Pharmacological treatment of insomnia
Insomnia is a widespread condition which affects approximately one-third of the general population. It is especially prevalent in the elderly. The treatment modalities of insomnia are varied and include nonpharmacological and pharmacological techniques. Insomnia is a symptom of an underlying condition. Before starting treatment, it is imperative to carefully assess the possible causes of insomnia, since the aetiology of the insomnia determines the treatment. Pharmacotherapy is indicated in transient insomnia which occurs in otherwise healthy, normal sleepers, and in the treatment of intermittent insomnia in the elderly. Pharmacotherapy is not indicated in chronic insomnia, except perhaps on an intermittent basis and as adjunctive treatment. If adjunctive pharmacotherapy is to be used in chronic insomnia, the possibility of a primary sleep disorder must be ruled out prior to the use of a sedative hypnotic. When using sedative hypnotic agents, the lowest possible dose should be used for the shortest possible time. Special care should be exercised when treating the elderly, because altered pharmacokinetics in this age group may impair tolerability. Benzodiazepines remain the recommended hypnotic agents, although newer, non-benzodiazepine agents may also be utilised. Despite the relative safety of benzodiazepines, the most common adverse effects include residual daytime sleepiness, rebound insomnia and anterograde amnesia. Short-acting benzodiazepines are more commonly associated with rebound insomnia and withdrawal symptoms, whereas the long acting benzodiazepines are more likely to produce residual daytime sleepiness. Anterograde amnesia may be seen with all benzodiazepines. Use of alcohol for its sedative properties, and over-the-counter preparations, are not recommended for the treatment of insomnia
Effects of triazolam on the perception of sleep and wakefulness in insomniacs
Examined whether triazolam (TRZ) altered the perception of being asleep in 15 chronic insomniacs. TRZ (.25 mg) resulted in increased EEG or behavioral arousal thresholds for 'lights out,' Stage 2 sleep, and waking time conditions. Arousal thresholds in Stage 2 on active drug nights exceeded the amplitude of common commercial smoke alarms. Ss reported having been awake during the Stage 4 trial in 50% of the cases after placebo, but only in 8% after TRZ. There were no drug-induced changes in accuracy of estimation of amount of sleep since the prior forced awakening. Although the only change in polysomnographic measures was an increase in non-REM sleep, morning subjective reports described less difficulty getting to sleep, increased depth and quality of sleep, and increased total sleep.