Neurotic Disorders

Question 1

Epidemiology of GAD?

Answer 1

Onset = generally In early adulthood, less commonly in middle age. F>M, 2:1

Question 2

Aetiology of GAD?

Answer 2

Genetic - modest, shared heritability with depression.

Neurochemical - Human studies limited. Animal work implicates NA system (diminished ANS responsiveness). ?Loss of regulatory control of cortisol.

Question 3

Psychological aetiology of GAD?

Answer 3

Generalised Psychological Vulnerability - Diminished sense of control – trauma or insecure attachment to primary caregivers, leading to intolerance of uncertainty.
Parenting – overprotective or lacking warmth –> low perceived control over events.

Specific Psychological Vulnerability
Stressful life events – trauma (e.g. early parental death, rape, war) and dysfunctional marital/family relationships.

Question 4

Presenting features (essence) of GAD?

Answer 4

Longstanding free-floating anxiety that may fluctuate but that is neither situational nor episodic. Apprehension about a number of events far out of proportion to the actual likelihood or impact of the feared events.

Question 5

ICD-10 criteria for diagnosis of GAD?

Answer 5

(At least 4 – with 1 from autonomic arousal) for at least SIX MONTHS.

Autonomic arousal – palpitations/tachycardia; sweating; trembling/shaking; dry mouth.
‘Physical symptoms’ – breathing difficulties; choking sensation; chest pain/discomfort; nausea/abdominal distress.
Mental state symptoms – feeling dizzy, unsteady, faint or light-headed; derealisation/depersonalization; irritability; fear of losing control, going crazy, passing out, dying.
General symptoms – hot flushes/cold chills; numbness or tingling.
Symptoms of tension – muscle tension/aches and pains; restlessness/inability to relax; feeling keyed up, on edge or mentally tense; a sensation of a lump in the throat or difficulty swallowing.
Other – exaggerated response to minor surprises/being startled.
Concentration difficulties/’mind going blank’ – due to worry or anxiety; persistent irritability; difficulty getting to sleep due to worrying.

Question 6

Biological treatment of GAD?

Answer 6

SSRIs – First line. Start low then increase dose. Some prone to discontinuation symptoms. SNRIs if not tolerated. Then Pregabilin.
BDZs – no more than 2-4 weeks if absolutely necessary. Avoid if alcohol dependent/hepatic impairment. Use sleep hygiene advice first.
Beta-blockers – for palpitations/tremor only.
Buspirone – 5-HT1A receptor agonist - can be considered as alternative to BDZs when sedative effects unwanted, in patients with personal/FH of drug misuse, or for those already taking CNS depressants. Beneficial effects can take 2-4 weeks. Low or absent risk of abuse or dependence.

Question 7

Psychological treatment of GAD?

Answer 7

Treatment of choice, although generally less effective than in the other anxiety disorders (lack of situational triggers). Some evidence for CBT combining behavioural methods (treat avoidance by exposure, use of relaxation and control of hyperventilation) and cognitive methods (teaching about bodily responses related to anxiety/education about panic attacks, modification of thinking errors).

Question 8

Prognosis of GAD?

Answer 8

Chronic and disabling, prognosis generally poor, remission rates low (30% after 3 years, with treatment).
6-year outcome – 68% mild residual symptoms, 9% severe persistent impairment. Often co-morbidity becomes more significant (esp. alcohol misuse) and worsens the prognosis.

Question 9

Epidemiology of Panic Disorder?

Answer 9

Lifetime prevalence = 1.5-4% for panic disorder, 7-9% for panic attacks. F>M 2/3:1.
Onset = bimodal distribution, highest peak incidence at 15-24 and second peak at 45-54. Rare after 65.

Question 10

Risk factors for panic disorder?

Answer 10

Being widowed/divorced/separated; living in a city; limited education; early parental loss; physical or sexual abuse.

Question 11

Neurochemical aeitology of panic disorder?

Answer 11

Serotonergic/noradrenergic (↑activity/response) and GABA (↓receptor sensitivity and inhibition) theories – based on successful pharmacological treatment.

Question 12

Genetic aetiology of panic disorder?

Answer 12

Moderate heritability – 25-50% in family and twin studies. Most studies suggest that vulnerability is genetically determined but critical stressors required to develop symptoms.

Question 13

Definition of panic attack and panic disorder?

Answer 13

Panic Attack = rapid onset of severe anxiety lasting for about 20-30 minutes. Attacks can be spontaneous or situational.

Panic Disorder = recurrent panic attacks, not secondary to substance misuse, medical conditions, or another psychiatric disorder. Not restricted to any particular situation or set of circumstances – unpredictable. Frequency may vary from many attacks a day to a few per year. Usually a persistent worry about having another attack or consequences of the attack (which may lead to phobic avoidance of places or situations).

Question 14

Symptoms of panic attack?

Answer 14

Autonomic arousal - Sudden onset palpitations, choking sensations, chest pain, dizziness and depersonalization/derealisation.
Concern of death from CVS/respiratory problems may be major focus – repeated presentation to emergency services. May be diagnosied in patients with ‘unexplained’ medical symptoms.
Thoughts of suicide (or homicide) should be elicited – can lead to impulsive acts; risk increased in comorbid depression/alcohol or substance misuse.

Question 15

Investigations in panic disorder?

Answer 15

Investigations to rule out physical causes – guided by history/examination.

Question 16

Pharmacological treatment of panic disorder?

Answer 16

SSRIs = 1st line. Citalopram, escitalopram, paroxetine and sertraline all licensed. Start low and gradually increase. Alternative antidepressants unlicensed in UK. 
2nd line = consider switching to different class agent (alternative antidepressant), addition of BDZ (or different BDZ), trial of bupropion, or for severe symptoms an atypical antipsychotic (olanzapine or risperidone). Little evidence to support use of bupropion, mirtazapine, inositol, reboxetine, atypical antipsychotics, anticonvulsants and propranolol. 

BDZs = use with caution or best avoided altogether. May be effective for severe, frequent, incapacitating symptoms.

Question 17

Psychological interventions in panic disorder?

Answer 17

CBT – Behavioural methods – treat phobic avoidance by exposure, use of relaxation and control of hyperventilation. Cognitive methods – teaching about bodily responses associated with anxiety/physchoeducation about panic attacks, modification of thinking errors.

Psychodynamic psychotherapy – some evidence for brief dynamic psychotherapy, particularly ‘emotion-focused’ treatment, where fears of being abandoned or trapped are explored.

Question 18

Prognosis of panic disorder?

Answer 18

Untreated, disorder runs a chronic course. With treatment, functional recovery seen in 25-75% after first 1-2 years, 10-30 after 5 years. Long term around 50% will experience only mild symptoms.
Poor responses associated with: very severe initial symptoms, marked agoraphobia, low SES, less education, long duration of untreated symptoms, restricted social networks, presence of personality disorder.

Question 19

Epidemiology of agoraphobia?

Answer 19

Prevalence = 2.8-5.8%, F>M 1:3. Bimodal distribution (like panic disorder) but first peak broader (15-35). Later in life agoraphobic symptoms may develop secondary to frailty.

Question 20

Aetiology of agoraphobia?

Answer 20

Genetic - predisposition towards overtly interpreting situations as dangerous may be genetic – evolutionary determined vulnerability to unfamiliar territory. First-degree relatives have increased prevalence of other anxiety/depressive disorders and alcohol misuse.

Psychoanalytical - unconscious conflicts are repressed and may be transformed by displacement into phobic symptoms.

Learning Theory - conditioned fear responses lead to learned avoidance.

Question 21

Presentation of agoraphobia?

Answer 21

Anxiety and panic symptoms associated with places or situations where escape may be difficult or embarrassing, leading to avoidance.
Often presents with panic disorder, depressive disorder, other anxiety and related disorders (55% have social phobia), alcohol and substance misuse. Some experience little anxiety because they are able to avoid their phobic situations.

Question 22

Management of agoraphobia?

Answer 22

Pharmacological - Rarely used. SSRIs as for panic disorder.

Psychological - Behavioural methods – exposure techniques, relaxation training, anxiety management. Cognitive methods – teaching about bodily responses associated with anxiety/education about panic attacks, modification of thinking errors.

Question 23

Epidemiology of social phobia?

Answer 23

Lifetime prevalence = 2.4-12.1%. F>M. Onset = bimodal distribution with peaks at 5yrs and 11-15 years – often don’t present until 30s.

Question 24

Aetiology of social phobia?

Answer 24

Genetic - MZ:DZ = 24%:15.3%. Predisposition to overly interpreting situations as dangerous may be genetic, whereas individual interpretations of social cues may be environmentally determined.

Neurochemical - imaging studies showed increased activity in fear networks (pre-frontal cortex, amygdala, hippocampus) during anxiety-provoking attacks in individuals with SP. Response to antidepressants suggests may be dysregulation of 5-HT, NA, or DA systems.

Psychosocial - Responses may be learned from observing parents.

Question 25

Presentation of social phobia?

Answer 25

Symptoms of incapacitating anxiety not secondary to delusional or obsessive thoughts and are restricted to particular social situations, leading to a desire for escape or inadequacy. Excessive fear of scrutiny by other people or others noticing how anxious they are; more pervasive social phobias are usually associated with low self-esteem and fear of criticism. Individuals often characteristically self-critical and perfectionistic. Situational avoidance may lead to difficulty in maintaining social/sexual relationships, educational/vocational problems.
May present as a complaint of blushing, hand tremor, nausea or urgency of micturition. Patient sometimes convinced that secondary manifestation of their anxiety is the primary problem.

Question 26

Pharmacological treatment for social phobia?

Answer 26

Beta-blockers – may reduce autonomic arousal, particularly for ‘specific social phobia’.
SSRIs – more generalized social anxiety. SNRIs (venlafaxine) also used. Addition of BDZ (avoid) or buspirone (to augment SSRI).

Question 27

Psychological treatment for social phobia?

Answer 27

CBT – either individual or group setting, is first line. Involves relaxation training/anxiety management, social skills training, integrated exposure methods and cognitive restructuring.

Question 28

Prognosis of socical phobia?

Answer 28

CBT – either individual or group setting, is first line. Involves relaxation training/anxiety management, social skills training, integrated exposure methods and cognitive restructuring.

Question 29

Epidemiology of specific/simple phobias?

Answer 29

Lifetime prevalence = 12.5%. M=F. Animal/situational phobias may be more common in women.
Mean onset = 15. Animals = 7yrs, blood/injection/injury = 8yrs, situational = 20yrs.

Question 30

Aetiology of simple/specific phobias?

Answer 30

Genetic
MZ:DZ = 25.9%:11.0% for animal phobia, situational phobia roughly equal suggesting stronger role for environment.

Psychoanalytical = Manifest fear is the symbolic representation of an unconscious conflict, which was has been repressed and displaced into phobic symptoms.

Learning Theory = Conditioned fear response related to a traumatic situation, with learned avoidance (trigger to conditioned response may be a reminder of original situation). ‘Preparedness’ theory = fear of certain objects may be evolutionarily adaptive, selectively acquired and difficult to extinguish.

Question 31

Presentation of specific/simple phobia

Answer 31

Recurring excessive and unreasonable psychological or autonomic symptoms of anxiety, in the (anticipated) presence of a specific feared object or situation leading, wherever possible, to avoidance.
Lifetime risk of experiencing at least one other psychiatric disorder is 80%. Rates of substance misuse considerably less than in other anxiety disorders.

Question 32

Management of specific/simple phobia?

Answer 32

Psychological (Medication generally not used except in severe cases to allow patient to engage in exposure)

Behavioural Therapy – Exposure is treatment of choice; methods aim to reduce the fear response with relaxation and graded exposure (imaginary or in vivo).
Other techniques – reciprocal inhibition, flooding, modelling.
Cognitive methods – education/anxiety management, coping skills/strategies, cognitive restructuring – may enhance long-term outcomes.

Question 33

Prognosis of simple/specific phobia?

Answer 33

Without treatment, tends to run a chronic, recurrent course. Individuals may not present unless life changes force them to confront the feared object or situation.

Question 34

Epidemiology of OCD?

Answer 34

Mean age = 20. 70% onset before 25, 15% after 35. M=F. Prevalence = 0.5-3% of general population.

Question 35

Biological aetiology of OCD?

Answer 35

Neurochemical - Dysregulation of 5-HT system.

Immunological - Cell-mediated autoimmune factors may be associated (e.g. against basal ganglia peptides) as in Sydenham’s chorea.

Imaging - CT/MRI - Bilateral reduction in caudate size. PET/SPECT – hypermetabolism in orbitofrontal gyrus, basal ganglia (caudate nuclei) and cingulum that ‘normalises’ following successful treatment.

Genetic - MZ = 80% DZ = 25%, 3-7% first degree relatives affected.

Question 36

Psychological aetiology of OCD?

Answer 36

Defective arousal system and/or inability to control unpleasant internal states. Obsessions are conditioned (neutral) stimuli, associated with an anxiety-provoking event. Compulsions are learned (and reinforced) as they are a form of anxiety-reducing avoidance.

Question 37

Essential feature of OCD?

Answer 37

Obsessional thoughts and compulsive acts

Question 38

Obsessional thoughts in OCD?

Answer 38

Ideas, images or impulses that enter the patient’s mind again and again in a stereotyped form. Invariably distressing and patient often tries unsuccessfully to resist them. They are however recognised as the patient’s own thoughts, even though they are involuntary and often repugnant – at some point the patient recognises the symptoms to be excessive or unreasonable.

Question 39

Examples of obsessional thoughts?

Answer 39

Fear of acquiring disease, coming to harm, causing harm to others, ‘an indecisive endless consideration of alternatives, associated with an inability to make trivial but necessary decisions in day-to-day living’.

Question 40

Compulsive acts in OCD?

Answer 40

Stereotyped behaviours that are repeated again and again. Not inherently enjoyable, nor do they result in the completion of inherently useful tasks. Function is to prevent some objectively unlikely event, often involving harm or danger to or caused by the patient, which they fear might otherwise occur (i.e. cancel out the obsessional thought). Recognised by patient as symbolic, pointless or ineffectual. Anxiety invariably present. Repeated attempts are made to resist but if acts are resisted the anxiety gets worse.

Question 41

Examples of compulsive acts?

Answer 41

Cleaning (particularly handwashing), repeated checking, orderliness and tidiness.

Question 42

Assessment of OCD?

Answer 42

NICE OCD Questions

• Do you wash or clean a lot?
• Do you check things a lot?
• Is there any thought that keeps bothering you that you’d like to get rid of but can’t?
• Do you daily activities take a long time to finish?
• Are you concerned about putting things in a special order or are you very upset by mess?

Question 43

Psychological management of OCD?

Answer 43

CBT – recommended by NICE, but essentially takes a behavioural approach, including exposure and response prevention (ERP).

Behavioural Therapy – response prevention useful in ritualistic behaviour; thought stopping may help in ruminations; exposure techniques for obsessions.

Psychotherapy – supportive - valuable (use of family members, use of groups); psychoanalytical – no unequivocal evidence of effectiveness.

Question 44

Pharmacological management of OCD?

Answer 44

SSRIs – fluoxetine, sertraline = first-line (at least 12 weeks for treatment response). Unlicensed = citalopram and venlafaxine.

Clomipramine = second-line (has specific anti-obsessional action).

Augmentation = antipsychotics (risperidone, haloperidol, pimozide) esp. if psychotic features, tics or schizotypal traits.

Question 45

Physical management of OCD?

Answer 45

ECT – if patient suicidal or severely incapacitated.

Psychosurgery – if suicidal or severely incapacitated. Theoretically disrupts neuronal loop between orbitofrontal cortex and basal ganglia.

Deep Brain Stimulation – efficacy remains to be established.

Question 46

Prognosis of OCD?

Answer 46

Often sudden onset (after stressful event). Presentation may be delayed by 5-10 years due to secrecy, symptom intensity may fluctuate or be chronic.
20-30% significantly improve, 40-50% show moderate improvement, 20-40% have chronic or worsening symptoms. Relapse rates higher after stopping medication.

Question 47

Good and poor prognostic factors in OCD?

Answer 47

Poor prognostic factors = giving in to compulsions, longer duration, early onset, male, presence of tics, bizarre compulsions, hoarding, symmetry, comorbid depression, delusional beliefs or over-valued ideas, personality disorder.

Good prognostic factors = good premorbid social and occupational adjustment, a precipitating event, episodic symptoms, less avoidance.