Primary Sleep Disorders. A Review
An
Honors Thesis (10 499)
By
Carol M. Anders
.Thesis Director
Dr. William Clark
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Ball state Un1versity
Munc1e, Indiana
February, 1978
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For most people, sleep is a regular and welcome period of rest
and unresponsiveness, sometimes punctuated by dreams, which occurs
daily and lasts about eight hours.
Americans
ha~ve
However, about one in five
1
one form or another of sleep rHsord er.
For them,
terrifyin~,
sleep can by
cases, fatal.
insufficient, overabundant, or, in some
The purpose of this paper is to take an in-depth
look at cond.itions in which disturbances of sleep are the primary,
and often only, symptoms.
Karacan calls these primary sleep
disorders, and lists them as insomnia, narcolepsy, chronic hypersomnia, the Klein-Levin syndrome, the Pickwickian syndrome, sleep
paralysis, a.nd nightmares 2 •
In addition, sleep apnea will also
be discussed.•
Many sleep disorders involve a complaint of excessive
daytime sleepiness (EDS)J.
The most common of these is narco-
lepsy, which is defined to be "an illness involving excessive
daytime sleepiness, sleep episodes, and cataplexy, with or without
sleep paralysis, frightening hypnag;ogic hallucinations, and
disturbed nocturnal sleep" (Guilleminault and Dement, 1977, p. 17).
Automatic behaviour can also be symptomatic of narcolepsy4,5.
Excessive daytime sleepiness usually consists of sudden,
irresistable periods of sleep, usually about fifteen minutes long
(although they may range from five to thirty minutes
the narcoleptic awakens feeling alert and refreshed.
6 ), from which
There is
usually a refractory period of one to five hours between sleep
attacks 7 ,8,
situationS.
;~nd they most often occur in boring or monotonous
Zarcone reports on a patient who fell asleep
"during a bombing run in a B-17"(Zarcone, 1973 p. 1158).
Somewhat more common are reports of falling asleep during inter-
5 B or whi I e driv i ng a car6,B.
course'
One study reported that 40%
of the narcoleptics surveyed had fallen asleep at the wheelB,
and another study found that more than 10% of the narcoleptics
they questioned had had at least one automobile accident due to
EDS6.
In ge'neral, narco1eptics also report feelin~ sleepy be-
tween sleep attacks 5 •
Although the presence of cataplexy, as well as EDS. is now
crucial to e. diagnosis of narcolepsy, it has not always been so.
Yoss and Daly reported that about one-fourth of all patients
diagnosed as narcoleptic suffered from excessive sleepiness
alone, and about B% more of all narcoleptic patients exhibited
sleep attacks with hypnagogic hallucinations and/or sleep
paralysis, but without cataplexy9.
Roth has used the term
"independent narcolepsy" for the cases of excessive sleepiness
only6, and, although independent narcolepsy is not a form of
narcolepsy proper, Roth's terminology will be used in this paper.
Cataplexy consists of sudden, full or partial loss of
muscle tone 8 , almost always trig~ered by some strong emotion,
such as laughter, ans:z;er, surprise, fright, exultation, or
e I ation 5,B.9 • Th e a tt ac k may range in severity from a feeling of subjective weakness to total paralysis 9 , and may affect
only certain groups of muscles, or virtually all muscles 8 •
The extraocular muscles are occasionally9, although rarely5,
affected; cataplexy usually occurs only in the voluntary
muscles, and therefore the respiratory system (as well as
other involuntary muscular systems) is almost never disrupted 5 •
The narcoleptic is most often fully conscious during the cataplectic attack and able to remember sounds heard during cataplexyS,
4
although unable to speak or move.
Electroencephalographic
8
recordings taken during cataplexy are normal.
A cataplectic
attack may last only a few seconds, is rarely longer than two
minutes S ,9, and may be terminated immediately if the narcoleptic
hi ts someth1.ng when he falls down 10 • An exception to this may
occur when a. narcoleptic is sitting or reclining during a
4
cataplectic attack, which then develops into a sleep attack •
The onset of' cataplexy rarely occurs before the onset of EDS,
and most often happens either the same year as the first sleep
attacks or in the five years immediately after EDS starts 9 •
Like
c~a taplexy,
sleep paralysis is usually experienced as
full conscic1usness coupled with normal electroencephalographic
recordings and the inability to move or speak, most often
lasting only a few seconds 8 ,9, although it may last aslong as
twenty minutes or develop into sleepS.
Un11ke cataplexy,
however, sleep paralys1s may be accompanied by hallucinations
and a fee11ng of helplessness and 1ntense fear 4 ,8.
Also unlike
cataplexy, sleep paralySis occurs only dur1ng the transition
between sleep and wakefulness 11 , and may 1nclude respiratory
arrests, although these are rare 9 .
Sleep paralysis occurs 1n
about 36:t of all narcolept1cs, in about 15% of all 1ndependent
9
narcoleptics , and fairly often in normal people.
The rate of
such occurance is unknown, although Dement reports that about
half of a. large group of Stanford students have experienced
sleep paralYSis at least once 12 •
Hypnagogic hallucinations often occur simultaneously
with sleep paralysis. although they can also occur separate 1 y
7.9
•
They happen. like sleep paralysis. in the state between wakefulness and sleep9,13. usually just before the onset of sleep4.5.
Hypnagogic hallucinations are false perceptions. predominantly
.
visual 13 • a.Lthough
often auditory or tacti 1 e 4.5.7.8.9 , that occur
both in normals and in narcoleptics 4 , 13.
The content of these
hallucinaticms may be benign or frightening 5 • 9.13. although in
8
narColeptics they are most often terrifying, They typically
involve the bedroom or sleeping area, and are often experienced
as an lmminEmt attack by some intruder (human. animal, or monster) from ~rhich escape is impossible because the limbs are
paralyzed 4 '-"" 14 • Hypnagogic hallucinations occur in about 37%
of all narcoleptics and in about 17% of all independent narcoleptics 9 • Incidence rates in normals are unknown, although the
frightening type are often associated with emotional stress 13 •
Disturbed nocturnal sleep may take anyone of several
forms.
An estimated 60% of all narcoleptics suffer from
repeated awakenings throughout the
ni~ht,
from which they have
no trouble returning to sleep5,8,15. Nightmares also occur
frequently in narcoleptics 8 , as do body movements during sleep2.
A less common disturbance is sleep apnea, which occurs in
approximately 20% of all male narcoleptics. although not in
female narcoleptics 4 • Mitchell and Dement have found that
disrupted nocturnal sleep occurs in most cases of narcolepsy
and usually precedes or occurs with the onset of EDS 16 •
Automatic behavior, estimated to occur in about half of
all case,s of narcolepsy, involves performance of an action which
cannot be r~~called afterwards 5 •
Such behavior may last moments
Q'r hourS' and mostly occurs late in the d8.y5.
It is sometimes
preceded by rolling eye movements and blinking 4 , although the
n8rcoleptic is unaware of this.
The automatic nature of the behav-
ior may be lmnoticed, since such behavior is often a continuation
4
of the previous behaviors ,5.
It has been estimated that there are about 250,000
narcolepticB in the United States, which yields an incidence
rate of approximately
.1%
of the general population, although
other estimates are as low as 50,000 or .02% of the population 1 ,4 •.
Narcolepsy occurs equally often in men and women 3 •
It most often
onsets at about puberty. with about half of all cases showing the
first symptoms between 10 and 20 years of age 1 ,4,8,9. In women,
onset may occur along with pregnancy5.
Onset of symptoms seldom
4 8'
occurs after the age of forty , •
Proper treatment of narcolepsy is, of course, dependent
on correct diagnosis.
If a person has a distinct history of
sleep attac}:s and cataplexy, no testing is needed to confirm
a diagnos is of narcolepsy • although. such tests may be used as
a guide to treatment 3 ,4.
When the history of cataplexy is not
distinct, the usual diagnostic procedure involves a sleep recording.
Whenever possible, the person is withdrawn from all
medication for several days before the test, and is awake during
the entire morning of the test.
In the afternoon, electrodes
are attached to the person so that the electroencephalographic',
electromyographic, electrooculographic, and, on some occasions,
the electroeardio$l:raphic responses may be recorded.
is then askE!d to take a nap4.
The person
Approximately 90% of all narco-
leptics (excluding independent narcolepsy) show ev1dence of a
sleep-onset REM period in this nap,
and all narcoleptics show
at least one sleep-onset REM period in a 24-hour polygraphic
recordin~4.
These sleep onset REM periods are not seen in normal
people, where there is a delay of ?O to 100 minutes between
sleep onset and the first REM period?, nor are they seen in
people with independent narcolepsy1?
Although this diagnostic procedure seems straightforward,
avera~e
the
time between the onset of narcoleptic symptoms and
the diagnosis of narcolepsy 18 fifteen years 4 , and is often more
than twenty years5.
Many narcoleptics will visit four or five
d1fferent doctors before receiving a correct diagnosis 4 .
Part
of this is undoubtedly due to the gradual onset of narcoleptic
4
symptoms ,5. Narcoleptics often do not seek medical attention
until the symptoms become severe, even incapaciting.
Another
factor, often leadlng to incorrect diagnoses, is that many
narcoleptlcs either wrongly report their symptoms 5 (e.g., tlredness or fatigue instead of EDS) or do not report all of their
4 18
symptoms'
•
The third reason that accurate diagnosis may
take so long is that many doctors are unable to identify and
4
treat narcolepsy •
In many cases, narcolepsy is mistakenly dlagnosed as
something else.
lsm
5
,9.
The most frequent mls-diagnosis ls hypothyroid-
Basal metabolism tests may indlcate hypothyroidism
slmply because the narcoleptlc falls asleep during the test,
even though other measures of thyroid functioning show no
abnormality5,9.
Even so, many narooleptios report having been
unsuocessfully treated with thyroid extract prior to correct
diagnOSis 5 ,B,9. Hypoglycemia may be diagnosed instead of narcolepsy if thE! narooleptic reports fatigue instead of sleePiness 5 ,8.
Although a
~~luoose
tolerance test should reveal the fals1ty of
this diagnosis, the problem may be compounded by the presence,
in some cas€!s, of functional hyperinsulinism,
t9
attacks •
alon~
with sleep
In solIte oases, narcolepsy may be diagnosed as another of
the sleep disorders, especially chronic hypersomnia, the Pick8
wickian syndrome, or apnea. The differentiation between
narcolepsy and apnea is oomplicated by the occuranoe of apnea
in narcoleptic males 4 , so that even a correot diagnosis of apnea
does not rule out the possibility of narcolepsy.
Narcoleptics may report their sleep attacks as 'blackouts',
or cataplexy may be confused with petit mal seizures, leading
to a diagnosis of epilepsy5,8,9.
Ocular symptoms, such as double
vision and ptosis, at the onset of a sleep attack may lead to
a false diagnosis of multiple sclerosis or myasthenia gravis 8 ,9.
Althou~h
there is no evidence that narcolepsy is symptomatic
of a psychological disturbance 6 ,9, it may be diagnosed as a
psychological disorder.
Especially if thyroid extract is unsuccess-
ful in treating EDS, narcolepsy may be incorrectly diagnosed as
a neurotic fatigue state 9 • If the narcoleptic reports only sleep
paralysis and/or hypnagogic hallucinations, an erroneous diagnosis
of schizophrf:mia may be made 18 • Such diagnoses have been noted
in children 5 • and differentiating between narcolepsy and schizo-
phrenla can be complicated by the presence of disordered sleep
2
in schizophrenics.
The narcoleptic may also show signs of
8
paranoia anel/or schizophrenia after prolonged amphetamine therapy •
A
dia~~nosis,
during childhood, of hyperact1v1ty has been
5
reported by about one-tenth of all narcoleptics.
This is probably
due to the narcolept1c child's attempts to resist EDS.
In child-
ren, narcolepsy may also be confused with viral encephalitis,
although the only similarity between the two is that the term
'sleeping stckness' is often used to describe both
conditions9~
When proper diagnosis does not occur soon after the onset
of symptoms,> the narcoleptic may be thought to be stupid, uncooperative, trresponsible, lazy, bored, unable to concentrate,
depressed, Clr mentally il1 1 ,5,6,24. The narcoleptic's abilities
to learn, to read, and to study are often impaired, als0 4 ,5.
These labe18 and impairments can seriously disorganize the
narcoleptic"s social and economic life, and result in a distorted
self-image 4 ,5,6.
The narcoleptic may be unable to participate
in sports ( and other activities that may involve surprise or
exultation) due to cataplexy9, and narcoleptics may restrict
their emotional responses in order to help control the cataplexy4.12.
They may also withdraw from relationships and situations that provoke cataplectic attacks 5 , thus generatin~ emotional disturbances.
Group therapy or family therapy may be helpful in treat-
ing these disturbances 5 •
Once narcolepsy has been diagnosed, treatment may be
instituted.
If the narcolepsy is mild and cataplexy causes few
problems, several short naps per day may be all that is needed to
control the sleepiness, enabling the narcoleptic to function
normally5.
This type of treatment is also recommended for
narcoleptic children, as the effects of other treatments on
development are unknown 5 •
The most common treatment for more severe narcolepsy
involves thEt use of analeptic drugs.
The preferred medication
for treating EDS is methylphenidate hydrochloride, 20-80 mg/day
and methamphetamines can also be used to treat EDS
especially methamphetamine hYdrOChloride 8 and dextroamphetamine
Amphetamine~1
sulPhate 6 , although they have many s1de effects.
4,5,9
4.8
.
,
If none of these
analeptios can oontrol the symptoms, monoamine oxidase (MAO)
inhibitors may be used 20 • They control not only EDS but also
cataplexy, hypnagog1c halluo1nations. and sleep paralys1s; however, MAO 1nhibitors have a large number of side effects. Including possible' optic damage, and 1nteract with many drugs.
Also.
consumption of any food rich in tyramine (an intermediate stage
in the synthes1s of ep1nephrine from tyrosine) while being treated with MAO inhibitors may result in intraoranial hemorrhages
and death 21 • Withdrawal from MAO inhibitors oan result in insomnia, extreme anxiety, depression, and suicidal thoughts, for this
reason, MAO inhibitors are best used only when all other treatments
fai1 8 •
In order to control cataplexy, imipramine or impraminic
compounds (des1m1pramine or chlorimipramlne) are usually used 4 • 5 • 6 • 8 •
Although they have little or no effect on EDS. they are very effective treatments for cataplexy, sleep paralYSiS, and hypnagogic
hallucinatio11s 4 • 5 • 6 ,8. The usual dosage of imIpramine for treat-
ment of cats,plexy is 75-100 mg/day 5,8 ,although ch 1 orimipram i ne
is more effE~ctive than either imipramine or desimipramine 4 .
S1de effectsl and interactions are less common with im1pram1n1c
compounds than w1th MAO inhib1tors 21 • The combination of amphetam1nes and i.mipramine i8 generally considered unsa f e 4,5 ,and
therefore
sE~ldom
used.
However, methylphenidate hydrochloride
may be used together with imipramin1c compounds w1thout deleterious s1de effects 4 ,5,21, although dosages must be carefully
adjusted since each drug tends to potent1ate the other21.
Prim1done he.s also been used to treat cataplexy22.
To treat
disrupted nocturnal sleep and/or sleep paralYSiS, 10 to 15 mg
of 41azepam at bedtime may be effective 8 , apparently due to the
sedative action of diazepam shortening the trans1tion between
wakefulness and sleep9.
No drug treatment currently in use 1s completely safe or
completely e'ffective.
Long-term treatment is usually required,
due to the fact that narcolepsy only rarely remits J • 9 , and
tolerances to most of these drugs may develop with long-term
usage 5 ,8.
!Ihis tolerance may be offset by w1thdrawing the med-
ication for a per10d of t1me and then readm1nister1ng the same
medication at a lower dosage leve1 5 •
Gamma hydroxybutyrate,
although still being studied and tested, seems to be effective
in treat1ng EnS, cataplexy, and disrupted nocturnal sleep5.
There 1s also the poss1b1l1ty that narcolept1cs may be able to
learn to modify the1r EEG responses and thus control narcolept1c
symptoms w1thout drUgs 2J •
Yoss and Daly cons1der narcolepsy to be an hereditary
disorder, cs,used by an autosomal dominant gene 9 •
The evidence
supporting this hypothesis comes from the observation of several
8
families in which more than one member has narcolepsy. However,
an early ana.lysis of 250 to JOO reported cases of narcolepsy
showed that approximately 81% of these cases were not familial,
i.e., these narcoleptics did not have any relatives who had narcolepsy.
When several cases of narcolepsy were reported in the
same family, the number of cases ranged from 2 to 8, with an
average of 2.8.
These familial cases usually consisted of parents
and children or of siblings 8 •
This is consistant with recent
research, which indicated that narcolepsy occurs about 200 times
more frequently (a rate of occurance of 4% to 19.4%) in the immed4
iate rela.tives of narcolept1cs than in the general population •
However, if Yoss and Daly are correct and narcolepsy is caused
solely by an autosomal dominant gene, all reported cases of naroQlepsy should cluster in familial groups, and the rate of oceurance
of narcolepsy in the immediate relatives of narcoleptics should
be approximately 50%.
Therefore, one may conclude that, although
there is probably a genetic predisposit1on to narcolepsy, the
cause of naroolepsy is not genetic.
There 1s no evidence that narcolepsy is caused by tumors
or lesions of the brain, severe head injuries, or viral encephalitis9, and significant pathology in the central nervous system
does not appE~ar to be a factor in narcolepsy24.
The observation that sleep onset REM periods occur in all
cases of nareolepsy proper J , when combined with other observations,
leads to the conclusion that narcoleptic symptoms are manifestations of a dlsturbance in the system controlling REM sleep.
The typical duration of narcoleptic sleep attacks is the same
as the typical duration of REM sleep episodes (5 to 30 minutes)6.
and narcole,tics show a much greater incidence of REM sleep in
afternoon naps than do those with independent narcolepsy25.
Cata-
plexy is st:::-ikingly like the motor inhibition that occurs with
REM slee!p, although it oceurs during wakefulness.
Sleep paralysis
and hypnagogic hallucinations can be considered premature expressions of REM sleep's motor inhibition and dream imagery.
nocturn~.l
Disrupted
sleep may also be a manifestation of a disturbance in
the system eontrolling REM sleep.
Many authorities on narcolepsy
agree that narcoleptics suffer from some disturbance o:f REK
sleep2. 6, 25-- 2 7, but there is disagreement as to whet'-1er or not
non-REM sleep is involved.
Roth till have concluded t lat non1
REM sleep disturbance, as well a8 REM sleep disturbance, occurs
in most cases of narcolepsy25,26.
The question of what neural centers are structurally or
functionally abnormal and thus create the narcoleptic symptoms
does not have a simple answer.
Early research implicated nor-
epinephrine circuits in t'-1e pontine reticular formation and the
locus cerulE!Us as the neurological areas controlling REM sleep28,
29
•
A report of a patient with some symptoms similar to narcolepsy
and severe neurological damage in the pontine tegmental nuclei
may be taken as partial
area in narcolepsy30.
suppo~t
for
involveme~t
of the pontine
However, many other areas of the brain
influence the pontine reticular f0rmation, and a dysfunction in
anyone of these may cause narcolepsy.
Other researchers have
suggested that some mechanism of wakefulness fails to inhibit
the reticul?',r formation areas controlling REM sleep7.
Narco-
lepsy has also been characterized as a disturbed circadian cycle
or as a regl'ession to infantile sleep patterns 8 • Passouant has
16
hypothesized that the narcoleptic either has regressed to the
polyphasic sleep pattern of sleep onset REM periods found in
8
infants or has not pro~ressed beyond this pattern •
Jouvet has postulated that REM sleep is controlled by the
28
caudal part of the pontine reticular formation
and the locus
ceruleus.
~~hese
areas are activated by cholinergic mechanisms
which in turn are activated by mechanisms in the caudal part of
the raphe system 29 •
The raphe system controls non-REM sleep,
while the pontine reticular formation controls REM sleep29.
locus ceruleus seems to be involved in REM motor inhibition
The
28
•
Although other areas in the central nervous system are also part
of the sleep system, the raphe system, the pontine reticular
formation, a.nd the locus ceruleus seem to be the central mechanisms.
Peri pheral a.reas of the sleep system include the septal-basal
forebrain area, which "exerts descending facilitatory influences
on the brainstem structures responsible for the various characteristics of paradoxical sleep" (Knauss, 1966, p. 1699).
The
basal forebrain also appears to influence the non-REM system J1 •
It is my contention that a disturbance in this system is
the cause of narcolepsy.
More specifically, in normal humans
there must be a functional link between the raphe system and the
pontine reticular formation such that inactivity in the former
inhibits activity in the latter and the locus ceruleus.
In narco-
leptics, this link does not function normally, i.e., does not
always inhibit REM phenomena,
althou~h
it sometimes does.
Thus,
descending facilitatory influences from the septal-basal forebrain area !Lre sometimes not counterbalanced by inhi bi tory
influenc.es from the raphe system, yielding REM phenomena during
wakefulness (i.e., cataplexy, sleep paralysis, and hypnagogic
hallucinati<ms).
In particular, the septal area (which is part
of the limbic system and therefore involved 1n emotional functioning) 1s
fun(~tionally
connected to the locus ceruleus, so that
strong emotion can trigger a d1sassociated state of REM motor
Inh1bitl.on, otherw1se known as cataplexy.
Furthermore. 1nfluences
which in a normal person would facilitate the raphe system and
thus 1nhibit the pontine reticular formation, producing non-REM
sleep, have other effects 1n narcoleptics.
While
facll~Ltating
These influences,
the raphe system, would also facilitate the
pont1ne retlcular formation, instead of inhibitIng 1t.
If there
were simultaneous influences from the septal-basal area, a sleeponset REM
pE~rlod
or a REM nap would result.
This dysfunction
1n the link between the raphe system and the pontine retioular
formation could result from a failure of the structure to mature,
from damage to the structure, from a genetic weakness of the
struoture, clr from any combinat10n of these.
Independent narcoleptics mayor may not develop cataplexy.
One study found that EDS onset preceded the first cataplect1c
a ttack by melre than five years in a bout 28% of all cases of
narcolePBy9.
Thus, some independent narcolept1cs are actually
narcoleptics whose full symptomatology has not yet developed.
They mayor may not show sleep onset REM per10ds J ,8.
Other cases
of independent narcolepsy actually be cases of apnea, as about
two-thirds of all cases of apnea report excessive sleepiness 12 •
In a recent study, no eases of independent narcolepsy without
)
sleep onset REM periods were reported , indicating that, as a
diagnosis, independent narcolepsy is no longer adequate.
Apnea may be either oentral, obstructive, or mixed, and
1,),)2,))
affects an f~stimated 50,000 Americans, mostly male
•
All apnea
v~lctim8
actually stop breathinQ; during their sleep
as many as l~OO to 900 times per night 1, )), in central apnea,
movement of the diaphragm stops during sleep, while in obstructive apnea the muscles in the upper airway collapse
1, )2
•
In
either case, the apnea victim is usually unaware of his nocturnal
cycle of falling asleep, ceasing to breathe, awakening, breathing,
and falling asleep again 1 ,)). The most common sign of apnea is
a history of extremely loud snorinQ;
1, )2
•
other symptoms include
high blood pressure, hypersomnia, insomnia, morning headaches,
a feeling of disorientation and drunkenness upon awaken1ng, and
frequent bod.y movements dur1n,cz; sleep1,),)2.
Apnea may result in
hypertens10T.l, hypoxia, cardiac abnormalities, chronic heart disease, and even death 5 ,)).
Apnea resulting in EnS may be d1fferentiated from narcolepsy because narcoleptics awaken from daytime sleep episodes
feeling refreshed, while the apnea v1ctim awakens feeling unrefreshed).
In most cases, the root cause of apnea is unknown.
although Ondine's CUrse (a form of central apnea) is caused by
a tumor of the brain or spinal cord 1 • Treatment for oentral
apnea usually includes medication.
Tricyclic antidepressants
(1ncluding the imipramine compounds) are sometimes effective
in central apnea. and carbamazepine has also been used with
some succesflJ4.
A recent development in the treatment of ob-
structive apnea is the tracheostomy, which places a valve in the
patient's throat.
This valve is closed during the day to permit
normal functioning and opened at night to permit breathing 1 • J2 ,JJ.
Hypnotic drug treatments for insomn1a, which also depress the
breathing mt!!chanism, should not be used w1th apnea, as they can
be fsta1 1 ,J].
The Pickwickian syndrome is characterized by periodic apnea,
2
as well as hypersomnia and obes1ty.
20 to JO
se(~onds
The apnea episodes, usually
long, are both preceded and followed by several
deep breathf,J5, with EEG arousal occuring just prior to the end of
2
the episode'.
Increased muscle tone, myoclonic jerking in the
arms, and cardiac acceleration may accompany the EEG arousal J5 •
The duratiorl of these apnea episodes appears to be directly
re 1ated to the depth of the seep
they occur i n 2,J6 • Fr equency
1
of ocCUranCE! of the Pickwick1an syndrome is unknown; however,
Gu111eminault and Dement found no cases of it in their stUdyJ.
Apparently, the symptoms of the Pickwickian syndrome are an
exaggeratior.l of a normal sleep phenomenon called Mayer's waves 2 ,J5,J6.
Perhaps this: exaggeration is triggered by obesityJ6.
Chronic hypersomnia also appears to be an exaggeration of
normal sleep phenomena.
Hypersomniacs, unlike narcoleptics, do
not find their sleep attacks irresistable, but they usually last
muck longer than the narcoleptic's sleep attacks, with a duration
of several hours to a few days6,7.
The hypersomn1ac msy exhibit
extended nocturnal sleep in addition to (or in place of) daytime
sleep attacks 2 ,6. Other symptoms 1nclude difficulty in awakening,
postdorm1tal confus10n, and increased heart and resp1rat10n rates
dur1ng sleep2,6.37.
The hypersomniac has a normal. though pro-
longed, c:yc1:lc pattern of nocturnal sleel>, and the proportions
of sleep splEmt in each stage of sleep are also norma1
2 , 6,37.
Gui11em1nault and Dement report several cases of hypersomnia
associated w1th increased levels of 5-hydroxyindo1eacetic acid,
and have successfully treated some of these cases with methysergide 3 •
6
Analeptic drugs are often used to treat hypersomnia.
Hypersomn1a
seems to be assoc1ated w1th injuries or damage to the central
nervous system or with a family history of hyperSomn1a 6 ,37.
Hypersomnia has also been reported in patients with manic-depressive i11nesses 38 •
The Kleine-Levin syndrome, first reported in the 1920's,
consists of periodic hypersomnia and excessive eating, associated
with alterations 1n the v1ctim's mental state, sometimes even
schizophrenic or confusional states 2 ,39. Episodes are usually
preceded by physiological stresses, such as illness, and many are
associated with
neurolo~ica1
or somatic abnormalities and/or
elevated 1e,,'els of sexual fantasy and behavior 39 •
Guil1eminault
and Dement f'ound no cases of the Kleine-Levin syndrome in their
stUdy3, but other sources report that most patients are adolescent
boys39.
Onset of the disorder 1s often preceded by febrile illnesses such as leukocytosis or enoePha11tis 40 • The Kleine-Levin
syndrome is generally thought to result from a dysfunction in
the thalamus or hypothalamus 2 •
Nightmares, or dreams "in which fear is of such intense
degree as to overwhelm the dreamer and force at least partial
awakening" {Boller
ll!l.
three categ()ries.
Two of these three types are relatively
1975. p.1026) may be divided into
normal phenc)mena of sleep, namely, REM anxiety dreams and those
42
associated 1fi th sleep paralySis • The third type, called night
2
terror, pavor nocturnus, or incubus ,7, 1s associated with non-REM.
sleep. more specifically, with arousal from stage J or 4 sleep42,4J.
These nightJl!l.ares most often occur in the first non-REM period of
the night, !Llthough they may also occur in the second 7 ,44,45.
Night terrors are character1zed by an alpha EEG pattern, loud
screams,
tac~hycardia,
increased respiratory amplitude and rate,
moti11 ty, arid somnambulism, lasting only a few minutes, often
coupled with subjective anxiety, a rap1d return to sleep, and,
7,44
usually, amnE!sia for most of the episode
• When amnesia is
incomplete, recalled themes are usually of dying, falling, choking, being crushed, abandoned, or enclosed, or fearing the
46
aggressive 8.ctions of others • The amount of delta sleep prior
to the night terror episode appears to be positively correlated
with the intenSity of the night terror.
The etiology of night
terrors is unknown, but they may be associated with epilepsy,
temporal lot~ lesions 11 , certain types of hypnotic drug treatment, confllot 42 • external orises 14 , or head injury48. Although
some psyohoanalysts have thought that the nightmare expressed
internal conflict over incestuous impulses 49 , there is little,
if any, evidence that night terrors are associated with the
buildup of i~nstlnctual roroes 14 • Night terrors are estimated to
occur in three to six percent of all young ohildren, and less
42
rrequently in adults ,5 0 • Children tend to eventually outgrow
night terrOl'S 7 , although removal of the adenoids. if they are
enlarged, mEiLy eliminate the night terrors 50 • Night terrors may
be treated lfi th imipramine 48 , diazepam 51 , 52, systematic desensi tization 45 , or implosive therapy5J,54.
Insomnia, or "the inability to obtain adequate sleep"
(Karacan and Williams, 1971, pp. 274-275) may stem from difficulty
in getting to sleep, multiple awakenings throughout the night,
early awakening in the morning, or any combination of these 7 • 56 •
Due to
thesf~
disturbances of nocturnal sleep, the insomniac' s
daytime activities may be impaired 57 •
The total amount of sleep
per night, however, is not a criterion for diagnosis of insomnia.
Jones and Onwald report two men who normally sleep about three
hours per night, and other researchers have found an elderly
woman who sleeps only 67 minutes per night 59 , but these people
find their
f~leep
adequate and thus are not insomniacs.
Insomlia may be divided into five types, based on causal
factors 60 • One type 1s phys1cal insomnia, the result of physical
symptoms preventing sleep.
Apnea, arthritis, asthma, ulcers,
kidney disease, heart disease, and m1graines are examples of
phYSical s~1ptoms causing insomnia 1 • A second type is
phYSiologic insomnia, caused by jet lag 1 , disruptions of the
c1rcadian cycle, tea, or cOffee 60 • A th1rd type is psychologic
insomnia, which is secondary to psychological disorders.
The
primary disorder associated with insomnia is depression 7 ,61.
Comparative psychological testing of insomn1acs and controls
has found that scores measur1ng depress10n, fear, hypochondriacal
concerns, selma tic concerns, dependent rej ection , obsessive worrying, and decreased control were elevated in 1nsomn1acs 62 - 64 •
High levels of anxiety may 62'01" may not
insomnia.
64
be associated w1th
'1'he type of depression associated w1 th insomn1a
changes with increas1ng age, and the proportion of insomniacs
who are depressed increases 61 • Yet another type of 1nsomnia is
iatrogenic, or caused by dru~s such as amphetamines, antidepressants 60 , or 8.lcohol 1 • Iatrogenic insomnia may be associated with
66
either chrortic use of 61 ,65 0r withdrawal from hypnotic drUgs ,67.
The fifth type, idiopathic insomnia, consists of all cases of
insomnia whose causes are unknown. In general, physiological
arousa1 68 , including sexual arousa1 69 , is associated with any
kind of insomnia.
In physical or physiologic insomnia, the logical treatment
is to allev1.a te or eliminate the cause of the insomnia.
For
iatrogenic insomn1a, gradual and medically supervised withdrawal
of the drug is recommended 7 ,61.
IdiopathiC and psychologic
insomnia may be treated with drugs.
The most effective drug
for treatmer:lt of insomnia is flurazepam, 15-)0 mg. at bedtlme 7 ,61.
This drug
both sleep latency and nocturnal awakenings,
and insomnia.cs do not develop tolerances to flurazepam 7.7 0 •
de~creases
Flurazepam a.lso does not disrupt REM sleep patterns 71,
Diazepam,
10 mg. at bedtime, is also effective in reducing sleep latency
and decreasing nocturnal awakenings 61 ,71. Some success has also
been reported with the tricyclic antidepressants doxepin hydrochloride 61 and desipramine hYdrOChloride 72 •
Some hypnotic drugs have been found to be effective in
reducing nocturnal awakenings and/or sleep latency over short
periods of time, but lose effectiveness when used for extended
72
These drugs include methaqualone, glutethlmide ,
chloral hydrate, and secobarbito1 61 • Extended use of any hypnotic
periods of time.
drug may lead to tolerance, Increased use of the drug, and, event4
ually, iatrog:enic insomnla 61 ,7 •
In some cases, electrosleep treatments may be helpful in
treating chronic insomnia 75 ,77; however, this does not always help78
and usually yields only short term effects 75 • The use of an airfluidized be~d may temporarily reduce insomnia 79.
The classical
80
conditioninQ: paradiQ;m has also been used to treat lnsomnia • It
has been
that biofeedback may be used to modify the EEG
pattern and reduce insomnla 23 • Attribution theory has also contributed possible treatments for insomnla 81 ,82.
su~:gested
Various forms of relaxation training have been generally
found to be effective in treating insomnia 83- 86 • These include
self-relaxation 8?-88, metronome-conditioned relaxation 89 , hypnotic
relaxation 8E1 , progressive relaxation 8 ?-91, progressive relaxation
with muscle-tension release 92 , desensitization 91 ,93, and autogenic
88
training 8 ?
Relaxation training may be done in a group setting ,
and positive results were reported
instead of a therapist 94 •
usin~
tape-recorded instructions
Some a~uthors recommend psychotherapy as a treatment for
1nsomnia 61 • The insomniac, however, often denies having any
psychologics.l problems and resists any form of psychiatric treatment 7 • 61 , ma.king such treatment difficult.
Although much research has been done in the field of sleep
and sleep disorders in the past twenty-five years, much is yet
unknown.
What we do know is difficult to apply so that it may
"make the w1dest possible contribution to the diagnosis, prog-
nosis, and treatment of patients" (Karacan et aI, 1973, p. 77).
One of the reasons for this is that our basic
questions about the function of sleep in
gE~neral, and of the various sleep stages in
~lrticular, remain to be answered.
And if
1m do not yet have answers to these questions,
i1; is obvious that we cannot fully appreciate
the significance of sleep disturbances.
~lrthermore, many of the sleep disturbances
have yet to be completely described, much
14~ss examined from some more mechanistic
p()int of view. (Martin et aI, 1973. p. 75)
Much work
rE~mains
to be done.
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