פרק 18 Chapter 18 Sleep and Its Abnormalities Flashcards
תיאור של בחור צעיר עם תקופות חוזרות לסירוגין בהן סובל מאירוע שינה רצופים של 24 שעות והתקפי רעב סביבם, פרט לכך תקין.
EEG מה נראה
1. כניסה מהירה לREM
2. הארכה של NREM
3. היעדר ספינדלים של שינה
4. EEG תקין
EEG תקין.
תסמונת קליין לווין
Episodic disorder characterized by somnolence and overeating.
For days or weeks, the patients, mostly adolescent boys, sleep 18 h or more a day, awakening only long enough to eat and attend to toilet needs.
They appeared dull, often confused, and restless, and were sometimes troubled
by hallucinations. The duration of nocturnal sleep may be greatly prolonged, or they may sleep for days on end. Food intake during and around the period of hypersomnia may exceed three times the normal (bulimia) and occurs almost compulsively during brief periods of semiwakefulness; to a variable extent, there are other behavioral changes such as social withdrawal, negativism, slowness of thinking, incoherence, inattentiveness, and disturbances of memory.
The somnolence has been well studied by modem laboratory methods; **except for the total duration of sleep, the individual components of the NREM and REM cycles
are normal. **
Between episodes these patients are behaviorally and cognitively normal.
The basis of this condition has never been clarified.
The syndrome usually disappears during adulthood, and there is limited pathologic Material a predominance of males, higher C-reactive protein than controls, and a history of early childhood developmental problems.
There was no human leukocyte antigen (HLA) clustering, but children of Jewish heritage were overrepresented.
- בן 30, סובל זה שנים מתחושה של משהו שנוגע בגוף שלו בשלב ההירדמות. לפעמים התחושה מלווה בהבזק של אור, או שמיעת רעש חזק. לפעמים יש קפיצה של הגוף. כל התופעות האלו מעירות אותו משינה ויכולות לחזור פעם או פעמיים במהלך ההירדמות. הדבר מדאיג אותו מאוד, מבקש טיפול. מה הטיפול המומלץ?
1. תכשיר טריציקלי
2. תכשיר אנטיאפילפטי
3. אנטי-פסיכוטי אטיפי
4. אין צורך בטיפול
אין צורך בטיפול- זו תופעה שפירה.
Sensory centers may be disturbed in a similar way to the earlier-described sleep starts, either as an isolated phenomenon or in association with motor phenomena. The patient, dropping off to sleep, may be roused by a sensation that darts through the body, a sudden flash of light, or a sudden crashing sound or thunderclap of head pain—cephalgia fugax, or “the exploding head syndrome” (Pearce). Sometimes there is a sensation of being turned or lifted, and dashed to the ground; conceivably, these are sensory paroxysms involving the labyrinthine-vestibular mechanism. Though obvious causes for concern by patients, these sensory paroxysms are benign.
נהג משאית לאחר 40 שעות במצב שלחסך שינה–מה לא יהיה?
א.אקסופוריה
ב. הפרעה בסאקדות
ג. אובדןהאקומודציה
ד.מיוזיס
ד. מיוזיס
פסיקולציות
lf deprived of sleep (NREM and REM) for periods of 60 to 200 h, human beings experience
increasing sleepiness, fatigue, irritability, and difficulty in concentration. Performance of skilled motor activities also deteriorates; if the tasks are of short duration and slow pace, the subject can manage them, but if speed and perseverance are demanded, he cannot. Self-care is neglected, incentive to work wanes, sustained thought and action are interrupted by lapses of attention, judgment is impaired, and the subject becomes decreasingly inclined to communicate. With sustained deprivation, sleepiness becomes increasingly more intense, momentary periods of sleep (“microsleep“) become more intrusive, and the tendency to all types of accidents becomes more marked. Eventually, subjects fail to perceive inner and external experiences accurately and to maintain their orientation. Illusions and hallucinations, mainly visual and tactile ones, intrude into consciousness and become more persistent as the period of sleeplessness is prolonged.
* Neurologic signs of sleep deprivation include a mild and inconstant nystagmus, impairment of saccadic eye movements, loss of accommodation, exophoria, a slight tremor of the hands, ptosis of the eyelids, expressionless face, and thickness of speech, with mispronunciations, and incorrect choice of words. The EEG shows a decrement of alpha waves, and closing of the eyes no longer generates alpha activity. The seizure threshold is reduced, and seizure foci in the EEG may be activated. Rarely and probably only in predisposed persons, loss of sleep provokes a psychotic episode. During recovery from prolonged sleep deprivation, the amount of sleep obtained is never equal to the amount lost. This is probably a result of the intrusion of brief sleep periods during the waking state and represents a sizable amount of time if summated (it is virtually impossible to deprive a human being or animal totally of sleep). When falling asleep after a long period of deprivation, the subject rapidly enters N3 (NREM) sleep, which continues for several hours at the expense of N2 and REM sleep. But by the second recovery night, REM sleep rebounds and exceeds that of the predeprivation period.
N3 seems to be the most important sleep stage in restoring the altered functions that result from prolonged sleep deprivation.
מה ההבדלת בין
Primary & secondary insomnia
Primary Insomnia
This term is reserved for the condition in which nocturnal sleep is disturbed for prolonged periods and none of the symptoms of anxiety, depression, pain, or other psychiatric or medical diseases can be invoked to explain the sleep disturbance. In some patients, the disorder is lifelong.
insomniacs suffer the effects of partial sleep deprivation and resort to medications or alcohol. Their lives come to revolve around sleep to such an extent that they have been called “sleep pedants” or “sleep hypochondriacs.” Although statements on the quantity and quality of sleep given by insomniacs are often not to be taken as entirely valid, most of them do, indeed, sleep for shorter periods, move and awaken more often, spend less time in N3 sleep than normal persons, and show a heightened physiologic arousal. Personality inventories have disclosed a high incidence of psychologic disturbances in this group, but whether these are cause or effect is not clear.
Furthermore, a category of “conditioned,” or “psychophysiological” insomnia has been denominated, in which a situational trigger for insomnia has ceased, but the sleep disorder persists. Although insomniacs, regardless of the cause, tend to exaggerate the amount of sleep lost, primary insomnia should be recognized as a valid entity.
חולהעםהיפותאירוידיזםוסכרת,תיאורשל
RLS.
מה לא לתת טיפול ?
א.קלונזפם
ב.אמיטריפטלין
ג.פרמיפרקסול
ד.גבהפנטין
אמיטריפטילין- טיפול בטריציקלים או
SSRI
גורמין להחמרה של
RLS ו- PLMDS
אגוניסט לדופמין
The syndrome is idiopathic and persists for years.
Iron-deficiency anemia and low ferritin levels are associated with the syndrome in many instances, as is thyroid disease, pregnancy, and certain drugs, such as antidepressants
and antihistamines
A search for iron deficiency, and its correction if present,
is indicated in almost all cases. A large number of symptomatic
medications have proved helpful in the treatment
of both the restless legs syndrome and periodic leg movements.
As a first choice, many practitioners favor treatment
with dopamine agonists such as prarnipexole (0.25 to 0.75 mg) or ropinirole (0.5 to 1 .5 mg), either one taken 1.5 to 2 h before bedtime. Long-acting combinations of
L-dopa/carbidopa (12.5/50 or 25/100 mg dose) taken at bedtime have also been successful, but L-dopa, and sometimes the dopamine agonists, causes some patients to develop the movements earlier, i.e., in the daytime, which become more intense and spread to other body
parts. A longer acting dopamine agonist, rotigotine patch is available to treat patients who have this augmentation phenomenon. The latter is also helpful for periodic leg movements.
אלו מבין התרופות הבאות עלולה לגרום להתפתחות של
Restless legs syndrome?
- נוגדני דיכאון
- אגוניסטים של קולטני אלפא
- גלולות למניעת הריון
- NSAIDS
- אופיאטיים
נוגדי דכאון
התרופות שגורמות ל
—RLS
הינם נוגדי דיכאון ואנטיהיסטמינים
סיבות נוספות: עייפות, מזג אויר חם, חסר ברזל, היפותירואידיזם, הריון, נוירופתיה אורמית.
טיפול: דופא, אגוניסטים. גאבאפנטין, ליריקה, קלונקס. טגרטול, אופיאטים, בקלופן
בת 25 סובלת מישנוניות יתר, התקפים של צניחת ראש ולסת בזמן צחוק, ואירועים מתועדים של התנהגות אוטומטית מורכבת. התרופה בעלת יעילות מוכחת לצניחת הראש ולסת:
1. Modafinil
2. Methylphenidate
3. Clomipramine
4. Dextroamphetamine
5. Pyridostigmine
clomipramine
No single therapy will control all the symptoms. Narcolepsy responds best to (1) strategically placed 15- to 20-min naps (during lunch hour, before or after dinner, etc.); (2) the use
of stimulant drugs in the daytime—modafinil, dextroamphetamine sulfate, or methylphenidate hydrochloride to heighten alertness; and
(3) antidepressants (sertraline,
venlafaxine, protriptyline, imipramine, or clomipramine for control of cataplexy
מה לא מאפיין נרקולפסיה?
1. לפעמים מלווה בשיתוק חולף בזמן צחוק
2. החולים עלולים להשלח לפסיכיאטר
3. שכיחה יותר אצל גברים
4. מתחילה ברוב המקרים לפני גיל 25
5. קיימת אסוציאציה לגן HLA
המחלה אינה שכיחה יותר אצל גברים!
Men and women are affected equally
a rule, narcolepsy has a gradual onset between theages of 15 and 35 years; in fully 90 percent of narcoleptics, the condition is established by the 25th year of life. Narcolepsy is usually the first symptom**, less often cataplexy; and rarely sleep paralysis.
Approximately 70 percent of narcoleptics first seeking help will report having some form of cataplexy, and about half of the remainder will develop cataplexy later in life. Cataplexy refers to a sudden loss of muscle tone brought on by strong emotion-that is, circumstances in which hearty laughter** or, more rarely; excitement, surprise, anger, or intense athletic activity cause the patient’s head to fall forward, the jaw to drop, the knees to buckle, even with sinking to the ground-all with **perfect preservation of consciousness**
A number of compelling observations implicate
**hypocretin* and its receptors in human narcolepsy. hypocretin-secreting
neurons are depleted in the brains of human
Narcoleptics, and CSF hypocretin levels are reduced or
absent in affected patients.
an autoimmune causation for narcolepsy. For
example, it has long been known that there is an
almost universal association with specific alleles of the histocompatibility antigen HLA-DQ (B1 -0602)
מה המשותף בין התקפי עייפות פוסט-פרנדיאל לבין נרקולפסיה?
1. תדירות גבוהה עד 6 פעמים ביום
2. מופיע לאחר אכילה
3. רצון עז לישון בזמן דיבור
4. מופיע בזמן פעילות
מופיע לאחר אכילה (פרנדיאל= קשור לאוכל)
Narcolepsy is usually the first symptom, less often cataplexy; and rarely sleep paralysis. The essential disorder is one of frequent attacks of irresistible sleepiness. Several times a day; usually after meals or while sitting in class or in other boring or sedentary situations, the affected person is assailed by an uncontrollable desire to sleep. The eyes close, the muscles relax, breathing deepens slightly, and by all appearances, the individual is dozing. A noise, a touch, or even the cessation of the lecturer ‘s voice is enough to awaken the patient. The periods of sleep rarely last longer than 15 min unless the patient is reclining, when he may continue to sleep for an hour or longer. At the conclusion of a nap, the patient feels somewhat refreshed.
מה לא ייגרם בפגיעה בהיפותלמוס?
1. הפרעת שינה מסוג RBD
2. שתיה מרובה והשתנה מרובה
3. בצקת ריאות נוירוגנית
4. סומנלובוליזם
HYPOTHALAMIC SYNDROMES
- Diabetes Insipidus
- Syndrome of Inappropriate Antidiuretic Hormone Secretion
- Cerebral Salt Wasting (Nelson Syndrome
- Precocious Puberty
- Failure of Puberty
- Adiposogenital Dystrophy (Froehlich Syndrome)
- Anorexia Nervosa and Bulimia
- Abnormalities of Growth
- Disturbances of Temperature Regulation
- Cardiovascular Disorders With Hypothalamic Lesions
- Neurogenic Pulmonary Edema
- Disorders of Consciousness and Personality
- Periodic Somnolence and Bulimia (Kleine-Levin Syndrome)
א. נראה סקאדות בתנועות עיניים.
מדובר ב
REM SLEEP BEHAVIOR DISORDER
The episodes, which occur exclusively during REM sleep, usually in the second half of the night, are out of keeping with the patient’s
waking personality. Polysomnographic recordings during these episodes have disclosed augmented muscle tone but no seizure activity.
variable but sometimes detailed recall of a nightmare of being attacked and fighting back or attempting to flee.
The episodes can be suppressed by the administration of clonazepam in doses of 0.5 to 1.0 mg at bedtime and by melatonin, 3 to 12 mg. The advantage of the latter is that sleep apnea is not affected as it is with benzodiazepines. Discontinuation of medication, even after years of effective control, has resulted in relapse. Antidepressants are said to exacerbate the disorder with the possible exception of bupropion.
It usually occurs soon after falling asleep,
during stage 3 or 4 sleep. The child awakens abruptly in a state of intense fright, screaming or moaning, with marked tachycardia (150 to 170 beats/min) and deep, rapid respirations. Children with night terrors are often sleepwalkers as well, and both kinds of attack may occur simultaneously. The entire episode lasts only a minute or two, and in the morning the child recalls nothing of it or only a vague unpleasant dream.
בןאדםבזמןשינה, בEEGישדלטאאיטי .
מה לא נכון ?
א. ירידה בטמפרטורה
ב. ירידה בדופק ושינה
ג. ירידה בהפרשתGH
ד. ירידה במטבוליזם
לא נראה ירידה בהפרשת
GH
אקטיבציה של
VLPO
The suprachiasmatic nucleus (SCN) of the hypothalamus has no direct influence on the sleep cycle but does integrate ambient light cues, and thereby affects various circadian rhythms, including sleep.
Experiments in animals and analyses of cases of von Economo encephalitis (that caused a pathologic sleep syndrome) have indicated that the ventrolateral preoptic nucleus of the hypothalamus (VLPO) sends fibers to all the other major cell groups of the hypothalamus and brainstem that are engaged in arousal. Damage to the VLPO results in pathologic
wakefulness, and the virtual absence of sleep. The SCN has only minimal projections to the VLPO and to orexin containing neurons (see further on), but it does strongly innervate the subparaventricular zone (SPZ) and the dorsomedial hypothalamic nuclei. The last of these areas integrates feeding, temperature, light, and other cues from SPZ and SCN.
The brain contains a three-stage pathway for the control of the sleep rhythm.
* the awake state is maintained by monoaminergic activity (locus ceruleus, tuberomammillary nucleus [TMN], and the
raphe nuclei) that inhibits the VLPO.
* Sleep occurs when the VLPO is activated, which reciprocally removes the tonic inhibitory action of the monoaminergic system.
* The orexin neurons act through the monoaminergic system as a stabilizing influence to prevent rapid transitions from one state to the other
transitions between NREM and REM sleep are governed by the pontine reticular formation and are influenced by acetylcholine.
Although it is generally agreed that cholinergic
mechanisms selectively promote REM sleep, and its components-rapid eye movements, absence of activity in the antigravity muscles (i.e., atonia), and desynchronized
EEG-the role of amines has been more difficult to
Establish.
ג. VLPO
- Fatal Familial Insomnia: The cerebral changes consist mainly of profound neuronal loss in the anterior or anteroventral, and mediodorsal thalamic nuclei.
-
Medullary lesions may affect sleep by altering automatic ventilation; the most extreme examples occur with bilateral tegmental lesions that may completely abolish breathing during sleep (“Ondine’s curse). Lesser degrees of tegmental damage-as might occur with Chiari malformations, unilateral medullary infarction, syringobulbia, or poliomyelitis-may cause sleep apnea, and daytime drowsiness. Patients with large hemispheric strokes may also be left with daytime
lethargy on the basis of inversion of sleep-wake rhythm. Certain instances of mesencephalic infarction that are characterized by vivid visual hallucinations (peduncular hallucinosis) may be associated with disruption of sleep. von Economo encephalitis, now an extinct illness, was usually associated with a hypersomnolent state but caused persistent insomnia in some instances. The latter was related to a predominance of lesions in the anterior hypothalamus and basal frontal lobes, in distinction to hypersomnia, which was related to lesions mainly in dorsal hypothalamus and subthalamus. - Regarding Normal Aging- Brain shrinkage is accounted for in part by the reduction in size of large neurons, not their disappearance. There is a more substantial reduction in neuronal number in the substantia nigra, locus ceruleus, and basal forebrain nuclei. It may be possible to differentiate normal aging from disease in the medial temporal lobe by distinguishing between cell loss in specific regions.
- animal studies have related acute anxiety to a disturbance of function of the locus ceruleus and the septal and hippocampal areas, the principal norepinephrine-containing nuclei.
The locus ceruleus is involved in rapid eye movement (REM) sleep and drugs such as the tricyclic antidepressants and monoamine oxidase inhibitors, which suppress REM sleep, also decrease anxiety. Certain of the serotonin receptors in the brain, different from those implicated in depression, have been related to anxiety. Other parts of the brain must also be involved; bifrontal orbital leukotomy diminishes anxiety, possibly by interrupting the medial forebrain connections with the limbic parts of the brain. Positron emission tomography (PET) studies in subjects who anticipate an electric shock show enhanced activity in the temporal lobes and insula, implicating these regions in the experience of acute anxiety.
Table 18-1
AMERICAN ACADEMY OF SLEEP MEDICINE (AASM) SLEEP SCORING SYSTEM
Table 18-2
CAUSES OF DAYTIME SLEEPINESS
Figure 18-1. Conventional EEG (30 mm/s) of a young healthy woman in stage 2 (N2) sleep showing vertex waves (large arrows) and sleep
spindles (small arrows), best seen in the central regions.
Figure 18-2. Representative polysomnographic recordings from adults in the awake state and various stages of sleep. Recordings are made at conventional sleep laboratory speed of 10 mm/s (i.e., at the paper speed of one-third standard clinical EEG recordings).
A. Upper tracings: Awake state (with eyes closed). Alpha rhythms are prominent in EEG. Normally active chin EMG.
B. Middle tracings: Stage 1 (N1) sleep. Onset of sleep is defined by the diminished amplitude of alpha waves in the occipital EEG channel (“flat” appearance).
C. Lower tracings: Stage 2 (N2) sleep, characterized by appearance of high-amplitude single-complex (K) waves and bursts of 13- to 16-Hz waves (sleep spindles) on a background of low frequency.
D. Upper tracings: Stage 3 (N3) sleep. Appearance of high-voltage slow (delta) waves.
E. Middle tracings: Deepest stage of N3 sleep, with predominant delta-wave activity occupying 50 percent of a 30-s tracing.
F. Lower tracings: Rapid eye movement (REM) sleep, characterized by episodes of REM and occasional muscle twitches in an otherwise flat chin EMG. Technical Note: Four sites from the same montage are illustrated in each recording: C3/A2, left central to right mastoid; O2/A1, right occipital to left mastoid; ROC/A1, right outer canthus to left mastoid; LOC/A2, left outer canthus to right mastoid. A chin EMG tracing is added to each recording. (Adapted with permission from Butkov N. Atlas of Clinical Polysomnography. Vol 1. Synapse Media, Medford, OR, 1996.)
Figure 18-3. Sleep architecture, or sleep cycles. REM sleep (darkened areas) occurs cyclically throughout the night at intervals of approximately 90 min in all age groups. REM sleep shows little variation in the different age groups, whereas stage 4 sleep decreases with age. Stages 3 and 4 are now considered N3. (Redrawn by permission from Kales, Kales, and Soldatos.)
Figure 18-4. Schematic representation of the “flip-flop” mechanism of transition between sleep and waking, which is determined by the state of activity of the ventrolateral preoptic nucleus (VLPO). Arrowheads denote excitation and perpendicular line ends are inhibitory. A. During wakefulness, the monoaminergic nuclei (LC, locus ceruleus; TMN, tuberomammillary nucleus; raphe nuclei) inhibit the VLPO, thereby relieving the inhibition of the monoaminergic cells, and that of the orexin (ORX) neurons. Because the VLPO neurons do not have orexin receptors, orexin serves to reinforce the monoaminergic tone, rather than directly inhibiting the VLPO. B. During sleep, firing of VLPO neurons inhibits the monoaminergic cell groups, thereby relieving their own inhibition. This inhibits the orexin neurons, further preventing monoaminergic activation that might interrupt sleep. The mutual inhibition between the VLPO and the monoaminergic cell groups forms a flip-flop switch, which produces sharp transitions in state, but is relatively unstable. The addition of the orexin neurons stabilizes the switch. (Reproduced with permission from Saper, Scammell, and Lu.)
