reducing psychological distress ^[2]. May be harmful — a single session of forced narrative reconstruction does not allow proper processing and may retraumatise
Pharmacotherapy ^[2]	Generally not considered helpful for ASD	Early benzodiazepine use may interfere with fear extinction and is associated with worse PTSD outcomes; early SSRI/SNRI use has not shown clear benefit for ASD specifically

Why Debriefing Doesn't Work (and Exposure Does)

Both involve talking about the trauma. The difference is how. CISD is a single, often mandatory session shortly after the event — the person may not be ready, and a single exposure is insufficient for extinction. Trauma-focused CBT uses graduated, repeated, controlled exposure over multiple sessions (typically 5–12), allowing systematic habituation and cognitive reprocessing. Extinction requires repeated, prolonged exposure until the fear response subsides — a single brief session actually reinforces the conditioned fear.

3. Post-Traumatic Stress Disorder — Management

PTSD management is the most comprehensive and commonly tested. The approach is multimodal.

A. Psychotherapy (First-Line)

Trauma-focused CBT: usually considered 1st line ^[2]

This is the same three-component model as for ASD (psychoeducation + cognitive restructuring + exposure therapy), but delivered over a longer course (typically 8–16 sessions) because the symptoms are more entrenched.

Component	Application to PTSD	Mechanism
Psychoeducation	Understanding the nature of PTSD, normalising symptoms, building a therapeutic alliance	Reduces shame and self-blame; improves treatment adherence
Cognitive restructuring	Challenging distorted trauma-related appraisals ("It was my fault," "The world is completely dangerous")	Targets Cluster D — persistent negative cognitions. Based on Beck's cognitive model: identify automatic negative thoughts → examine evidence → develop balanced alternative thoughts
Exposure therapy	Imaginal exposure (narrating the trauma in detail) + in vivo exposure (gradually confronting avoided real-world situations/places)	Targets Clusters B and C. Prolonged, repeated exposure in a safe setting allows extinction of the conditioned fear response. The patient learns that the trauma-related cues are not dangerous in the present moment. Habituation occurs within and between sessions

Why does CBT work in PTSD? From first principles:

PTSD is maintained by two key mechanisms: (1) unprocessed trauma memories (stored by amygdala without hippocampal contextualisation) and (2) avoidance (prevents extinction)
CBT directly targets both: exposure forces processing of the trauma memory and breaks avoidance; cognitive restructuring corrects the distorted meaning attached to the event
The hippocampus "re-stamps" the memory with context ("this happened then, I am safe now"), integrating it into the normal autobiographical memory system

EMDR is the other well-established first-line psychotherapy for PTSD.

Aspect	Detail
Procedure	Patient imagines a scene from the trauma, focusing on accompanying cognition and arousal, while the therapist moves two fingers across the patient's visual field and instructs the patient to track the fingers ^[2]
Sequence	Sequence repeated until anxiety decreases, with patient instructed to generate a more adaptive thought ^[2]
Mechanism	Not fully understood. Hypotheses: (a) bilateral eye movements tax working memory → the trauma memory becomes less vivid and emotional when recalled; (b) bilateral stimulation mimics REM sleep processing → facilitates memory consolidation and integration; (c) the dual-attention task (tracking + remembering) forces "adaptive information processing"
Efficacy	Most studies show that it is efficacious in PTSD, superior to other less specific psychotherapy ^[2]
Sessions	Typically 6–12 sessions
Advantages	Does not require detailed verbal narration of the trauma (useful for patients who cannot tolerate prolonged exposure); structured protocol

Other psychotherapy: coping skills training, stress management, hypnotherapy, interpersonal therapy, mindfulness-based stress reduction, psychodynamic ^[2]

Psychotherapy	Role in PTSD
Coping skills training	Teaches practical strategies for managing arousal, distress tolerance, and interpersonal difficulties. Not directly trauma-processing but improves daily functioning
Stress management / relaxation training	Progressive muscle relaxation, controlled breathing — targets autonomic hyperarousal. Adjunctive rather than standalone
Mindfulness-based therapy ^[1]	Developing non-judgemental awareness of present-moment experience; reduces avoidance and emotional reactivity. Growing evidence base as adjunct
Interpersonal therapy	Addresses interpersonal difficulties arising from PTSD (estrangement, relationship conflict). Useful when social functioning is a primary concern
Psychodynamic therapy	Explores unconscious meanings attached to trauma and how early life experiences shape vulnerability. Longer-term; less evidence base than CBT/EMDR

B. Pharmacotherapy (Second-Line or Augmentation)

Pharmacotherapy: usually as augmentation or 2nd line to psychotherapy ^[2]

The key principle: drugs do NOT cure PTSD — they manage symptoms (particularly hyperarousal, mood, and sleep) to enable the patient to engage in psychotherapy. Think of pharmacotherapy as the scaffolding, and psychotherapy as the actual construction.

Antidepressants: SSRIs, SNRIs → hyperarousal, mood ^[2]

Drug Class	Examples	Mechanism	Target Symptoms	Evidence	Notes
SSRIs ^[1]^[2]^[3]	Sertraline, paroxetine (both FDA-approved for PTSD), fluoxetine, citalopram	Block serotonin reuptake transporter (SERT) → ↑synaptic 5-HT → modulates amygdala reactivity, improves prefrontal regulation, normalises HPA axis	All 4 PTSD clusters: intrusion, avoidance, mood/cognition, arousal	Strongest evidence; first-line pharmacotherapy internationally	Start low, go slow (initial ↑anxiety in first 1–2 weeks). Continue ≥12 months after response. Sertraline and paroxetine are the only FDA-approved medications for PTSD
SNRIs ^[2]^[3]	Venlafaxine	Blocks both SERT and noradrenaline reuptake transporter (NRT) → ↑5-HT and NA	All 4 clusters; may have additional benefit for fatigue, concentration (via NA)	Good evidence; recommended by NICE as first-line alongside SSRIs	Monitor BP (NA-mediated hypertension at higher doses)

Why SSRIs work in PTSD — from first principles:

Serotonin (5-HT) modulates the amygdala's threat response. Low serotonergic tone → amygdala is "uninhibited" → exaggerated fear, irritability, impulsivity
↑synaptic 5-HT → ↑serotonergic inhibition of amygdala → ↓re-experiencing, ↓hyperarousal
5-HT also modulates prefrontal cortex function → improved cognitive reappraisal and emotional regulation
Additionally, SSRIs promote neuroplasticity (↑BDNF) → may help restore hippocampal volume lost in chronic PTSD

Drug Class	Examples	Mechanism	Target Symptoms	Indications / Notes
Second-generation antipsychotics (SGAs) ^[2]	Quetiapine, risperidone, olanzapine, aripiprazole	D₂ and 5-HT₂A antagonism; quetiapine also has antihistaminic (sedation) and α₁-blocking effects	Treatment-resistant PTSD, particularly hyperarousal, paranoia, sleep disturbance	As monotherapy or augmentation of antidepressants ^[2]. Used when PTSD has prominent anger, paranoia, or psychotic features. Watch for metabolic syndrome
α-blockers ^[2]	Prazosin	α₁-adrenergic receptor antagonist → blocks noradrenaline-mediated activation in the CNS, particularly during sleep	Can ↓PTSD symptoms, nightmares, sleep disturbance ^[2]	Specifically targets trauma-related nightmares and sleep disruption. The rationale: nightmares in PTSD are driven by elevated noradrenergic tone during sleep; blocking α₁ receptors reduces this. Start low (1 mg nocte), titrate slowly. Monitor for orthostatic hypotension
Benzodiazepines (BDZs) ^[1]^[2]^[3]	Diazepam, clonazepam, lorazepam	Positive allosteric modulator of GABA-A receptor → ↑inhibitory neurotransmission → anxiolysis, sedation, muscle relaxation	May be useful in treatment of anxiety and hyperarousal symptoms ^[2]	Use with extreme caution in PTSD: (a) may interfere with fear extinction (GABA-A enhancement blocks the learning required for exposure therapy); (b) high dependence/abuse potential especially in a population prone to substance use; (c) evidence does NOT support routine use in PTSD. Use only short-term, specific indications
TCAs ^[3]	Amitriptyline, imipramine	Block SERT + NRT + muscarinic/histaminic/α₁ receptors	Mood, sleep, hyperarousal	Third-line due to side effect burden (anticholinergic, cardiac, sedation). Lethal in overdose — avoid in suicidal patients
MAOIs ^[3]	Phenelzine	Inhibit monoamine oxidase → ↑5-HT, NA, DA	Mood, hyperarousal	Rarely used due to dietary restrictions (tyramine crisis) and drug interactions. Reserved for refractory cases
Beta-adrenergic antagonists ^[3]	Propranolol	β-receptor blockade → ↓peripheral and some central adrenergic effects (tachycardia, tremor)	Performance anxiety, autonomic arousal	Propranolol ^[3] has been studied for secondary prevention of PTSD (given shortly after trauma to block consolidation of fear memories). Results are mixed. Not standard treatment for established PTSD. Contraindicated in asthma
Buspirone ^[3]	—	5-HT₁A partial agonist → anxiolytic without sedation or dependence	Chronic anxiety, augmentation	Slow onset (2–4 weeks); no abuse potential; limited evidence specifically for PTSD
Pregabalin ^[3]	—	Binds α₂δ subunit of voltage-gated calcium channels → ↓excitatory neurotransmitter release	Anxiety, hyperarousal, sleep	Some evidence for GAD; limited but growing evidence for PTSD. May help with comorbid pain
Mood stabilisers ^[1]	Valproate, lamotrigine	Various — valproate ↑GABA; lamotrigine blocks voltage-gated Na⁺ channels	Irritability, emotional dysregulation, impulsivity	Mood stabilizers ^[1] mentioned as a treatment approach. Used off-label for PTSD with prominent affective instability or comorbid bipolar features

Benzodiazepines in PTSD: A Double-Edged Sword

BDZs may seem logical for PTSD hyperarousal, but they are NOT recommended as first-line or routine treatment. Three reasons: (1) They enhance GABA-A → this blocks the new learning required for fear extinction during psychotherapy; (2) PTSD patients have high rates of substance use disorders → BDZs have high abuse/dependence potential; (3) They do NOT treat the core pathology (unprocessed trauma memories, conditioned fear). Use only briefly for acute crisis management, not as ongoing therapy ^[2].

Treat comorbid conditions, e.g., alcohol/substance use disorders, sleep disorders, psychosis ^[2]

This is critical because comorbidities are the rule in PTSD, not the exception:

Comorbidity	Management Approach
Depression	SSRIs address both PTSD and comorbid depression simultaneously; add psychotherapy targeting depressive cognitions
Substance use disorders	Must be addressed concurrently — "stabilise-then-process" model. Motivational interviewing, relapse prevention, consider naltrexone/acamprosate for alcohol dependence. Avoid BDZs
Sleep disorders	Sleep hygiene education; prazosin for nightmares; consider trazodone (low-dose) for insomnia; avoid long-term BDZ hypnotics
Psychosis	SGA (e.g., risperidone, quetiapine) for PTSD with psychotic features or comorbid psychotic disorder
Chronic pain	Common comorbidity; SNRIs (duloxetine, venlafaxine) address both PTSD and neuropathic pain; avoid opioids (abuse risk)

Adjustment disorder is generally self-limiting and requires less intensive treatment than PTSD.

Management ^[2]:

Intervention	Detail	Mechanism / Rationale
Problem-solving counselling ^[2]	Encouraging patient to seek solutions to stressful problems, and to consider advantages and disadvantages of various kinds of actions ^[2]	Targets the core issue: the patient feels overwhelmed by the stressor. Problem-solving therapy empowers them to regain a sense of control by systematically breaking down the problem, generating options, evaluating consequences, and implementing solutions
Other psychotherapy ^[2]	Psychodynamics, supportive ^[2]	Supportive therapy provides empathic listening, validation, and reinforcement of healthy coping. Psychodynamic therapy explores how early relational patterns may be shaping the patient's response to the current stressor
Psychoeducation	Explain the nature of the adjustment process; normalise distress; provide realistic expectations	Reduces secondary anxiety about symptoms; frames the experience as time-limited and manageable
Pharmacotherapy ^[2]	Anxiolytics/hypnotics may be helpful for a few days ^[2]	Short-term symptomatic relief of insomnia or acute anxiety. Must NOT become long-term. BDZ use should be limited to a few days — the condition is self-limiting and long-term medication use is inappropriate

Adjustment Disorder: Less Is More

Unlike PTSD, adjustment disorder typically does NOT require intensive trauma-focused therapy or long-term medication. The stressor is not traumatic, and the symptoms are subthreshold. The prognosis is usually good ^[2], but be aware that adjustment disorder may herald future development of anxiety/depression ^[2]. Monitor the patient and reclassify if symptoms persist beyond 6 months of stressor resolution.

	Acute Stress Reaction	Acute Stress Disorder	PTSD	Adjustment Disorder
First-line	Supportive care, safety, psychoeducation	Trauma-focused CBT ^[2]	Trauma-focused CBT or EMDR ^[2]	Problem-solving counselling ^[2]
Second-line	Usually none needed	—	SSRIs (sertraline, paroxetine) or SNRIs (venlafaxine) ^[2]^[3]	Other psychotherapy (supportive, psychodynamic) ^[2]
Augmentation	—	—	SGAs, prazosin, BDZs (short-term) ^[2]	Anxiolytics/hypnotics (few days only) ^[2]
NOT recommended	CISD	CISD; pharmacotherapy generally not helpful ^[2]	Long-term BDZs as monotherapy	Long-term medication
Duration of Rx	Days	Weeks	≥12 months pharmacotherapy; psychotherapy 8–16+ sessions	Weeks to few months
Comorbidity Mx	—	Monitor for PTSD	Treat comorbid substance use, depression, sleep disorders, psychosis ^[2]	Monitor for MDD/GAD development

Treatment	Contraindications / Cautions
CISD	NOT evidence-based; may worsen outcomes; avoid mandatory debriefing
BDZs	Avoid in PTSD patients with substance use disorders (high abuse potential); may block fear extinction and impair psychotherapy effectiveness; risk of dependence
TCAs	Avoid in suicidal patients (lethal in overdose due to cardiotoxicity — QT prolongation, Na⁺ channel blockade); anticholinergic effects problematic in elderly
MAOIs	Dietary restrictions (tyramine — risk of hypertensive crisis); extensive drug interactions (serotonin syndrome with SSRIs, sympathomimetics); avoid in non-adherent patients
Propranolol	Contraindicated in asthma (β₂ blockade → bronchospasm), heart block, severe peripheral vascular disease
SSRIs	Caution in first 2 weeks (initial ↑anxiety, ↑suicidality in young adults — black box warning); serotonin syndrome risk with MAOIs; GI side effects, sexual dysfunction
SGAs	Metabolic syndrome (weight gain, dyslipidaemia, hyperglycaemia — especially olanzapine); QT prolongation (especially quetiapine); extrapyramidal symptoms (especially risperidone at higher doses)
Prazosin	Orthostatic hypotension (start 1 mg nocte, titrate slowly); dizziness; avoid in patients already on multiple antihypertensives

Consider referral to secondary care if ^[2]:

Risk of self-harm or suicide
Marked self-neglect
Non-response to at least two treatments (stepped care principle)
Significant comorbidity (e.g., substance use, physical health problems)
Complex PTSD (prolonged, repeated trauma — e.g., childhood abuse, human trafficking)
Diagnostic uncertainty

High Yield Summary

There are many effective treatments including psychotherapy and psychopharmacology ^[1]
Trauma-focused CBT is first-line for both ASD and PTSD ^[2] — components: psychoeducation, cognitive restructuring, exposure therapy
EMDR is an equally effective first-line psychotherapy for PTSD ^[2] — most studies show it is efficacious, superior to other less specific psychotherapy
CISD has NOT shown to be helpful in reducing psychological distress ^[2] — do NOT use mandatory debriefing
Pharmacotherapy for ASD is generally not considered helpful ^[2]
Pharmacotherapy for PTSD is usually augmentation or second-line to psychotherapy ^[2]: SSRIs (sertraline, paroxetine) are first-line drugs
Prazosin (α₁-blocker) can reduce PTSD symptoms, nightmares, sleep disturbance ^[2]
SGAs can be used as monotherapy or augmentation ^[2] for treatment-resistant PTSD
BDZs: may be useful for anxiety and hyperarousal but use with extreme caution ^[2] — risk of dependence, may block fear extinction
Adjustment disorder management: problem-solving counselling first-line; anxiolytics/hypnotics may be helpful for a few days only ^[2]
Treat comorbid conditions ^[2]: substance use, depression, sleep disorders, psychosis
General treatment approaches for anxiety-spectrum disorders ^[1]^[3]: antidepressants, anxiolytics, antipsychotics, mood stabilisers; CBT, mindfulness-based therapy

Active Recall - Management of Stress-Related Disorders

1. Psychiatric Comorbidities

There are significant comorbid psychiatric conditions associated with anxiety disorders ^[1].

Co-morbidities of PTSD ^[1]:

Depression
Other anxiety disorders
Substance use disorders
Somatization
Dissociative disorders

These are not merely "associated conditions." They are mechanistically linked complications that develop as consequences of the chronic pathophysiology of PTSD.

Aspect	Detail
Prevalence	Up to 50% of PTSD patients develop comorbid major depressive disorder; this is the single most common comorbidity
Mechanism	Chronic HPA axis dysregulation + serotonin depletion + learned helplessness (repeated exposure to uncontrollable threat → belief that one cannot influence outcomes) + social withdrawal and anhedonia from Cluster D (negative cognitions/mood) → progressive depressive syndrome. The Cluster D symptoms of PTSD (guilt, shame, diminished interest, emotional numbing, inability to experience positive emotions) are essentially depressive symptoms embedded within the PTSD framework
Why it matters	Comorbid depression dramatically worsens PTSD prognosis: ↑chronicity, ↑functional impairment, ↑treatment resistance, and critically, ↑suicide risk. The combination is more than additive
Clinical implication	Always screen PTSD patients with PHQ-9. SSRIs treat both conditions simultaneously, which is why they are first-line pharmacotherapy for PTSD

Disorder	How It Develops	Pathophysiology
GAD	The hypervigilance and threat-scanning of PTSD generalises beyond trauma-related cues → free-floating, pervasive worry about multiple life domains	Amygdala sensitisation → lowered threshold for threat detection → chronic "worry mode" that extends beyond the original trauma context
Panic disorder	Trauma-related autonomic arousal (tachycardia, diaphoresis, chest tightness) becomes misinterpreted as catastrophic → "Am I dying?" → panic attacks	Catastrophic misinterpretation of trauma-induced somatic symptoms; conditioned autonomic responses to internal cues
Agoraphobia / specific phobias	Avoidance behaviours in PTSD generalise → patient avoids not only trauma-specific cues but increasingly wider situations → functional constriction	Operant conditioning: avoidance is negatively reinforced → avoidance repertoire expands progressively
Social anxiety	Estrangement, shame, guilt from PTSD Cluster D → social withdrawal → fear of scrutiny and judgement → social avoidance	Trauma-related shame ("I should have done something") → belief that others will judge negatively → avoidance of social situations

Aspect	Detail
Prevalence	25–50% of PTSD patients develop comorbid substance use disorders; alcohol is the most common, followed by cannabis, opioids, and benzodiazepines
Mechanism — Self-medication hypothesis	Patients use substances to dampen hyperarousal (alcohol, BDZs), numb emotional pain (opioids), or cope with insomnia (alcohol, cannabis). The short-term relief negatively reinforces substance use → dependence
Neurobiological basis	Chronic stress → dysregulation of the reward circuitry (ventral tegmental area → nucleus accumbens). The depleted dopaminergic tone in PTSD creates a state of anhedonia that substances temporarily relieve. Additionally, ↑CRF in PTSD drives stress-induced relapse
Alcohol-induced anxiety disorder ^[5]	Symptoms occur while patient on heavy alcohol consumption; symptoms subside gradually on abstinence, but may persist up to 6 months. Must be distinguished from alcohol withdrawal syndrome ^[5]. This creates a diagnostic challenge: is the anxiety from PTSD driving the drinking, or is the alcohol causing the anxiety?
Alcohol comorbid psychiatric disorders ^[5]	Alcohol can temporarily reduce symptoms of anxiety, depression, and insomnia but causes increased psychotic symptoms and mood swings, disruptive behaviour, suicide, treatment non-compliance, drug abuse, poor clinical outcome ^[5]
Why it matters	Substance use worsens every aspect of PTSD: ↓treatment engagement, ↓medication adherence, ↑impulsivity and violence, ↑suicide risk, ↑medical morbidity. It also interferes with psychotherapy (impaired memory consolidation prevents trauma processing)

The Vicious Cycle of PTSD and Substance Use

PTSD → hyperarousal/nightmares/emotional pain → self-medication with alcohol/substances → temporary relief (negative reinforcement) → tolerance and dependence → withdrawal symptoms mimic/worsen PTSD (tremor, anxiety, insomnia, irritability) → ↑PTSD symptoms → ↑substance use. Breaking this cycle requires treating BOTH conditions simultaneously, not sequentially.

Aspect	Detail
Mechanism	Chronic autonomic hyperarousal manifests as somatic symptoms (palpitations, chest pain, headaches, GI disturbance, musculoskeletal pain). When patients lack the psychological vocabulary to express distress (alexithymia), or when cultural norms discourage emotional expression, distress is channelled into bodily complaints
Clinical presentation	Chronic pain syndromes (headache, back pain, fibromyalgia), functional GI disorders (IBS), chronic fatigue, medically unexplained dizziness. These patients often present to medical rather than psychiatric services
Hong Kong context	Somatisation is particularly common in Chinese populations, where mental health stigma may lead to presentation with physical rather than emotional symptoms. Chronic pain and fatigue are common "somatic masks" of underlying PTSD
Complication risk	Unnecessary invasive investigations and procedures with iatrogenic complications; substance use (narcotic analgesics, benzodiazepines prescribed for somatic complaints) ^[2]

Aspect	Detail
Mechanism	Dissociation begins as a peri-traumatic protective mechanism (the brain "disconnects" from overwhelming reality via endogenous opioid release and prefrontal-limbic disconnection). In some patients, this becomes a habitual, maladaptive coping strategy that persists long after the trauma
Presentations	Depersonalisation (feeling detached from own body), derealisation (feeling the world is unreal), dissociative amnesia (gaps in memory), dissociative identity disorder (in severe chronic childhood trauma)
DSM-5 recognition	The dissociative subtype of PTSD (with dissociative symptoms — derealisation or depersonalisation) ^[1] acknowledges that dissociation is a core complication in a substantial subset of PTSD patients
Clinical significance	Dissociative patients may appear "calm" or "emotionally flat" during assessment, masking severe underlying distress. They may respond differently to treatment — some evidence suggests the dissociative subtype may respond better to psychotherapy that addresses dissociation specifically before trauma processing

This is the most feared and most important complication.

Aspect	Detail
Risk magnitude	PTSD is associated with a 2–3-fold increase in suicide risk compared to the general population. When comorbid with depression and substance use, risk escalates dramatically
Mechanism	Multiple converging pathways: (a) Reckless or self-destructive behaviour ^[1] is a DSM-5 criterion — the disorder itself drives risk-taking; (b) Comorbid depression → hopelessness, suicidal ideation; (c) Substance intoxication → disinhibition; (d) Trauma-related guilt and shame → "I deserve to die"; (e) Chronic hyperarousal → emotional exhaustion → desire for escape; (f) Impaired impulse control from prefrontal hypofunction
Self-harm patterns	Non-suicidal self-injury (cutting, burning) may serve as an attempt to "feel something" in the context of emotional numbing (Cluster D) or to provide a sense of control over pain. Deliberate self-harm is also a feature of adjustment disorder — behavioural changes include deliberate self-harm, suicidal behaviour ^[2]
Clinical implication	Risk assessment is mandatory at every clinical encounter with stress-related disorder patients. Use structured tools (Columbia Suicide Severity Rating Scale). Assess for access to lethal means

Suicide Risk in PTSD

Never underestimate suicide risk in PTSD. The combination of PTSD + depression + substance use + access to firearms (particularly in veterans) represents one of the highest-risk profiles in all of psychiatry. Always ask directly about suicidal ideation, intent, plan, and access to means.

PTSD causes significant impairment in function ^[1]. The disability burden is enormous and affects every domain of life.

Domain	How PTSD Impairs Function	Mechanism
Occupational	Poor concentration → ↓work performance; hypervigilance → inability to focus; avoidance → missing work; irritability → interpersonal conflict with colleagues; substance use → unreliability	Attentional resources hijacked by threat-monitoring (Cluster E); avoidance of work environments if associated with trauma cues (Cluster C)
Social / Interpersonal	Emotional numbing → inability to connect; estrangement → social isolation; irritability/anger → relationship conflict and breakdown; trust impairment → difficulty forming new relationships	Cluster D (detachment, estrangement, inability to experience positive emotions) + Cluster E (irritability, angry outbursts). In interpersonal trauma, the fundamental sense of trust in other humans is shattered
Self-care	Neglect of hygiene, nutrition, medical appointments; reckless behaviour (driving, unsafe sex)	Depressive symptoms, anhedonia, self-destructive behaviour (Cluster E); dissociative episodes impairing awareness
Academic	In younger patients: ↓concentration, avoidance of school, behavioural disturbances	Cognitive resources consumed by intrusive memories and hypervigilance

Chronic PTSD is associated with significant medical morbidity. This is NOT coincidental — the sustained neurobiological perturbation has direct physiological consequences.

System	Complication	Mechanism
Cardiovascular	↑risk of hypertension, coronary artery disease, myocardial infarction, stroke; ↑CVS mortality ^[2]	Chronic sympathetic activation (↑noradrenaline) → sustained ↑HR, ↑BP, ↑vascular tone → accelerated atherosclerosis. Chronic inflammation (↑IL-6, CRP, TNF-α) → endothelial dysfunction
Metabolic	Obesity, metabolic syndrome, type 2 diabetes	Dysregulated HPA axis → altered cortisol pulsatility → visceral fat deposition; emotional eating as coping; reduced physical activity; medication-related weight gain (SGAs)
Immune	Chronic low-grade inflammation; impaired wound healing; ↑susceptibility to infections	Chronic stress → shift from Th1 to Th2 immune response (immunosuppression); ↑pro-inflammatory cytokines paradoxically coexist with impaired cellular immunity
Neurological	Cognitive decline, ↑risk of dementia in later life; chronic pain syndromes	Neurotoxic effects of sustained cortisol/NA on hippocampus → ↓hippocampal volume → memory impairment. Central sensitisation → chronic pain
Gastrointestinal	IBS, functional dyspepsia, peptic ulcer disease	Autonomic dysregulation of gut motility (brain-gut axis); stress-induced ↑gastric acid secretion; altered gut microbiome
Sleep	Chronic insomnia, nightmares, obstructive sleep apnoea (in obese patients)	Locus coeruleus hyperactivation → disrupted sleep architecture; ↑REM density; cortical hyperarousal preventing deep sleep. Insomnia follows the Spielman 3P model: predisposing vulnerability + precipitating trauma + perpetuating factors (maladaptive sleep habits, conditioned arousal in bed) ^[2]

PTSD Is Not Just a 'Mental' Illness

The cardiovascular mortality data should shift your thinking: PTSD kills people through heart disease, not just suicide. Chronic sympathetic overdrive and inflammation are as real and as damaging as the psychological symptoms. This is why comprehensive PTSD management must include cardiovascular risk factor screening and management.

Complication	Mechanism
Relationship breakdown / divorce	Emotional numbing → partner feels rejected; irritability/anger → domestic conflict; avoidance → inability to engage in family life; sexual dysfunction (↓libido from depression/SSRIs, or avoidance of intimacy if trauma was sexual)
Domestic violence	Irritable behaviour and angry outbursts ^[1] with little or no provocation → verbal or physical aggression towards family members. Impaired impulse control from prefrontal hypofunction
Intergenerational transmission	Children of PTSD parents are at increased risk of developing anxiety, behavioural problems, and PTSD themselves. Mechanisms: (a) disrupted attachment (emotionally unavailable parent); (b) modelling of avoidant/hypervigilant behaviour; (c) genetic vulnerability; (d) exposure to parental substance use and domestic violence
Social isolation	Progressive avoidance → shrinking social world → loneliness → worsened depression → further withdrawal. The social isolation itself becomes a perpetuating factor that maintains the disorder

Adjustment disorder is generally milder but carries its own complications ^[2]:

Complication	Detail
Progression to MDD or GAD	Prognosis is usually good, but may herald future development of anxiety/depression ^[2]. Adjustment disorder may be a prodrome or early manifestation of a more serious psychiatric condition
Deliberate self-harm and suicidal behaviour	Behavioural changes in adjustment disorder include deliberate self-harm, suicidal behaviour ^[2]. This is frequently underestimated — adjustment disorder is the most common diagnosis in suicide attempters presenting to emergency departments
Substance misuse	Misuse of alcohol or drugs ^[2] as a maladaptive coping strategy
Occupational and academic impairment	Inability to cope with the precipitating stressor (e.g., job change, relationship breakdown) → cascading dysfunction

Don't Dismiss Adjustment Disorder

Despite being considered a "milder" condition, adjustment disorder accounts for a disproportionate number of suicide attempts. In some studies, it is the most common psychiatric diagnosis associated with deliberate self-harm. Always assess suicide risk even in adjustment disorder.

Complication	Source	Mechanism
Medication side effects	SSRIs: sexual dysfunction, GI symptoms, initial anxiety worsening, serotonin syndrome if combined with MAOIs. SGAs: metabolic syndrome (weight gain, dyslipidaemia, hyperglycaemia). TCAs: anticholinergic effects, cardiac toxicity in overdose. Prazosin: orthostatic hypotension	Direct pharmacological effects of medications used to treat PTSD
Benzodiazepine dependence	BDZs prescribed for PTSD anxiety/insomnia → tolerance → dose escalation → dependence → withdrawal symptoms mimic PTSD (anxiety, tremor, insomnia)	GABA-A receptor downregulation with chronic use; negative reinforcement maintains use
Unnecessary investigations	Somatisation leads to repeated medical consultations → over-investigation → false positives → invasive procedures → iatrogenic harm	Patients present with somatic symptoms; clinicians pursue organic workup repeatedly without recognising the underlying stress-related disorder
Retraumatisation in therapy	Poorly conducted exposure therapy or premature trauma processing → worsening of symptoms, dropout	If exposure is too intense, too fast, or without adequate preparation and safety, it can overwhelm rather than help. This is why trauma-focused CBT requires trained therapists

Disorder	Natural History	Key Prognostic Factors
Acute Stress Reaction	Self-limiting within hours to days	Universal recovery expected
Acute Stress Disorder	~40–80% develop subsequent PTSD ^[2]	Severity of acute symptoms, dissociation, peritraumatic arousal
PTSD	~50% remit within 3 months; ~40% run a chronic course ^[2]	Good prognosis: early treatment, strong social support, single discrete trauma, no comorbidities. Poor prognosis: chronic/repeated trauma, comorbid depression/substance use, personality disorder, avoidant coping, ongoing stressors
Adjustment Disorder	Most will last for a few months after stressor is removed; prognosis is usually good ^[2]	May herald future development of anxiety/depression ^[2]. Worse if personality vulnerability, ongoing stressor, comorbid substance use

High Yield Summary

PTSD comorbidities: Depression, other anxiety disorders, substance use disorders, somatization, dissociative disorders ^[1]
There are significant comorbid psychiatric conditions associated with anxiety disorders ^[1] — comorbidity is the rule, not the exception
PTSD is associated with 2–3× increased suicide risk; always assess suicidality; reckless or self-destructive behaviour is a DSM-5 criterion ^[1]
Self-medication hypothesis: patients use alcohol/substances to dampen hyperarousal → dependence → worsened PTSD (vicious cycle)
Alcohol temporarily reduces symptoms of anxiety, depression, insomnia but causes increased psychotic symptoms, mood swings, disruptive behaviour, suicide, treatment non-compliance, poor clinical outcome ^[5]
Physical health: chronic sympathetic activation → ↑cardiovascular mortality, metabolic syndrome, chronic pain, immune dysregulation, cognitive decline
Interpersonal: emotional numbing + irritability → relationship breakdown, domestic violence, intergenerational transmission to children
Adjustment disorder complications: often underestimated; may herald future development of anxiety/depression ^[2]; significant association with deliberate self-harm and suicide attempts
Iatrogenic risks: BDZ dependence, medication side effects, unnecessary investigations from somatisation, retraumatisation from poorly conducted therapy
ASD: 40–80% develop subsequent PTSD; PTSD: ~50% remit within 3 months but ~40% chronic course ^[2]

Active Recall - Complications of Stress-Related Disorders

High Yield Summary

Stress-related disorders include Acute Stress Reaction, Acute Stress Disorder, PTSD, and Adjustment Disorder ^[1]
The stress-vulnerability model explains individual susceptibility: disorder occurs when stress overwhelms vulnerability threshold ^[2]
Traumatic stress occurs outside range of normal human experience → ASD/PTSD. Psychosocial stress is subjective → adjustment disorder ^[2]
Time course is critical: ASD = 3 days–4 weeks; PTSD = > 1 month; Adjustment disorder = ≤3 months of stressor, resolves within 6 months
PTSD neurobiology: ↑amygdala, ↓hippocampus, ↓PFC, ↑NA, ↑CRH, ↓cortisol ^[1]^[2]
PTSD has LOW cortisol (unlike depression) due to upregulated glucocorticoid receptors and enhanced negative feedback ^[2]
Autonomic arousal immediately after trauma predicts PTSD ^[1]
Risk factors: female gender, neuroticism, prior trauma, pre-existing psychiatric disorder, lack of social support, trauma severity ^[1]^[2]
PTSD clusters: Intrusion + Avoidance + Negative cognition/mood + Arousal (mnemonic: I-A-N-A or think "I Avoid Negative Arousal")
Conditioned fear (classical conditioning) drives re-experiencing; avoidance (operant conditioning, negative reinforcement) maintains the disorder ^[1]^[2]
Mild TBI mimics PTSD (irritability, startle, poor concentration) but lacks re-experiencing and avoidance ^[2]
Adjustment disorder = distress out of proportion to stressor + does NOT meet criteria for another specific disorder ^[2]

High Yield Summary

Adjustment disorder is a residual category — only diagnose when criteria for other specific disorders (MDD, GAD, PTSD, etc.) are NOT met ^[2]
PTSD vs. Adjustment Disorder: PTSD requires traumatic stressor + specific symptom clusters (re-experiencing, avoidance, hyperarousal). Adjustment disorder can follow any stressor and has subthreshold/non-specific symptoms ^[2]
PTSD vs. TBI: TBI mimics arousal symptoms but lacks re-experiencing and avoidance; may show persistent disorientation and confusion ^[2]
PTSD vs. OCD: Intrusive thoughts in OCD are unrelated to a traumatic event; compulsions are ritualistic and excessive ^[2]
PTSD co-morbidities: Depression, other anxiety disorders, substance use disorders, somatization, dissociative disorders ^[1]
Always exclude medical causes (thyroid, epilepsy, cardiac, phaeochromocytoma, TBI) and substance causes (intoxication, withdrawal, medication side effects) before diagnosing a stress-related disorder ^[2]^[3]
The focus/theme of anxiety helps differentiate: trauma memory = PTSD, imminent death = panic, free-floating = GAD, embarrassment = social phobia, intrusive ideas = OCD ^[3]
ASD vs. PTSD: identical symptom content; duration is the sole distinguishing feature (ASD: 3 days–4 weeks; PTSD: > 1 month) ^[1]^[2]

High Yield Summary

PTSD DSM-5 minimum counts: Criterion B ≥1 intrusion + C ≥1 avoidance + D ≥2 cognition/mood + E ≥2 arousal → "1-1-2-2" mnemonic. Plus: > 1 month duration, impairment, not substance/medical
ASD DSM-5: ≥9 symptoms from 5 categories (intrusion, negative mood, dissociation, avoidance, arousal) ^[1], duration 3 days–1 month
PTSD specifiers: with dissociative symptoms (derealisation/depersonalisation) and with delayed expression (criteria not met until > 6 months) ^[1]
Adjustment disorder = onset ≤3 months of stressor, distress out of proportion OR functional impairment, does NOT meet criteria for another disorder, NOT normal bereavement ^[2]
Adjustment disorder is a residual category — never diagnose it if MDD/GAD/PTSD criteria are met ^[2]
ICD-10 ASR = normal response (hours–days); DSM-5 ASD = abnormal response (3 days–4 weeks) that may predict PTSD
CAPS-5 is the gold standard diagnostic tool for PTSD
Investigations are to exclude organic mimics, NOT to diagnose PTSD: TFTs, BGL, UDS, CBP, LFT are the key baseline bloods ^[2]^[4]
Screening questions can help identify or rule out diagnoses ^[1] — use PCL-5, PHQ-9, GAD-7, AUDIT in clinical practice

High Yield Summary

There are many effective treatments including psychotherapy and psychopharmacology ^[1]
Trauma-focused CBT is first-line for both ASD and PTSD ^[2] — components: psychoeducation, cognitive restructuring, exposure therapy
EMDR is an equally effective first-line psychotherapy for PTSD ^[2] — most studies show it is efficacious, superior to other less specific psychotherapy
CISD has NOT shown to be helpful in reducing psychological distress ^[2] — do NOT use mandatory debriefing
Pharmacotherapy for ASD is generally not considered helpful ^[2]
Pharmacotherapy for PTSD is usually augmentation or second-line to psychotherapy ^[2]: SSRIs (sertraline, paroxetine) are first-line drugs
Prazosin (α₁-blocker) can reduce PTSD symptoms, nightmares, sleep disturbance ^[2]
SGAs can be used as monotherapy or augmentation ^[2] for treatment-resistant PTSD
BDZs: may be useful for anxiety and hyperarousal but use with extreme caution ^[2] — risk of dependence, may block fear extinction
Adjustment disorder management: problem-solving counselling first-line; anxiolytics/hypnotics may be helpful for a few days only ^[2]
Treat comorbid conditions ^[2]: substance use, depression, sleep disorders, psychosis
General treatment approaches for anxiety-spectrum disorders ^[1]^[3]: antidepressants, anxiolytics, antipsychotics, mood stabilisers; CBT, mindfulness-based therapy

High Yield Summary

PTSD comorbidities: Depression, other anxiety disorders, substance use disorders, somatization, dissociative disorders ^[1]
There are significant comorbid psychiatric conditions associated with anxiety disorders ^[1] — comorbidity is the rule, not the exception
PTSD is associated with 2–3× increased suicide risk; always assess suicidality; reckless or self-destructive behaviour is a DSM-5 criterion ^[1]
Self-medication hypothesis: patients use alcohol/substances to dampen hyperarousal → dependence → worsened PTSD (vicious cycle)
Alcohol temporarily reduces symptoms of anxiety, depression, insomnia but causes increased psychotic symptoms, mood swings, disruptive behaviour, suicide, treatment non-compliance, poor clinical outcome ^[5]
Physical health: chronic sympathetic activation → ↑cardiovascular mortality, metabolic syndrome, chronic pain, immune dysregulation, cognitive decline
Interpersonal: emotional numbing + irritability → relationship breakdown, domestic violence, intergenerational transmission to children
Adjustment disorder complications: often underestimated; may herald future development of anxiety/depression ^[2]; significant association with deliberate self-harm and suicide attempts
Iatrogenic risks: BDZ dependence, medication side effects, unnecessary investigations from somatisation, retraumatisation from poorly conducted therapy
ASD: 40–80% develop subsequent PTSD; PTSD: ~50% remit within 3 months but ~40% chronic course ^[2]

Stress-related Disorders

Epidemiology

Anatomy and Neurocircuitry of the Stress Response

Aetiology

Clinical Features

1. Acute Stress Reaction (ICD-10) / Acute Stress Response

2. Acute Stress Disorder (DSM-5)

3. Post-Traumatic Stress Disorder (PTSD)

4. Adjustment Disorder

Active Recall - Stress-Related Disorders: Definition, Epidemiology, Aetiology, Classification, Clinical Features

Active Recall - Differential Diagnosis of Stress-Related Disorders

References

Diagnostic Criteria

3. Post-Traumatic Stress Disorder (DSM-5: 309.81)

5. Adjustment Disorder

Step-by-Step Explanation of the Algorithm

Investigation Modalities

Assessment Tools

Active Recall - Diagnostic Criteria, Algorithm, and Investigations for Stress-Related Disorders

Treatment Modalities by Disorder

2. Acute Stress Disorder — Management

3. Post-Traumatic Stress Disorder — Management

A. Psychotherapy (First-Line)

B. Pharmacotherapy (Second-Line or Augmentation)

Active Recall - Management of Stress-Related Disorders

1. Psychiatric Comorbidities

Active Recall - Complications of Stress-Related Disorders

On this page

Stress-related Disorders

Definition

Epidemiology

Acute Stress Disorder (ASD)

Post-Traumatic Stress Disorder (PTSD)

Adjustment Disorder

Risk Factors

Anatomy and Neurocircuitry of the Stress Response

The Fear Circuit

The HPA Axis in PTSD

Neurochemical Changes

Aetiology

Biological Factors

Psychological Factors

Social Factors

Classification of Stress-Related Disorders

By Nature of Stressor

By Time Course

Clinical Features

1. Acute Stress Reaction (ICD-10) / Acute Stress Response

Symptoms

Signs

2. Acute Stress Disorder (DSM-5)

Symptoms

Signs

3. Post-Traumatic Stress Disorder (PTSD)

Symptoms

Signs

DSM-5 Specifiers

Important Clinical Distinctions

4. Adjustment Disorder

Subtypes (DSM-5)

ICD-10 Subtypes

Symptoms

Signs

Diagnostic Boundaries

Concussion / Mild TBI — Differential Consideration

Summary of Key Pathophysiological Mechanisms Across Stress-Related Disorders

Active Recall - Stress-Related Disorders: Definition, Epidemiology, Aetiology, Classification, Clinical Features

References

Differential Diagnosis of Stress-Related Disorders

Diagnostic Hierarchy and Approach

Differential Diagnosis Table for PTSD

Differential Diagnosis Table for Adjustment Disorder

Comorbidities of PTSD (Important for DDx Thinking)

Differentiating Stress-Related Disorders From Each Other

Medical and Substance-Related Differentials (Must Exclude First)

Medical Conditions Mimicking Stress-Related Symptoms

Substance-Related Differentials [2]

Differentiating by the Focus/Theme of Anxiety

Differentiating Intrusive Thoughts: PTSD vs. OCD vs. Depression

Summary: Decision Framework for Differential Diagnosis

Active Recall - Differential Diagnosis of Stress-Related Disorders

References

Diagnostic Criteria

1. Acute Stress Reaction (ICD-10: F43.0)

2. Acute Stress Disorder (DSM-5: 308.3)

3. Post-Traumatic Stress Disorder (DSM-5: 309.81)

Criterion A: Exposure

Criterion B: Intrusion — Presence of 1 or more after the event [1]

Criterion C: Avoidance — Persistent avoidance by 1 or both [1]

Criterion D: Negative Alterations in Cognitions and Mood — 2 or more [1]

Criterion E: Arousal and Reactivity — 2 or more [1]

Criteria F–H

Specifiers [1]

4. PTSD — ICD-10 Criteria (F43.1) for Comparison

5. Adjustment Disorder

DSM-5 Criteria [2]

ICD-10 Criteria (F43.2) [2]

ICD-10 Subtypes [2]

Diagnostic Algorithm

Step-by-Step Explanation of the Algorithm

Investigation Modalities

Why Investigations Are Needed

Assessment Tools

Clinical Assessment (The Core of Diagnosis)

Standardised Screening and Rating Instruments

Laboratory Investigations (To Exclude Organic Mimics)

Neuroimaging (Selective — Not Routine)

Other Investigations as Indicated