INTRODUCTION — Infantile spasms are an age-specific epileptic disorder of infancy and early childhood. The epidemiology, etiology, pathogenesis, and pathology of infantile spasms are reviewed here.
Although rare, infantile spasms are a significant disorder because of the strong association with developmental delay or regression, high mortality rate, refractoriness to conventional antiseizure medications, and responsiveness to hormonal therapy. The clinical features, diagnosis, management, and prognosis of infantile spasms are discussed separately. (See "Infantile epileptic spasms syndrome: Clinical features and diagnosis" and "Infantile epileptic spasms syndrome: Management and prognosis".)
TERMINOLOGY
●Infantile epileptic spasms syndrome (IESS) – IESS is a term adopted by the International League Against Epilepsy (ILAE) in 2022 to encompass both infants with West syndrome and infants with epileptic spasms who do not fulfill all criteria for West syndrome [1].
●West syndrome – Children with infantile spasms typically exhibit epileptic spasms along with the electroencephalographic (EEG) pattern known as hypsarhythmia. The triad of epileptic spasms, arrest of psychomotor development, and hypsarhythmia is known as West syndrome.
●Epileptic spasms – Epileptic spasms are seizures that consist of brief, tonic, mostly symmetric contractions of flexor or extensor axial or limb muscles, typically lasting less than three seconds, and often occurring in clusters [1]. They vary in pattern, intensity, duration, and extent. (See "Infantile epileptic spasms syndrome: Clinical features and diagnosis", section on 'Infantile spasms'.)
●Infantile spasms – The term "infantile spasms" is the traditional term for describing the ictal events of epileptic spasms with onset in infancy. However, as a minority of patients can develop these seizures outside of infancy, the "epileptic spasms" term used is more inclusive of other age groups.
EPIDEMIOLOGY — Infantile epileptic spasms syndrome (IESS), also known as "infantile spasms," is a rare disorder with an incidence of 1.6 to 4.5 per 10,000 live births [2-5]. Infantile spasms occur in children of all ethnic groups. Some studies have found that male and female infants appear to be affected equally [2,6], while others suggest that males are somewhat more likely to be affected [3,4].
In a cross-sectional, population-based surveillance system that included 21 electroencephalography (EEG) laboratories in Atlanta, Georgia, the incidence was 2.9 per 10,000 live births among children born in 1975 to 1977 [2]. Infantile spasms occurred in similar proportions in White and Black children. The prevalence among 10-year-old children was 2.0 per 10,000; the lower prevalence than incidence likely reflecting the substantial mortality of the disorder [2,5]. However, a history of infantile spasms was found in a substantial proportion, 12 percent, of children with profound intellectual disability.
Period changes in incidence rates of infantile spasms are stable over time in some reports but variable in others [3,4,6,7]. The differences are likely due in part to the relatively small number of patients. In a study of 57 patients from Finland during the period of 1960 to 1992, the incidence remained stable [7]. In a report from Canada that included 75 patients recorded over a 20-year period, annual and five-year incidence rates varied [6]. During two consecutive periods (1979 to 1992 and 1993 to 1998), the estimated average annual incidence decreased from 3.31 to 1.73 per 10,000 live births.
PATHOGENESIS — The pathophysiology of infantile spasms is not well understood [5,8]. Multiple diverse insults may cause or be associated with the occurrence of infantile spasms. These include pathogenic genetic variants and acquired factors such as hypoxic-ischemic injury, infectious processes, and structural abnormalities of the brain.
One hypothesis suggests that infantile spasms result from a nonspecific insult at a critical point in the ontogenetic development of the brain [9]. The age at onset of spasms appears to correlate with the location of focal cerebral lesions and follows the normal sequence of brain maturation. This correlation was illustrated by a series of 93 patients who had lesions confined to one of three regions [10]. The mean age of onset of infantile spasms was 3.4, 6.3, and 9.8 months for occipital, centro-temporo-parietal, or frontal lesions, respectively, which follows the pattern of functional brain development.
The responsiveness of infantile spasms to treatment with corticotropin (ACTH) suggests a possible role for abnormalities in the hypothalamic-pituitary-adrenal axis in the pathogenesis of infantile spasms (perhaps a brain insult activating a neuroendocrine stress response), but this has not been specifically elucidated [11,12]. Disturbed immune activation has also been hypothesized to play a role [13,14].
It is uncertain whether the epileptic spasms are generated primarily in the cerebral hemispheres or the brainstem. A cortical origin is supported by neuropathologic changes in the cerebral hemispheres in autopsy studies and surgical specimens, as well as abnormalities seen on neuroimaging studies and electroencephalography (EEG) [15-25]. Resolution of infantile spasms following cortical surgical resection also supports this origin. However, other findings suggest that infantile spasms may originate in the brainstem or in other subcortical structures [8]. These findings include some autopsy studies, the prominent sleep disturbance in infantile spasms, as well as observed patterns of neurotransmitter abnormalities [26-28].
Useful animal models should recapitulate the unique clinical features in humans: onset in the first year of life; the character of the epileptic spasms; the EEG features, including the ictal pattern and the pattern of hypsarhythmia; neurodevelopmental disabilities; and therapeutic responsiveness including ACTH [29].
Existing animal models of infantile spasms include those resulting from genetic engineering [29]:
●The aristaless-related homeobox (Arx) protein knock-in and knock-out mouse models. Arx protein is a homeobox transcription factor important in the maturation and migration of developing GABAergic interneurons.
●The adenomatous polyposis coli (APC) knock-out mouse model. APC is a negative regulator of beta-catenin; genetically removing APC from excitatory forebrain neurons results in increased dendritic spines on hippocampal CA1 neurons and increased excitatory neurotransmission.
●The multiple hit mode. Acquired mouse models have been developed using unilateral infusion of the sodium channel blocker tetrodotoxin into the dorsal hippocampus and the infusion of doxorubicin and lipopolysaccharide followed by intraperitoneal injections of p-chlorophenylalanine (fenclonine). This method causes structural lesions in the brain.
In view of these diverse models, the question remains as to whether a common pathway or mechanism can be identified. These models suggest that inhibitory interneurons may have a role in the mechanism; brain regions that have been implicated include the cortex, hippocampus, and the hypothalamic-pituitary-adrenal axis [29].
GENETICS — While some patients with infantile epileptic spasms syndrome (IESS) have an inherited disorder, such as tuberous sclerosis, most cases are sporadic. There is a family history of infantile spasms in 1 to 7 percent of cases [8]. A genetic susceptibility that is multifactorial appears to exist [30-32]. However, environmental factors such as anoxia or birth trauma may be required to precipitate seizures.
Recurrence rates with families without a defined genetic syndrome vary depending upon the features associated with infantile spasms. In one study of 77 families, the empiric recurrence risk of infantile spasms among siblings was estimated as 15 per 1000 [30]. In a report that excluded familial diseases, the recurrence risk for infantile spasms was <1 percent [33].
De novo pathogenic variants in various genes are being increasingly recognized as a cause of infantile spasms in some children with otherwise unexplained infantile spasms. (See 'Genetic causes' below.)
CLASSIFICATION — The International League Against Epilepsy (ILAE) has presented a revised framework for the classification of the epilepsies and for the classification of seizures [34,35]. Three levels of diagnosis characterize this framework: seizure type, epilepsy type, and epilepsy syndrome (figure 1). As an example, a child with infantile epileptic spasms syndrome (IESS) might be classified as follows: seizure type, generalized; epilepsy type, generalized; epilepsy syndrome, IESS. A fourth level, etiology, is also considered if the etiology can be determined as due to a genetic, structural, metabolic, immune, or infectious cause. Additionally, the term developmental and epileptic encephalopathy seems appropriate to apply. (See "ILAE classification of seizures and epilepsy".)
Traditionally, infantile spasms have been classified as "symptomatic" (known cause) versus "cryptogenic" (no known cause):
●Patients with "symptomatic" infantile spasms have an identified etiology and/or significant developmental delay at the time of spasm onset
●Patients with "cryptogenic" infantile spasms have no known etiology and normal development at the time of spasm onset
However, based on the ILAE Commission on Classification and Terminology, these terms are best replaced in modern literature by specific etiologic categories (ie, genetic, structural, metabolic, immune, infections, or unknown) (figure 1).
ETIOLOGY — The proportion of etiologic categories of infantile epileptic spasms syndrome (IESS) reports. This wide range results from use of different definitions, the early age at diagnosis when neurodevelopmental status may be difficult to assess, and the increased use of neuroimaging studies that may reveal an underlying cause.
Infantile spasms of identified etiology — Infantile spasms of identified etiology (previously known as "symptomatic") result from a known or suspected central nervous system (CNS) disorder. One or more etiologic factors can be identified in the majority (60 to 70 percent) of cases of infantile spasms [36,37]. Follow-up evaluation with neuroimaging and positron emission tomography may increase the proportion with a known cause to as high as 90 percent [37-40].
In a prospective, multicenter study on the evaluation of new-onset infantile spasms from the National Infantile Spasms Consortium, 251 infants were enrolled, and a cause was identified in 161 patients (64 percent) [36]. The most commonly identified causes were structural-acquired (22 percent), genetic (14 percent), structural-congenital (11 percent), genetic-structural (10 percent), metabolic (5 percent), and infection (2 percent). Clinical evaluation and magnetic resonance imaging (MRI) provided a specific diagnosis in 55 percent of infants. These results emphasize the importance of initial clinical evaluation and MRI in the evaluation of newly diagnosed infantile spasms, followed by genetic and metabolic testing if no obvious etiology is identified. (See "Infantile epileptic spasms syndrome: Clinical features and diagnosis", section on 'Etiologic evaluation'.)
The causative insult typically occurs in the prenatal, perinatal, or early postnatal period. Prenatal factors account for the greatest proportion of cases of West syndrome, 43 percent in one series [41,42]. The most common prenatal abnormality is a malformation of the CNS. Others include chromosome and other genetic disorders, neurocutaneous disorders, inborn errors of metabolism, and intrauterine infections.
CNS malformations — Cortical dysplasia is the most common identified etiology, estimated to account for up to 30 percent of prenatal causes of infantile spasms [37]. Other CNS malformations that may result in infantile spasms include cerebral dysgenesis (eg, Aicardi syndrome), lissencephaly (eg, Miller-Dieker syndrome), polymicrogyria, holoprosencephaly, hydranencephaly, and hemimegalencephaly. Nearly all patients with Miller-Dieker syndrome and Aicardi syndrome have infantile spasms at some stage.
Miller-Dieker syndrome — Miller-Dieker syndrome is caused by a disturbance in neuroblastic migration during CNS development, resulting in lissencephaly. Other features include growth retardation, microcephaly, craniofacial abnormalities (bitemporal grooving, micrognathia, ear anomalies, anteverted nares), renal and cardiac defects, and neurologic abnormalities (eg, hypotonia, infantile spasms, and intellectual disability) [43-52]. Most patients with this disorder have a deletion of the gene located at 17p13.3. (See "Microdeletion syndromes (chromosomes 12 to 22)", section on '17p13.3 deletion including PAFAH1B1 (Miller-Dieker syndrome)'.)
Aicardi syndrome — Aicardi syndrome is an X-linked dominant disorder. Because the condition is lethal in affected males, females are affected exclusively. The syndrome is characterized by infantile spasms (usually the presenting sign), complex brain malformation with agenesis of the corpus callosum and other neuronal migration abnormalities, a distinctive chorioretinopathy, vertebral anomalies, and severe intellectual disability [53-56]. Patients typically develop partial seizures before the age of three months; asymmetric infantile spasms develop some weeks to months later. EEG also often shows asymmetric hypsarhythmia.
Hemimegalencephaly — Hemimegalencephaly is characterized by enlargement of one cerebral hemisphere with thickened and abnormal cortical structure on the affected side [57]. As many as half of patients with hemimegalencephaly develop infantile spasms, often in addition to other seizure types.
Tuberous sclerosis complex — Tuberous sclerosis complex (TSC) is the neurocutaneous disorder most frequently associated with infantile spasms and accounts for 10 to 30 percent of prenatal causes [37]. Infantile spasms occurs in as many as 68 percent of patients with TSC, and 7 to 25 percent of patients with infantile spasms have TSC [58-63]. The actual incidence of TSC in children with infantile spasms may be even higher because the clinical signs of TSC may not be apparent when spasms first present. (See "Tuberous sclerosis complex: Clinical features", section on 'Seizures and epilepsy'.)
Cognitive disability is a primary feature of TSC; risk factors include a history of infantile spasms and/or refractory epilepsy. (See "Tuberous sclerosis complex: Clinical features", section on 'Intellectual disability'.)
The most common and difficult aspect of management in TSC is the control of seizures. The management of TSC is reviewed in detail separately. (See "Tuberous sclerosis complex: Management and prognosis".)
Other neurocutaneous disorders — Other neurocutaneous syndromes associated with infantile spasms include linear nevus sebaceous syndrome, incontinentia pigmenti, pigmentary mosaicism of Ito, Sturge-Weber syndrome, and neurofibromatosis type 1 (NF1). (See "The genodermatoses: An overview" and "Neurofibromatosis type 1 (NF1): Pathogenesis, clinical features, and diagnosis".)
Patients with NF1 and infantile spasms generally have symmetric spasms, typical hypsarhythmia on EEG, and no focal features. Compared with the combination of TSC and infantile spasms, outcome is better in patients with NF1, with resolution of infantile spasms with treatment in 87 percent [64].
Chromosome abnormalities — Chromosomal abnormalities accounted for 15 percent of prenatal etiologies of West syndrome in one series [41]. Down syndrome (trisomy 21) was the most common. (See "Down syndrome: Clinical features and diagnosis".)
Infantile spasms are a common seizure type in patients with Down syndrome [65,66]. In one series of 350 children with Down syndrome, 28 (8 percent) had seizures; 13 had infantile spasms [66]. In general, neurodevelopmental outcome in these patients is poor [66,67]. This may be modifiable with early recognition and treatment; in one retrospective study of infantile spasms in children with Down syndrome, longer lead times to treatment of infantile spasms were associated with lower developmental quotient and higher scores of autism [68]. (See "Infantile epileptic spasms syndrome: Management and prognosis", section on 'Outcomes'.)
Other chromosome abnormalities linked to infantile spasms include 15q duplication, 18q duplication, 7q duplication, deletion of the MAGI2 gene on chromosome 7q11.23-q21.11, and partial 2p trisomy [69].
Genetic causes — Genetic studies have identified pathogenic variants in over 30 genes as causes of infantile spasms. Whole-genome and whole-exome sequencing in children with otherwise unexplained infantile spasms have revealed a variety of potentially pathogenic de novo genetic variants. Specific genes that have been associated with infantile spasms include those encoding the following, among others [31,70-76]:
●Adenylosuccinate lyase (ADSL)
●ALG13 UDP-N-acetylglucosaminyltransferase subunit (ALG13)
●Aristaless-related homeobox protein (ARX)
●Calcium/calmodulin-dependent serine protein kinase (CASK)
●Cyclin-dependent kinase-like 5 gene (CDKL5)
●Doublecortin (DCX)
●Forkhead box G1 (FOXG1)
●Glutamate ionotropic receptor NMDA type subunit 2A (GRIN2A)
●Glutamate ionotropic receptor NMDA type subunit 2B (GRIN2B)
●Membrane-associated guanylate kinase, WW and PDZ domain containing 2 (MAGI2)
●NEDD4 E3 ubiquitin protein ligase (NEDD4)
●Nuclear receptor binding SET domain protein 1 (NSD1)
●Phosphatase and actin regulator 1 (PHACTR1)
●Phospholipase C-beta 1 (PLCB1)
●Platelet-activating factor acetylhydrolase 1b regulatory subunit 1 (PAFAH1B1)
●Potassium voltage-gated channel subfamily Q member 2 (KCNQ2)
●Pyridoxamine-5'-phosphate oxidase (PNPO)
●Syntaxin-binding protein 1 (STXBP1)
●Ryanodine receptors (RYR1, RYR2, RYR3)
●Solute carrier family 1 member 4 (SLC1A4)
●Spectrin alpha, non-erythrocytic 1 (SPTAN1)
●Tubulin alpha 1a (TUBA1A)
Rare families demonstrate X-linked inheritance of infantile spasms. Pathogenic variants in the ARX gene are associated with a familial syndrome of infantile spasms, severe intellectual disability, and subsequent epilepsy [77-79]. Other affected members within the same family may have variant syndromes with some combination of intellectual disability along with dystonia, myoclonic seizures, lissencephaly, and/or abnormal genitalia [80,81].
Many of these genetic causes of infantile spasms are extremely rare. In a study that used targeted sequencing to screen candidate genes in 92 individuals with infantile spasms, a genetic diagnosis was identified in 8 percent of this cohort and included pathogenic variants in KCNB1 (n = 2), GNAO1 (n = 1), STXBP1 (n = 1), SLC35A2 (n = 1), TBL1XR1 (n = 1), and KIF1A (n = 1). These findings emphasize the genetic heterogeneity of infantile spasms [82].
Other loci have been identified. Two severely affected unrelated female patients with infantile spasms had balanced X:autosome translocations disrupting the gene encoding cyclin-dependent kinase-like 5 (CDKL5) [83,84]. Pathogenic variants in this gene have been reported in individuals with severe neurodevelopmental disorders, including a Rett syndrome-like phenotype and early-onset seizures including infantile spasms [84].
Accurate genetic testing is available for X-linked infantile spasms [85]. Further information is available at the Genetic Testing Registry. Counseling for genetic testing is discussed separately. (See "Genetic testing".)
Inborn errors of metabolism — Infantile spasms have been associated with more than 25 inborn errors of metabolism (see "Inborn errors of metabolism: Epidemiology, pathogenesis, and clinical features" and "Metabolic emergencies in suspected inborn errors of metabolism: Presentation, evaluation, and management") [86]. These include:
●Phenylketonuria
●Dihydropteridine reductase deficiency [87]
●Menkes disease [88,89]
●Pyruvate dehydrogenase complex deficiency [90]
●Cytochrome C oxidase deficiency (Leigh syndrome) [91]
●Histidinemia [92]
●Pyridoxine deficiency [93]
●Pyridoxamine-5'-phosphate oxidase (PNPO) deficiency [94]
●Urea cycle disorders [95]
●Congenital disorders of glycosylation [96]
In countries where phenylketonuria is not detected by newborn metabolic screening, infantile spasms are a common manifestation of this disorder. In a report from Beijing, China, West syndrome occurred in 62 of 503 patients (12 percent) with phenylketonuria [97]. In this series, the diagnosis of phenylketonuria was made in patients four months to seven years of age, with the onset of infantile spasms occurring prior to diagnosis in most cases. Dietary intervention reduced the frequency of spasms and improved cognitive outcome [93,97]. (See "Overview of phenylketonuria".)
Congenital infections — Infantile spasms can occur in infants with congenital infections affecting the CNS (table 1). These include toxoplasmosis, syphilis, cytomegalovirus, and Zika virus [7,98,99]. (See "Overview of TORCH infections", section on 'Clinical features of TORCH infections' and "Congenital Zika virus infection: Clinical features, evaluation, and management of the neonate".)
Perinatal causes — Infantile spasms may be associated with perinatal insults, including hypoxic-ischemic encephalopathy, neonatal hypoglycemia, and perinatal arterial ischemic stroke [7,100,101]. In one series of 32 patients with infantile spasms and a history of perinatal insults, 15 had porencephalic lesions, 12 (all premature) had periventricular leukomalacia, and 5 had diffuse bilateral cerebral atrophy [102]. In one study of 17 term and near-term infants with hypoxic ischemic encephalopathy, 5 developed West syndrome [103]. Prolonged EEG depression over 21 days of age was an important predictor of West syndrome in this small series. (See "Clinical features, diagnosis, and treatment of neonatal encephalopathy" and "Stroke in the newborn: Classification, manifestations, and diagnosis".)
The relationship between infantile spasms and preterm birth is uncertain. Among children with infantile spasms, the rate of low birth weight is approximately three to four times that of the general population, although the rate of prematurity is similar [7,104]. This may be because infantile spasms are more likely to occur in infants who are small for gestational age than in preterm infants of appropriate weight [105]. However, the apparent increase in infantile spasms attributed to perinatal causes may result from the improved survival of very-low-birth-weight infants, including those with periventricular leukomalacia [37].
Postnatal insults — Infantile spasms have been attributed to postnatal insults in 15 to 67 percent of cases [7,42,100,104]. These include traumatic injury, near drowning, tumors, and CNS infections, including bacterial meningitis and viral encephalitis. In one literature review, these events typically occurred within the first year of life, but were reported as late as 31 months [100]. The latency between the insult and the onset of infantile spasms ranged from 1.5 to 11 months (mean 5.1 months).
However, in rare cases, infantile spasms occur after a later event, as illustrated by case reports of two children with previously normal development who developed infantile spasms at 20 and 34 months of age after near drowning at 16 and 31 months, respectively [106].
No data support a causal relationship between infantile spasms and immunizations for pertussis or other childhood diseases [107,108].
Infantile spasms of unknown cause — The etiologic categorization of infantile spasms continues to evolve, as many instances of infantile spasms with unknown cause (previously known as "cryptogenic" or "idiopathic" infantile spasms) may have further testing and reclassification as the patient's neurologic disorder progresses.
Traditionally, criteria for infantile spasms of unknown cause include [109]:
●Normal development before onset of symmetric spasms
●No other kind of seizure
●Normal examination
●Normal head CT and MRI
●Recurrence of hypsarhythmia between consecutive spasms of a cluster
●Lack of any focal interictal or ictal EEG abnormality
The proportion of affected infants with infantile spasms of unknown cause ranges from 4 to 42 percent [5,37,110]. This wide range results from the use of different definitions, the early age at diagnosis when neurodevelopmental status may be difficult to assess, and the increased use of neuroimaging and neurogenetic studies that may reveal an underlying cause. (See "Infantile epileptic spasms syndrome: Clinical features and diagnosis", section on 'Neuroimaging'.)
Although infantile spasms may appear to have no clear etiology at the initial presentation, additional neuroimaging and/or genetic testing can identify an etiology in many cases, as the list of genes implicated continues to grow, and reimaging after myelination is complete may reveal structural changes not detected on earlier imaging [38,111]. In a report from the Canadian provinces of Nova Scotia and Prince Edward Island from 1978 to 1998, the proportion of etiologic categories was 68, 24, and 8 percent for symptomatic, cryptogenic, and idiopathic, respectively [6]. However, in a series of 140 affected patients whose evaluation included computed tomography (CT), MRI, and/or positron emission tomography, 96 percent of the cases were classified as symptomatic (having an identified cause) [38]. The medical evaluation of these patients was somewhat more extensive than is typical; it is unlikely that as high a proportion of patients evaluated in the community would be classified as having an identified etiology.
This subset of infantile spasms with unknown cause appears in some reports to have a better prognosis than patients with symptomatic infantile spasms. (See "Infantile epileptic spasms syndrome: Management and prognosis", section on 'Outcomes'.)
SUMMARY
●Description and terminology – Infantile epileptic spasms syndrome (IESS), also known as "infantile spasms," is an age-specific epileptic disorder of infancy and early childhood consisting of seizures typically with symmetric contractions of flexor or extensor axial or limb muscles. (See 'Terminology' above.)
●Epidemiology – IESS is a rare disorder with an incidence of 1.6 to 4.5 per 10,000 live births. Infantile spasms occur in children of all ethnic groups. There is no clear predilection for either sex. (See 'Epidemiology' above.)
●Pathogenesis – The pathogenesis of IESS is not well understood but is likely to be multifactorial. (See 'Pathogenesis' above.)
●Genetic susceptibility – While most cases of IESS are sporadic, infantile spasms may be a manifestation of certain inherited disorders including tuberous sclerosis and other neurocutaneous syndromes. Nonetheless, a genetic susceptibility is believed to play a role in the pathogenesis of the disorder. (See 'Genetics' above.)
●Classification – IESS was traditionally classified as "symptomatic" (having an identified etiology) versus "cryptogenic" (having no known etiology and normal development at the time of spasm onset). However, ILAE terminology recommends replacing these terms in modern literature with specific etiologic categories (ie, genetic, structural, metabolic, immune, infections, or unknown). (See 'Classification' above.)
●Infantile spasms with an identified cause – Most cases (with best estimates between 60 to 70 percent) of IESS have an identifiable etiology. Prenatal factors (eg, brain malformations, chromosomal and other genetic disorders, neurocutaneous disorders) account for the greatest proportion of symptomatic cases. Perinatal and postnatal insults are causative in others. (See 'Infantile spasms of identified etiology' above.)
●Infantile spasms of unknown cause – The proportion of affected infants with IESS of unknown cause in some studies is as high as 40 percent. (See 'Infantile spasms of unknown cause' above.)
●Significance – Although rare, IESS is a significant disorder because of the strong association with developmental delay or regression, high mortality rate, refractoriness to conventional antiseizure medications, and responsiveness to hormonal therapy. These issues are discussed separately. (See "Infantile epileptic spasms syndrome: Clinical features and diagnosis" and "Infantile epileptic spasms syndrome: Management and prognosis".)
ACKNOWLEDGMENT — The editorial staff at UpToDate acknowledges Daniel G Glaze, MD, who contributed to an earlier version of this topic review.
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