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Cerebral cortical function in infants at risk for sudden infant death syndrome.

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Cerebral Cortical Function in Infants
at Rsk for Sudden Infaant Death Syndrome
Robert R. Clancy, MD, and Alan R. Spitzer, MD
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~
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Cerebral cortical function was prospectively examined by electroencephalography (EEG) in 3 subgroups of 257 infants
at risk for sudden infant death syndrome (SIDS). Group 1 consisted of apparently healthy infants with near-miss SIDS
episodes; Group 2 consisted of siblings of SIDS victims; and Group 3 consisted of neurologically suspect infants with
apnea. The usual abundance and distribution of sharp EEG transients (SETs) were determined from 69 Group 1
infants. EEGs were interpreted as abnormal in the presence of ictal apnea, excessively abundant SETs, or immaturity of
EEG background for conceptional age. Ninety percent of infants in Group 1 had entirely normal EEGs. There was no
significant difference in the abundance or distribution of SETs between infants with normal breathing patterns and
those with excessively periodic respirations. Nonictal apnea was recorded in 7% of Group 1 infants. The unexpected
diagnosis of ictal apnea was confirmed in 2 Group 1 infants (1.2%), and 5 (2.9%) had excessive SETs but no recorded
seizures. Only 4 infants (2.3%) had abnormally immature EEGs for conceptional age. Nonictal apnea occurred in 5 of
33 (15.2%) Group 3 infants and ictal apnea was confirmed in 2 others (6.1%). We conclude that the majority of Group 1
and 2 infants have normal cerebral cortical activity between and during apnea and that central nervous system cortical
immaturity, as measured by EEG, plays no important role in the pathogenesis of SIDS. SETs are commonly recorded in
these infants and must be conservatively interpreted. However, an EEG examination was critical in establishing the
unexpected diagnosis of ictal apnea in a small percentage of Group 1 and 3 infants and materially influenced subsequent evaluation, management, and prognosis.
Clancy RR, Spitzer AR: Cerebral cortical function in infants at risk for sudden
infant death syndrome. Ann Neurol 18:41-47, 1985
Apnea is a potentially lethal respiratory disturbance in
infants that may presage the sudden infant death syndrome (SIDS). Although the cause of SIDS is unknown, faulty central nervous system regulation of
breathing is suspected to play an important role in its
patho,genesis C14, 151. Few reports have detailed the
participation of the cerebral cortex in SIDS [ l l , 181.
This study evaluates cerebral cortical function, examined b y electroencephalography (EEG), in 257 infants
at high risk for SIDS to: (1) clarify the interpretation of
sharp EEG transients (SETs) in EEGs recorded from
these infants; (2) determine the incidence of “ictal
apnea” as a specific cause of infant apnea; and (3) ascertain whether functional immaturity of the cerebral cortex, as measured by BEG, plays an important role in
this disorder.
Methods
Patieizt Population
Infants evaluated by the Children’s Hospital of Philadelphia
Apnea Screening Program between 1982 and 1984 were
included in the study. Each infant was hospitalized and
From rhe Divisions of Neurology and Neonatology, The Children’s
Hospiral of Philadelphia, and the Departments of Neurology and
Pediatrics, University of Pennsylvania School of Medicine, Philadelphia, PA.
underwent a minimum evaluation including a detailed history and physical examination, chest x-ray studies, electrocardiogram (EKG), EEG, complete blood count, and determinations of serum electrolytes, glucose, calcium, magnesium,
phosphate, and blood urea nitrogen. A 6- to 24-hour thermistor pneumocardiogram was obtained and sometimes a
pH probe study and barium swallow. Patients were divided
into 3 groups according to their clinical characteristics:
Group 1 was composed of apparently healthy children with
near-miss SIDS episodes, Group 2 consisted of siblings of
SIDS victims, and Group 3 included neurologically suspect
infants with recurrent apnea. This last group included infants
with disorders that may adversely affect the central nervous
system such as intrauterine growth retardation, sepsis, or
intraventricular hemorrhage.
Themistor Pneumocardiogram Stzldies
Simultaneous recordings of heart rate, impedance pneumography, and nasal airflow were monitored in all patients. Standard lead placement of the lateral upper right side of the
chest wall below the clavicle, lower left side of the chest wall
in the anterior axillary line, and upper left side of the chest
wall was used for these recordings. Airflow at the nose was
determined by taping a thermistor 2 to 5 mm below the
Received Oct 1, 1984, and in revised form Dec 4. Accepted for
publication Dec 7, 1984.
Address reprint requests to Dr Clancy, Division of Neurology,The
Children’s Hospital of Philadelphia, 34th Street and Civic Center
Boulevard, Philadelphia, PA 19104.
41
nostril. The thermistor was connected to a bridged resistor
circuit and amplified through the polygraph to provide a
qualitative signal of air exchange.
Each recording was analyzed for periods of bradycardia
and prolonged apnea. Prolonged apnea has been previously
defined by the American Academy of Pediatrics Task Force
f201 as “cessation of breathing for 20 seconds or longer, or as
a brief episode associated with bradycardia, cyanosis or pallor.” In the present study, prolonged apnea included any
cessation of respiratory airflow of more than 5 seconds associated with bradycardia or any cessation of respiratory airflow
of more than 20 seconds, regardless of heart rate. Bradycardia was defined as a heart rate less than 100 beats per minute.
Periodic breathing was defined as periods of respiration of
less than 2 0 seconds separated by periods of apnea of less
than 10 seconds’ duration occurring at least three times in
succession. Periodic breathing was defined as excessive when
it occurred during more than 20% of total sleep time.
Electroencephalograms
EEGs were recorded in the laboratory o r at the patient’s
bedside with a 2 1-channel Grass electroencephalograph. An
array of twelve surface electrodes was applied with electrode
paste according to the International 10-20 System modified
for neonates 1213. Sixteen channels were devoted to EEG
and five recorded polygraphic parameters including extraoculogram, EKG, and nasal and chest respirations. The technologist made frequent notations of small and large body
movements, apnea, skin color changes, and rapid eye movements. Behavioral states (awake, active [rapid-eye-movement) sleep, quiet [non-rapid-eye-movement) sleep, and
indeterminant sleep) were recognized using previously
described criteria fll.Quiet sleep was further classified into
two varieties: immature (traci. alternant) o r mature (continuous slow wave).
Each EEG was visually analyzed and graded as normal o r
abnormal for conceptional age (determined by adding the
postnatal age to the estimated gestational age) according to
predetermined and previously published criteria 131. EEGs
were judged abnormally immature if the observed background cerebral activity implied a conceptional age that was
3 or more weeks younger than the conceptional age determined by maternal dates or Dubowitz examination. Special
note was made of apnea that occurred while the EEG was
being recorded. Ictal apnea was defined as a definite electrographic seizure clinically accompanied by apnea. Nonictal
apnea was recognized as a cessation of breathing in the absence of electrographic seizure patterns.
The usual abundance and distribution of SETs were determined by a detailed analysis of EEG samples recorded from
69 Group 1 infants. Each infant was considered medically
and neurologically well except for apnea and each had normal background EEG activity. Some of these 69 infants had
normal thermistor pneumocardiograms (Group lNR), and
the others had excessive periodic breathing (Group 1 p ~ ) .
SETs were defined as monophasic, diphasic, or polyphasic
sharply contoured waves (duration less than 300 to 500 ms)
that were clearly distinguishable from the background activity. Typical peak-to-peak amplitude was 50 to 150 p v (Fig 1).
A representative portion of active sleep was chosen from
each record, and the SET frequency (number of SETs per 10
42
Annals of Neurology
Vol 18 No 1 July 1985
Fig 1. Typical morphologiej of sharp eiectroencephalographic
transients recorded from the temporal and central regions during
active sleep in 4 healthy Gronp 1 infants. (Calibration:5 0 pv,
2 seconds.)
minutes of active sleep) in the left and right central (C3 and
Cq) and temporal (Tj and Tq) regions was measured. For each
individual tracing, randomness of SET distribution was determined by calculating the probability of the observed distribution among locations Cj, Cq, T3, and T,, by the cumulative
binomial probability function. Comparisons were made between the left and right central and temporal regions (C3
versus Cq and T3 versus Td), the left and right hemispheres
(Cj
T3 versus C4 + Tq), and between the central and
temporal regions (C,
C4 versus T3
T4). SET distribution was considered nonrandom (i.e., “focal”) if the probability of the observed distribution was less than 0.05.
Statistical analysis of the data was performed by the twotailed Student’s t test, chi-squared analysis, and the cumulative binomial probability function.
+
+
+
Results
Patient Population
Two hundred fifty-seven infants were included in the
study. Table 1 summarizes the range and mean estimated gestational ages and conceptional ages of the
infants at the time of EEG examination. The clinical
diagnoses of the 3 3 Group 3 infants with recurrent
apnea included: multiple congenital anomalies (7 infants), intrauterine growth retardation (4) and status
post intraventricular hemorrhage (11), asphyxia (8), or
sepsis-meningitis (3). No patient had a known active
seizure disorder at the time of the EEG examination
for recurrent apnea.
Table I . Clinical and Electroencephalog~aphi~
Characteristics of Infants at
Risk for Sudden Infant Death
Type of EEG Abnormality
Patient Group
Group 1
Healthy infants with near-miss
SIDS episodes (n = 173)
Group 2
Siblings of SIDS victims
(n = 51)
Group 3
Neurologically suspect infants
with apnea rn = 33)
EEG
=
Estimated
Gestational
Age:
Mean, Range
(wk)
Conceptional
Age at Time
of EEG:
Mean, Range
(wk)
Immaturity
Mild, Nonspecific
Abnormalities of
Background
18 (10.496) 2 (1.296) 5 (2.9%)
4 (2.3%)
7 (4%)
4 (7.8%)
1 (2.0%)
2 (3.9%)
Gender
Ratio
(MF)
Normal
EEGs
37.6 (27 to 43) 42.2 (31 to 53)
1.06
155 (89.6%) 12 (7%)
38.4 (30 to 43)
42.6 (34 to 52)
1.68
47 (92.2%)
1(2.0%)
34.8 (26 to 42)
39.6 (28 to 48) 3.13
13 (39.4%)
5 (15.2%) 20 (60.6%) 2 (6.1%) 10 (30.3F) 0
electroencephalogram; SlDS
=
Nonictal
Apnea
Total
Abnormal
EEGs
Ictal
Apnea
0
Excessive
SharpEEG
Transients
I (2.0%)
8 (24.2%)
sudden infant death syndrome.
The Usual Frequency and Distribution
of SETJ in Group 1 Infants
The EEGs from 67 Group 1 infants were visually
analyzed to determine the usual abundance and distribution of SETs during active sleep. Thermistor
pneumocardiogram studies yielded normal results in
44 infants (Group lNR). The remaining 25 infants had
excessive periodic breathing (Group 1 p ~ ) A
. total of
871 minutes of active sleep was selected from these
two groups for analysis (mean active sleep sample time
in Group INR = 12 minutes, range 8 to 24 minutes;
mean active sleep sample time in Group l p B = 14
minutes, range 8 to 28 minutes). Table 2 displays the
abundance of SETs per 10 minutes of active sleep for
these two groups stratified by conceptional age. There
was no significant difference in SET frequency between
Groups 1 N B and l p g at any conceptional age.
SETs were most abundant in the temporal regions
(T3 and T4) where they persisted until conceptional age
45 weeks, then gradually disappeared from the background by conceptional age 50 weeks. Fewer SETs
appeared in the central regions (C3 and C,) where they
peaked in abundance by conceptional age 37 weeks
and also disappeared from the tracings by conceptional
age 50 weeks.
SETs were randomly distributed between the left
and right temporal areas (T, versus T*),central areas
(C3versus C4>,and hemispheres (T3 C3 versus T4 +
C4) for the majority of Group ~ N and
R
Group l p g
infants (Table 3). Hgwever, SETs were distributed
preferentially (nonrandomly) to the temporal rather
than the central regions (T3 T4 versus C3 + C4) in a
sizable and comparable portion of both Group 1 N R and
Group 1pB infants (27.3% and 4496, respectively).
+
+
EEGs in Group 1, 2, and 3 Infants
GROUP 1 INFANTS. Ninety percent of Group 1 infants had entirely normal EEGs (see Table 1).Nonictal
apnea was recorded in 7% of the group and was unac-
companied by any alteration of the EEG except for
normal sleep transition or arousal patterns.
The unexpected diagnosis of ictal apnea was
confirmed in 2 Group 1 infants, representing 1.2% of
these patients (Tables 1 and 4). Both displayed a
definite electrographic seizure that was clinically manifested solely or primarily by apnea, and both had an
abnormal interictal EEG displaying an excessive number of SETs.
Five Group 1 infants had abnormal EEG backgrounds and excessive SETs for conceptional age, but
no electrographic seizures or apnea was recorded.
None of these infants subsequently had seizures on 1year follow-up examination.
Immaturity of the background EEG activity was
present in only 4 (2.3%) Group 1 infants. The transition from immature (traci. alternant) to mature (continuous slow wave) quiet sleep was completed in all
infants by conceptional age 46 weeks.
2 INFANTS. Forty-seven of 5 1 (72.2%)
Group 2 infants had entirely normal EEGs (Table 1).
Nonictal apnea was recorded in 1 infant (1.9%) and
was unaccompanied by any EEG changes. N o electrographic seizure was recorded. Only 1 infant (1.7%)
had an abnormally immature EEG for conceptional
age.
GROUP
3 INFANTS. The majority of Group 3 infants
had abnormal EEGs (see Table 1). Nonictal apnea was
recorded in 5 of 33 infants. The unexpected diagnosis
of ictal apnea was confirmed in 2 of 33 patients (6.1%)
(Tables 1 and 4). The first infant suffered birth asphyxia and neonatal seizures that resolved by the
seventh day of life. At 8 weeks of age, he was
reevaluated by EEG for new-onset apnea at which time
the diagnosis of ictal apnea was confirmed (Fig 2). Ictal
apnea continued sporadically despite treatment until
age 5 months. The second infant was small for gesta-
GROUP
Clancy and Spitzer: Cortical Function in Near-Miss SIDS 43
Table 2. Mean Number of Sharp Electroencephalographic Transients in Group 1 Infants per 10 Minutes of Actizie Sleep
Conceptional Age
5
Location of SET
+
Central regions (Cj C,)
Temporal regions (T3 + T,$)
All regions (C, C4 T3
+
+ Td)
+
37 wk
38-41 wk
PB
(n = 7 )
NR
Both”
(n = 1 3 )
PB
(n = 9 )
NR
(n = 6 )
(n = 11)
Both
(n = 20)
2.55
7.13
9.68
2.85 ? 2.05
7.03 -+ 2.90
9.90 5 4.05
2.69 ? 2.48
7.08 ? 4.90
9.78 t 5.36
1.73
3.24
8.17 ? 8.71
9.91 2 9.35
1.04 i 1.14
1.94 ? 3.23
4.98 -+ 3.70
1.35 i 2.29
5.84 t 6.49
7.20 2 7.10
?
?
?
2.!?6‘
6.40
6.61
’Since there was no significant difference in SET abundance between NR and PB for any location or conceptional age, figures for both groups were combined
hNumbers are mean 2 I SD.
CA
=
conceptional age; SET
=
sharp electroencephalographic transients, PB = infants with excessive periodic breathing; NR
=
infants with normd respirations.
tional age but otherwise appeared well except for recurrent sleep apnea. A right temporal electrographic
seizure was recorded that was accompanied solely by
apnea. Ten other Group 3 infants (30.36%) had excessively abundant SETS but no electrographic seizure,
and none had subsequent clinical seizures on follow-up
examination.
yet been established, although dysfunction of the
brainstem {19], vagal nerve [B, 131, and carotid body
chemoreceptors 14, 14, 151 has been investigated. Few
studies have examined the participation of the cerebral
cortex in SIDS [ l l , 181. EEGs have been recommended as part of the full medical evaluation of infants
Discussion
Infants may experience apnea for a variety of specific
identifiable reasons, such as pneumonia, upper airway
obstruction, hypoglycemia, sepsis, anemia, or gastroesophageal reflux [16, 17). When apnea occurs
without apparent cause, the event is labeled “near-miss
SIDS,” and the cause is generally suspected to be
faulty central nervous system regulation of respiration
112, 14, 151. The neurological basis of SIDS has not
Fig 2. Electroencephalogram recorded during active sleep in a 44week conceptional age infant because of new-onset sleep apnea beginning 7 weeks after birth asphyxia and resolved neonatal seizures. An electrographic seizure arose from the right temporal
region and spread at lower voltage to the occipital regions. There
was no change in the infant’s ongoing active sleep behavior, but
extremely subtle eye deviation was noted. Prolonged apnea and
facial cyanosis were the predominant clinical manifstations of
the seizure. (Calibration: SO pv, 2 seconds.) (EKG = electrocardiogram.)
Chest Wall
Move rnents
EKG
-w
44 Annals of Neurology Vol 18 No I July 1985
Conceptional Age
42-45 wk
46-49 wk
3
PB
(n = 6)
NR
(n = 16)
Both
(n = 22)
PB
(n = 0 )
NR
(n = 6)
Both
(n = 6)
PB
(n = 3)
1.38 f 1.17
8.13 5 6.92
9.52 5 7.34
0.71
5.98
6.69
0.90 f 1.07
6.57 f 7.29
7.47 2 7.75
...
...
1.08 f 1.39
2.42 5 2.75
3.50 2 3.89
1.08 f 1.39
2.42 5 2.75
3.50 f 3.89
0
0.48
0.48
f
5
?
1.01
7.55
7.99
...
5
2
0.83
0.83
50 wk
NR
(n = 5)
Both
(n = 8)
0
0
0.18
0.18
0
0
5
5
0.51
0.51
Table 3. Incidence of Random and Nonrandom Distribution of Sharp
Electroencephalographic Transients during Active Sleep in Group 1 Infants
Scalp Locations Compared
Left and Right
Temporal
(T3 vs T4)
Left and Right
Central
(C3 vs C4)
Patient
Group
Pattern of SET
Distribution
1PB
Random
Nonrandom
96% (24125)
96% (24125)
4% (1/25)
4% (1125)
Random
Nonrandom
97.7% (43144)
2.3% (1144)
~ N R
“Yates corrected &squared
SET
=
with 1 df
=
100% (44/44)
0
Left and Right
Hemispheres
(T3 + C3 vs
T4 + C4)
Temporal and
Central
(T? + T4 vs
c3 + C4)
92% (23125)
8% (2125)
56% (14125)
44% (11125)”
97.7% (43144)
2.3% (1144)
72.7% (32144)
27.3% (12/44)”
1.325; p > 0.05.
sharp electroencephalographic transients; PB
=
periodic breathing; NR
=
normal respirations.
Table 4. Infants with Ictal Apnea
PatiendGroup
EGA
(wk)
CA
(wk)
Behavioral State
during Seizure
Site of Origin and
Spread of Seizure
Interictal EEG
IIGroup 1
37
43
Active sleep
Left temporal -+
left occipital region
Abnormal; excessive multifocal
SETs
2iGroup 1
40
52
Active sleep
3/Group 3 (status
post birth asphyxia)
36
44
Active sleep
Central vertex +
right central occipital region
Right temporal -+
right occipital region
Abnormal; excessive slowing and
SETs
Abnormal; excessive multifocal
SETs
4/Group 3 (small
for dates)
40
41
Active sleep
Right temporal -+
right occipital region
Abnormal; excessive multifocal
SETs
EGA = estimated gestational age; CA
=
Clinical Signs
during Seizure
Apnea; staring, facia1 cyanosis;
mild bradycardia
to 100 beadmin
Apnea
Apnea; facial cyanosis; brief and
subtle ocular deviacion to the left
Apnea
conceptional age; EEG = electroencephalogram; SETs = sharp EEG transients.
Clancy and Spitzer: Cortical Function in Near-Miss SIDS 45
with near-miss SIDS 1171 as apnea may accompany
seizures in early infancy. The interpretation of these
EEGs, however, is hampered by a lack of clear guidelines to judge the significance of SETs in this age
group. Furthermore, although isolated reports of ictal
apnea have been described [ 5 , 22, 23, 251,the incidence of ictal apnea mimicking near-miss SIDS episodes has not been determined.
The cerebral cortex functioned normally in most infants at risk for SIDS. The majority of Group 1 and 2
infants had entirely normal EEGs during and between
apnea. Furthermore, most Group 3 infants had no
pathological change in the EEG during apnea. Only
2% of Group 1 infants displayed any electrographic
marker of cortical immaturity. The conceptional age at
transition from immature (traci. alternant) to mature
(continuous slow wave) quiet sleep was normal for
most infants [GI. kttle attention has been paid previously to systematic electrophysiological examinations
of cerebral cortical function in this patient population.
Sterman and associates { 181 have reported normal or
accelerated cerebral electrical maturity in a small
cohort of infants with apnea followed longitudinally.
Although Lacey [I 11 has measured excessive variability of the frequency of sleep spindles in infants with
apnea, the significance of this finding was not apparent,
and no other important abnormalities were recorded.
Apparently healthy infants with nonictal apnea frequently display SETs that interrupt an otherwise normal EEG background. SETs are relatively common
during active sleep in infants of conceptional age 37 to
45 weeks, then decline in abundance and virtually disappear by 50 weeks of conceptional age. Karbowski
and Nencka [lo} reported a mean interval of 1 minute, 48 seconds, between SETs appearing at all locations within the first week of life in healthy full-term
infants. This is comparable to our determination of a
mean incidence of 7.20 SETs per 10 minutes (1 minute, 23 seconds, between SETs) in similar aged infants.
When SETs interrupt the ongoing background cerebral activity, they arise in a random fashion for most
locations in the majority of patients. There is no persistent laterality of SETs comparing the left and right
central regions, left and right temporal regions, and left
and right hemispheres. However, there is commonly a
preferential (nonrandom) distribution of SETs to the
temporal rather than the central regions. This “focal”
assortment of SETs is also reflected in the higher mean
abundance of SETs occurring in the temporal regions
(see Table 2). The predominance of SETs in the temporal regions may cause special concern because electrographic seizures recorded in the neonate commonly
arise there 1241. Nevertheless, there are recognized
EEG criteria that help distinguish between SETs in
healthy babies and those recorded in infants with sei-
46 Annals of Neurology Vol 18 No 1 July 1985
zures 12,81. The significance of the excessively abundant SETs recorded in a small number of Group 1 and
3 infants is unclear (see Table 1). There was no
confirmation of ictal apnea and none of these infants
later experienced clinical seizures. It is possible that
their excessive SETs indicated a mild encephalopathy
resulting from apnea rather than evidence of seizures
provoking apnea. It is apparent that a conservative approach to the interpretation of SETs should be
adopted to avoid the inaccurate diagnosis of ictal apnea.
Previous reports have described apnea as the sole or
predominant clinical manifestation of seizures in neonates, infants, and children [ 5 , 22, 23, 251, but the
incidence of ictal apnea in the whole population of
infants with apnea has not been previously determined. In contrast to the frequent appearance of SETs
in infants with apnea, the incidence of seizures
mimicking near-miss SIDS episodes was low, approximately 1% of Group 1 infants and 6% of Group 3
infants. In our patients, the diagnosis of ictal apnea
was unexpected and would have been missed without
an EEG examination. Despite the low incidence of
confirmed ictal apnea, EEG was valuable in the full
assessment of infants at risk for SIDS as it materially
and uniquely affected subsequent evaluation and treatment for some patients. Conversely, a normal EEG
was helpful in refuting the diagnosis of ictal apnea in
infants who displayed abnormal motor signs accompanying apnea such as sometimes occurred with gastroesophageal reflux 17, 161.
Presented in part as a poster presentation at the Child Neurology
Society Meeting, Phoenix, AZ, Oct 11-13, 1984.
We thank Bruce Kassie, Eileen Shupak, Denise Conicella, Sharon
Butterworth, and Kathy Peeke for their expert technical assistance
and Lisa Dieni for preparing the manuscript.
References
1. Anders T, Emde R, Parmelee A: A manual of standardized
terminology techniques and criteria for scoring of states of sleep
and wakefulness in newborn infants. U.C.L.A. Brain Information Service. NINDS Neurological Information Network, Los
Angeles, 1971
2. Clancy RR. Sharp electroencephalographic transients in neonates with seizures (abstract). Ann Neurol 14:377-378, 1983
3. Clancy RR, Tharp BR, Enzman D: EEG in premature infants
with intraventricular hemorrhage. Neurology (Cleveland)
34~583-590, 1984
4. Cole S, Lindenberg LB, Galisto JR, et al: Ultrastructure abnormalities of the carotid body in sudden infant death syndrome.
Pediatrics 63:13-17, 1979
5. Coulter DL: Partial seizures with apnea and bradycardia. Arch
Neurol 41:173-174, 1984
6. Ellingson RJ, Peters JF: Development of EEG and daytime sleep
patterns in normal full-term infants during the first 3 months of
life: longitudinal observations. Electroencephalogr Clin Neurophysiol 49:112-124, 1980
7. Herbst JJ: Gastroesophageal reflux. J Pediatr 98:859-870, 1981
8. Hughes JR, Fino J, Gagnon L The use of the electroencephalogram in the confirmation of seizures in premature and
neonatal infants. Neuropediatrics 14:2 13-2 19, 1983
9. Kahn A, Riazi J, Blum D: Oculocardiac reflex in near miss for
sudden infant death syndrome infants. Pediatrics 7 1:49-52,
1983
10. Karbowski K, Nencka A Right mid-temporal sharp EEG transients in healthy newborns. Electroencephalogr Clin Neurophysiol 48:461-469, 1980
11. Lacey DJ: Sleep EEG abnormalities in children with near miss
sudden infant death syndrome, in siblings, and in infants with
recurrent apnea. J Pediatr 1022355-859, 1983
12. McCulloch K, Brouillette RT, Guzzetta AJ, Hunt CE Arousal
responses in near miss sudden infant death syndrome and in
normal infants. J Pediatr 101:911-917, 1982
13. Sachis PN, Armstrong DL, Becker LE, Bryan AL: The vagus
nerve and sudden infant death syndrome: a morphometric
study. J Pediatr 98:278-280, 1981
14. Shannon DC, Kelly DH: Medical progress: SIDS and near
SIDS. N Engi J Med 306959-765, 1982
15. Shannon DC, Kelly DH: Medical progress: SIDS and near
SIDS. N Engl J Med 306:1022-1028, 1982
16. Spitzer AR, Boyle JT, Tirchmen DT, Fox WW: Awake apnea
associated with gastroesophageal reflux. J Pediatr 104:200-205,
1984
17. Spitzer AR, Fox WW: Infant apnea: an approach to management. Clin Pediatr 7:374-380, 1984
18. Sterman MB, McGinty DJ, Harper RM, et al. Developmental
comparison of sleep EEG power spectral patterns in infants at
low and high risk for sudden death. Electroencephalogr Clin
Neurophysiol 53: 166- 18I, 1982
19. Takashima S, Armstrong D, Becker L, Bryan C: Cerebral hypoperfusion in the sudden infant death syndrome? Brainstem
gliosis and vasculature. Ann Neurol 4:257-262, 1978
20. Task Force on Prolonged Apnea, American Academy of Pediatrics: Prolonged apnea. Pediatrics 61:651-652, 1978
2 1. Tharp B R Neonatal pediatric electroencephalography. in
Aminoff MJ (ed): Electrodiagnosis in Clinical Neurology. New
York, Churchill Livingstone, 1980, pp 67-117
22. Watanabe K, Hara K, Hakamada S, et ai: Seizures with apnea in
children. Pediatrics 7987-90, 1982
23. Watanabe K, Hara K, Miyazaki S, et al: Apneic seizures in the
newborn. Am J Dis Child 136:980-984, 1982
24. Watanabe K, Hara K, Miyazaki S, et al: Electroclinicalstudies of
seizures in the newborn. Folia Psychiatr Neurol Jpn 31:383392, 1977
25. Willis J, Gould JB: Periodic alpha seizures with apnea in a newborn. Dev Med Child Neurol 22:214-222, 1980
Clancy and Spitzer: Cortical Function in Near-Miss SIDS 47
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infant, death, syndrome, cortical, function, risk, sudden, cerebral
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