Drugs can either alleviate or induce nightmares. Some of the widely known drugs that evoke nightmares in patients are the beta-blockers, reserpine, cholinesterase inhibitors, and L-Dopa. Since the membranes of the cells in human bodies are made out of lipids, it has been suggested that drug and physiological interactions usually favor fat-soluble drugs, rather than water-soluble ones; thus, those that are able to easily pass through the cell membranes tend to result in more serious side effects. However, studies comparing fat-soluble and water-soluble beta-blockers have found that both drugs cause an equally significant increase in nightmares. Thus, it would appear that fat solubility is not the critical property involved in causing nightmares; this is particularly true with beta-blockers. It has been hypothesized that side-effects due to beta-adrenergic-blocking drugs are caused by the resulting decrease in melatonin level. Melatonin is secreted primarily during the night, and decreased melatonin secretion has been found in patients with sleep disturbances. Bearden quoted that Brismar discovered that the hypertensive patients (treated with beta-blockers) who reported the most nightmare distress also had the lowest melatonin levels. Another hypothesis is that the decrease or blocking of norepinephrine receptors may be the cause of nightmares, since it appears to be involved in dreaming.
The actions of reserpine provide further evidence for the involvement of biologenic amines in nightmares, in that it produces its effects by preventing intraneuronal storage of dopamine, norepinephrine, and serotonin.
Cholinesterase inhibitors prevent the destruction of acetylcholine by acetylcholinesterase, and are used in the treatment of neuromuscular diseases, such as myasthenia gravis. Historically, they have also been employed as neurotoxins and poisons because of their potent effect on the central and peripheral nervous system. These have also been shown to produce long, intense dreams and nightmares.
L-Dopa, a direct precursor to dopamine, is used to treat Parkinsons disease, a disease caused by decreased dopamine levels. One of the side effects of L-Dopa includes unusually vivid dreams and nightmares and, occasionally, full-blown psychotic episodes. This lends credence to the notion that nightmares may in fact be an intermediate stage between ordinary dreaming and psychosis. A study found that dreams induced by L-Dopa were significantly more dreamlike, vivid, and detailed than under placebo conditions. Further evidence supporting dopamine-inducing nightmares is that dopamine blockers have been reported to reduce the incidence of nightmares in chronic nightmare sufferers. Interestingly, the overactivation of dopamine in schizophrenia, and the tendency toward schizophrenia in frequent nightmare sufferers and their families, also supports this hypothesis. It would appear that dopamine somehow play a key role in the itnerconnection between nightmares and psychopathology.
Another form of drug that influences traumatic nightmares in PTSD patients is clonidine, an alpha-2 receptor blocker in the locus ceruleus, which decreases norepinephrine levels. This lowering of norepinephrine contributes to the propensity of nightmares by acting on the forebrain. Clonidine also reduced the level of CNS arousal and puts the patients into deeper sleep with fewer awakenings in general, thus making it less likely that the patient would awaken suddenly from a traumatic nightmare, which contributes to lengthening of disturbing dreams.
Withdrawal from certain depressant drugs, such as barbiturates, alcohol, and benzodiazopines, can also induce nightmares. As these drugs are administered in increasing doses over time, the receptors in the CNS are changed. When the drug is finally withdrawn, the changes in sensitivity and numbers of receptors often result in hyper-reactivity. This causes longer REM-sleep with frequent awakenings - conditions that are likely to generate nightmares.
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Other Types of Nightmares