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INFANTILE SPASMS: A FRONTLINE GUIDE FOR PEDIATRICIANS

Apr 17, 2023
Eric H Kossoff, MD
Seva G. Khambadkone, MD, PhD
Contemporary PEDS JournalApril 2023




Delaying diagnosis and treatment for this early childhood disorder can lead to
worse outcomes, so early recognition is crucial.

Newborn baby| Image Credit: © Gary - © Gary - stock.adobe.com.



“[He] was a remarkably fine, healthy child when he was born, and continued to
thrive till he was 4 months old. It was at this time that I first observed
slight bobbings of the head forward…these bobbings increased in frequency, and
at length became so frequent and powerful, as to cause a complete heaving of the
head forward to the knees, and then immediately relaxing into the upright
position.”1

British physician William James West wrote the above in an 1841 letter to the
editor of The Lancet, begging for the medical profession’s attention to a
condition afflicting his infant son James.1 This letter was the first published
description of what became known as West syndrome, or infantile spasms. The
clinical features described—repeated attacks of “bowings and relaxings”
increasing in severity and accompanied by developmental regression—are still
deeply familiar to any parent or physician caring for a child with infantile
spasms.

The primary care pediatrician is the front line for early recognition and
treatment initiation in these children. This guide is designed to equip
pediatricians with focus on the clinical features, workup, and management of
this challenging disorder.

Diagnostic criteria and clinical importance

West syndrome is historically defined as an epilepsy of infancy and early
childhood characterized by a triad of (1) pathognomonic seizures (infantile
spasms), (2) hypsarrhythmia on an electroencephalogram (EEG), and (3) associated
neurodevelopmental arrest or regression. The term “infantile spasms” has been
used inconsistently in the literature, to encompass the syndrome or to refer to
the seizures alone.2 Given inconsistent terminology as well as variability in
clinical and encephalographic presentations, the International League Against
Epilepsy proposed a new consensus term for the syndrome: infantile epileptic
spasms syndrome (IESS), an epileptic encephalopathy defined by the onset of
infantile spasms in infants aged between 1 and 24 months, with peak onset
between 3 and 12 months.3 Spasm onset is associated with developmental
plateauing or regression. EEG is generally abnormal, often but not always with
the chaotic rhythm known as hypsarrhythmia.

The estimated incidence for IESS is 1 in 2400 to 5500 live births.4 Evidence
suggests that provider comfort in identifying and managing IESS is lacking, with
direct consequences for affected infants and families. In a cross-sectional
study of 100 parents of children with infantile spasms, the median time from
spasm onset to first visit with any health care provider was 5 days, but the
median time from onset to first visit with an “effective provider” (one who
provided both accurate diagnosis and prescription for appropriate first-line
treatment) was 24.5 days, a delay attributed at least in part to poor awareness
of the condition among providers.5 Given that worse outcomes may be associated
with even a 1-week delay in treatment from onset, it is critical that pediatric
health care providers are proficient in recognizing this condition.6,7

Clinical features
Infantile spasms



An infantile spasm is brief and abrupt, generally 1 to 3 seconds, with muscle
contraction that can include the head, neck, trunk, and/or extremities. Spasms
can occur in clusters, repeating every 5 to 10 seconds over minutes but,
especially early in the disease course, may be isolated and infrequent. They may
also be subtle, ranging from a brief head nod or facial/eye movement to a
jackknifing of the torso at the waist with contraction of the trunk and
extremities. When clustering, they often follow a crescendo-decrescendo pattern
of intensity in a series of 2 to 100 spasms. See Table 1 for a summary of spasm
features.

The context of the spasm episode may provide other helpful clues for
recognition. While spasms can occur anytime, they commonly occur soon after the
infant awakens. Behavioral changes around the spasm are common. Caregivers may
notice that the infant looks scared or surprised during or immediately before an
episode. Following the episode, it is common for the infant to cry, scream, or
seem upset.

Home video recording as a clinical tool

Given the length of a typical clinic visit, it is unlikely that the infant will
have a spasm in the office. This is where home video recordings (eg, via
smartphones) can be extremely helpful. Home video recording, first advised by
the Child Neurology Society to streamline IESS management at the onset of the
COVID-19 pandemic, has since been endorsed as a continued recommendation toward
timely intervention.4 In preparing to evaluate a patient with possible IESS,
pediatricians should ask caregivers to record suspected events. Videos should be
reviewed prior to the scheduled visit if possible and filed to share with
consulting providers including child neurologists. Shortened clips can easily be
shared through patient/provider portals in most electronic medical records,
whereas longer videos may require secure cloud services.

Age of onset

While the diagnostic criteria for IESS defines an age range of 1 to 24 months,
the average age of spasm onset is 6 to 7 months, and most infants will have
onset between 3 and 12 months. Although it is possible for IESS to first present
after 18 months or before 3 months, it is very uncommon, and spasm-like events
should raise concern for another etiology, including conditions other than
epilepsy.

Neurodevelopmental changes



Many infants will appear developmentally normal at spasm onset, with
neurodevelopmental consequences becoming more apparent as spasms continue. In
addition, as risk for IESS is significantly increased in infants with
preexisting developmental delay, including some conditions independently
associated with developmental delay (eg, tuberous sclerosis complex or trisomy
21), it may be difficult for the caregiver or physician to distinguish initially
subtle neurodevelopmental consequences of IESS from antecedent developmental
abnormalities.

The differential diagnosis for IESS is broad and includes both neurologic and
non-neurologic considerations. Table 2 provides some common mimics for spasms
with clinical clues. Given the possible consequences of untreated IESS and
evidence for frequent misdiagnosis, it is important to maintain high clinical
suspicion, especially in the setting of suspicious features.5,7 Red flag
features are highlighted in Table 3.

Workup

Urgency

Clinical suspicion for IESS requires urgent action. Next steps in workup and
management should begin within 24 hours, starting with an EEG. Ideally, the
pediatrician should immediately reach out to a child neurologist for rapid
assessment and EEG. This is best done by phoning the on-call neurologist line at
a regional children’s hospital. It is extremely helpful to provide a video clip
during this communication. If concerned, the child neurologist will coordinate a
same-day EEG, either outpatient or through the emergency department, followed by
possible admission.

The national shortage of child neurologists and uneven distribution across the
country can make this option difficult. If it is not possible to connect
directly with a child neurologist for urgent assessment, other options include
directly sending the infant to the emergency department (ED) of a regional
children’s hospital with child neurologists on staff for EEG and possible
admission (preferred) or sending them to the ED of a local hospital with adult
neurologists on staff for the same. If a pediatrician can order a same-day EEG
with access to rapid results, that can also help guide the urgency of a
neurological consultation.

EEG

The interictal EEG finding most commonly associated with IESS is hypsarrhythmia,
which describes a chaotic, disorganized, and high-amplitude background rhythm
with asynchronous slowing and multifocal epileptiform discharges. Of note,
classic hypsarrhythmia is not always seen nor a requirement for IESS diagnosis.
Some infants may show 1 of several variations known together as modified
hypsarrhythmia, and others may show epileptiform discharges without altered
background. The EEG pattern during the spasm itself is a high-amplitude sharp or
slow wave followed by a relative electrodecrement.

Because the interictal EEG is generally abnormal, it is not necessary to capture
a spasm during the EEG recording to support the diagnosis. The ideal EEG
recording captures a full sleep-wake cycle and so is generally a few hours long.
This is because the interictal abnormalities associated with IESS are
potentiated during non–rapid eye movement sleep.8 However, EEG abnormalities are
often still detectable in the absence of sleep, so shorter EEGs (eg, routine
30-minute) can sometimes be sufficient.

Other elements in workup

Once diagnosis confirmed, the next step in workup is to evaluate for an
underlying etiology. Diagnostic workup and treatment initiation are often
conducted inpatient, which allows for rapid coordination of the various steps.
However, this is not always necessary, especially in cases of clear IESS
diagnosis (ie, clinically evident spasms and classic hypsarrhythmia on EEG) with
an obvious underlying etiology (ie, previously established trisomy 21
diagnosis).

A list of common underlying etiologies is presented in Table 4. Workup for an
underlying etiology if not known is important not only because some are
associated with other health concerns requiring monitoring and intervention, but
also because it can guide management, as some etiologies may respond better to
different treatment approaches.9 Identification may also guide appropriate
counseling of families, including prognostication and possible genetic
counseling.

A detailed clinical history and physical exam should be conducted in all
patients. MRI is strongly recommended if not previously obtained, even in cases
where etiology appears evident (eg, a child with trisomy 21). This initial
workup will identify an underlying etiology in over 50% of presenting
infants.10,11 Genetic testing followed by potential metabolic testing will be
informative in most of the remaining cases.11 Despite thorough diagnostic
evaluation, in a sizable minority of cases a clear etiology will not be
identified; with a growing list of genes implicated in IESS, it is likely that
many of these are genetic in origin.12

Management

Though etiology can help guide management, it is not necessary to wait for MRI
or genetic/metabolic evaluations to initiate therapeutic intervention. The 3
recommended first-line medications for IESS are oral corticosteroids (OCS),
adrenocorticotropic hormone (ACTH), and vigabatrin.10,13 In the United States,
either oral corticosteroids (typically high-dose prednisolone) or ACTH are
generally preferred as initial therapies over vigabatrin in part because of the
latter’s adverse effect profile, though there have historically been few trials
evaluating their head-to-head efficacy.

A 2021 multicenter study by the National Infantile Spasms Consortium responded
to this need by prospectively following 423 children aged 2 to 24 months with
new-onset infantile spasms to compare treatment response among ACTH, OCS,
vigabatrin, and nonstandard therapy.14 The study concluded that initial
treatment with ACTH or OCS is superior to nonstandard therapy. Vigabatrin
efficacy was estimated to be between that for ACTH/OCS and nonstandard therapy,
but the study was underpowered to evaluate whether vigabatrin was statistically
inferior. As previously reported and detailed below, vigabatrin was the superior
initial therapy in the setting of tuberous sclerosis complex (TSC).

Two weeks after initiation of first-line therapy, infants should undergo an exam
including possible EEG to evaluate for electroclinical treatment response. This
is generally done in an outpatient child neurology clinic. Clinical and EEG
improvement will guide continued management, including possible dosage
modifications, switching of therapies, and combining of therapies. In the
following subsections, we will review major therapies with focus on what the
primary care pediatrician needs to know.

Steroids (hormonal therapy)



ACTH and OCS were initially used empirically and their mechanisms of action in
IESS remain somewhat unclear. ACTH is given via intramuscular injection with
dosing based on body surface area. Dosing protocols vary and there is evidence
that low to moderate doses (eg, 120 units/m2) may be as effective as high-dose
protocols (eg, 40 units/m2), with improved adverse effects.15,16 Standard
protocols include daily injections at static dose over 2 to 3 weeks followed by
a several-week taper. OCS are given orally and can include prednisolone,
prednisone, dexamethasone, and others; in the United States, prednisolone (15
mg/5 mL solution) is generally preferred. For OCS, there is evidence that
high-dose therapy (4 to 8 mg/kg/day) is superior to low-dose therapy (1 to 2
mg/kg/day). Similar to ACTH, treatment is generally given for 2 weeks, followed
by a gradual taper over 2 to 4 weeks. Dose may be increased if spasms continue
after 1 week. In the United Kingdom Infantile Spasms Study (UKISS), infants with
continued spasms after 1 week of 40 mg/day prednisolone had the dose increased
to 60 mg/day prednisolone for week 2.17 For most infants, we suggest an initial
dose of 45 mg/day prednisolone divided 3 times a day (15 mg/dose), with an
increase to 60 mg per day prednisolone divided 4 times a day (15 mg/dose) if
ineffective after 1 week.18



Both ACTH and high-dose prednisolone have significant adverse effects, including
immunosuppression, hypertension, hyperglycemia, stress ulcers and other
gastrointestinal irritation, behavioral irritability, disturbed sleep, increased
appetite, and adrenal insufficiency. Precautions are taken prior to, during, and
following treatment toward these risks, including glucose and blood pressure
monitoring and stress ulcer prophylaxis. Following hospital discharge, this will
largely fall to the primary care pediatrician, who should aim to see the patient
regularly. Patients must also be followed closely for spasm recurrence; even
with initially effective treatment response, recurrence rate with steroids is
about 33%. Along with an outpatient child neurologist, the pediatrician is a
critical ally in this monitoring.

Vigabatrin

Vigabatrin is an irreversible inhibitor of GABA-transaminase that acts by
increasing GABA concentration in the central nervous system. Starting dosage is
50 mg/kg/day divided twice daily, which can be slowly uptitrated to a maximum
dosage of 150 mg/kg/day divided twice daily. Treatment generally continues for 6
months but in the absence of clinical and/or EEG improvement at the 2-week mark,
it may be discontinued in favor of another therapy. Vigabatrin is associated
with considerable adverse effects, the most serious being permanent peripheral
visual field loss secondary to retinal toxicity. Children on vigabatrin must
receive a baseline eye exam within 4 weeks of treatment initiation and
subsequent exams every 3 months through treatment and 3 to 6 months following
treatment. This exam should be conducted by a pediatric ophthalmologist and
should include visual field testing whenever possible. Caregivers should be
counseled on other adverse effects including sedation, behavior changes, sleep
changes, and weight gain. Vigabatrin is also associated with MRI changes in the
brain, which have unclear clinical significance but are generally reversible
after conclusion of treatment.19

Vigabatrin is particularly effective in infants with TSC, where it has been
found to be superior to ACTH or OCS, and should be the first-choice therapy in
these patients. Up to 95% of children with TSC-related IESS will have a complete
treatment response.20

Other therapies

Several antiseizure medications have been trialed in IESS, including topiramate,
zonisamide, phenobarbital, and levetiracetam. These medications are inferior to
first-line therapies and should not typically be used as initial therapies.14 In
some cases, children with IESS may have other types of seizures at presentation
or will evolve to other seizure types or disorders, precipitating a need for
additional medications. Many children with IESS will go on to develop a
subsequent seizure disorder. Antiseizure medications in these children should be
managed by a child neurologist.

The ketogenic diet is a high-fat, low-carbohydrate diet extensively used in the
management of refractory epilepsy, either as a monotherapy or in conjunction
with medications. There is considerable evidence that the ketogenic diet can be
effective in IESS, and its availability as a liquid formula makes it a viable
option for infants. Most of this work has been done in patients with IESS
refractory to standard first-line treatment.21,22 In a systematic review of
ketogenic diet therapy for IESS, a median of about two-thirds of patients had an
over 50% reduction in spasms, and a median of one-third were seizure free.21

Follow-up and prognosis

Unfortunately, even in some cases with spasm resolution, long-term prognosis is
often poor. Outcomes include subsequent epilepsy and neurodevelopmental
impairment. Etiology may be the most important predictor of outcome.23 Lead time
to treatment is another critical and modifiable prognostic factor.23 Several
studies to date have found improved developmental/intellectual outcomes with
shorter delays between spasm onset and treatment, highlighting the importance of
early intervention.6,7,24 In the UKISS study, this relationship was suggested to
be dose dependent, where longer lead time durations were associated with a
stepwise decline in developmental assessment scores at aged 4 years.6

Children with history of IESS should be followed closely for developmental and
neurological sequelae. Psychomotor development should be monitored until at
least kindergarten, even in children who appear to have excellent prognoses. It
is best to involve a developmental pediatrician in this care as well as to have
a low bar for the recruitment of allied specialists including physical,
occupational, and speech therapists. While outcomes can be challenging, close
allyship among the family, primary pediatrician, neurologist, and broader care
team will go far toward creating an environment of support and resilience.

To read more from the April, 2023, issue of Contemporary Pediatrics®, click
here.

References

1. West WJ. On a peculiar form of infantile convulsions. The Lancet.
1841;35(911):724-725. doi:10.1016/S0140-6736(00)40184-4

2. Mytinger JR. Definitions and diagnostic criteria for infantile spasms and
West syndrome - historical perspectives and practical considerations. Semin
Pediatr Neurol. 2021;38:100893. doi:10.1016/j.spen.2021.100893

3. Zuberi SM, Wirrell E, Yozawitz E, et al. ILAE classification and definition
of epilepsy syndromes with onset in neonates and infants: position statement by
the ILAE Task Force on Nosology and Definitions. Epilepsia.
2022;63(6):1349-1397. doi:10.1111/epi.17239

4. Grinspan ZM, Mytinger JR, Baumer FM, et al. Management of infantile spasms
during the COVID-19 pandemic. J Child Neurol. 2020;35(12):828-834.
doi:10.1177/0883073820933739

5. Hussain SA, Lay J, Cheng E, Weng J, Sankar R, Baca CB. Recognition of
infantile spasms is often delayed: the ASSIST Study. J Pediatr.
2017;190:215-221.e1. doi:10.1016/j.jpeds.2017.08.009

6. O'Callaghan FJ, Lux AL, Darke K, et al. The effect of lead time to treatment
and of age of onset on developmental outcome at 4 years in infantile spasms:
evidence from the United Kingdom Infantile Spasms Study. Epilepsia.
2011;52(7):1359-1364. doi:10.1111/j.1528-1167.2011.03127.x

7. Auvin S, Hartman AL, Desnous B, et al. Diagnosis delay in West syndrome:
misdiagnosis and consequences. Eur J Pediatr. 2012;171(11):1695-1701.
doi:10.1007/s00431-012-1813-6

8. Watanabe K, Negoro T, Aso K, Matsumoto A. Reappraisal of interictal
electroencephalograms in infantile spasms. Epilepsia. 1993;34(4):679-685.
doi:10.1111/j.1528-1157.1993.tb00446.x

9. Messer R, Knupp KG. Infantile spasms: opportunities to improve care. Semin
Neurol. 2020;40(2):236-245. doi:10.1055/s-0040-1705121

10. Pellock JM, Hrachovy R, Shinnar S, et al. Infantile spasms: a U.S. consensus
report. Epilepsia. 2010;51(10):2175-2189. doi:10.1111/j.1528-1167.2010.02657.x

11. Wirrell EC, Shellhaas RA, Joshi C, et al. How should children with West
syndrome be efficiently and accurately investigated? Results from the National
Infantile Spasms Consortium. Epilepsia. 2015;56(4):617-625.
doi:10.1111/epi.12951

12. Yuskaitis CJ, Ruzhnikov MRZ, Howell KB, et al. Infantile spasms of unknown
cause: predictors of outcome and genotype-phenotype correlation. Pediatr Neurol.
2018;87:48-56. doi:10.1016/j.pediatrneurol.2018.04.012

13. Wilmshurst JM, Gaillard WD, Vinayan KP, et al. Summary of recommendations
for the management of infantile seizures: task force report for the ILAE
Commission of Pediatrics. Epilepsia. 2015;56(8):1185-1197. doi:10.1111/epi.13057

14. Grinspan ZM, Knupp KG, Patel AD, et al. Comparative effectiveness of initial
treatment for infantile spasms in a contemporary US cohort. Neurology.
2021;97(12):e1217-e1228. doi:10.1212/WNL.0000000000012511

15. Fayyazi A, Eslamian R, Khajeh A, Dehghani M. Comparison of the effect of
high and low doses of adrenocorticotropic hormone (ACTH) in the management of
infantile spasms. Iran J Child Neurol. 2020;14(2):17-25.

16. Riikonen R, Lahdetie J, Kokki H. ACTH treatment of infantile spasms:
low-moderate- versus high-dose, natural versus synthetic ACTH-a retrospective
cohort study. Pediatr Neurol. 2020;111:46-50.
doi:10.1016/j.pediatrneurol.2020.06.010

17. Lux AL, Edwards SW, Hancock E, et al. The United Kingdom Infantile Spasms
Study comparing vigabatrin with prednisolone or tetracosactide at 14 days: a
multicentre, randomised controlled trial. Lancet. 2004;364(9447):1773-1778.
doi:10.1016/S0140-6736(04)17400-X

18. Kossoff EH, Hartman AL, Rubenstein JE, Vining EP. High-dose oral
prednisolone for infantile spasms: an effective and less expensive alternative
to ACTH. Epilepsy Behav. 2009;14(4):674-676. doi:10.1016/j.yebeh.2009.01.023

19. Dracopoulos A, Widjaja E, Raybaud C, Westall CA, Snead OC 3rd.
Vigabatrin-associated reversible MRI signal changes in patients with infantile
spasms. Epilepsia. 2010;51(7):1297-1304. doi:10.1111/j.1528-1167.2010.02564.x

20. Hancock E, Osborne JP. Vigabatrin in the treatment of infantile spasms in
tuberous sclerosis: literature review. J Child Neurol. 1999;14(2):71-74.
doi:10.1177/088307389901400201

21. Prezioso G, Carlone G, Zaccara G, Verrotti A. Efficacy of ketogenic diet for
infantile spasms: a systematic review. Acta Neurol Scand. 2018;137(1):4-11.
doi:10.1111/ane.12830

22. Kossoff EH, Pyzik PL, McGrogan JR, Vining EP, Freeman JM. Efficacy of the
ketogenic diet for infantile spasms. Pediatrics. 2002;109(5):780-783.
doi:10.1542/peds.109.5.780

23. Riikonen R. Infantile spasms: outcome in clinical studies. Pediatr Neurol.
2020;108:54-64. doi:10.1016/j.pediatrneurol.2020.01.015

24. Kivity S, Lerman P, Ariel R, Danziger Y, Mimouni M, Shinnar S. Long-term
cognitive outcomes of a cohort of children with cryptogenic infantile spasms
treated with high-dose adrenocorticotropic hormone. Epilepsia.
2004;45(3):255-262. doi:10.1111/j.0013-9580.2004.30503.x

Download Issue PDF
Articles in this issue

--------------------------------------------------------------------------------

Donna Hallas says follow these steps to improve your NP practice

Infantile spasms: A frontline guide for pediatricians

Biologics to the rescue: changing the treatment paradigm in juvenile idiopathic
arthritis

Juvenile spring eruption in a young boy

The Great Resignation: Survival strategies for pediatric practice

Conference highlights from the National Association of Nurse Practitioners

Kudos to WHO

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ASSOCIATION BETWEEN PRENATAL COVID-19 EXPOSURE AND NEURODEVELOPMENT

April 20th 2023

PODCAST: AUDITORY BRAIN STEM IMPLANTS IN YOUNG CHILDREN.

January 14th 2016

THEORETICAL INPUT ON EATING BEHAVIORS COULD TRANSFORM DATA INTO CLINICAL
GUIDANCE

April 11th 2023

DRUG-RESISTANT PATIENTS HAVE IMPROVED HEALTH-RELATED QUALITY OF LIFE POST
PEDIATRIC EPILEPSY SURGERY

April 6th 2023

LINKING PARENTAL AGE AND PRENATAL DEVELOPMENT

April 5th 2023

NEURODEVELOPMENTAL DISORDERS FROM IN UTERO COVID-19 EXPOSURE BASED ON SEX 

March 28th 2023

ASSOCIATION BETWEEN PRENATAL COVID-19 EXPOSURE AND NEURODEVELOPMENT

April 20th 2023

PODCAST: AUDITORY BRAIN STEM IMPLANTS IN YOUNG CHILDREN.

January 14th 2016

THEORETICAL INPUT ON EATING BEHAVIORS COULD TRANSFORM DATA INTO CLINICAL
GUIDANCE

April 11th 2023

DRUG-RESISTANT PATIENTS HAVE IMPROVED HEALTH-RELATED QUALITY OF LIFE POST
PEDIATRIC EPILEPSY SURGERY

April 6th 2023

LINKING PARENTAL AGE AND PRENATAL DEVELOPMENT

April 5th 2023

NEURODEVELOPMENTAL DISORDERS FROM IN UTERO COVID-19 EXPOSURE BASED ON SEX 

March 28th 2023
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Association between prenatal COVID-19 exposure and neurodevelopment


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PODCAST: Auditory brain stem implants in young children.


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At 2 years post-pediatric epilepsy surgery, 72% of patients were seizure-free
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Neurodevelopmental disorders from in utero COVID-19 exposure based on sex 


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In a recent study, female offspring of mothers with a positive COVID-19 test
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