Sleep and other diseases

[1], [2], [3], [4], [5], [6]

Sleep and stroke

In 75% of cases of strokes develop during the day, the remaining 25% are for the period of night sleep. The frequency of subjective sleep disorders in strokes is 45-75%, and the frequency of objective violations reaches 100%, and they can manifest themselves in the form of the appearance or increase of insomnia, sleep apnea syndrome, sleep cycle inversion. Changes in the structure of sleep in the acute period of stroke have an important prognostic value, are non-specific, consisting in a decrease in the duration of deep stages and an increase in superficial stages and wakefulness. There is a parallel decrease in quality indicators. In certain clinical conditions (an extremely difficult condition or an acute stage of the disease), specific phenomena may occur in the structure of sleep, which practically do not occur in other pathological conditions. In some cases, these phenomena indicate an unfavorable prognosis. Thus, the discovery of the absence of deep sleep stages, extremely high activation, segmental indicators, as well as gross asymmetry (one-sided sleepy spindles, K-complexes, etc.) of brain activity indicates an unfavorable prognosis. It is believed that these changes may be associated with diffuse gross dysfunction of stem and cortical somnogenic generators (indicating their organic lesion), as well as with excessive function of activating systems reflecting the release of a large number of excitatory neurotransmitters (glutamate and aspartate) in the acute period of stroke. In cases of an unfavorable (fatal) outcome of the disease, the disappearance of sleep stages occurs in the following sequence: fast sleep - δ-sleep - stage II. It is shown that the survival rate of patients in whom all stages of sleep are represented is 89%. In the absence of fast sleep, the survival rate drops to 50%. With the disappearance of fast sleep and δ-sleep, the survival rate is only 17%. If you can not identify the stage of sleep mortality reaches 100%. It follows from this that the complete and final destruction of the structure of sleep occurs exclusively in cases incompatible with life. An important prognostic factor for the course of a stroke is sleep analysis over time. Thus, an improvement in the structure of night sleep with repeated research after 7–10 days is associated with an increase in survival rate of up to 100%, even in the absence of positive dynamics of neurological manifestations. The presence of sleep apnea syndrome in patients before the onset of cerebral stroke worsens the course of the disease. The appearance of breathing disorders in sleep after a stroke indicates diffuse brain damage, which is a prognostic adverse factor.

Taking into account the obligatory nature of sleep disorders in stroke, there is an obvious need to include sleeping drugs in the treatment regimen. In case of night sleep disorders in patients with stroke, the most appropriate is the prescription of zopiclone, zolpidem, melatonin (in the inversion of the “sleep-wake” cycle). One should also take into account the high incidence of sleep apnea in stroke. On the one hand, stroke can develop in patients with sleep apnea syndrome, which worsens its prognosis, on the other hand, sleep apnea syndrome can develop during a stroke as a result of damage to certain brain areas (for example, the brainstem). In any case, in the presence of sleep apnea, adequate diagnostic and therapeutic measures are necessary.

[7], [8], [9], [10], [11], [12], [13]

Sleep and epilepsy

Previously, the terms "sleep epilepsy" and "wakefulness epilepsy" reflected only the fact of the daily affiliation of the manifestations of the disease. After the introduction of the functional neurological approach, it became clear that there are fundamental pathogenetic differences between these forms of seizures. The sleep structure of patients with wakefulness epilepsy was characterized by an increase in δ-sleep representation and a decrease in the frequency of spontaneous activation shifts to this stage. A deficiency of activating effects, which manifests itself in all functional states (in wakefulness and in sleep), is found. In patients with sleep epilepsy, an increase in thalamocortical synchronization was revealed during sleep.

Other features of epileptic seizures occurring in different functional states of the brain have also been found. For wakefulness epilepsy, the typical left-hemispheric location of the lesions (or it is represented by idiopathic generalized forms), during an attack, motor phenomena are more often noted. When sleep epilepsy is dominated by foci in the right hemisphere, during an attack, sensory phenomena are usually noted.

[14], [15], [16]

Epileptic syndromes associated with sleep

There are several forms of epilepsy information associated with the period of sleep: izhymicheskikh-delica-sylicisms, which resembled an ear-to-ear-to-one-to-one-to-one-to-one family of mammothylic anaphytosexia, infantile spasms, benign partial epilepsy with centrally-temperate epilepsy and centrally occurring epilepsy. Paroxysm. Recently, an interest in autosomal dominant frontal epilepsy with nocturnal paroxysms and Landau-Kleffner syndrome has increased.

Complicated partial seizures that occur during sleep are more often associated with nocturnal frontal epilepsy. Quite often, night temporal epilepsy is also observed.

Paroxysmal, unexplained awakenings during sleep may be the only manifestation of nighttime seizures. As a result, the patient is mistakenly diagnosed with sleep disorders. These paroxysmal arousals can occur in the presence of deep epileptic focus, especially in frontal epilepsy.

[17], [18]

Epileptic activity during sleep

Back in 1937, FA Gibbs, EL Gibbs, WG Lenoex noted that “recording an EEG for one minute of superficial sleep provides more information for diagnosing epilepsy than an hour of research in the waking state.” Given the presence of different functional states in sleep, it plays a dual role in the diagnosis of epilepsy. On the one hand, some functional states during sleep have an antiepileptic effect (δ-sleep and PBS). On the other hand, stage II of the FMS has a pro-epileptic effect. In fact, stage II of the PMS is a set of paroxysmal elements - sleepy spindles, vertex sharp potentials, positive occipital sharp sleep waves (λ-waves), K-complexes, etc. In a patient with epilepsy due to the deficiency of GABA-ergic systems, these elements can be transformed into typical epileptic phenomena (peak-slow wave complexes).

Superficial sleep has been found to play an important role in identifying epileptic activity. After the discovery of PBS, it was revealed that slow-wave sleep selectively facilitates the occurrence of generalized seizures, and PBS - partial, especially of temporal origin. Sometimes, temporal epilepsy is manifested only by paroxysms on EEG, without clinical manifestations, and with the cessation of epileptic activity, the normal pattern of PBS is restored. In recent years, it has been established that adhesions arising in PBS allow more precisely localize an epileptic focus than adhesions occurring during slow-wave sleep. Temporal epileptic paroxysms, which appear selectively in PBS, indicate a possible connection between the dream and the epileptic activity of this type.

Lack of sleep enhances epileptic activity and the frequency of attacks, which was demonstrated during sleep deprivation. However, in patients with refractory epilepsy therapy, sleep deprivation may not have a significant effect on the course of the disease.

The latest generation anticonvulsants (valproic acid, lamotrigine, gabapentin, levetiracetam) generally have a less pronounced effect on sleep patterns than barbiturates and benzodiazepines, which contribute to the effectiveness of therapy, better tolerance and normalization of quality of life in patients with epilepsy.

[19], [20]

Sleep and Parkinsonism

The clinical picture of parkinsonism has a number of features that allow us to speak about the presence of specific mechanisms of pathogenesis in this disease, which are not characteristic of other forms of organic brain pathology. First of all, the phenomenon of disappearance of most symptoms during sleep should be attributed to the “mysteries” of parkinsonism. The situation is all the more surprising because dopaminergic systems during sleep reduce their activity, as evidenced, in particular, by an increase in the levels of prolactin, somatotropic hormone and melatonin during this period. In other words, it is impossible to explain the disappearance of symptoms of parkinsonism in a dream from the point of view of activation of dopaminergic systems. Symptoms of parkinsonism weaken or disappear completely in a hypnotic state, during a sleepwalking, with paradoxical kinesies and in some other situations characterized by a particular emotional state. The connection of rigidity and tremor with the “sleep-wakefulness” cycle, as well as with the peculiarities of the emotional state, is not accidental and reflects the role of non-specific brain systems in their pathogenesis.

Analysis of the structure of night sleep has improved the understanding of the main features of wakefulness in parkinsonism. It is no coincidence that the history of the study of parkinsonism is closely connected with the history of the study of the brain mechanisms of sleep and wakefulness. Recall that epidemic of lethargic encephalitis Economo not only stimulated a more intensive study of parkinsonism, but also became a reason for physiological studies of cerebral sleep patterns. The existence of fairly close functional and morphological connections between the brain systems of wakefulness and sleep and structures, which causes Parkinson's disease, is evidenced by the clinical picture of the acute and chronic stages of lethargic encephalitis. The combination of drowsiness with oculomotor disturbances has already made it possible for Econom to assume that the apparatus regulating sleep is in the region of the third ventricle near the sylvian aqueduct.

The most frequent phenomenon detected by polysomnography in Parkinsonian patients is the reduction of carotid spindles. It is assumed that the severity of carotid spindles correlates with muscle tone and that the regulation of carotid spindles and muscle tone is carried out by some common extrapyramidal structures. In the treatment with levodopa, in parallel with a decrease in akinesia or rigidity, the representation of carotid spindles increases.

Among other features of a night's sleep in parkinsonism, a reduction in the presence of PBS (characteristic only for patients with marked muscular rigidity) should be mentioned. To explain this phenomenon, the idea of a violation in Parkinson's mechanisms of mechanisms that reduce muscle tone and play an important role in the implementation of REM has been proposed. The qualitative abnormalities of PBS are also described: decrease in the frequency of dreams, insufficient drop in muscle tone, appearance of blepharospasm, etc.

It should be noted the high frequency of sleep disorders in parkinsonism (difficulty falling asleep, a decrease in the total duration of night sleep, frequent spontaneous awakenings, daytime sleepiness). The effect of levodopa therapy on sleep structure is made up of an increase in the representation of sleep spindles (as well as the total duration of sleep) and an improvement in its cyclical organization. These data indicate a normalizing effect of the drug on the structure of sleep. Moreover, in the structure of night sleep of patients with parkinsonism, one can find sensitive parameters suitable for determining the optimal dose and therapeutic efficacy of levodopa.

[21], [22], [23], [24], [25], [26], [27]