- Significant mental health problems nearly always interfere with sleep
- Conversely, poor quality sleep almost certainly directly contributes to many psychiatric disorders, particularly those involving low mood
- Major depression is reliably associated with an altered pattern of sleep architecture, including a short latency to REM sleep and early morning waking
- Sedative drugs used to treat anxiety and associated insomnia may lengthen sleep time but do not always improve sleep quality
- A defining symptom of post-traumatic stress syndrome (PTSD) is recurring vivid dreams, replicating the memory of the initial stressful event together with the associated negative emotion
- Sleep disorders associated with psychotic disorders such as schizophrenia are variable and poorly defined but can cause major concerns, especially if there is reversal of the sleep–wake cycle
- Antipsychotic drugs may cause significant daytime somnolence, occasionally as a result of weight gain and associated sleep-disordered breathing
- Subjects addicted to a variety of drugs whether stimulating or sedative will usually report sleep disturbance either as a direct consequence of drug misuse or when attempting to withdraw
The vast majority of psychiatric disorders co-exist with a disturbed sleep–wake cycle. Insomnia is the most closely associated problem but excessive sleepiness or even parasomnias may also be intimately linked to an underlying psychiatric condition or its drug treatment.
Increasingly, it is appreciated that the link between sleep and mental health problems, particularly those affecting mood, is ‘bi-directional’. Depression and anxiety may commonly fuel poor quality sleep resulting in sleep deprivation that, in turn, promotes further mood disturbance. Moreover, reports of worsening insomnia are well recognised as an independent risk factor for either the development of major depression within the subsequent year or a clinical relapse in established depression.
Depression
All types of insomnia are extremely common in depressed patients, particularly if they are female. Indeed, 90% of depressed subjects report unrefreshing sleep that usually arises from a combination of delayed sleep onset and impaired sleep maintenance. Waking 2–4 hours earlier than desired with an inability to fall back to sleep is also a commonly recognised pattern.
Depressed patients with insomnia usually report daytime fatigue in the absence of objective evidence for excessive sleepiness. However, in atypical depression, reflecting around 10% of all cases, frank daytime somnolence and increased appetite may replace the more typical pattern of insomnia with anorexia.
There are interesting changes in REM sleep that typically characterise the sleep architecture of depressed patients. The latency to enter REM sleep is shorter than average, a feature which may persist even with successful treatment and which is also seen in unaffected first-degree relatives. This feature has been used as predictor for a good response both to pharmacological and psychotherapeutic management. The density of REM sleep overnight is also generally increased although the initial REM sleep period is shorter than average.
It is of interest that the vast majority of routinely used antidepressant drugs are effective at supressing REM sleep. Whether this property is directly relevant to their action on mood elevation remains unclear, however.
Other recognised changes in sleep architecture, such as reduced deep non-REM (slow wave) sleep, appear less specific to depression.
Seasonal depression is seen particularly in higher latitudes. There is typically an increased need for sleep, enhanced appetite and weight gain during the winter months. Morning bright light therapy with or without selective serotonin reuptake inhibitor (SSRI) therapy is often an effective treatment strategy. There is some evidence that abnormalities of melatonin secretion, usually suppressed by light exposure, may be aetiologically important.
The inability to sleep during a manic phase of bipolar depression may present as insomnia if there is reduced insight into the underlying mood disturbance.
Antidepressants vary considerably in their sedative properties (Table 10.1). Significantly sedating agents such as mirtazapine might be considered preferential if insomnia is a major feature. The new agent agomelatine also appears to lengthen nocturnal sleep time in depression and may improve sleep quality by increasing levels of deep non-REM sleep.
Table 10.1 Sedative properties of selected antidepressant drugs.
| Usually sedating | Neutral | Usually stimulating |
| Mirtazapine | Paroxetine | Fluoxetine |
| Trazodone | Citalopram | Sertraline |
| Amitriptyline | Escitalopram | Venlafaxine |
| Nortriptyline | Phenelzine |
Anxiety disorders
Chronic generalised anxiety may affect at least 4% of the population. It is characterised by persistent symptoms of unease, dread or anticipation occurring on a daily basis for a period of months. Although usually considered a primary psychiatric condition, there may well be underlying medical or social reasons for anxiety which exacerbate the problem. Anxiety and associated increased muscle tension almost invariably produce insomnia, which may dominate the clinical picture.
Cognitive therapies are aimed at reducing distorted perceptions about future threats and minimising the tendency to ‘catastrophise’. Together with relaxation techniques, a non-pharmacological approach often improves sleep quality as well as the underlying anxiety.
Drugs used to treat anxiety are invariably sedative. Although traditional anxiolytic agents, such as benzodiazepines, may increase sleep time, the effects on subjective sleep quality may be mixed.
Some newer agents licensed for generalised anxiety, such as pregabalin, may reduce anxiety yet improve sleep quality, potentially by directly enhancing the deep non-REM sleep elements of nocturnal sleep.
Panic disorders may present as nocturnal phenomena although symptoms are rarely exclusive to sleep. Discriminating nocturnal panic attacks from agitated arousals due to non-REM sleep parasomnia can be difficult. Because the former usually arise from light (stage 2) non-REM sleep, subjects awake quickly and often have major problems returning to sleep. By contrast, confusion and variable amnesia for the event would be expected after a non-REM sleep parasomnia which develops from deep non-REM sleep. If medication is considered appropriate, sedating antidepressant drug therapy rather than benzodiazepines may be preferable for nocturnal panic attacks although controlled evidence from trials is lacking.
Post-traumatic stress disorder (PTSD) is strongly associated with sleep-related problems, notably insomnia and nightmares arising from fragmented REM sleep (Box 10.1). The nightmares in PTSD are physiologically and emotionally arousing, typically with vivid replication of the triggering traumatic event. Treatments include supportive psychotherapy aimed at reducing arousal levels when exposed to reminders of the traumatic event. However, drug therapy may also be appropriate and recent evidence suggests prazosin, a centrally active alpha-adrenergic antagonist, as a particularly useful agent. It has been proposed that this drug may actually enhance REM sleep activity but attenuate the emotional character of the associated dream or nightmare. More commonly used drugs to promote sleep, such as benzodiazepines, paradoxically, may increase the chances of developing PTSD in some patients if given after traumatic events. It has been proposed this reflects REM sleep suppression and subsequent impaired ability to process emotional memories appropriately.
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