G. BROWNE GOODE, M.D.
Sleep Paralysis OKLAHOMA CITY
Sleep paralysis is an unusual neurologic
phenomenon which may be described as
"brief accesses of inability to move one's
limbs, to speak and even to open one's eyes
on awakening (hypnapompic or postdormital
sleep paralysis) or more rarely when falling
asleep (hypnagogic or predormital sleep
paralysis)."11 The patient is fully aware of
his state and has complete recall for the
event. Sleep paralysis is occasionally pre-
ceded or accompanied by vivid and terrifying
hallucinations in the pre- or postdormital
stages of sleep. Rarely, it may be preceded
by cataplexy. The paralysis always dis-
appears suddenly, either spontaneously, after
intense effort by the patient to "break" the
paralysis, or after some sensory stimulation,
such as being touched or spoken to. The
duration of the episode is usually a few
seconds, but may be a few minutes. The
only sequelae are an occasional relapse into
the paralyzed state if the patient does not
stand and move about, and, rarely, numbness
and tingling of the extremities. The first
episode of sleep paralysis is commonly ac¬
companied by extreme anxiety, which us¬
ually subsides with subsequent episodes as
the patient finds that they are brief, pain¬
less, and without significant residua, Ex¬
amination of the patient during the episode
reveals flaccid paralysis; further information
Received for publication Aug. 9, 1961.
From the Departments of Medicine, Duke Medi-
cal Center, Durham, N.C., and The University
of Oklahoma Medical Center.
Downloaded from jamanetwork.com by Boston University user on 04/30/2024
is difficult to obtain because touching the
patient ends the episode.
Sleep paralysis apparently was first de¬
scribed in 1876 by Mitchell,18 who reported
cases of sleep paralysis in 2 healthy white
male adults. Adie1 and Wilson25 were
among the first in the literature to report
the association of sleep paralysis with nar¬
colepsy and cataplexy. "Nocturnal hemi¬
plegia," "nocturnal paralysis," and "sleep
numbness"18 were 3 terms used before
"sleep paralysis" 25 was introduced by Wil¬
son around 1925. Other terms used since
have been "delayed psychomotor awaken¬
ing," 8 "cataplexy of awakening,"8 and
"postdormital chalastic fits." 1X
Numerous cases of sleep paralysis, oc¬
curring both as an isolated phenomenon and
in association with several neurologic dis¬
eases, have been reported.5'16'17'20,26 How¬
ever, the incidence, distribution, and nat¬
ural history of sleep paralysis are not
known. The primary purpose of this paper
is to present the results of surveys of several
population groups concerning the occurrence
of sleep paralysis. This is the first such
survey reported. The present state of
knowledge about this disorder is summa¬
rized.
Methods
To determine the incidence of sleep paralysis in
various population groups, a questionnaire was
circulated. It follows :
 "QUESTIONNAIRE"
"In a study of sleep and its mechanisms I am
surveying several "normal" population groups to
t~ CM «OMO determine the rough incidence of certain symptoms
^13 SS " O O »O -1 00
00 »O associated with variations from normal sleep.
O)
fe
OS
"1. Have you ever experienced transient paral¬
o
ò O O O 00 00 ysis—inability to speak and move any muscle
OS
»O
oo
groups—while entering or awaking from sleep?
co
.—I
c3
"2. Have you ever experienced sudden transient
O o !>·
—I
i-i O O 0O "
O i—I OS
weakness of muscle groups while awake, or
« 1-1 l-H
sudden transient inability to speak while awake,
occurring either with laughter, startle, or without
13 ££
t~
ei
CO OS CM
associated event?
* c
SOí "3. Have you ever experienced hypersomnolence
fe
* —sudden episodes of brief or long-lasting sleep
*

»
i—t o o os t"«· oo
rt H occurring frequently and/or inappropriately—in
>
—
spite of normally adequate amounts of nocturnal
«O
a sleep ?
(M O O (M O (N
0O 0O
"4. Have you ever experienced very vivid and
realistic "dreams" upon falling asleep or awaking
from sleep? (Exclude the ordinary dreams of
F—t
as
^ ^ w ei
^ ei sleep. )
s.
a « M N
"5. Have you ever experienced walking in your
fe
0O
»O fe sleep ?
00
d o o o eo oo oo
^i1 i—i oo "6. Have you ever experienced talking in your
»o
•s sleep?"
a The questions were used to determine possible
O o o
O O O CO 00 00
'S O
" T-l 00 relationships among 6 phenomena: sleep paralysis,
cataplexy, narcolepsy, sleep hallucinations, sleep¬
oo
walking, and sleeptalking. Two groups of medical
—I
& t^ o o
o »o »o
oó i- oó students (Groups I and II), one group of student
Tf M IO
«o
a nurses (Group III), and one group of hospital
fe
"
_ *
i-t
inpatients (Group IV) were surveyed (Table 1).
o O O <M i-t 00
00
CO The questionnaire was explained to all groups
studied except Group I, which received the ques¬
s s
o o IO O O CN t-t OS
tionnaire by mail. Although *there was not a 100%
o 0O CN 0O
response in Group I, as there was in all the other
groups, Group I was included in this study be¬
cause of the cases of sleep paralysis found, and

!
r-t CO > - -<

13
ìS co ·*
— because the results in this group were very similar
a to Group III, another medical student group in
fe
00
<µ *
which there was 100% participation.
oo
CO
Those subjects in all groups who answered any
H a of the first questions "yes" were interviewed indi¬
o
s- - © < t^ vidually.
O OS ( 00

Group I the entire student body of Duke

was
Medical School, comprising 287 persons in resi¬
dence. Of these questionnaires, 163 (56%) were
returned.
en

i Group II comprised 68 University of Oklahoma

co
—
08 Medical School junior and senior students who
co ¿3 were present at a lecture.
f3 M >i á^3
Group III consisted of the 53 Duke University
a a a School of Nursing sophomore students in at¬
o3
53 ,
ce
m w 53 tendance at a lecture.
Group IV consisted of 75 Duke Hospital private
inpatients (medicine, 67, open-ward psychiatry, &)
available for questioning on one day.

Downloaded from jamanetwork.com by Boston University user on 04/30/2024

 Table 2.—Information About Sleep Paralysis Cases in Surveys of Population Groups
Pre- Post¬ Estimated
Age Onset dormital dormital Duration Sleep
Case of Sleep Sleep Sleep in Hallu¬ Sleep¬ Sleep-
Group No. Age Paralysis Paralysis Paralysis Seconds Frequency cinations walking talking

I 1 22 9 Yes Yes 30-60 10/Yr. No No Yes

2 23 10 No Yes 10-30 2-3/Yr. No No Yes
3 25 22 No Yes 15-30 1-2/Mo. Yes * No Yes
4 24 18 No Yes 10-15 1/Mo. No No Yes
5 27 18 Yes No 30-60 4-5/Yr. Yes* No No
6 23 16 Yes Yes 30-60 4-5/Yr. Yes No Yes
7 21 21 No Yes 30-60 Once Yes No Yes
8 24 20 No Yes 30-60 2-3 /Yr. Yes No Yes
9 25 8 No Yes 10-30 4-5/Yr. Yes Yes Yes
10 26 16 Yes No 30-60 Once No No No
II 11 29 10 Yes Yes 30-60 4-5/Yr. No No Yes
12 24 16 No Yes 30-60 Once No Yes No
13 25 12 No Yes 30-60 <1/Yr. No No Yes
14 24 14 No Yes 60-120 2-3/Yr. Yes* No Yes
15 25 18 No Yes 30-60 Once No No No
IV 16 67 45 No Yes 30-60 1/Mo. Yes * No No
17 58 50 No Yes 60-120 Once No No No

*
With sleep paralysis
Results experienced it less than 5 times, and 2
Table 1 shows the results of surveys of had experienced it more than 5 times. Four
all 4 groups, and Table 2 gives a tabulation had experienced only postdormital sleep
of all the sleep paralysis cases. paralysis and 1 had experienced both pre-
In Group I the average age of onset in and postdormital sleep paralysis. There was
the 10 (all men) with sleep paralysis was no- family history. One experienced pre-

16. In all 10, the initial episode was ac¬ dormital sleep hallucinations with sleep
companied by fear and intense concentration paralysis.
to overcome the paralysis. None was ever In Group III there were no cases of
touched or spoken to during an episode. The sleep paralysis.
frequency varied greatly: 3 had experienced In Group IV the age range was 18 to
sleep paralysis only once, 3 had experienced 73, with an average of A6. Only 2 of the
it less than 5 times, and the other 4 ex¬ 75 had experienced sleep paralysis. One
perienced it from 5 to 15 times a year. The was a 68-year-old white woman who- had
durations in all cases were less than 60 depressive and anxiety neurosis. Sleep
seconds, and most were estimated at 15 paralysis had occurred for 15 years, pre-
seconds. Seven experienced sleep paralysis dormitally only, and usually associated with
only predormitally, 2 experienced it only hallucinations. This patient's 45-year-old
postdormitally, and 1 experienced it both daughter and 40-year-old son both had ex¬
pre- and postdormitally. One student with perienced sleep paralysis for approximately
sleep paralysis stated that his father had 20 years. The patient had no> other asso¬
experienced sleep paralysis for many years. ciated symptoms.
Six of the 10 had also experienced sleep- The second patient with sleep paralysis
talking, one had experienced sleepwalking, was a 58-year-old whitewho· was
man
and 5 had experienced sleep hallucinations. hospitalized for treatment of chronic bron¬
In 2 patients the sleep hallucinations oc¬ chitis and emphysema. At age 56 he had a
curred with sleep paralysis. single episode of sleep paralysis which oc¬
Group II contained 4 men and 1 woman curred in the postdormital state, lasted
who had experienced sleep paralysis. The several minutes, and terminated when he
average age at onset was 14. Two- students was touched. He has had no recurrence and
had experienced sleep paralysis once, 1 had no associated symptoms.

Downloaded from jamanetwork.com by Boston University user on 04/30/2024

 Fifteen of the 32 patients in Group IV not coded in the Duke Hospital Medical
(Table 1) who had had sleep hallucinations Library, and the cases were gathered from
recalled a sensation of falling during the personal experience and from reviewing the
episode. Nine of these 32 often felt unable charts of patients with narcolepsy, akinetic
to move during the hallucination, but were seizures, pyknolepsy, and undiagnosed ill¬
able to move when they tried. nesses.
There 27 patients known to have
were
Comment
sleep paralysis in Duke Hospital from 1930
Sleep paralysis is an apparently
benign to November, 1959. Two of these cases
phenomenon occurring more commonly than occurred without related symptoms and the
usually appreciated, especially in healthy other 25 (Table 4) were associated with
young adults, but also- in older age groups. narcolepsy.
The sex distribution of subjects with sleep One case of isolated sleep paralysis was
paralysis in the groups surveyed is ap¬ seen in a 46-year-old white man admitted
proximately 80% males to 20% females. for treatment of bronchial adenoma. He ex¬
No subject had cataplexy or narcolepsy as¬
sociated with sleep paralysis, but there was
perienced postdormital sleep paralysis on
the ward in my presence. The episode was
one case of mild narcolepsy without other
ended by a light touch on his hand. It was
symptoms. Those individuals with sleep found that he had experienced sleep paral¬
paralysis had sleep hallucinations, somnam¬ ysis, both pre- and postdormitally, for about
bulism, and somniloquism about as frequent¬ 15 years. Neurological examination im¬
ly as those patients without sleep paralysis. mediately after the episode was normal.
The brief duration of the symptom, the
A second case of isolated sleep paralysis
absence of sequelae, and its frequent as¬
was that in a 42-year-old white man ad¬
sociation with sleep hallucinations all con¬
mitted for evaluation of multiple complaints
tribute to the patient's lack of concern and
and anxiety. One of his most prominent
its infrequent mention in routine medical
was postdormital sleep paralysis
histories. It is only when sleep paralysis is symptoms
associated with more dramatic events, such following sleep
hallucinations. His mother
had had the same experience.
as cataplexy and narcolepsy, that it is likely
to be mentioned by the patients.
Table 4.—Occurrence of Sleep Paralysis and Other
Symptoms in Duke Hospital Cases of Narcolepsy
Review of Charts (140)
The known Duke Hospital cases of sleep
Primary Secondary
paralysis were reviewed. Sleep paralysis is Narcolepsy Nareolepsy
No. % No. %
Table 3.—Duke Hospital Cases of Sleep Paralysis
Associated with Narcolepsy
N, total 120 100 26 100
C, total 85 70 7 27
I. Types of Narcolepsy No. % SP, total 21 18 4 15
HH, total 28 23 3 12
A. Primary (idiopathic) 21 84 O, total 24 20 10 38
13. Secondary (symptomatic) 4 16 N, alone 28 23
1. Postencephalitie 2 8 & C 43 36
2. Pickwickian syndrome 2 8 & SH 1 1
& SP 1 1
II. Symptoms Additional to Narcolepsy & & O 5 4
Sleep Paralysis & C & SH 6 5
A. Cataplexy 22 88 N&C&SH&SP 8 7
B. Sleep hallucinations 18 72 N&C&SH&SP&O 8 7
C. Obesity 8 32 N & C & SP 4 3
N & C & SH & O 5 4
III. Sex Distribution N & C & O 11 9
. M 20 80
B. F 5 20
N =
narcolepsy; C cataplexy; SP
= =
sleep paralysis; SH =

sleep hallucinations: O obesity.

=

Downloaded from jamanetwork.com by Boston University user on 04/30/2024

 Comment
While little has been written about pri¬
mary or idiopathic sleep paralysis, there
are many studies mentioning its association
with other states.1'8'15'21,25'26 For many years,
sleep paralysis has been known to< occur
frequently in the narcolepsy syndrome.1'8'
15,25 Tfae recent review of
narcolepsy by
Daly26 reports sleep paralysis in 24% of
241 cases. As shown in Table 4 this figure
is slightly higher than the incidence of sleep
paralysis in the Duke Hospital cases of nar¬
colepsy. When occurring with narcolepsy,
sleep paralysis is usually also associated
with cataplexy and sleep hallucinations. It
has been proposed that the narcolepsy syn¬
drome is a forme fruste of the pickwickian
syndrome,21 and that both are primary hy-
poventilation syndromes. Sleep paralysis
occurs with the pickwickian syndrome,13 but
the incidence is not known well enough to
allow any inferences. However, sleep
paralysis does occur often enough with
narcolepsy to' be considered part of the
narcolepsy syndrome.
Narcolepsy 12 and cataplexy 9'10 each has
been reported to occur singly in association
with structural lesions of the hypothalamus,
diencephalon, and frontal lobe. The only
known case of sleep paralysis in conjunction
with intracranial structural lesion was
an
reported by Ethelberg.11 The case was seen
in a young female patient who sustained a
depressed fracture of the right anterolateral
frontal bone and soon afterward had the
onset of sleep paralysis. It occurred fre¬
quently, but only postdormitally, was not
associated with sleep hallucinations, cata¬
plexy, or narcolepsy, and was followed by
a "strange feeling" which ascended from
the hands to the shoulders. The patient
also- developed frontal headaches and epi¬
sodes of bilateral paresthesias which were
unrelated to the sleep paralysis. Surgery 2
years after the accident revealed a small
epidermoid cyst under the fracture site.
Soon after removal of the cyst, sleep
paralysis and the other symptoms disap¬
peared.
Downloaded from jamanetwork.com by Boston University user on 04/30/2024
The only psychiatric study of sleep paraly¬
sis found in a review of past reports dealt
with 3 young white soldiers during World
War II.24 All 3 were thought to have severe
"combat neuroses," but had no antecedent
psychopathological disorder. It was felt that
the sleep paralysis was an expression of
severe anxiety, similar in meaning to terri¬
fying dreams and sleep hallucinations. The
results of psychotherapy with these patients
were equivocal.
Langworthy and Betz14 postulated that
sleep paralysis, sleep hallucinations, cata¬
plexy, and narcolepsy are similar to hysteri¬
cal reactions, being "neurotic defences, with
symbolic significance, against primary anx¬
ieties associated with difficulties in realistic
adjustments in personal relationships with
others." Several authors 14>23'24 have re¬
ported a high incidence of psychiatric
illnesses in patients with narcolepsy syn¬
drome. However, the evidence for a
psychogenic origin of sleep paralysis is in¬
conclusive.
Many writers 2'9'19 have in the past pro¬
posed that sleep paralysis is a form of
epilepsy. There are clinical similarities be¬
tween certain types of seizures and sleep
paralysis.19 However, there is no electro¬
encephalographic evidence for this belief. In
one study of electroencephalograms on nar¬
colepsy patients,7 recordings were made
while several patients experienced sleep
paralysis. Except for the pattern of light
sleep during conscious awareness, the rec¬
ords were normal. In a similar study21 it
was reported that painful stimulation of a
narcolepsy patient during the catapletic epi¬
sode did not block the alpha rhythm on the
electroencephalogram, but that, otherwise,
the record was normal.
Sleep paralysis is rarely bothersome
enough for the patient to seek medical treat¬
ment. In a series6 of 25 patients with the
narcolepsy syndrome who- were treated with
methyl phenidate hydrochloride (Ritalin),
the narcolepsy in all patients improved
greatly. The 13 with cataplexy improved
moderately, but the 6 with sleep paralysis
 did respond impressively. Only 3 of tion is the decided male predominance of
not
the 6 with sleep paralysis experienced more sleep paralysis in the narcolepsy syndrome
than 50% reduction in frequency of the (males 4:1), while the sex distribution of
symptom. No other reports were found of cataplexy in the narcolepsy syndrome is
the medical drug treatment of a series of the same as for narcolepsy itself (males
patients with sleep paralysis. 3:2). Primary sleep paralysis is not an
The neurologic phenomenon most similar uncommon phenomenon, whereas primary
to sleep paralysis is cataplexy. Many au¬ cataplexy is very infrequent.
thors 2'8'26 consider sleep paralysis a variant Any theory of the etiology of sleep
of cataplexy. Both symptoms are charac¬ paralysis must also encompass a possible
terized by decreased or absent muscle tone, explanation for cataplexy and narcolepsy,
in spite of complete mental awareness. The because they are so frequently associated.
muscle weakness in sleep paralysis is a paral¬ However, the fact that any one of these
ysis of voluntary muscles, but cataplexy is symptoms may occur alone permits an ex¬
merely a hypotonia of some voluntary muscle planation for sleep paralysis that does not
groups. While cataplexy is usually pre¬ treat all the symptoms as being dependently
cipitated by an emotional stimulus during interrelated.
consciousness, sleep paralysis often follows While the etiologies of sleep paralysis,
or is accompanied by sleep hallucinations cataplexy, and narcolepsy are unknown,
during the "twilight" stages of sleep. most investigators now believe that the most
Cataplexy almost always accompanies sleep likely explanation is some dysfunction of
paralysis in the narcolepsy syndrome, but the reticular activating system.2,21 A plausi¬
the reverse is not true (Table 3).26 The ble theory is that sleep paralysis and
incidence of isolated cataplexy would seem cataplexy represent dysfunctions of the de¬
to be exceedingly low, as reflected in Table scending portions of the reticular activating
1 and in the paucity of reports in the litera¬ system, either by a block of facilitatory im¬
ture. pulses, by a stimulation of inhibitory im¬
Brain3 and Brock4 considered sleep pulses, or both.2 To extend this theory,
paralysis and cataplexy to be episodes of narcolepsy, sleepwalking, and sleeptalking
dissociation between the mental and physical may represent dysfunctions of the same kind
components of sleep. The physical part in the ascending portion of the reticular
consists of loss of muscle tone, decreased activating system.
respiration and blood pressure, and hypo- Conversely, but not in contradiction, sleep
ventilation. The mental part consists of paralysis may also- be conceived as the ex¬
loss of conscious awareness. Predormital pression of dysfunction in the ascending
sleep paralysis and cataplexy are interpreted reticular activating system. In the perform¬
as the initiation of physical sleep before the ance of voluntary movement, sensation and
mental part, and postdormital sleep paraly¬ motion are thought to' form "a single indi¬
sis is viewed as arousal of consciousness visible continuous process."13 A disturb¬
prior to volitional actvity. Sleep paralysis ance in integration of afferent impulses in
and cataplexy (mentally awake and physi¬ the reticular activating system theoretically
cally asleep) have their antithesis in nar¬ could produce inhibition of volitional con¬
colepsy, sleepwalking, and sleeptalking trol of skeletal muscles in advance of in¬
(mentally asleep and physically awake). hibition of conscious awareness (predormital
If sleep paralysis and cataplexy represent sleep paralysis), or the persistence of mus¬
essentially the same phenomenon, resulting cle control inhibition after release of
from different precipitating factors, it is inhibition of conscious awareness (post¬
puzzling why individuals who have experi¬ dormital sleep paralysis). Cataplexy might
enced one symptom have not always at some then represent an exaggeration of the normal
time experienced the other. Another ques- response to sensory inputs (i.e., hypotonia

Downloaded from jamanetwork.com by Boston University user on 04/30/2024

 from intense emotional experience such as
fear), resulting in increased inhibition of
muscle tone.
Sleep paralysis has been
studied and many lines of
could be opened. Information about the in¬
cidence, age of onset, sex distribution, and
natural history in large population groups
is needed. Those with frequent sleep
paralysis could be studied during the at¬
tacks, especially in regard to- techniques for
ending the episodes. Drug trials with anti-
convulsants and cortical stimulators might
prove rewarding. Intensive psychologic
analysis of a number of unselected sleep
paralysis patients would help in answering
the question of psychogenic factors.
Summary
Sleep paralysis is defined and its history
discussed briefly. In a survey of 2 groups
of medical students, 1 group of student
nurses, and 1 group of hospital inpatients,
sleep paralysis is found to occur fairly fre¬
quently as an isolated symptom, and more
often in males than females. The Duke
Hospital cases of sleep paralysis are re¬
viewed. The association of sleep paralysis
with several illnesses is discussed, and sleep
paralysis and cataplexy are compared. Pos¬
sible etiologic mechanisms are considered,
with special emphasis on the occurrence of
sleep paralysis as a dy s functioning either
in the ascending or descending portion of
the reticular activating system.
I am indebted to Dr. E. Charles Kunkle, Dr.
Gunter R. Haase, Dr. Stewart Wolf, and Dr.
E. M. Brandt for their helpful criticism.
G. Browne Goode, M.D, 800 N.E. 13th
Oklahoma City 4.
REFERENCES
1.
Adie, W. J.: Idiopathic Narcolepsy,
257, 1926.
2. Aird, R. B.: Use of Phenacemide (Phen-
urone) in the Treatment of Narcolepsy and
Cataplexy, Arch. Neurol. Psychiat. 70:510, 1953.
3. Brain, W. R.: Sleep: Normal and Patho-
logical, Brit. Med. J. 2:4046, 1939.
4. Brock, S.: The Narcoleptic-Cataplectic Syn-
drome\p=m-\AnExcessive and Dissociated Reaction of
the Sleep Mechanism\p=m-\and Its Accompanying
Mental States, J. Nerv. Ment. Dis. 94:700, 1941.
Downloaded from jamanetwork.com by Boston University user on 04/30/2024
5.Chodoff, P. : Sleep Paralysis, J. Nerv. Ment.
Dis.100:278, 1944.
6.Daly, D. D.: Treatment of Narcolepsy with
Methyl-Phenylpiperidylacetate, Proc. Mayo Clin.
inadequately 32:320, 1957.
investigation 7. Daly, D. D., and Yoss, R. E.: The Electro-
encephalogram in Sleep, Electroenceph. Clin. Neu-
rophysiol. 9:109, 1957.
8. Daniels, L. E. : Narcolepsy, Medicine 13:1,
1934.
9. Ethelberg, S. : Symptomatic Cataplexy or
Chalastic Fits in Cortical Lesions of the Frontal
Lobe, Brain 73 :499, 1950.
10. Ethelberg, S.: Obscurations and Further
Time-Related Paroxysmal Disorders in Intracranial
Tumors : Syndrome of Initial Herniation of Parts
of the Brain Through the Tentorial Incision, Arch.
Neurol. Psychiat. 68:130, 1952.
11. Ethelberg, S.: Sleep Paralysis or Post-
Dormital Chalastic Fits in Cortical Lesions of the
Frontal Pole, Acta Psychiat. Neurol. Suppl. 108:
121, 1956.
12. Fulton, J. F.: Tumors in the Region of the
Third Ventricle\p=m-\TheirDiagnosis and Relation to
Pathological Sleep, J. Nerv. Ment. Dis. 69:1, 1929.
13. Gooddy, W. : Sensation and Volition, Brain
72:312, 1949.
14. Langworthy, O. R., and Betz, B. J. : Narco-
lepsy as a Response to Emotional Conflicts, Psycho-
som. Med. 6:211, 1944.
15. Levin, M.: Narcolepsy (Gelineeu's Syn-
drome) and Other Varieties of Morbid Somnolence,
Arch. Neurol. Psychiat. 22:1172, 1929.
16. Levin, M.: The Pathogenesis of Narcolepsy
with Consideration of Sleep Paralysis and Local-
ized Sleep, J. Neurol. Psychiat. 14:1, 1933.
17. Lichtenstein, B. W. : Sleep Paralysis, J. Nerv.
Ment. Dis. 95:153, 1945.
18. Mitchell, S. W.: Some Disorders of Sleep,
Amer. J. Med. Sc. C:109, 1890.
19. Notkin, J. : The Narcolepsies, Arch. Neurol.
Psychiat. 31:615, 1934.
20. Schneck, J. M. : Sleep Paralysis Without
Narcolepsy or Cataplexy : Report of a Case,
J.A.M.A. 173:1129, 1960.
St., 21. Sieker, H. O., et al.: The Effects of Natural
Sleep and Hypersomnolent States on Ventilatory
Functions, Ann. Intern. Med. 52:500, 1960.
22. Smith, C. : Psychosomatic Aspects of Narco-
Brain 19:
lepsy, J. Ment. Sci. 104:593, 1953.
23. Spiegel, L. A.: Narcolepsy as a Psychogenic
Symptom, Psychosom. Med. 8:28, 1948.
24. Vanderheide, C. : Sleep Paralysis with Com-
bat Fatigue, Psychosom. Med. 7:330, 1945.
25. Wilson, S. A. K. : The Narcolepsies, Brain
21:63, 1928.
26. Yoss, R. E., and Daly, D. D. : Criteria for
the Diagnosis of the Narcolepsy Syndrome, Proc.
Mayo Clin. 32:320, 1957.