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incident should probably be a short course of a benzodiazepine to promote sleep and help minimise mental rehearsal of the trauma that may lead to its perpetuation. Long-term therapy appears to be indicated at doses in the same range as for other anxiety disorders.


Acute stress disorder is anxiety in response to a recent extreme stress. Although in some respects it is a normal and understandable reaction to an event, the problems associated with it are not only the severe distress the anxiety causes but also the risk that it may evolve into a more persistent state.

Treatment. A benzodiazepine used for a short time is the preferred approach for treating overwhelming anxiety that needs to be brought rapidly under control. It particularly relieves the accompanying anxiety and sleep disturbance. A drug with a slow onset of action such as oxazepam (60-120 mg/day p.o.) causes less dependence and withdrawal, and is preferred to those that enter the brain rapidly, e.g. diazepam, lorazepam. Some patients find it hard to discontinue the benzodiazepine, so its use should be reserved for those in whom extreme distress disrupts normal coping strategies.


The essential feature of this condition is chronic anxiety and worry. To the nonsufferer the focus of the worry often seems to be trivial, e.g. getting the housework done or being late for appointments, but to the patient it is insurmountable. The anxiety is often associated with other symptoms, which include restlessness, difficulty in concentrating, irritability, muscle tension and sleep disturbance. The course of the disorder is typically chronic with exacerbations at times of stress and is often associated with depression. Its chronic nature with worsening at times of stress helps to distinguish GAD from anxiety in the form of episodic panic attacks with associated anticipatory anxiety (panic disorder). Hyperthyroidism and caffeinism should also be excluded.

Treatment. Historically benzodiazepines have been seen as the most effective treatment for GAD for they rapidly reduce anxiety and improve sleep and somatic symptoms. Consequently patients like taking them but the chronic nature of GAD raises issues of duration of treatment, tolerance, dependence and withdrawal reactions.

Buspirone is structurally unrelated to other anxiolytics and was the first nonbenzodiazepine to demonstrate efficacy in GAD. Its mode of action is unclear, although we know it suppresses 5HT neurotransmission through a selective activation of the inhibitory presynaptic 5HTlA-reactor. Buspirone has a t'/2 of 7 h, and is metabolised in the liver; it has an active metabolite that may accumulate over weeks. Twice daily dosing is suitable, with the usual range being 15-30 mg/d p.o., maximum 45 mg/d.

Buspirone is generally less effective and slower in action than benzodiazepines and does not improve sleep; it does not benefit benzodiazepine withdrawal symptoms. The advantages are that it does not seem to cause dependence or withdrawal reactions and does not interact with alcohol. It appears to be less effective in patients who have previously received benzodiazepines and is therefore probably best used in benzodiazepine naive patients. A disadvantage is that useful anxiolytic effect is delayed for 2 or more weeks.

Adverse effects can include dizziness, headache, nervousness, excitement, nausea, tachycardia and drowsiness.

Paroxetine (SSRI) and venlafaxine (SNRI) are effective (and are licenced for GAD in the UK), and TCAs have also been shown to give benefit. These drugs have a slower onset of action than benzodiazepines, are less well tolerated but cause fewer problems of dependence and on withdrawal.

A delayed response in GAD is not as critical as with acute situational anxiety. A sensible approach (especially in benzodiazepine naive patients) is to start with buspirone for 6-8 weeks, at least 30 mg day increasing over 2-3 weeks to minimise unwanted actions; patients should be warned not to expect an immediate benefit. Those who do not respond should receive an antidepressant (SSRI or venlafaxine) for 6-8 weeks at full therapeutic dose. There remain some patients, including those with a long history of benzodiazepine use, who yet fail to respond. A benzodiazepine may be the only medication that provides relief for such resistant cases, and can be used as the sole treatment.

The duration of therapy depends on the nature of the underlying illness. If symptoms are intermittent, i.e. triggered by anxiety-provoking situations, then intermittent use of a benzodiazepine (for a few weeks) may be sufficient. More typically GAD requires treatment over 6-8 months with gradual withdrawal of medication thereafter. This may suffice but some patients experience severe, unremitting anxiety and the best resort is to chronic maintenance treatment with a benzodiazepine (analogous to long-term drug use in epilepsy). Such clinically supervised benzodiazepine use is justified because, without treatment, patients often derive comfort from the most widely accessible, easily available anxiolytic, alcohol.

Specific phobia

A specific phobia is a fear of a circumscribed object or situation, for instance fear of spiders, fear of flying. The diagnosis is not usually in doubt. A course of treatment by a trained therapist, involving graded exposure to the feared stimulus is the treatment of choice and can be very effective. By its nature such therapy generates severe anxiety and a benzodiazepine may permit patients fully to engage in therapy.

Obsessive-compulsive disorder (OCD)

Obsessive-compulsive disorder has two main components:

• the repetition of acts or thoughts which are involuntary, recognised by the sufferer to be generated by their own brain but are not in keeping with their usual thought processes, morals or values, and are therefore very distressing and

• anxiety provoked by the occurrence of such acts or thoughts.

OCD on its own often starts in late adolescence and has a chronic and pervasive course unless treated. OCD starting later on in life is often associated with affective or anxiety disorders. Symptoms often abate briefly if the individual is taken to a new environment.

Treatments are cognitive behavioural therapy and an SSRI or clomipramine (i.e. an antidepressant that enhances serotonergic function), used at higher doses and for much longer periods than for depressive disorders. Neuroleptics, atypical antipsychotics in low dose and benzodiazepines can be used successfully to augment the SSRIs if they are not wholly effective, especially in patients with tics (habitual, repeated contraction of certain muscles). Psychosurgery is still occasionally used for severe and treatment resistant cases. Interestingly, the brain pathways targeted by the surgeon are those that show abnormalities in neuroimaging (PET) studies of OCD, i.e. the basal ganglia/orbitofrontal pathways.

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