Insomnia causes and treatment

Dysomnias they can be defined as primary disorders of the initiation or maintenance of sleep or excessive sleepiness. They are characterized by significantly altering the quantity, quality or schedule of sleep. Here 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 required is variable in each subject and is genetically determined, generally 7-8 hours in an adult. Insomnia affects the subject at night and during the day when he suffers 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.

Index

1. Causes of insomnia
2. Psychophysiological insomnia
3. Insomnia Treatment
4. Psychiatric disorders associated with insomnia
5. Chronobiological disorders of insomnia
6. Types of insomnia and treatment

Insomnia is defined by a lack of nighttime sleep and can be of two main types: Conciliation insomnia: Difficulty getting to sleep Insomnia from early awakening: You fall asleep easily, but wake up very early, unable to fall asleep:

Insomnia is probably the most common disorder in humanity and affects a third of the population. It's more prevalent in the elderly and women. Almost half of patients with chronic insomnia have a psychiatric cause and about 20% of cases insomnia is primary.

Insomnia from poor sleep hygiene and inconvenient habits. As with any biological rhythm:

• the harmful habits of the subject can alter the periodicity of a function.
• irregularity of sleep-wake cycles with absence of stable times for going to bed and getting up, along with variations in social customs and times for breakfast, lunch and dinner, etc., cause "weakness" or desynchronization of rhythms sleep-wake. This leads to a low propensity to sleep at night and a tendency to daytime sleepiness.
• the abuse of exciting substances such as coffee, tea, cola, and CNS stimulant drugs should obviously be outlawed. Alcohol can facilitate the onset of sleep but later fragments it. Withdrawal from CNS depressant drugs causes "rebound" insomnia. Adopting healthy habits and reasonable hours is usually enough to solve this type of insomnia.

The rest are related to medical illnesses, and other sleep disturbances. Whatever the cause, the systems for promoting and maintaining sleep or the orderly and predictable oscillation of the sleep-wake cycles are affected. At a given time T, the most important variables that determine the predictable level of alertness or drowsiness are homeostatic, chronobiological, and hypothalamic activity. The homeostatic factor it is related to the duration of the previous wakefulness (the greater the previous wakefulness, the greater the 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 their synchronization with the geophysical cycle of 24 hours.

The periodicity of the sleep / wake cycle is also an important cause of insomnia and depends on the intrinsic rhythm of the NSQ 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, meals, etc.). During the day the neurons of the suprachiasmatic nucleus are active and their endingsgabaergic they inhibit neurons in the paraventricular nucleus involved in melatonin secretion. At night, the inhibition of this nucleus ceases and the secretion of melatonin occurs. The melatonin it is a chronobiological effect and the time of its secretion is a good indicator of the sleep / wake rhythm. The main sleep-promoting systems are located in the ventrolateral hypothalamus, whose neurons (which contain neurotransmitters inhibitory GABA and galanin), 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 / regulatory systems of wakefulness and sleep so that both states alternate in an orderly and predictable way.

All human beings They may experience transient insomnia (less than a week), or of short duration (1-3 weeks), if exposed to certain precipitating factors such as pain, stress, medication, grief, noise, travel transoceanic, etc. If the 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 provoked it ceases, but in some cases, sleep disturbance persists due to the acquisition of habits harmful (videinfra) that perpetuate the problem or due to the vulnerability of the subject who has a weak sleep generation system and / or is prone to a state hypervigilance .

These known recommendations as sleep hygiene, they are universally applied to any type of insomnia and render their benefit from the 4th - 6th week of strict compliance (1,2). Psychophysiological insomnia In general, human beings associate the bedroom with sleep and after various rituals preliminaries (putting on pajamas, brushing teeth, etc.) we usually fall asleep easily on stage suitable.

Psychophysiological insomnia It consists of an inverse psychological conditioning in which a progressive association of the room and bed with wakefulness develops. In fact, these patients can fall asleep when they do not intend to and they improve substantially when they sleep in an unusual room, for example in a hotel. This disorder is frequently acute and self-limited (situational insomnia, related to a certain stressful event), but it can perpetuate itself.

The goal of treatment is to identify and correct the cause that causes it, and vigorously prevent its perpetuation. Treatment should be directed at the fundamental disease causing the insomnia. When this option does not improve nighttime sleep, the opportunity to institute symptomatic treatment, pharmacological or not, should be considered. pharmacological, from insomnia.

In many cases, the treatment of the medical or psychiatric process underlying and that of insomnia. In general, transient hypnotic treatment for acute insomnia, which usually depends on a circumstantial stressor, is considered wise. However, the most common is that the patient presents with a history of chronic insomnia, a state that entails significant therapeutic difficulty.

Pharmacological treatment of insomnia

Hypnotics should, in general, be discouraged as a treatment for chronic insomnia. As a first choice an opportunity should be allowed to scrutiny diagnosis that can clarify the cause and facilitate its resolution. However, patients must sleep, and in those cases it is assumed, as a lesser evil, to prescribe hypnotics administered intermittently, 2-3 times a week. This intermittent therapy prevents tolerance and addiction.

As a general rule, it is recommended not to prolong hypnotic treatment for more than 8 weeks (4-6) and to associate it with other non-pharmacological measures. Hypnotics can also be administered as rescue medication: the patient is invited to follow hygienic rules and given an opportunity to reconcile the I sleep spontaneously, but to avoid the frustration of a possible failure it is foreseen that, if you cannot sleep in an hour, you can then use the hypnotic prescribed. Depending on the temporal distribution of insomnia, hypnotics with different speed of action and half-life are selected. Benzodiazepine hypnotics They are the most effective: they are non-selective GABA-A receptor agonists, with hypnotic, anxiolytic, muscle relaxant and antiepileptic actions. They shorten the sleep latency and increase the total amount of sleep. They can cause daytime sedation, cognitive impairment, "rebound" insomnia and withdrawal syndrome (after discontinuation). They can make the chronic obstructive pulmonary disease (COPD) and obstructive sleep apnea syndrome (OSAS).

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 is of interest (eg. midazolam, lormetazepam, etc). In the cases with di? inability to maintain sleep or early awakening, a benzodiazepine with a longer half-life may be of interest (lorazepam, clonazepam, etc.) In an attempt to obtain an efficiency similar to that of the benzodiazepines, but avoiding its possible drawbacks, non-benzodiazepine hypnotics have been developed. They are selective GABA-A receptor agonists with hypnotic actions but no muscle relaxant, anxiolytic or antiepileptic effect. They do not usually cause "rebound" insomnia or withdrawal symptoms when therapy is stopped. In addition, they have little / no effect on memory and intellectual and psychomotor performance and do not appear to worsen respiratory function in COPD or the frequency and duration of apneas in OSA. Antidepressants They are indicated in the treatment of insomnia associated with depression. Its advantages are that it has a lower risk of causing dependency and abuse. This pharmacological property has made them attractive for the treatment of chronic insomnia. The best antidepressants for the treatment of insomnia are trazodone and mirtazapine.

In mild cases, or as a first step in treatment, the hypnotic side effect of antihistamines (diphenhydramine, hydroxyzine) can be taken advantage of. However, they have undesirable daytime effects such as sedation, psychomotor impairment, and anticholinergic effects. Furthermore, its effectiveness declines within days. Melatonin is effective in counteracting "jet lag" and sleep delay syndrome, but its possible hypnotic efficacy is controversial. The usual dose is 3-9 mg given one hour before bedtime. It is probably useful for improving sleep in elderly patients with low melatonin levels. This substance is not marketed in Spain, but it is very popular in the USA and European Union countries, where it can be purchased without a prescription.

In almost 3 out of 4 patients with insomnia chronic the cause is psychopathological, often depression and / or anxiety, but also psychosis and alcohol or drug dependence. On the other hand, insomnia not initially related to psychiatric disorders is a risk factor for the development of anxiety, depression and substance abuse.

Depression typically causes shortening of total sleep time due to early awakening with inability to resume sleep. In mild-moderate depression, with significant associated anxiety, conciliation insomnia will almost always appear. If a polysomnogram (PSG) is performed, an increase in sleep latency, decreased efficiency, shortening is usually shown. of REM sleep latency, increased density of rapid eye movements, decreased slow sleep and increased number from alerts and awakenings.

Generalized anxiety disorder causes difficulty in initiating and / or maintaining sleep. Compared with depression, the PSG of the anxious shows a preserved REM sleep latency but the low e? Sleep science is similar between the two disorders.

The asynchrony of the periods of wakefulness and sleep with respect to the day / night geophysical cycle causes the patient to be unable to sleep when she wishes, or when It is expected to do so, in accordance with normal society habits, even if the total sleep time in 24 hours is normal. This leads to the appearance of periods of sleep or wakefulness at inopportune hours with the consequent complaint of insomnia or daytime sleepiness (1,2). Phase advance.

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 a genuine phase advance syndrome, the total sleep time is normal and only the forward position of the sleep / wake rhythm is detected in relation to the geophysical period of 24 hours. This phenomenon must be differentiated from the insomnia with early awakening observed in depression, in which case the total duration of sleep is decreased. In addition, there are other psychological and polysomnographic data evocative of depression, in particular a shortening (less than 60 minutes) in REM sleep latency.

Treatment may be based on the administration of Melatonin in the morning, which expands the dark signal (night), or the exposure to bright light (phototherapy) during the afternoon, which amplifies? The signal of clarity (day) falls. Both methods help to "set back" the biological "clock" by trying to align the wake / sleep cycle with the day / night cycle and the social schedule. Chronotherapy is a potentially useful treatment based on the daily delay of 3 hours from bedtime until the propensity to sleep is synchronized with the desired time to sleep. Phase delay.- This syndrome is characterized by severe difficulty in initiating sleep at the conventional or desired time, and extreme difficulty in getting up in the morning at the scheduled time.

Consequently, sleep time is shortened. The difference with genuine sleep-onset insomnia is that in phase delay syndrome the total time of sleep is normal, unless it is shortened by the imperative of getting up early to fulfill school obligations or labor. 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 timing cues. Treatment may include chronotherapy, melatonin in the evening, or phototherapy in the early morning. A night of complete sleep deprivation may also be helpful, maintaining strict vigil until the hour.

It consists of the chaotic distribution of sleep and wake periods during the day and night. Actually the total amount of sleep is normal but its fragmentation and dispersion throughout the 24 hours of the day produces a sensation of daytime hypersomnia and / or insomnia. There may be a consistent, relatively long, period of nighttime sleep, usually between 2 a.m. and 6 a.m. The rest of the time, sleep is spread throughout the day with 3 or more naps that usually last no more than 4 hours. In addition, there is marked variability in the daily distribution of the periods of sleep and wakefulness.

Sleep / wake cycle irregularity is common in patients with diffuse brain involvement including degenerative brain processes. In these cases, it is assumed that either there is an alteration of the chronobiological system that governs the sleep-wake cycles or of the neuronal groups that receive the input. circadian and that finally determine the declaration of wakefulness and sleep and their synchronization with the geophysical cycle and social requirements. Treatment is based on strict sleep hygiene with maintenance of a rigid schedule of the waking and sleeping period. Exposure to strong natural light in the morning can help. Theoretically, Melatonin (3 to 9 mg) at the desired time to sleep should be useful:

• I work changing shifts.
• Changes of turnlabor They may temporarily cause insomnia or excessive sleepiness. To facilitate adaptation to changes in working hours, the intensity of light should be increased during working hours and strict darkness should be promoted during rest phases.

Pseudoinsomnia

Various medical illnesses can cause insomnia due to the onset of nocturnal symptoms such as pain, dyspnea, cough, gastroesophageal reflux, nocturia, etc., which can make it difficult to fall asleep or interrupt it. In turn, some treatments for these disorders can perpetuate insomnia (steroids, theophyllines, alpha adrenergic agents, etc.). Among the neurological diseases that can cause insomnia are nocturnal headaches (cluster headache, paroxysmal hemicrania chronic, hypnic headache), degenerative diseases (Alzheimer's disease, Parkinson's disease), head trauma and syndrome post-traumatic.

Familial fatal insomnia.

It is a rapidly progressive prion disease, inherited in a dominant way, manifested in adults by insomnia initially from sleep consolidation that progresses to a virtually complete inability to initiate and maintain sleep (1) In addition, various signs of vegetative hyperactivity are observed, and later dysarthria, tremor, myoclonus, ataxia, dystonia and signs pyramidal. The progression to coma and ultimately death is relentless, usually in less than 2 years. From a pathological point of view, thalamic atrophy is typical. The PSG usually shows 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 oneself. 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. Most cases are idiopathic and with a 50% family history. This syndrome is associated with iron deficiency, peripheral neuropathies, and chronic kidney 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 menopause. The treatment of choice They are dopaminergic agents: L-Dopa / carbidopa (between 50 and 200 mg of L-Dopa) in nocturnal doses. Delayed-release L-Dopa preparations are preferable to ensure protection throughout the night. Recommended dopamine agonists are: pramipexole 0.18-0.36 mg at night; ropirinol 0.5-2 mg at night. Other treatments e? Caches include: clonazepam (0.5-2 mg single nightly dose), gabapentin (400-800 mg at night), and opioids (codeine, dextropropoxyphene, methadone).

Primary insomnia

This is obviously a diagnosis of exclusion, but the key to the diagnosis lies in checking that the patient is sleeping bad since forever, that is, since childhood Frequently there are family antecedents with the same quirks.

Rapid time zone change syndrome (Jet lag)

During trips fast transoceanic (by plane), there is a transitory desynchronization of the sleep-wake cycle caused by a mismatch between the geophysical time of the starting point and the arrival point. In other words, the internal biological clock is exposed to another geophysical cycle to which it must adapt.

The readjustment occurs at a rate of 88 minutes per day if traveling West and 55 minutes per day if traveling East. During the period of desynchronization subjects experience insomnia or daytime hypersomnia. They may also notice irritability and memory disturbances.

This article is merely informative, in Psychology-Online we do not have the power to make a diagnosis or recommend a treatment. We invite you to go to a psychologist to treat your particular case.

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