- 1 Causes And Treatment Of Insomnia And Psychophysiological Insomnia
- 2 Causes Of Insomnia
- 3 Psychophysiological Insomnia
- 4 Insomnia Treatment
- 5 Psychiatric Disorders Associated With Insomnia
- 6 Chronobiological Alterations Of Insomnia
- 7 Types Of Insomnia And Treatment
Causes And Treatment Of Insomnia And Psychophysiological Insomnia
Dyssomnias can be defined as primary disorders of the onset or maintenance of sleep or excessive sleepiness. They are characterized by significantly altering the quantity, quality or schedule of sleep. Below are some of the most common.
Insomnia is the inability to sleep in sufficient quantity or quality to feel rested and operational the next day. The amount of sleep needed is variable in each subject and is genetically determined, in general 7-8 hours in an adult. Insomnia affect the person at night and during the day when they suffer the consequences of insufficient rest. This differentiates true insomnia from the “short sleeper” that requires few hours of sleep but feels rested in the morning and remains fully operational during the day.
Causes Of Insomnia
Insomnia is defined by the lack of nighttime sleep and can be of two types mainly: Initial insomnia: Difficulty falling asleep Insomnia of early awakening: You fall asleep easily, but wake up very early, without the possibility of falling asleep.
Insomnia is probably the most frequent disorder of humanity and affects a third of the population. It is more prevalent in the elderly and women. Almost half of the patients with chronic insomnia have a psychiatric cause and about 20% of cases insomnia is primary.
Insomnia is due to poor sleep and inconvenient habits. As with any biological rhythm:
- The harmful habits of the subject can alter the periodicity of a function.
- The irregularity of the sleep-wake cycles with the absence of stability of bedtime for going to bed and getting up, together with variations in the social customs and schedules of breakfast, lunch, and dinner and etc. And it causes weakness or desynchronization of the sleep-wake rhythms. This leads to a low desire to sleep at night and a tendency to daytime sleepiness.
- The abuse of stimulant substances such as coffee, tea, cola and CNS stimulant drugs should obviously be banned. Alcohol can facilitate the onset of sleep but later affect it. Withdrawal of CNS depressant drugs causes “rebound” insomnia. The adoption of healthy habits and reasonable schedules is usually enough to solve this type of insomnia.
The rest is relatedto medical illnesses and other sleep disorders. Whatever the cause, sleep promotion and maintenance systems or the orderly and predictable oscillation of sleep-wake cycles are affected. At a given time T, the most important variables that determine the foreseeable level of alertness or drowsiness are homeostatic, chronobiological and hypothalamic activity.
The homeostatic factor is related to the duration of the last vigil (the greater the last vigil, the greater propensity to sleep). The chronobiological factor depends on the function of the biological pacemaker: the suprachiasmatic nucleus (SCN) of the hypothalamus, which determines the periodicity of the sleep/wake cycles and its synchronization with the 24-hour geophysical cycle.
The periodicity of the sleep/wake cycle is also an important cause of insomnia and depends on the intrinsic rhythm of the suprachiasmatic nucleus (SCN) and training by external markers that allow the biological pacemaker to be synchronized with the day/night cycle. The synchronizing factors are light, physical activity and social schedules (work, food, etc.). During the day the suprachiasmatic nucleus neurons are active and their gabaergic endings inhibit the paraventricular nucleus neurons involved in melatonin secretion.
At night, the inhibition of this nucleus ceases and melatonin secretion occurs. Melatonin is a chronobiological effect and the secretion schedule is a good indicator of the sleep/wake rhythm. The main sleep-promoting systems are located in the ventrolateral hypothalamus, whose neurons (containing GABA and galanin inhibitory neurotransmitters) send projections to the hypothalamic and brainstem neuronal groups involved in the maintenance of wakefulness.
Hypocretinergic neurons related to the promotion and regulation of wakefulness are located in the posterolateral hypothalamus. A precise mechanism modulates the activity of all these promoter/regulator systems of wakefulness and sleep so that both states alternate in an orderly and predictable manner.
All human beings may experience transient insomnia (less than a week), or short duration (1-3 weeks), if they are exposed to certain precipitating factors such as pain, stress, medication, grief, noise, transoceanic travel and etc. If insomnia persists for a few weeks it is called acute; If it persists for more than a month it is chronic. Acute insomnia usually resolves when the cause that caused it ceases, but in some cases, sleep disturbance persists due to the acquisition of harmful habits that perpetuate the problem or because of the subject’s own vulnerability that has a weak sleep generation system and/or is prone to a state of hypervigilance.
These recommendations known as sleep hygiene are universally applied to any type of insomnia and yield their benefit from the 4th – 6th week of strict compliance. In general, Psychophysiological insomnia and human beings associate the bedroom with sleep and after various preliminary rites (putting on pajamas, brushing teeth, etc.) we usually fall asleep easily in the appropriate situation.
Psychophysiological insomnia consists of inverse psychological conditioning in which a progressive association of the room and bed with wakefulness develops. In fact, these patients may fall asleep when they do not intend it and improve substantially when they sleep in an unusual room, for example in a hotel. This disorder is often acute and self-limited (situational insomnia, related to a particular stressful event), but it can be perpetuated.
The goal of treatment is to identify and correct the cause that causes it, and vigorously prevent its perpetuation. Treatment should be directed to the fundamental disease that causes insomnia. When this option does not improve nighttime sleep, the opportunity to establish symptomatic, pharmacological or non- pharmacological treatment of insomnia should be considered.
In many cases, the treatment of the underlying medical or psychiatric process and that of insomnia should be combined. In general, transient hypnotic treatment for acute insomnia is considered appropriate, which usually depends on a circumstantial stressor.
However, the most frequent is that the patient presents with a history of chronic insomnia, a condition that entails a significant therapeutic difficulty.
Pharmacological Treatment Of Insomnia
Hypnotics shouldn’t, in general, be suggested as a treatment for chronic insomnia. As a first choice, an opportunity should be allowed for diagnostic scrutiny that can clarify the cause and facilitate its resolution. However, patients should sleep, and in those cases, it is assumed, as a minor illness, to prescribe hypnotics administered intermittently, 2-3 times per week. This intermittent therapy avoids tolerance and addiction.
As a general rule, it is recommended not to prolong the hypnotic treatment for more than 8 weeks (4-6) and associate it with other non-pharmacological measures. Hypnotics can also be administered as rescue medication: the patient is invited to follow hygienic standards and is given an opportunity to fall asleep spontaneously, but to avoid the frustration of a possible failure it is expected that, if they fail to sleep in time, they can then use prescribed hypnotics.
Depending on the temporary distribution of insomnia, hypnotics are selected with different speed of action and half-life. Benzodiazepine hypnotics are the most effective: they are non-selective agonists of the GABA-A receptor, with hypnotic, anxiolytic, muscle relaxant and antiepileptic actions. They shorten sleep latency and increase the total amount of sleep. They can cause daytime sedation, cognitive impairment, “rebound” insomnia and withdrawal symptoms. They can make chronic obstructive pulmonary disease (COPD) and obstructive sleep apnea syndrome (OSAS) worse.
At high doses, they can cause dependence and tolerance. In the case of sleep-onset insomnia, a drug with rapid action and short half-life (eg midazolam, lormetazepam, etc.) is of interest. They are selective agonists of the GABA-A receptor with hypnotic actions but without a muscle relaxant, anxiolytic or antiepileptic effect. They do not usually cause “rebound” insomnia or withdrawal syndrome when therapy is discontinued. In addition, they have little / no effect on memory and intellectual and psychomotor performance and do not seem to worsen respiratory function in COPD or the frequency and duration of OSA apneas.
They are indicated in the treatment of insomnia associated with depression. The advantages are that they have a lower risk of causing dependence and abuse. This pharmacological property has made them attractive for the treatment of chronic insomnia. The best antidepressants for insomnia treatment are trazodone and mirtazapine.
In some cases, or as the first step of treatment, the hypnotic side effect of antihistamines (diphenhydramine, hydroxyzine) can be used. However, they have undesirable diurnal effects such as sedation, psychomotor impairment, and anticholinergic effects. In addition, their effectiveness declines in days. Melatonin is effective in counteracting jet lag and delayed sleep phase syndrome, but its possible hypnotic efficacy is controversial. The usual dose is 3-9 mg administered one hour before bedtime. It is probably useful for improving sleep in elderly patients with low levels of melatonin. This substance is very popular in the USA and countries of the European Union, where it can be purchased without a prescription.
Psychiatric Disorders Associated With Insomnia
In almost 3 out of 4 patients with chronic insomnia, the cause is psychopathological, often depression and/or anxiety, but also psychosis and alcohol or drug dependence. On the other hand, insomnia isn’t initially related to psychiatric disorders but a risk factor for the development of anxiety, depression and substance abuse.
Depression typically causes shortening of total sleep time by waking early with an inability to resume sleep. Repetitive insomnia will almost always appear in mild-moderate depression with significantly associated anxiety.
A polysomnogram (PSG) usually shows an increase in sleep latency, decreased efficiency, reduced REM sleep latency, increased density of rapid eye movements, decreased slow sleep and increased number of alerts and awakenings.
Generalized anxiety disorder causes difficulty in initiating and maintaining sleep. Compared to depression, the Polysomnography (sleep study) shows a preserved latency of REM sleep but the low sleep efficiency is similar between both disorders.
Chronobiological Alterations Of Insomnia
The asynchrony of the periods of wakefulness and sleep cause the patients to not be able to sleep when they wish, or when they are expected to do so, according to the normal habits of society, with respect to the day/night geophysical cycle, although the total time of sleep in 24 hours is normal.This leads to the appearance of periods of sleep or wakefulness in untimely hours with the consequent complaint of insomnia or daytime sleepiness.
Stages Of Development
The intrinsic period of the human circadian pacemaker shortens with age, probably from the 6th decade of life, causing the characteristic pattern of falling asleep early and waking up early.In the case of advanced sleep phase disorder, the total sleep time is normal and only the advanced position of the sleep/wake rhythm is detected in relation to the 24-hour geophysical period. This phenomenon must be distinguished from insomnia with early awakening observed in depression, in which case the total duration of sleep is diminished. In addition, there are other psychological and polysomnographic data reminiscent of depression, in particular, a shortening (less than 60 minutes) of REM sleep latency.
Treatment may be based on the administration of Melatonin in the morning, which expands the signal of darkness (night), or exposure to bright light (Phototherapy) during the afternoon, which amplifies the signal of clarity (day). Both methods help to “delay” the biological “clock” trying to align the wake/sleep cycle with the day/night cycle and social time. Chronotherapy is a potentially useful treatment based on the daily delay of 3 hours of bedtime to synchronize the propensity to sleep with the desired bedtime.
This syndrome is characterized by severe difficulty in starting sleep at the conventional or desired time, and extreme difficulty in getting up in the morning at the scheduled time.
Consequently, the sleep time is shortened. The difference with the genuine insomnia of the onset of sleep is that in the phase delay syndrome the total sleep time is normal unless it is shortened by the imperative to get up early to meet school or work obligations. This disorder is typical of adolescents and is apparently due to a weakness of the circadian system to advance the phase in response to geophysical time keys. Treatment may include chronotherapy, melatonin at night or phototherapy in the early morning. It may also be helpful to have a night of complete deprivation of sleep while keeping vigil up to the hour strictly.
Types Of Insomnia And Treatment
It consists of the chaotic distribution of periods of sleep and wakefulness during the day and night. Actually, the total amount of sleep is normal but its fragmentation throughout the 24 hours of the day produces a feeling of diurnal hypersomnia and/or insomnia. There may be a consistent, relatively prolonged period of nighttime sleep, generally between 2 and 6 in the morning. The rest of the time, the dream spreads during the day with 3 or more naps that do not usually last more than 4 hours. In addition, there is a marked variability in the daily distribution of sleep and awake periods.
Irregularity of the sleep/wake cycle is common in patients with diffuse brain involvement including degenerative brain processes. In these cases, it is assumed that there is either an alteration of the chronobiological system that manages the sleep-wake cycles or the neuronal groups that receive the circadian input and ultimately determine the declaration of wakefulness and sleep and their synchronization with the geophysical cycle and social requirements. The treatment is based on strict sleep hygiene with the maintenance of a rigid schedule of the waking and sleeping period. Exposure to natural intense light in the morning may be helpful. Theoretically, Melatonin (3 to 9 mg) should be useful at the desired time of sleep:
- Changes in shift work cause insomnia or excessive sleepiness temporarily. To facilitate adaptation to changes in working hours, the intensity of light must be increased during working hours and provide strict obscurity during the rest phases.
Various medical diseases can cause insomnia due to the emergence of nocturnal symptoms such as pain, dyspnea, coughing, gastroesophageal reflux, nocturia, etc., which can make it difficult to sleep or interrupt. In turn, some treatments of these disorders can perpetuate insomnia (steroids, theophyllines, alpha-adrenergic agents, etc.). Among the neurological diseases that can cause insomnia are nighttime headaches (cluster headache, chronic paroxysmal hemicrania, hypnic headache), degenerative diseases (Alzheimer’s disease, Parkinson’s disease), head trauma and post-traumatic syndrome.
Fatal Familial Insomnia
It is a rapidly progressive prion disease, inherited dominantly, manifested in the adult by an insomnia initially of sleep consolidation that evolves into a practically complete inability to initiate and maintain sleep. In addition, various signs of hyperactivity are observed vegetative, and later dysarthria, tremor, myoclonus, ataxia, dystonia and pyramidal signs. From the pathological point of view, thalamic atrophy is typical. The PSG usually shows the absence of slow sleep (stages III and IV), REM sleep without atony and signs of myoclonus or tremor.
Restless Legs Syndrome
It consists of the perception of discomfort in the legs with an irresistible need to move them, or even wander, to relieve themselves. This discomfort appears in periods of inactivity, particularly at night, in the transition from wakefulness to sleep. Clinically, it causes sleep onset insomnia. This disorder is common and affects 10% of the population and therefore constitutes one of the frequent causes of insomnia. The majority of cases are idiopathic and have a 50% family history. This syndrome is associated with iron deficiency, peripheral neuropathies, and chronic renal failure. The hormonal influence has been verified, and it has been observed that almost a quarter of pregnant women suffer from it.
In addition, exacerbations have been observed during menstruation and in menopause. The treatment of choice is the dopaminergic agents: L-Dopa / carbidopa (between 50 and 200 mg of L-Dopa) at night dose. Delayed-release L-Dopa preparations are preferable to ensure overnight protection. The recommended dopamine agonists are: pramipexole 0.18-0.36 mg at night; ropinirole 0.5-2 mg at night. Other treatments: clonazepam (0.5-2 mg in a single night dose), gabapentin (400-800 mg at night) and opioids (codeine, dextropropoxyphene, methadone).
Rapid Time Zone Change Syndrome (Jet Lag)
During rapid transoceanic trips (by plane), there is a temporary de-synchronization of the sleep-wake cycle caused by a mismatch between the geophysical time of the starting point and the arrival time. In other words, the internal biological clock is exposed to another geophysical cycle to which it must adapt.