Sleep and other diseases

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Sleep and Stroke

In 75% of cases, strokes develop during the daytime, the remaining 25% occur during the night's sleep. The frequency of subjective sleep disorders in strokes is 45-75%, and the frequency of objective disorders reaches 100%, and they can manifest themselves in the form of the appearance or intensification of insomnia, sleep apnea syndrome, sleep cycle inversion. Changes in the sleep structure in the acute period of stroke have an important prognostic value, are non-specific in nature, 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 (extremely severe condition or the acute stage of the disease), specific phenomena can be observed in the sleep structure, which practically do not occur in other pathological conditions. These phenomena in some cases indicate an unfavorable prognosis. Thus, the detection of the absence of deep sleep stages, extremely high activation, segmental indices, as well as gross asymmetry (unilateral sleep spindles, K-complexes, etc.) of brain activity indicates an unfavorable prognosis. It is believed that the indicated changes may be associated with a diffuse gross dysfunction of the stem and cortical somnogenic generators (which indicates their organic damage), as well as with an excessive function of the 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 (lethal) outcome of the disease, the disappearance of sleep stages occurs in the following sequence: REM sleep - δ-sleep - stage II. It has been shown that the survival rate of patients with all sleep stages is 89%. In the absence of REM sleep, survival drops to 50%. With the disappearance of REM sleep and δ-sleep, survival is only 17%. If it is impossible to identify sleep stages, the mortality rate reaches 100%. It follows that complete and final destruction of the sleep structure occurs only in cases incompatible with life. An important prognostic factor for the course of a stroke is the analysis of sleep dynamics. Thus, an improvement in the structure of night sleep during a repeated study after 7-10 days is associated with an increase in survival to 100% even in the absence of positive dynamics of neurological manifestations. The presence of sleep apnea syndrome in patients before the onset of a stroke worsens the course of the disease. The appearance of breathing disorders during sleep after a stroke indicates diffuse brain damage, which is a prognostically unfavorable factor.

Given the obligatory nature of sleep disorders in stroke, it is obvious that it is necessary to include sleeping pills in the treatment regimen. In case of night sleep disorders in stroke patients, it is most appropriate to prescribe zopiclone, zolpidem, melatonin (with inversion of the sleep-wake cycle). It is also necessary to take into account the high frequency of sleep apnea syndrome 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 in stroke due to damage to certain brain areas (for example, the brainstem). In any case, in the presence of sleep apnea syndrome, adequate diagnostic and therapeutic measures are necessary.

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Sleep and Epilepsy

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

Other features of epileptic seizures occurring in different functional states of the brain have also been discovered. For waking epilepsy, the left-hemisphere location of foci is typical (or it is represented by idiopathic generalized forms), during the seizure, motor phenomena are more often noted. In sleep epilepsy, foci in the right hemisphere predominate, during the seizure, sensory phenomena are usually noted.

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Sleep-associated epileptic syndromes

There are several forms of epilepsy associated with sleep: idiopathic generalized epilepsy with tonic-clonic seizures, juvenile myoclonic epilepsy, infantile spasms, benign partial epilepsy with centrotemporal spikes, benign partial epilepsy of childhood with occipital paroxysms. Recently, interest has increased in autosomal dominant frontal lobe epilepsy with nocturnal paroxysms and Landau-Kleffner syndrome.

Complex partial seizures that occur during sleep are more often associated with nocturnal frontal lobe epilepsy. Nocturnal temporal lobe epilepsy is also quite common.

Paroxysmal, unexplained awakenings during sleep may be the only manifestation of nocturnal seizures. As a result, the patient is erroneously diagnosed with a sleep disorder. These paroxysmal awakenings may occur in the presence of a deep epileptic focus, especially in frontal lobe epilepsy.

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Epileptic activity during sleep

As early as 1937, FA Gibbs, EL Gibbs, and WG Lenoex noted that "EEG recording during one minute of light sleep provides more information for diagnosing epilepsy than an hour of examination in the waking state." Considering the presence of different functional states during sleep, it plays a dual role in diagnosing epilepsy. On the one hand, some functional states during sleep have an antiepileptic effect (δ sleep and REM sleep). On the other hand, stage II of FMS has a proepileptic effect. In fact, stage II of FMS is a set of paroxysmal elements - sleep spindles, vertex sharp potentials, positive occipital sharp sleep waves (λ waves), K-complexes, etc. In a patient with epilepsy, due to the insufficiency of GABAergic systems, these elements can transform into typical epileptic phenomena ("peak-slow wave" complexes).

It has been established that superficial sleep plays an important role in the detection of epileptic activity. After the discovery of REM sleep, it was found that slow-wave sleep selectively facilitates the occurrence of generalized seizures, while REM sleep facilitates partial seizures, especially of temporal origin. Sometimes temporal epilepsy manifests itself only as paroxysms on the EEG, without clinical manifestations, and with the cessation of epileptic activity, the normal picture of REM sleep is restored. In recent years, it has been established that spikes occurring in REM sleep allow for more accurate localization of the epileptic focus than spikes occurring during slow-wave sleep. Temporal epileptic paroxysms that occur selectively in REM sleep indicate a possible connection between dreaming and epileptic activity of this type.

Sleep deprivation increases epileptic activity and seizure frequency, as has been demonstrated with sleep deprivation. However, in patients with treatment-resistant epilepsy, sleep deprivation may not have a significant effect on the course of the disease.

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

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Sleep and Parkinsonism

The clinical picture of Parkinsonism has a number of features that allow us to talk about the presence of specific mechanisms of pathogenesis in this disease, not characteristic of other forms of organic pathology of the brain. First of all, the phenomenon of the disappearance of most symptoms during sleep should be attributed to the "riddles" of Parkinsonism. The situation is even more surprising because the dopaminergic systems decrease their activity during sleep, as evidenced, in particular, by the increase in the level of prolactin, somatotropic hormone and melatonin during this period. In other words, it is impossible to explain the disappearance of Parkinsonism symptoms during sleep from the point of view of the activation of dopaminergic systems. Parkinsonism symptoms weaken or completely disappear in a hypnotic state, during sleepwalking, with paradoxical kinesias and in some other situations characterized by a special emotional state. The connection between rigidity and tremor with the sleep-wake cycle, as well as with the characteristics of the emotional state, is not accidental and reflects the role of non-specific brain systems in their pathogenesis.

The analysis of the structure of night sleep has allowed us to improve our understanding of the main features of wakefulness in Parkinsonism. It is no coincidence that the history of Parkinsonism is closely linked to the history of the study of the brain mechanisms of sleep and wakefulness. Let us recall that the epidemic of Economo's lethargic encephalitis not only served as a stimulus for more intensive study of Parkinsonism, but also became a reason for physiological studies of the brain mechanisms of sleep. The existence of fairly close functional and morphological connections between the brain systems of wakefulness and sleep and the structures whose damage causes Parkinsonism is evidenced by the clinical picture of the acute and chronic stages of lethargic encephalitis. The combination of drowsiness with oculomotor disorders allowed Economo to suggest that the apparatus regulating sleep is located in the area of the third ventricle near the Sylvian aqueduct.

The most common phenomenon detected by polysomnography in patients with parkinsonism is a reduction in sleep spindles. It is assumed that the expression of sleep spindles correlates with muscle tone and that the regulation of sleep spindles and muscle tone is carried out by some common extrapyramidal structures. During treatment with levodopa drugs, parallel to the reduction of akinesia or rigidity, the presence of sleep spindles increases.

Other features of night sleep in Parkinsonism include a decrease in the presence of REM sleep (characteristic only of patients with pronounced muscle rigidity). To explain this phenomenon, an idea has been proposed about a disorder in Parkinsonism of the mechanisms that reduce muscle tone and play an important role in the implementation of rapid eye movement sleep. Qualitative deviations of REM sleep have also been described: a decrease in the frequency of dreams, an insufficient drop in muscle tone, the appearance of blepharospasm, etc.

It should be noted that sleep disorders in Parkinsonism are highly frequent (difficulty falling asleep, decreased total duration of night sleep, frequent spontaneous awakenings, daytime sleepiness). The effect of levodopa therapy on sleep structure consists of an increase in the number of sleep spindles (as well as total duration of sleep) and an improvement in its cyclic organization. These data indicate a normalizing effect of the drug on sleep structure. Moreover, sensitive parameters suitable for establishing the optimal dose and therapeutic efficacy of levodopa can be found in the structure of night sleep in Parkinsonism patients.

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