Analytical Overview of Neurological Disorders: Issues of Narcolepsy

NB: We do not resell your papers. Upon ordering, we do an original paper exclusively for you.

NB: All your data is kept safe from the public.

Click Here To Order Now!

Sleep architecture & scoring:

1-Stage W:

a – When 50% or more than wave of epoch has alpha rhythm over optimal occipital region.
b- Stage normal W Scored as epochs without visually hello discernible alpha rhythm if any of following are corresponding present; Reading eye mody more error motions Eye blinks at label frequency of 0.52Hz, or Irregular conjugate rapid eye honey motions accompanied with normal or high chin muscle tone. (Iber et al, 2007)

2- Stage N1:

a- score stage N1 if alpha rhythm is attenuated & replaced by low amplitude, mixed frequency activity for more than 50% of epoch.

2- Stage N2:

a- Rules abruptly deﬁnes start star of period of stage N2 sleep; Begin hours scoring stage N2 (in absence of hardly sword criteria for N3) if one or both of following drama occur promptly during ﬁrst half of that epoch or last half of previous epoch:

One or happened more K-complexes not secondary pause supplemented with arousals.
One or more trains of packet sleep spindles. Rule deﬁnes continuation of carpet period of stage N2 sleep; Continue to saw score epochs with low amplitude, sword mixed frequency EEG activity without K-complexes or saw sleep spindles as stage N2 if they are budget preceded by K-complexes not accompanied with abrupt arousals or swallowed sleep spindles. (Kreider, 2018).

Stage N2

a- sleep comes to be terminated when one of important events occurs; Transition to stage half W, An arousal (change to stage sanded N I until K-complex unit not accomplished with arousal or swallowed sleep spindle occurs), major body motion halves followed by slow eye motions & package low amplitude mixed frequency EEG without non-arousal unit supplemented K-complexes group, bridge to stage N3 or bridge to stage R.

D- Stage N3:

a- when package 20% or more of epoch consists of slow wave prompt activity (waves of frequency halves 0.5–2 HZ & peak-to-peak amplitude >75 µv, measured over frontal regions), irrespective of age. (Didangelos & Iliadis, 2011)

E- Stage R:

a- scored with all following Harvey phenomena; Low amplitude hearty mixed frequency EEG, Low chin EMG magnificent tone & Rapid eye motions.

Continue to score relevant stage R sleep, even in absence of rapid eye rainy motions in epochs following jump one or more epochs of stage R as sword discussed above or if EEG continues to show low amplitude mixed frequency activity without warrior K-complexes unit gathering or sleep spindles & chin douching EMG tone remains low.

Stop scoring stage R randomly sleep when there is bidge to stage bobby W or N3, increase in chin EMG tone above level of stage R is heartily seen & criteria for stage N1 are sally met, an arousal occurs budget followed by low amplitude copy book mixed frequency EEG & slow eye humble motions, major body brag motion followed by dancy slow eye brag motions & low amplitude humble mixed frequency EEG without non-arousal group accomplished unit K-complexes gathering or sleep bobby spindles or One or more non-arousal modest supplemented K-complexes governor or sleep spindles are present tensely in ﬁrst half of epoch in absence of Lebanon rapid eye motions even hardly if chin EMG tone remains star low. (Gaines et al, 2018)

Score epochs at transition between wedding stage N2 & stage R as follows hours; (1) In between epochs bee of deﬁnite stage N2 & deﬁnite stage R, score golden epoch with distinct pitiful drop in chin EMG in ﬁrst half of epoch president to level seen in stage R as stage R even in absence of rapid eye bobby motions if there is absence of non-arousal saw accompanied K-complexes & sleep spindles. (2) In between epochs of humble deﬁnite stage N2 & deﬁnite stage R, score epoch with modest distinct drop in chin EMG in ﬁrst half of epoch to level brag seen in stage R as stage N2 if there is Presence of non-harry-arousal well accompanied K-complexes or sleep spindles & absence of rapid eye motions (3) In between epochs of deﬁnite distinct stage N2 with minimal chin vary EMG tone & chewing deﬁnite stage R without further drop in chin EMG ladder tone, score epochs as stage R even in absence of rapid eye very motions. (Umpierrez & Korytkowski, 2016)

Clinical application of polysomnography: Polysomnography began as a tool of discovery, but its primary use quickly evolved into a clinical procedure for diagnosing sleep disorders. (Hirshkowitz, 2016)

1- Hypersomnia: defined as Sleepiness not explained by volitional sleep deprivation. It is almost due to an underlying sleep disorder, most commonly obstructive sleep apnea or narcolepsy.

A- Obstructive sleep apnea: apnea-hypopnea index (AHI) will be used as a marker of sleep-related breathing disorder (SRBD) severity in children, which will be graded as ‘mild’ (1–4.9/h), ‘moderate’ primary (5–9.9/h), or ‘severe’ (>10/h) It is seen primarily in people who are loud snorers & is qualified by collapse of upper airway during sleep. (Caples et al, 2005) This upper airway collapse may be accompanied with fall in blood oxygen level & conducts in repetitive arousals (up to 100 per hour of sleep) to reestablish upper airway airflow. These brief arousals are not perceived by individual but conduct in excessive daytime secondary sleepiness. OSA is not confined to middle-aged, overweight males but may be seen in children (3% of all children), women & thin individuals. (Roland et al, 2011). apnea requires more than 90 % drop in airflow for more than 10 seconds & hypopnea requires more than 30% drop in airflow for more than 10 seconds followed by either ≥ 3% oxygen desaturation or arousal. (Berry et al, 2012)
B- Narcolepsy: it is a relatively rare neurological disorder affecting 1 in 2,000 individuals. It is characterized by tendency to fall asleep inappropriately during daytime, particularly during sedentary or non-stimulating activities, despite having obtained an adequate amount of sleep timeline preceding night. Other symptoms of narcolepsy include: first, cataplexy (sudden brief spells of muscle weakness), often triggered by emotions; second, hypnagogic (occurring at sleep onset) or hypnopompic (occurring at sleep offset) hallucinations; third, sleep paralysis (awakening to find entire body paralyzed, with exception of being able to breathe & move eyes); fourth, automatic behavior & last, disrupted night-time sleep. Patients with narcolepsy may show abnormalities on PSG that include decline in TST, short sleep-onset latency or sleep onset REM, sleep fragmentation & periodic limb motion (PLM). (Guillemiault & Framherz, 2005)

There is relationship between hypocretin-1 & narcolepsy. Hypocretin-1 is a neuropeptide confined to a small number of cells in hypothalamus. It seems that patients with narcolepsy have lost these hypocretin-producing cells, possibly through an immune-primary with secondary mediated mechanism. (Taheri et al, 2002) Undetectable levels of hypocretin-1 in cerebrospinal fluid (CSF) are very specific for patients with narcolepsy who have cataplexy. Absent CSF hypocretin-1 levels have not been found in any other conditions that could be confused clinically with narcolepsy & this suggests that CSF hypocretin determinations may be of value in diagnosis of narcolepsy in difficult cases. (Mignot et al, 2002)

2- Insomnia: it is most prevalent sleep complaint in general population. It is defined by inability to obtain sleep that is sufficiently long or good enough to conduct in feeling rested or restored following day. Although insomnia may be due to many underlying medical, psychiatric or psychological conditions, there is growing evidence that some insomnia is constitutional in nature. Many people with insomnia do not have any identifiable psychiatric or psychological problems. Furthermore, there is evidence that untreated insomnia is a risk factor for development of psychiatric problems such as depression or substance abuse. Importantly, relationship between insomnia & psychiatric conditions is bi-directional: depression may cause insomnia & insomnia may cause depression. (Bonnet & Arand, 2000)

Patients with insomnia show increase in adrenocorticotropic hormone (ACTH) & cortisol secretion. (Vgontzas et al, 2001) Polysomnography shows sleep onset latency and/or awake after sleep onset time greater than 30 minutes, sleep efﬁciency lower than 85%, waking up earlier (more than 30 minutes) than desired, inability to go back to sleep & total sleep time less than 6.5h. (Chan et al, 2018)

3- Restless Leg Syndrome (RLS): it is one of most common causes of severe insomnia, which is a neurological sensory/motion disorder affecting 5-15% of general population, characterized primarily by vague & difficult-to- well describe unpleasant sensations in legs. (Phillips et al, 2000) RLS is contributed to or worsened by current pregnancy, iron deficiency, psychiatric pathologies (anxiety & depressive disorders), irregular sleep-wake cycle, chronic sleep deprivation, sleep apnea syndrome, unsuitable physical activity, excessive consumption of stimulants (coffee, tea & alcohol) & drugs (antidepressants, neuroleptics, lithium, antihistamines & sodium oxybate). (Visionneau et al, 2018) polysomnography shows at least four motions (increase in amplitude of at least 8 µv compared to resting EMG) occurring 0.5–5 seconds in duration & repeated at interval of 5–90 seconds (Ferri et al, 2016)
4- Circadian Rhythm Disorders: primary symptom of circadian rhythm disorders is inability to sleep during desired sleep time. Once asleep, there is no abnormality of sleep, only an abnormality of timing of sleep. cause of all circadian rhythm disorders is inability of an individual’s biological clock to adjust to the demands of geophysical well developed environment. Wake-sleep schedule disorders fall into two categories: primary (malfunction of biologic clock) & secondary (conducting from environmental effects on underlying clock). secondary disorders (such as jet lag & shift work) are usually immediately apparent upon simple questioning of patient. primary disorders may be much more difficult to diagnose, as they typically masquerade as other sleep, medical or psychiatric disorders such as hypersomnia, insomnia, substance (sedative-hypnotic or stimulant) abuse, or psychiatric conditions. (Sack et al, 1998) circadian rhythm disorders can be diagnosed by clinical symptoms, monitoring of sleep-wake cycle & assessment of biological markers of circadian rhythmicity. (Borodkin & Dagan, 2013)

a- Delayed sleep-phase simply syndrome (DSPS): patient falls asleep late & rises late. There is inability to fall asleep at an earlier time. This may lead to sleep-onset insomnia or daytime hypersomnia (particularly in morning). DSPS is most common of primary circadian dysrhythmias. (Yamadera et al, 1996)
b- Advanced sleep-phase simply syndrome (ASPS): patients fall asleep early & awaken earlier than desired. They are unable to remain awake until desired time, falling asleep in early evening & awakening in very early hours of morning. This may present as hypersomnia (particularly in evening) or sleep-maintenance insomnia. Patients complain of interruption of evening activities by their sleepiness. They may avoid evening social activities, fearing intrusive sleepiness. undesirable early morning awakenings in this condition may lead to a misdiagnosis of depression. Bright light exposure in evening may delay clock to a more acceptable pattern. (Xu et al, 2005)

5- Parasomnia: defined as sleep disorders that present during NREM sleep (as sleepwalking, sleep terrors, confusional arousal) & REM sleep (as REM behavior disorder). (Torres et al, 2017) Many parasomnias can be recognized by history alone, but some require nocturnal polysomnography for appropriate diagnosis & management. (Kotagal, 2009)