Clinical Disorders of SleepISMET KARACAN, M.D., (Med.) D.Sc., PATRICIA J. SALIS, M.A. AND

ROBERT L. WILLIAMS, M.D.

The modem era of sleep research can beconsidered to have begun in 1935, whenLoomis, Harvey, and Hobart! first describedfive stages into which electroencephalographic(EEG) activity during sleep could be cate­gorized. The next major discovery did notoccur until 1953, when Aserinsky and Kleit­man2 reported that bursts of conjugate, rapideye movements (REM) periodically appearduring sleep. The later report of these sameauthors:! that subjects awakened during REMperiods recalled dreaming much more oftenthan when they were awakened from otherstages of sleep, was the primary stimulus forthe truly immense activity which has charac­terized the field of sleep research during thelast 20 years.

As a result of this activity, it has beenlearned that normal, healthy individuals alter­nate between REM and the other, non-REM(NREM), stages of sleep throughout eachnight. NREM sleep consists of stages 1, 2, 3,and 4 sleep, with each successive stage repre­senting progressively more synchronized EEGactivity. REM sleep consists of stage 1 lowvoltage, fast activity in the EEG and REM inthe eye movement channels. S!ages 3 and 4sleep are typically concentrated during thefirst part of the night, while REM sleep pre-

The preparation of this review and some of thework described were aided by Public Health Servicegrant MH 15508, Veterans Administration researchfunds, and Clinical Research Center grant FR-82.

This paper was presented at the Annual Meeting ofthe Academy of Psychosomatic Medicine, San Diego,California, October, 1972.

Dr. Karacan is from Department of Psychiatry,University of Florida, and Psychiatry Service, Vet­erans Administration Hospital, Gainesville, Florida.

Patricia Salis is from Department of Psychiatry,University of Florida, and Research Service, VeteransAdministration Hospital, Ganesville, Florida.

Dr. Williams is from Department of Psychiatry,Baylor College of Medicine, Texas Medical Center,Houston, Texas.

March-April, 1973

dominates during the later part of the night.4

Each individual exhibits a relatively consistentand characteristic sleep pattern from night tonight. However, the precise sleep pattern isvery much dependent upon the individual's age,for there are quite definite changes in character­istic sleep patterns with increasing age.4•8 Itis presently believed that REM and slow-wavestages 3 and 4 sleep serve particularly impor­tant functions, because selective deprivation ofthem is followed by compensatory increases intheir amounts on recovery nights.9,lo REMsleep is the parameter which has been mostconsistently found to be affected by pharma­cological agents: A vast majority of the com­pounds evaluated suppress REM sleep to atleast a mild extenLll-13

In addition to the studies which have pro­vided this type of information, a great numberof sleep researchers have been engaged in anintensive exploration of the relevance of sleepdisturbances to the understanding of the etiol­ogy and process of numerous disease states.These efforts have produced literally thousandsof miles of EEG data. As you will shortly see,they have also provided many intriguing piecesof information, and hypotheses concerningthem. However, perhaps more so than in manyother fields, much of this information has yetto become understood by the general popula­tion of physicians, and thus it has yet to makethe widest possible contribution to the diag­nosis, prognosis, and treatment of patients.

In the hopes of helping correct this situation,we will spend the next several minutes reviewingsome of the major findings ~rom the sleeplaboratory concerning various clinical condi­tions. As in other fields, obtaining the mostcoherent picture of such data would be greatlyaided by a satisfactory classification system.Such a system does not yet exist in the field ofsleep research. We believe that the most efficientmanner of deriving a useful system would be to

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PSYCHOSOMATICS

construct a sort of "Periodic Table" of sleepdisorders, with various neurophysiological,physiological, biochemical and psychologicalvariables listed along one axis and the clinicalsyndromes listed along the other. Naturally, theEEG characteristics would be the most impor­tant neurophysiological variables to consider.We should include categories not only relat­ing to the conventional measures of sleep,such as the percentages of each sleep stage,total sleep time, etc., but also categories relat­ing to the basic waveforms of the sleep EEG.Numbers and distributions of sleep spindlesand delta activity are examples of these vari­ables. With recent advances in the computeranalysis of the sleep EEG, the derivation ofsuch quantities is becoming more and morefeasible. With these same computer techniques,we could also derive information on quali­tative changes in the various waveforms of thesleep EEG. Among the other variables whichwe might include are measures of electromyo­graphic (EMG) activity, eye movement activ­ity, including eye movement density, nocturnalpenile tumescence, blood pressure, heart rate,and respiration rate. Changes in the variousbiochemical and neurohormonal concomitantsof sleep should also be noted, as well as findingsrelated to the personality characteristics of thepatients, the natural history of each clinicalcondition, and the type and outcome of re­sponses to different treatment modalities.

If we were to construct such a table today,we would quickly see that most of the cellswould be blank. However, preparing this tablenow might not be a wasted effort, for it wouldcertainly graphically illustrate the areas inwhich further research should be concentrated.When enough information had been gatheredto complete this table, an evaluation of thesimilarities and dissimilarities among and be­tween the clinical syndromes on all of the vari­ables would form the logical empirical basisfor a useful classification system.

But since we are not yet able to constructa complete table of sleep disorders, we mustmake do with rather arbitrarily determinedclassification systems which seem to best ac­count for the data we possess at present. The

78

classification scheme we will employ here issuch an attempt. It is presented in Table I. Forconvenience, we have divided the diseases onwhich we currently have data into four generalcategories. The first, which we have called Pri­mary Sleep Disorders, includes conditions inwhich abnormalities of sleep constitute theprincipal, and frequently only, symptoms.In the Secondary Sleep Disorders, specific ornon-specific sleep disturbances may accompanythe chronic clinical problem. The Parasomniasrepresent sleeping behaviors or automatismswhich are normal during wakefulness but con­sidered abnormal, or at least unusual, duringthe sleeping state. The last category, Sleep­Modified Disorders, is something of a "catch­all" category, but it generally includes the nu­merous disorders which are known to bechanged, either for better or worse, during thesleeping state, but which appear not to havesignificant effects on, or be accompanied bychanges in, sleep itself.

PRIMARY SLEEP DISORDERS

It is becoming increasingly evident to manyphysicians and researchers that primary insom-

TABLE ICLINICAL DISORDERS OF SLEEP

Primary Sleep DisordersInsomniaNarcolepsyChronic HypersomniaKleine-Levin SyndromePickwickian SyndromeSleep ParalysisNightmares

Secolldary Sleep DisordersSchizophreniaDepressionChronic AlcoholismPostpartum Emotional DisturbancesChronic Renal InsufficiencyNutritional DisordersThyroid DysfunctionNeurological Disorders

PlIrllsomlliasSleepwalkingSleeptalkingNocturnal EnuresisBruxism

Sleep-Modified DisordersCardiovascular DisordersRespiratory DisordersEpilepsiesNeuromuscular Disorders

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DISORDERS OF SLEEP-KARACAN. ET AL.

nia is a distinct disease entity, and is to be dis­tinguished from an inability to sleep which isassociated with some other chronic physical ormental disturbance. Although recent evidenceindicates that some form of psychological dis­turbance probably accompanies primary insom­nia or the related "poor sleep" syndrome,14.17there is also good evidence of a physiologicalbasis for the insomniac's often rather vaguecomplaint of inability to sleep. Sleep laboratorystudies have shown that these patients exhibitEEG signs of disturbances in sleep induction,sleep maintenance, and/or sleep quality.16,18-20Furthermore, Monroe16 has reported that hissample of "poor sleepers" exhibited heightenedphysiological activation (heart rate, peripheralvasoconstriction, and rectal temperature) bothbefore and during sleep. Our own concentratedstudy of insomniacs has impressed us with sev­eral facts. The first is that within any some­what random sample of insomniacs there is astriking degree of heterogeneity, both in termsof the patients' complaints and in terms oft;~e EEG signs of sleep disturbance. This hasled us to speculate that there are at least severalsubtypes of insomnia which further researchwill allow us to describe according to EEGcharacteristics. Another finding is that a par­ticular patient may show an abnormally highdegree of variability in his EEG sleep patternsfrom one night to the next. This suggests thatat least part of the insomniac's problem may behis inability to rely on a night's sleep properlypreparing him for the next day. A third findinghas been that some patients who may not exhib­it any quantitative EEG sleep disturbances,nevertheless exhibit certain qualitative EEGsleep disturbances, such as an intermingling ofalpha and delta activity. These qualitativechanges could conceivably be the basis for theircomplaints of inadequate sleep. Our prelim­inary irr.pression is that pharmacologic treat­ment is often ineffective in such patients.

Narcolepsy is one of the most dramatic ofthe primary sleep disorders. The modem diag­nostic criteria, elucidated by Voss and Daly in1957,21 delineate the narcoleptic tetrad as con­sisting of sleep attacks, cataplexy, sleep paraly­sis, and hypnagogic hallucinations. AU patientsdo not exhibit all four elements of the tetrad,

March-April. 1973

but most do exhibit sleep attacks. As withinsomnia, there is some indication that psycho­logical factors may play a role in narcolepsy,but in this case it would appear to be the roleof a precipitator22 rather than of a chronic dis­turbance. 23,24 From sleep laboratory studies itappears that most narcoleptics who exhibitsleep attacks and at least one of the auxiliarysymptoms in the tetrad, suffer from a distur­bance of the REM sleep system. This is sug­gested by the finding that both daytime andnocturnal sleep in these patients are frequentlycharacterized by a REM period very near theonset of sleep.25-30 Such sleep-onset REM pe­riods are rarely observed in normal subjects.Furthermore, the auxiliary symptoms of sleepparalysis, cataplexy, and hypnagogic hallucina­tions appear to be exaggerated and dissociatedforms of REM sleep.26,27,29.32 On the otherhand. narcoleptics who suffer only from sleepattacks seem to have a primary disturbanceof the NREM sleep system, for their sleep at­tacks are generally indistinguishable from typi­cal NREM sleep periods, and the patientsrarely exhibit the sleep-onset REM periodscharacteristic of the first type of narcoleptic. 26.29

A further distinction between these two typesof narcoleptics is the quality of their nocturnalsleep. Patients with several of the narcolepticsymptoms show numerous and long awaken­ings, decreased sleep time, frequent body move­ments, and decreased slow-wave sleep.25.3o,33.36Patients with only sleep attacks seem to sleepquite normally at night.25,34 Although it is gen­erally agreed among sleep researchers that nar­coleptics with auxiliary symptoms do sufferfrom a REM sleep disturbance, there is somecontroversy about whether or not all narcolep­tics suffer from a NREM sleep disturbance.Some evidence 29,37,38 suggests that this is thecase, but the issue remains to be resolved.

A distinct clinical disorder of chronic hy­persomnia has only recently been recognized,and this has been largely due to the studiesby Roth and Rechtschaffen and their col­leagues.23 ,:19,40 The principal complaints areextended nocturnal sleep periods and/or nu­merous and lengthy daytime sleep periods. Al­though nocturnal sleep appears to be undis­turbed, a frequent complaint is postdormital

'79

PSYCHOSOMATICS

confusion, or "sleep drunkenness." Daytimesleep attacks are generally longer and less com­pelling than those of the narcoleptic. Sleeplaboratory studies of samples of these patientsrevealed that their nocturnal sleep was essen­tially normal, though somewhat longer than isusually observed in the sleep laboratory. Theextended sleep consisted of a continuation ofthe expected pattern of REM and NREM sleep.Daytime sleep attacks were characterized byalternations between stages I and 2 sleep andwakefulness, although the recording times andprocedures may have biased against the appear­ance of REM and slow-wave sleep. Two epi­sodes of postdormital confusion were recorded,and seemed to consist of a mixture of stage Isleep and wakefulness. Perhaps the mostintriguing finding was that hypersomniacs ex­hibited higher heart and respiration rates thanthe investigators had recorded in various othertypes of normal and abnormal sleepers. Therewas even the suggestion that the severity of thehypersomnia was related to the degree of ele­vation of these physiological responses.

The Kleine-Levin syndrome is a rare dis­order consisting primarily of periodic hyper­somnia and excessive eating.41,4~ Among re­searchers there is currently some debate aboutwhether this is indeed a distinct clinical en­tity,4:1.4;; and, what is even more important,whether these patients really sleep excessively.In one series of patients the daytime sleep dur­ing exacerbations was described as natural;4G ina second study it was light and unstable, butessentially normal;47 and in two other studiesthere was no evidence of sleep spindles.4;;,48Since the presence of sleep spindles is requiredby current sleep EEG scoring methods to de­termine the presence of sleep, this latter resultwould indicate that the patients may in fact notbe asleep during their exacerbations. However,the few results from studies of nighttime sleepin these patients indicate that they do sufferfrom some sleep abnormality. During anexacerbation, one patient's nocturnal sleep waslight and unstable, with decreased amounts ofREM and stage 4 sleep.47 This and one otherpatient49 were studied between exacerbations,and although deep sleep had attained normallevels, REM sleep continued to be depressed.

80

The systems disturbed in this syndrome-sleep,alimentary, and sexual-support the currentnotion that the disorder stems from some dys­function in hypothalamic or diencephalicareas, 4~,4G.48,;;0.;;r. although some authors main-tain that psychological factors interact with thisorganic defect to produce the characteristicsymptom complex.56.58

Another syndrome characterized by hyper­somnia is the Pickwickian syndrome. Pick­wickian patients also exhibit obesity and per­iodic respiration.:w.62 Rather extensive studiesof the relationships between the sleep andrespiratory disturbances have revealed a uniqueinteraction between these two systems.60,62.G5Throughout his daytime and nocturnal sleepthe Pickwickian exhibits cycles of the followingevents: entry into sleep, appearance of apneawhile sleep patterns continue, EEG arousalresponse just prior to the return of respiration,and several deep breaths signalling the returnof respiration. The arousal may not be a com­plete awakening, although periodically through­out the sleep period there are complete arousalsat this p8int. The length of the apneic intervalseems to be directly related to the depth of theac.:ompanying sleep. Furthermore, sleep pro­gressively deepens with successive apneiccycles. As would be expected from this descrip­tion, the cardinal characteristic of the sleep ofPickwick ian patients is its fragmentation, eventhough patients may obtain greater than normaloverall amounts of sleep.64,6G,G7 They alsoseem to obtain only low amounts of REM andslow-wave sleep.6o,GI,G4.GG,68 Although there arecurrently debates concerning the pulmonaryfunction status of these patientsGO,61,G3,G4,G7,G9and the nature of the mechanisms controllingthe apneic episodesGO,G4,1i1i and the hypersomno­lence,GO,G3.G5 it seems clear that the Pickwick­ians' respiratory disturbances during sleep areat least in part merely exaggerations of changesin respiration which occur during normalsleep.62,65,68,70.75

Sleep paralysis, in addition to being one ofthe elements of the narcoleptic tetrad, has beenmore and more often described as an isolated,though benign, disturbance. 76·87 It is charac­terized by an inability to move while apparently

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DISORDERS OF SLEEP-KARACAN, ET AL.

fully conscious, and occurs during the transi­tion between sleep and wakefulness. It is oftenaccompanied by anxiety and hypnagogic hal­lucinations. Although it has yet to be deter­mined whether isolated sleep paralysis attacksare identical to those experienced by narcolep­tics, data from studies of the latter indicate thatnarcoleptic sleep paralysis attacks occur dur­ing these patients' sleep-onset REM peri­odsP,37 This fact, along with the facts thatboth normals88 and narcoleptics89 lose spinalreflexes during REM sleep, and that relativelylight sleep characterizes the early part of thenarcoleptic's sleep-onset REM period,27 sug­gest indeed that sleep paralysis attacks repre­sent a dissociation of REM sleep phenomena,i.e., the occurrence of muscular inhibition andthe dreamlike state during a relative wakingstate. It has been suggested that this mecha­nism accounts both for the narcoleptic's sleepparalysis attacks as well as for those of other­wise normal individuals.37,90 It has yet to besuggested how this mechanism might accountfor post-dormital sleep paralysis attacks.

Two types of nightmares, or frighteningdreams, can be distinguished on the basis ofclinical and sleep laboratory descriptions. Thenight terror (pavor nocturnus in children, in­cubus attacks in adults) is a slow-wave sleeparousal phenomenon91 ,o2 and is characterizedby a sudden scream and arousal with a com­plex of unpleasant emotions and autonomicchanges. Some evidence suggests that thelength of the slow-wave sleep interval precedingthe arousal, and the quantity of delta activityduring this interval, are positively related tothe intensity of the attack.91 Dream contentelicited following the arousal usually consistsof a single vivid scene.91 In contrast, the dreamanxiety attack occurs during REM sleep91 andis less panic-provoking than the night terror.It is characterized by much more elaboratedream content, and even when mild to markedanxiety accompany the arousal there may be nosigns of autonomic activation.91

SECONDARY SLEEP DISORDERS

Based on early evidence that experimentaldeprivation of REM sleep produced some psy­chological changes in normal subjects,10,93,94

March-April, 1973

numerous investigators began to explore thehypothesis that the delusions and hallucinationsof schizophrenia might represent an eruptionof REM phenomena into the waking state. Al­though some patients have been described asexhibiting isolated abnormalities of REMsleep,05.08 more recent evidence concerningthe effects of REM deprivation in normals99.101and studies of the REM sleep and waking char­acteristics of schizophrenicsIl5,OG,98,102.108 havegenerally failed to consistently support theoriginal findings with respect to both REM dep­rivation in normals and the presence ofsevere REM abnormalities in schizophrenics.However, this research endeavor has produceda most interesting finding: It has been shownthat remitted schizophrenics exhibit normalor exaggerated REM compensation followingexperimental REM deprivation, but that active­ly ill patients fail to exhibit such a REM re­bound.wo.lll It has been suggested that a de­fect in the neurochemical regulation of pontine­geniculate-occipital spike activity might ac­count for these findings and for many of thesymptoms of the schizophrenic psychosis,u0.112Evidence of a deficit in slow-wave sleep inschizophrenics102,1I3 and of their failure to ex­hibit normal slow-wave recovery following ex­perimental deprivation of this type of sleep,ll4further suggests that these patients possessseveral fundamental defects in sleep mecha­nisms.

Since sleep disturbances are part of the symp­tomatology of the depressive illnesses, it wasnatural that depressed patients would be studiedin the sleep laboratory. These studies haverather consistently demonstrated that variousarousal disturbances of sleep, as well as deficitsin slow-wave sleep, are characteristic of thisdisease. 115.127 Some patients exhibit REM sleepabnormalities, but others do not.1I6.126,128­tal Although not all depressed patients respondnormally to experimental REM sleep depriva­tion, those who do, as well as those whose REMsleep is depressed by pharmacological means,exhibit a parallel improvement in their clinicalstate.l:l2,133 Whatever the means of producingclinical improvement, it is usually accompaniedby an improvement in most of the EEG sleepdisturbances. 116,117,119,120,123,134 It has gener-

81

PSYCHOSOMATICS

ally been found that there is great variability inthe sleep patterns of depressed patients,118,121­1~3,12;; and there is some evidence that differencesin the severity of the illness, the age of the pa­tient, and the diagnostic sub-type may accountfor some of this variability.135,136

In normal subjects,13i.140 as well as in chronicalcoholics,141-1H the administration of alcoholinitially produces a suppression of REM sleep.With administration of constant doses of alcoholover several nights, REM may return to normallevels, but administration of increasing doses ofthe drug may produce a continued suppressionof this type of sleep. Occasionally, however,the chronic alcoholic will exhibit excessiveamounts of REM sleep while chronically in­ebriated. Furthermore, some chronic alcoholicsshow an initial suppression of slow-wave sleepand then a return to normal levels duringcontinued alcoholization. Other patients maynot obtain any slow-wave sleep. Total sleeptime may increase in the inebriated alcoholic,but sleep may be noticeably fragmented. Whenthe chronic alcoholic is withdrawn from alco­hol, REM sleep usually rebounds for severalnights and stage 4 sleep may be absent. It hasbeen suggested that the REM rebound may ac­count for the delirium, hallucinations, and sei­zures characteristic of alcohol withdrawal, andthat the complaints of sleep disturbance duringthis phase result from the absence of stage 4sleep. Other evidence suggests, however, thatdeficits in stage 4 sleep are a persistent char­acteristic of chronic alcoholism.

Motivated at least partially by an interest inpostpartum emotional disturbances, severalstudies have been made of sleep patterns duringpregnancy and the postpartum period. 145·148The most promising finding has been that bothREM and stage 4 sleep may show sizeablechanges during pregnancy, particularly duringthe last trimester. Certain arousal disturbanceswhich are observed during pregnancy, as wellas the disturbances in REM and stage 4, maypersist past the time of the first postpartummenses. These findings have suggested to usthat the return of the menses does not neces­sarily signal the complete normalization of allphysiological processes. Furthermore, it is pos-

82

sible that continued, exaggerated disturbancesof REM and/or stage 4 sleep during the post­partum period may be important factors in thepostpartum emotional disturbances.

Patients suffering from chronic renal insuf­ficiency, either untreated or treated with hemo­dialysis, often complain of sleep distur­bances.H~.Ir.:l Various EEG sleep disturbanceshave been described in untreated patients. l54

In addition, two studiesl:H ,155 have shown thathemodialysis may produce at least some im­provement in sleep patterns. We have recentlyfound that renal transplant patients also showsome improvement in sleep patterns. However,from the evidence available it appears thatneither of these therapeutic procedures,hemodialysis or renal transplantation, fully re­stores normal sleep to uremic patients.

A still relatively unexplored area in sleepresearch is the effect of various nutritional andmetabolic disorders on sleep patterns. It isknown that clinical improvement in anorexianervosa patients is accompanied by improve­ment in previously disturbed sleep patterns. 156

Furthermore. paradoxical as it may seem, itappears that both hypothyroid and hyperthy­roid patients obtain abnormally low amountsof slow-wave sleep.15i,158

A wide variety of neurological disorders hasbeen shown to affect EEG sleep patterns. Aswould be expected, lesions of the spinal cord,subcortical regions, and the cortex, as well assome brain tumors. produce numerous changesin sleep and eye movement patterns.1511.1i5 Sev­eral types of more or less well-organized sleeppatterns have been described for patients suf­fering from post-traumatic coma, and well­organized sleep patterns during comatose statesseem to be related to a favorable prog­nosis.liG.181 Infections and intoxications, suchas sleeping sicknessl82,183 and carbon monoxidepoisoningl84 ,185 also produce polygraphic sleepmodifications. Chronic brain syndrome pa­tientsl86,18i and some, but not all, mental re­tardatesl88-191 exhibit rather interesting sleepabnormalities.

PARASOMNIAS

A majority of sleep laboratory evidence hasdemonstrated that sleepwalking occurs prim-

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DISORDERS OF SLEEP-KARACAN, ET AL.

arily during arousal from slow-wave sleep.92,192.196 During the event, sleep-walkers exhibitinvestigatory eye movements but are generallynonreactive. They are often amnesic for theevent and do not report any dream recall ifquestioned following it. In one study196 sleepwalkers up to age 16 showed more frequentbursts of high-voltage delta activity duringslow-wave sleep than normal, which was inter­preted as representing an immaturity factor inthese subjects' brain function. More complexthan normal slow-wave sleep gestural move­ments and unusual confusion if awakened fromslow-wave sleep also seem to characterize sleep­walkers.192 The finding that sleepwalking canbe induced in some normals and in sleepwalkersif they are stood up during slow-wave sleep192,196lends further support to the conceptualization ofthis phenomenon as one of slow-wave sleeparousal.

Sleeptalking occurs predominantly dur­ing NREM sleep,92,197.199 but some subjectsstudied in the sleep laboratory have been ob­served to talk almost exclusively during REMsleep.197,200 The muscle tension artifact whichusually accompanies NREM speeches has madeit difficult to pinpoint the specific sleep stagesduring which they occur.198,19!! However, inseveral cases it was possible to determine thatthe speeches were accompanied by waking orstage 1 sleep EEG patterns.199,201,202

Nocturnal enuresis is another parasomniawhich appears to be a slow-wave sleep arousalphenomenon.1!!2 Various EEG studies92,203.20!! had indicated that micturition could occurduring any stage of sleep or wakefulness, buta more thorough description of the "enureticepisode"I!!2 has suggested that this may reflectthe fact that enuresis occurs at some point alonga continuum of progressive arousal from slow­wave sleep. There is little evidence that enuresisis closely related to REM sleep, 92,206,207 asmight have been expected from certain psy­chological explanations of the disorder, andthere has been no substantial evidence thatabnormally deep sleep characterizes theenuretic.

Bruxism, or teethgrinding, also appears torepresent a partial arousal phenomenon, sim-

March-April, 1973

Har to the slow-wave sleep arousal phenomenadiscussed above.210.212 In the case of teeth­grinding, however, the event occurs primarilyduring stage 2 sleep.200,211,212 Various auto­nomic changes may accompany the bruxismepisodes,200,211.213 and bruxism has been pro­voked in some subjects by administering soundstimuli during sleep.212

SLEEP-MODIFIED DISORDERS

From the long list of physiological functionswhich have been shown to change during sleep,one would naturally expect that some diseaseswould be either exacerbated or improved con­comitantly. There are, indeed, many suchdiseases, but we will just mention here that byand large various cardiovascular and respira­tory disorders and epilepsies are exacerbatedduring sleep. Certain neuromuscular disordersalso appear only during sleep or are worsenedduring it. However, in some others, such asthe choreas, there is at least a lessening ofsymptoms during sleep.

This review of a truly massive amount ofliterature has necessarily been quite selectiveand brief, but we hope it has been sufficient toconvey to you the extent of the sleep research­er's interest in, and potential contribution to, theresolution of some of the mysteries still sur­rounding many clinical disorders. In no areais there a complete understanding of the signifi­cance of the sleep disturbances to the overallclinical picture, and undoubtedly this must inpart await a more complete understanding of thebasic nature and function of sleep itself. Never­theless, the information obtained in the sleeplaboratory has already added a new dimensionto our continuing exploration of many diseaseprocesses, and we are confident that future workwill contribute to the elucidation both of themechanisms of these disorders and of morerational treatments for them.

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