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Author
Daniel G Glaze, MD
Section Editor
Douglas R Nordli, Jr, MD
Deputy Editor
April F Eichler, MD, MPH
Clinical features and diagnosis of infantile spasms
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: May 2014. | This topic last updated: Aug 09, 2012.
INTRODUCTION Infantile spasms (IS) is an age-specific convulsive disorder of infancy and early childhood.
Children with IS typically exhibit the electroencephalographic pattern known as hypsarhythmia. Infantile
spasms were described first by West in 1841 [1]. The triad of spasms, arrest of psychomotor development,
and hypsarhythmia is known as West syndrome.
The clinical features and diagnosis of IS are reviewed here. The etiology and pathogenesis, and management
and prognosis are discussed separately. (See "Etiology and pathogenesis of infantile spasms" and
"Management and prognosis of infantile spasms".)
CLINICAL FEATURES IS is characterized by epileptic spasms with onset in infancy or early childhood that
are usually associated with the electroencephalographic (EEG) pattern of hypsarhythmia, and also
developmental regression [2].
Age of onset The majority (90 percent) of affected children present at less than one year of age, with a
range from one day to 4.5 years of age (figure 1) [2-4]. The peak incidence of onset (50 to 77 percent) is
between three and seven months; onset after 18 months is rare. The true age of onset may be uncertain
because IS may be initially mistaken for other conditions, such as hyperirritability, exaggerated startle
responses, and/or colic [5]. (See 'Differential diagnosis' below.)
Spasms Spasms can involve the muscles of the neck, trunk, and extremities [2]. They are usually
symmetric and synchronous, but there can be variant clinical patterns. Two phases of muscle activity typically
occur. The first phase consists of sudden, brief contractions of one or more muscle groups. This is followed by
a longer tonic phase. The initial phasic contraction lasts less than two seconds. The less intense tonic
contraction that follows usually is two to ten seconds in duration. Less often, phasic contraction lasts less than
0.5 second and occurs without a tonic phase [6].
Three clinical types of spasms have been characterized using time-synchronized video and polygraphic
recording [6,7]. In one report, 5042 seizures in 24 infants were classified as flexor, extensor, and mixed flexor-
extensor in 33.9, 22.5, and 42.0 percent, respectively [6]. Most infants have more than one type of spasm.

Flexor spasms consist of sudden flexion of the neck, trunk, arms, and legs, and contraction of the
abdominal muscles. The latter may be severe enough to cause the torso to jackknife at the waist. The
intensity of the contraction and the number of muscle groups involved vary in different attacks and from
infant to infant.

Extensor spasms consist of abrupt extension of the neck and trunk, with abduction or adduction of the
arms or legs.

Mixed flexor-extensor spasms usually consist of flexion of the neck, trunk, and arms, and extension of the
legs. Less commonly, they involve flexion of the legs and extension of the arms.

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The extent and intensity of seizures varies [2]. The ictal event can range from a precipitous, massive
contraction of flexor and/or extensor muscles of the neck, trunk, and extremities to an evanescent contraction
confined to the rectus abdominis muscles or a brief head nod. Body position can affect the type of spasm.
Motor arrest, or episodes of attenuated responsiveness, sometimes occurs after the spasm and can last as
long as 90 seconds. These episodes also can occur independently as a seizure without a preceding motor
spasm. Deviation of the eyes or rhythmic nystagmoid eye movements occurs in approximately 55 percent of
seizures [6]. Asymmetric spasms occur almost exclusively in patients with focal brain lesions.
Changes in respiratory pattern occur frequently during spasms. Changes in heart rate are rare. A cry or
scream frequently occurs after an attack, but it is not considered to be part of the seizure [6].
Most infantile spasms (80 percent) occur in clusters consisting of 2 to 125 spasms at a rate of as many as 13
per minute [8]. The intensity and frequency of the spasms in each cluster often increase progressively to a
peak, then decline until they stop (a crescendo-decrescendo pattern). Although the average duration of an
individual spasm is four to ten seconds, a cluster may last for several minutes [2]. Different seizure types may
occur within a cluster. Parents may observe a behavioral change at the onset of clusters.
Spasms occur more frequently in the waking state and in the daytime [9]. Clusters tend to occur following
arousal, rather than during sleep [8]. One video-EEG monitoring study noted that spasms in younger patients
(< 3 years) were more frequent between 9 am to noon and between 3 pm to 6 pm, while older children have
spasms mostly between 6 am and 9 am [9]. The sleep pattern in affected infants is characterized by frequent
arousals during the night. Photic stimulation, handling, feeding, or loud sounds do not precipitate spasms
although they may appear to do so [6,7].
Recognition and accurate reporting of spasms can be difficult for both parents and medical personnel [6,7].
Although massive muscular contractions are easy to recognize, brief contractions confined to the abdominal
muscles may be detectable only with video EEG monitoring. Single spasms and even some clusters may be
short-lived and can occur on arousal from sleep when the infant is not observed. When parental reports of
seizure activity have been compared to video EEG monitoring, most parents underestimated seizure frequency
by five- to tenfold [10].
Other clinical manifestations Neurodevelopmental delay and/or regression with motor and cognitive
manifestations is evident in most patients.
Seizure types other than spasms occur in one-third to one-half of patients with IS [11,12]. These include
partial, myoclonic, tonic, and tonic clonic seizures.
Clinical course IS typically progresses through several stages [13]. During the initial stage, spasms may
occur infrequently and be isolated and relatively mild. Abrupt developmental regression may begin in infants
who previously were normal.
In the next stage, which is the most severe, spasms increase in frequency and appear in series or clusters. As
peak activity is reached, hundreds of spasms may occur in a 24-hour period. Developmental regression or
arrest is most pronounced during this stage.
The third stage is characterized by a progressive and sustained decrease in the frequency and severity of
spasms, which may be rapid or gradual. Resolution of spasms may be followed by the appearance of other
types of seizures.
In a retrospective review of 44 children with untreated IS the cumulative spontaneous remission rate of
spasms was 2 percent at one month, 5 percent at three months, and 25 percent at twelve months [14]. In
most patients, spasms disappear by age three to four years [12]. Other seizure types frequently emerge and
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persist, and permanent neurodevelopmental disability is common. (See "Management and prognosis of
infantile spasms".)
DIFFERENTIAL DIAGNOSIS The differential diagnosis of infantile spasms includes colic, gastroesophageal
reflux, excessive startles, exaggerated Moro reflexes, repetitive body arching, spasticity, benign myoclonus of
early infancy, benign neonatal sleep myoclonus, tonic reflex seizures of early infancy, and benign and severe
myoclonic epilepsies [6,7,10]. These conditions also may occur in patients who previously had or currently
have IS.
Visual observation alone often cannot distinguish IS from other normal and abnormal infant behaviors [6,7]. The
random, often abrupt, uncoordinated movements of infants with brain damage may be especially difficult to
differentiate from IS [6,7]. Video EEG monitoring is usually necessary to differentiate these conditions from IS,
evaluate the persistence or recurrence of IS, or identify other seizures (eg, myoclonic) [6,10].
IS should be distinguished from benign myoclonus of early infancy [15,16], benign neonatal sleep myoclonus
[17], and tonic reflex seizures of early infancy [18]. Similar to IS, these disorders occur in infants and are
characterized by sudden jerky movements.
Benign myoclonus of early infancy Benign myoclonus of early infancy is a rare condition characterized
by brief series of nonepileptic spasms that occur during wakefulness [15,16]. The episodes are characterized
by tonic and/or myoclonic activity of the truncal or limb musculature. Spasms typically result in flexion,
extension, or abduction of the arms and rarely involve the legs. The neck musculature often is involved with
flexor or extensor components and/or aversive jerking movements of the head. (See "Nonepileptic paroxysmal
disorders in infancy", section on 'Benign myoclonus of infancy'.)
In contrast to IS, infants with benign myoclonus of early infancy have normal neurologic examinations, EEGs,
and development. The myoclonic episodes typically resolve before the child reaches two years of age and no
other seizures develop.
Sleep myoclonus Benign neonatal sleep myoclonus is characterized by abnormal jerky movements that
occur only during sleep [17]. The myoclonus is bilateral, synchronous, and repetitive and affects the distal
parts of the upper extremities causing flexion of the fingers, wrists, and elbows, with occasional dorsiflexion of
the ankle. In contrast to IS, infants with sleep myoclonus present within the first week of life and have a normal
neurologic examination and EEG. The disorder resolves spontaneously during the child's first year, often within
the first three months, with no sequelae. (See "Nonepileptic paroxysmal disorders in infancy", section on
'Benign neonatal sleep myoclonus'.)
Tonic reflex seizures of early infancy Tonic reflex seizures of early infancy is a nonepileptic movement
disorder that presents at one to three months of age [18]. Affected infants have episodes of generalized tonic
contraction with extension of all limbs, accompanied by apnea and cyanosis and lasting three to ten seconds.
In the initial description, the episodes occurred only when the infants were awake and held in a vertical position
[18]. They were provoked by shaking or tactile stimulation. This disorder is distinguished from IS by the normal
ictal and interictal EEGs. The prognosis is benign, with spontaneous resolution within one to two months.
DIAGNOSIS
Electroencephalography The diagnosis of IS in a patient with clinical features is confirmed by EEG [2]. A
full EEG evaluation should capture an ictal event and include a full sleep-wake cycle. The recommended
approach is an overnight inpatient 24-hour video EEG; a two or four-hour EEG study may be sufficient in some
cases [19]. Prolonged or repeated monitoring may be required if the initial evaluation is not diagnostic.
Hypsarhythmia Most affected patients have an interictal EEG pattern known as hypsarhythmia. In the
2010 consensus report, this EEG pattern was identified as a defining feature of IS. The classic pattern of
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hypsarhythmia consists of very high voltage, random, slow waves and spikes in all cortical areas [2,20]. The
spikes vary in duration and location. They appear to originate from one part of the cortex at one moment, then
from another or from multiple foci a few seconds later. The spike discharges occasionally are generalized but
never are rhythmically repetitive or highly organized, as is the pattern in childhood absence epilepsy, for
example. The chaotic appearance of hypsarrhythmia suggests significant cortical dysfunction [20].
Hypsarrhythmia is usually seen in the early stages of IS and can precede the onset of spasms [21]. In some
cases, clinical spasms may precede the onset of hypsarhythmia. Longitudinal studies using prolonged
monitoring show a highly variable and dynamic EEG pattern [22]. The initial multifocal and chaotic pattern
evolves into a more organized pattern known as modified or atypical hypsarrhythmia, which is characterized
by features such as greater hemispheric synchronization and symmetry. Variations of this EEG pattern include
hypsarhythmia with increased interhemispheric synchronization, an asymmetrical pattern, a consistent focus of
abnormal discharge, episodes of attenuation (electrodecremental response), and hypsarhythmia comprised
primarily of high-voltage slow activity with little sharp-wave or spike activity [22,23]. The hypsarrhythmic
pattern may disappear with hormonal therapy while the infantile spasms persist [10,22]. Hypsarhythmia tends
to disappear later in childhood, sometimes evolving into other abnormal EEG patterns [12].
The hypsarrhythmic pattern changes with the state of the patient, and varies if the infant is awake or in
slow-wave quiet (non-REM) or active (REM) sleep [7,10,22]. The classic pattern is most pronounced in quiet
sleep and often is markedly reduced or absent during REM sleep. Patients with hypsarhythmia often have very
reduced amounts of non-REM sleep, and as a result, long-term monitoring studies may be required in some
cases to capture hypsarhythmia.
Other interictal patterns in patients with IS include focal or multifocal spikes and sharp waves, diffuse or focal
slowing, paroxysmal slow or fast bursts, and slow spike and wave [8]. These may occur singly or in
combination; the latter EEG features suggest evolution towards Lennox-Gastaut syndrome. It is rare for the
interictal EEG to appear normal.
Ictal EEG An ictal EEG typically shows a high-voltage, slow-wave transient followed by attenuation of
activity. Variations in these EEG events do not predict the type of spasm (flexor, extensor, or mixed). Episodes
of generalized attenuation (electrodecremental response) also may occur in both waking and sleeping states
without clinical evidence of a seizure.
Immediately after either a clinical or electrographic seizure, the EEG sometimes shows a marked decrease of
abnormal activity [6,22]. It may transiently appear normal for age. No consistent clinical changes are seen
during these periods.
Lateralized findings Focal or lateralized EEG findings may indicate the presence of a structural brain
lesion [23,24]. In one report of 77 patients with IS, 38 percent had focal or lateralized features on video EEG
[23]. Unilateral hypsarhythmia and asymmetric ictal EEG changes often occurred together. Both of these
features consistently indicated the side of a focal or asymmetric structural cerebral lesion that was visible on
computed tomography (CT) or magnetic resonance imaging (MRI) of the brain.
Asymmetric EEG changes occur with asymmetric IS, which is uncommon. Lateralized hypsarhythmia also
occurs with bilateral structural lesions that are more severe on one side.
Neuroimaging Neuroimaging studies should be performed in all patients with IS to identify lesions
associated with the disorder, as this may influence treatment decisions [2,25-27]. Approximately 70 percent of
patients will have an established etiology after clinical evaluation, EEG, and MRI. (See "Management and
prognosis of infantile spasms".)
CT may demonstrate cerebral atrophy, ventricular enlargement, calcium deposits, tubers, or
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encephalomalacia. However, CT has a limited role in patients with IS due to the higher sensitivity of MRI [2].
MRI is recommended for all patients with IS [2]. Children younger than one year require special MRI
sequences due to immature myelination patterns; these should included high-resolution coronal and axial
T2-weighted sequences, along with sagittal, axial, and coronal T1-weighted sequences [28]. Ideally, MRI
should be obtained prior to the initiation of therapy, which can sometimes cause imaging changes. If MRI is
normal and no other etiology is identified, then repeat imaging at six month intervals is recommended,
particularly if there is not an expected treatment response or if there is clinical deterioration.
MRI may detect cerebral malformations, cerebral atrophy, delayed myelination, and other focal lesions not
visible on CT scan [26]. MRI also may provide information regarding prognosis, especially with regard to
motor development. Patients with normal findings on MRI have better outcomes compared to those with
lesions [29].
Most patients with IS and symmetric hypsarhythmia have diffuse structural brain diseases that are not
lateralized. They rarely have focal or lateralizing features visible on imaging studies. Positron emission
computed tomography (PET) may help identify an etiology in these cases, as illustrated by a study of 140
affected patients referred for evaluation [30]. A specific disease or syndrome was diagnosed at presentation
in 9.3 percent. CT and/or MRI detected lesions in 20.7 percent of cases without a clinical diagnosis. Among
the 97 patients whose underlying condition remained uncertain, PET scanning detected unifocal or multifocal
abnormalities in 92 (65.7 percent). As a result, an etiology was identified in 96 percent of cases. Specialized
MRI studies, including magnetization transfer imaging and magnetic resonance spectroscopy may also identify
lesions not visible on a standard MRI.
Other studies In the 30 percent of patients whose etiology is not established after clinical evaluation, EEG,
and MRI, a metabolic etiology will be established in less than half; the remainder will be labeled idiopathic or
cryptogenic, or by the more inclusive term non-symptomatic.
Studies that can establish a metabolic etiology include, among others [2]:
SUMMARY AND RECOMMENDATIONS Infantile spasms (IS) is an age-specific convulsive disorder of
infancy and early childhood.
Pyridoxine challenge
Urine for organic acids
Serum for amino acids
Biotinidase determination
Cerebrospinal fluid analysis of neurotransmitters, lactic acid, amino acids, folate metabolites, glucose,
glycine

Chromosomal studies
Most children with IS present between three and seven months of age; onset after 18 months is rare.
(See 'Age of onset' above.)

Spasms are symmetric contractions of flexor or extensor axial or limb muscles. They vary in pattern,
intensity, duration and extent. Most spasms occur in clusters of two to more than 100 over one to several
minutes. (See 'Spasms' above.)

When spasm or spasm clusters are brief and involve limited musculature they may be unrecognized.
Parents typically underestimate seizure frequency by a factor of 5 to 10 (See 'Spasms' above.)

EEG is essential for the diagnosis of IS and should capture an ictus as well as the characteristic interictal
pattern of hypsarhythmia. A 24-hour inpatient video EEG monitoring study is ideal. (See

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REFERENCES
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Pellock JM, Hrachovy R, Shinnar S, et al. Infantile spasms: a U.S. consensus report. Epilepsia 2010;
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Trevathan E, Murphy CC, Yeargin-Allsopp M. The descriptive epidemiology of infantile spasms among
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3.
Vigevano F, Fusco L, Cusmai R, et al. The idiopathic form of West syndrome. Epilepsia 1993; 34:743. 4.
Lthvgsson P, Olafsson E, Sigurthardttir S, Hauser WA. Epidemiologic features of infantile spasms in
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Kellaway P, Hrachovy RA, Frost JD Jr, Zion T. Precise characterization and quantification of infantile
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Kellaway P, Frost JD Jr, Hrachovy RA. Infantile spasms. In: Antiepileptic Drug Therapy in Pediatrics,
Morselli PL, Pippenger CE, Penry JK (Eds), Raven Press, New York 1983.
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Hrachovy RA, Frost JD Jr. Infantile epileptic encephalopathy with hypsarrhythmia (infantile spasms/West
syndrome). J Clin Neurophysiol 2003; 20:408.
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Ramgopal S, Shah A, Zarowski M, et al. Diurnal and sleep/wake patterns of epileptic spasms in different
age groups. Epilepsia 2012; 53:1170.
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Glaze DG, Zion TE. Infantile spasms. Curr Probl Pediatr 1985; 15:1. 10.
Koo B, Hwang PA, Logan WJ. Infantile spasms: outcome and prognostic factors of cryptogenic and
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Lacy JR, Penry JK. Infantile spasms, Raven Press, New York 1976. 13.
Hrachovy RA, Glaze DG, Frost JD Jr. A retrospective study of spontaneous remission and long-term
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Maydell BV, Berenson F, Rothner AD, et al. Benign myoclonus of early infancy: an imitator of West's
syndrome. J Child Neurol 2001; 16:109.
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Lombroso CT, Fejerman N. Benign myoclonus of early infancy. Ann Neurol 1977; 1:138. 16.
Coulter DL, Allen RJ. Benign neonatal sleep myoclonus. Arch Neurol 1982; 39:191. 17.
Vigevano F, Lispi ML. Tonic reflex seizures of early infancy: an age-related non-epileptic paroxysmal
disorder. Epileptic Disord 2001; 3:133.
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Gaily E, Liukkonen E, Paetau R, et al. Infantile spasms: diagnosis and assessment of treatment
response by video-EEG. Dev Med Child Neurol 2001; 43:658.
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'Electroencephalography' above.)
Hypsarhythmia on interictal EEG is an essential feature of West syndrome. Hypsarhythmia varies with
the sleep-wake cycle. The classic pattern is most pronounced in quiet sleep and may be reduced or
absent when the patient is awake or in REM sleep. NonREM sleep may be reduced in patients with IS.
(See 'Hypsarhythmia' above.)

Other diagnostic studies in IS focus on etiology. Etiology is critical to determining treatment and
prognosis. An MRI is essential in this regard. If an etiology is not identified after clinical evaluation, EEG,
and MRI, further studies to assess a metabolic origin should be obtained. (See 'Neuroimaging' above and
'Other studies' above.)

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Gibbs, FA, Gibbs, EL. Atlas of Electroencephalography, Addison-Wesley, Reading, MA 1952. 20.
Philippi H, Wohlrab G, Bettendorf U, et al. Electroencephalographic evolution of hypsarrhythmia: toward
an early treatment option. Epilepsia 2008; 49:1859.
21.
Hrachovy RA, Frost JD Jr, Kellaway P. Hypsarrhythmia: variations on the theme. Epilepsia 1984; 25:317. 22.
Donat JF, Lo WD. Asymmetric hypsarrhythmia and infantile spasms in west syndrome. J Child Neurol
1994; 9:290.
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Drury I, Beydoun A, Garofalo EA, Henry TR. Asymmetric hypsarrhythmia: clinical
electroencephalographic and radiological findings. Epilepsia 1995; 36:41.
24.
Haginoya K, Kon K, Takayanagi M, et al. Heterogeneity of ictal SPECT findings in nine cases of West
syndrome. Epilepsia 1998; 39 Suppl 5:26.
25.
van Bogaert P, Chiron C, Adamsbaum C, et al. Value of magnetic resonance imaging in West syndrome
of unknown etiology. Epilepsia 1993; 34:701.
26.
Aydinli N, Cali!kan M, Ozmen M, Tongu E. Neuroradiologic aspects of West syndrome. Pediatr Neurol
1998; 19:211.
27.
Gaillard WD, Chiron C, Cross JH, et al. Guidelines for imaging infants and children with recent-onset
epilepsy. Epilepsia 2009; 50:2147.
28.
Saltik S, Kocer N, Dervent A. Informative value of magnetic resonance imaging and EEG in the
prognosis of infantile spasms. Epilepsia 2002; 43:246.
29.
Chugani HT, Conti JR. Etiologic classification of infantile spasms in 140 cases: role of positron emission
tomography. J Child Neurol 1996; 11:44.
30.
Topic 6145 Version 7.0
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GRAPHICS
Ages at onset of infantile spasms for 257 infants
studied during the period 1963-1980
Parents and physicians often do not recognize infantile spasms as
seizures, particularly when they first occur, and it is probable that the age
distribution should be shifted somewhat to the left.
Data from: Kellaway, P, Frost, JD Jr, Hrachovy, RA, Infantile spasms. In:
Antiepileptic Drug Therapy in Pediatrics, Morselli, PL, Pippenger, CE, Penry, JK
(Eds), Raven Press, New York 1983.
Graphic 82370 Version 2.0
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Disclosures: Daniel G Glaze, MD Nothing to disclose. Douglas R Nordli, Jr, MD Grant/Research/Clinical Trial Support: NIH-RO1
(Febrile seizures). Consultant/Advisory Boards: Eisai (Rufinamide). April F Eichler, MD, MPH Equity Ownership/Stock Options:
Johnson & Johnson [Dementia (galantamine), Epilepsy (topiramate)]; Employee of UpToDate, Inc.
Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are addressed by vetting
through a multi-level review process, and through requirements for references to be provided to support the content. Appropriately
referenced content is required of all authors and must conform to UpToDate standards of evidence.
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