DEVELOPMENTAL MEDICINE & CHILD NEUROLOGY INVITED REVIEW

Current understanding of febrile seizures and their long-term

outcomes
LEENA D MEWASINGH 1 | RICHARD F M CHIN 2,3, * | ROD C SCOTT 4,5, *
1 Department of Paediatric Neurology, Imperial College Healthcare NHS Trust, London; 2 Muir Maxwell Epilepsy Centre, Centre for Clinical Brain Sciences and MRC
Centre for Reproductive Health, The University of Edinburgh, Edinburgh; 3 The Royal Hospital for Sick Children, Edinburgh, UK. 4 Department of Neurological Sciences,
University of Vermont, Burlington, VT, USA. 5 Department of Neurology, Great Ormond Street Hospital NHS Trust, London, UK.
Correspondence to Leena D Mewasingh, The Bays Building, 1st Floor, St Mary’s Hospital, Imperial College Healthcare NHS Trust, South Wharf Street, London W2 1NY, UK.
E-mail: l.mewasingh@nhs.net

*These authors contributed equally.

In this paper we reframe febrile seizures, which are viewed as a symptom of an underlying
PUBLICATION DATA brain disorder. The general observation is that a small cohort of children will develop febrile
Accepted for publication 28th June 2020. seizures (2–5% in the West), while the greater majority will not. This suggests that the brain
Published online 3rd August 2020. that generates a seizure, in an often-mild febrile context, differs in some ways from the brain
that does not. While the underlying brain disorder appears to have no significant adverse
ABBREVIATIONS implication in the majority of children with febrile seizures, serious long-term outcomes (cog-
FSE Febrile status epilepticus nitive and neuropsychiatric) have been recently reported, including sudden death. These
MTS Mesial temporal sclerosis adverse events likely reflect the underlying intrinsic brain pathology, as yet undefined, of
SUDC Sudden unexplained death in which febrile seizures are purely a manifestation and not the primary cause. A complex inter-
childhood action between brain–genetics–epigenetics–early environment is likely at play. In view of this
emerging data, it is time to review whether febrile seizures are a single entity, with a new
and multidimensional approach needed to help with predicting outcome.

Febrile seizures, the most common form of childhood sei-
zure, have a prevalence in the West of 2% to 5%.1 They
are an age-related phenomenon, usually occurring between
6 months and 5 years of age. Most febrile seizures are
short and outcomes in children with short febrile seizures
are usually favourable leading to the widely held view that
they are benign.2 This view has become rather controver-
sial given recent studies that have identified relationships
between febrile seizures and psychiatric disease3 and sud-
den unexplained death in childhood (SUDC).4 In addition,
it has been argued that prolonged seizures can lead to
brain injury and consequent adverse outcomes.5,6
The relevant clinical question is whether febrile seizure
causes adverse outcomes. If the relationship is directly cau-
sal, aggressive therapy could alter the prevalence of adverse
outcomes. However, correlation does not necessarily imply
causation. It is clear that only a subset of children experi-
ence febrile seizures, even though almost all children will
experience a significant fever during early childhood. This
suggests that there is something different about the brains
of children who experience febrile seizures. In this con-
struct, it is possible that factors predisposing the brain to
febrile seizures could also be predisposing the brain to var-
ious adverse outcomes. Hence, it is essential that available
data on febrile seizure outcomes are critically reviewed and
interpreted in the light of either of the possible
pathophysiological sequences described above. This will
ensure appropriate therapeutic and prognostic advice is
available.
DEFINITION
Despite the high prevalence of febrile seizure, its definition
has not elicited consensus, with variation in: (1) age at
onset, (2) whether there is an a priori requirement for pre-
viously typical development, and (3) the accepted longest
duration for a simple febrile seizure (10 or 15mins). Hence,
it is key to establish which definition has been used in any
given study as the types of children included can have a
major impact on perceived outcomes.
Age at onset
According to the National Institute for Health and Care
Excellence in the UK and the American Academy of Pedi-
atrics,7,8 febrile seizures are defined as occurring in chil-
dren older than 6 months of age. However, an earlier
definition by the International League Against Epilepsy
states that febrile seizures can occur from 1 month of age.9
Although this may seem like an unimportant difference, a
lower age limit of 1 month has implications regarding the
likelihood of a genetic epilepsy such as Dravet syndrome
or PCDH19, given that both of these genetic disorders are
associated with seizures occurring below the age of 6

© 2020 Mac Keith Press DOI: 10.1111/dmcn.14642 1245


months in a febrile context. These children have adverse
outcomes that are a function of the underlying genetic dis-
order and thus have the potential to confound outcome
studies and lead to incorrect assertions about brain injury
caused by febrile seizure.
Prior development
The American Academy of Pediatrics7,8 define a febrile sei-
zure as a seizure occurring in the context of fever without
central nervous system infection in a child without prior
history of afebrile seizures, pre-existing neurological disor-
der, or disorder that predisposes to an increased risk of sei-
zures. In contrast, the International League Against
Epilepsy defines febrile seizure as ‘a seizure occurring in
childhood after 1 month of age associated with a febrile ill-
ness not caused by an infection of the central nervous sys-
tem, without previous neonatal seizures or a previous
unprovoked seizure, and not meeting the criteria for other
acute symptomatic seizures’.9 Although similar, the defini-
tions are not identical. The American Academy of Pedi-
atrics definition explicitly excludes children with
neurological disorders that predispose to later seizures (e.g.
cerebral palsies). This is not the case with the International
League Against Epilepsy definition although this may be
implied by exclusion of acute symptomatic seizures. Never-
theless, inclusion of children with significant pre-existing
neurological disorders could confound outcome studies if
this subset of children is not explicitly described. Cur-
rently, neither of the above definitions explicitly exclude
children with pre-existing neurodevelopmental disorders
such as autism spectrum disorders, some of which could
become manifest in later years.
Thus, the requirement for previously typical develop-
ment is in place to attempt to confirm a causative relation-
ship between febrile seizures and adverse outcomes, but
even with best intentions, this may be impossible to
achieve.
Duration
Febrile seizures have traditionally been divided into sim-
ple febrile seizures, complex febrile seizures, and febrile
status epilepticus (FSE) or prolonged febrile seizures
(Table 1).10–12 The terms ‘febrile status epilepticus’ and
‘prolonged febrile seizure’ are used interchangeably, as dif-
ferent studies use different terminologies to describe the
same phenomenon. These distinctions are currently
accepted as having prognostic value. The definition of FSE
has traditionally been at least 30 minutes of continuous sei-
zure activity or 30 minutes of recurrent seizures without
full recovery of consciousness in between the seizures.
However, in 2015, an International League Against Epi-
lepsy taskforce10 redefined the time periods for status
epilepticus, including FSE, as: (1) 5 minutes for general-
ized tonic–clonic seizures; (2) 10 minutes for focal seizures;
and (3) 10 to 15 minutes for absence seizures.
This definition change could have an impact on per-
ceived outcomes. If FSE does cause brain injury as a
1246 Developmental Medicine & Child Neurology 2020, 62: 1245–1249
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What this paper adds
• A febrile seizure is due to a brain’s aberrant response to high temperature.
• Problems in a small group of children are now being identified later in life.
• There is no clear correlation between duration or other characteristics of
febrile seizures and subsequent mesial temporal sclerosis.
function of seizure length, then changing the definition to
include children with shorter seizures will dilute those
effects and give an overly optimistic view of FSE.
Thus, studies need to be interpreted in light of the actual
definition used, as differences in outcomes could in part be
due to the inclusion of children with pre-existing neurologi-
cal or behavioural disorders thereby leading to incorrect
assertions about causative effects of febrile seizures.
ADVERSE OUTCOMES ASSOCIATED WITH FEBRILE
SEIZURES
Psychological impact on families
Febrile seizures can be frightening for parents and families,
despite being seen by professionals as essentially ‘benign’.
Studies looking at parental reaction to febrile seizures have
documented behaviours and physiological manifestations
affecting the carers’ physical, psychological, and beha-
vioural responses as well as disruption in the family’s qual-
ity of life.13 Appropriate and careful interpretation of
existing data is important to guide advice to families in
order to manage these psychological impacts.
Mesial temporal sclerosis associated with temporal lobe
epilepsy
Prospective studies from two separate groups have
addressed this issue, FEBSTAT in the USA6 and the Lon-
don status epilepticus group.5 They examined FSE because
it is more likely to be harmful than short febrile seizures
and examined the clinical and radiological outcomes at dif-
ferent time periods after FSE. FEBSTAT had the larger
sample size of the two studies but included children with
previous neurological abnormalities and thus their findings
may be biased towards overestimation.
Both groups identified quantitative magnetic resonance
imaging (MRI) abnormalities suggestive of acute hip-
pocampal oedema within 5 days of FSE. Follow-up MRI
at 4 to 8 months in the London group5 showed recovery
of the hippocampal oedema, but no evidence of mesial
temporal sclerosis (MTS). One-year post-complex febrile
seizure, the London group found no children who had
FSE had MTS (0%, 95% confidence interval [CI] 0–85).14
At 1-year follow-up, amongst the children in FEBSTAT,
nine (4.5%, 95% CI 2–8%) had evidence of hippocampal
sclerosis not apparent on their acute MRIs.6 However,
importantly, only four children in FEBSTAT that devel-
oped MTS had otherwise normal MRI and no evidence of
developmental delay at time of FSE. Inclusion of only
these children results in a similar incidence of MTS as
identified in the London study at 1-year follow-up. It
remains possible that a longer lag time beyond 1 year is
needed for the development of MTS after FSE but even 9
 14698749, 2020, 11, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/dmcn.14642 by Nat Prov Indonesia, Wiley Online Library on [13/12/2023]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License
Table 1: Current definitions of febrile seizure

Simple febrile
seizure Complex febrile seizure Febrile status epilepticus

Duration <15mins in USA 15mins >30mins

Onset
Recurrence within 24h
Postictal state
Previous neurological deficits
Seizure stopped by emergency
medication (even if <15mins)
<10mins in UK Or shorter serial seizures without recovery
of consciousness in between11
Generalized Focal or generalized + recurrent Definition based on duration not onset
or generalized + prolonged (i.e. focal or generalized tonic–clonic)
None Can recur > once
Quick recovery Can have neurological
abnormalities including
Todd’s paresis
None May have pre-existing deficits
Classified as complex
febrile seizures11,12

years post-FSE, the London group found only one child
had MTS (3%, 95% CI 0.6–16%).15 It will be interesting
to see what the long-term findings of FEBSTAT will be.
Possible explanations for the low incidence of MTS at 9
years post-FSE are that: (1) an even longer period of evo-
lution may be required before MTS emerges, (2) MTS
post-FSE is not as common as has long been believed, or
(3) other factors not specifically studied/reported in either
FEBSTAT or the London group such as genetics, an
autoimmune phenomena, or a central cause for the fever in
some children (e.g. viral encephalitis due to human herpes
virus type 6) are involved.
In summary, the evidence for a causative relationship
between MTS and febrile seizures is weak.
Long-term outcome of febrile seizures including
neurological, cognitive, and memory impairments
It is well accepted that short febrile seizures are not associ-
ated with an increased risk of neurological or cognitive
impairments, although there is a small increased risk of
developing afebrile seizures. This is more controversial for
children with FSE and therefore children in this group
have been studied specifically. In a 9-year follow-up study,
the incidence of epilepsy after FSE is 14% (95% CI 6–29),
with diagnosis of epilepsy often being made within 2 years
post-FSE. It will be of interest to know from ongoing
studies of children who had FSE what proportion will
develop epilepsy.16
In the London study, within 6 weeks and persisting at 1
year post-FSE, children showed similar cognition, motor,
and language scores as normative means of the control
population on the Bayley Scales of Infant Development
but lower scores than typically developing controls.17 The
FEBSTAT study found that the Bayley subscale scores
were similar at 6 weeks between children with FSE when
compared with children with simple febrile seizures. How-
ever, at 1-year follow-up, the scores were lower in the
group with FSE.18 But this finding is also likely to be
biased by inclusion criteria. It is plausible that the London
study findings were partly attributable to typically develop-
ing controls being offspring of ‘high achievers’. On the
other hand, the Flynn effect in which there is a tendency
of IQ scores to increase over time and the failure of mea-
suring tools to keep up with this change may contribute to
lack of difference with normative mean scores.19 In the
London study, within 6 weeks and still present at 1 year
post-FSE, children were also found to have impaired
recognition memory.20
The same London group, but in a different longitudinal
cohort of patients taken from the same geographical
region, found that at 9 years post-FSE, the full-scale IQ
findings were similar to that reported in the short term
post-FSE (i.e. full-scale IQ comparable to the normative
population mean but lower than controls).21 However,
contrary to the shorter term memory findings, children
with FSE had similar general memory scores to controls
and population norms. It is possible that the unexpected
finding is because the incidental recognition memory para-
digm adopted for the early outcomes study recruits differ-
ent brain structures and cognitive processes than that used
in the longer term outcomes study.21 Alternatively, the
memory problems seen in the first year are transient.
Longitudinal tract-based spatial statistics in children
with FSE at 1, 6, and 12 months in one London cohort14
complemented and supplemented by data in a separate
FSE cohort22 would suggest there are acute white matter
changes with ‘normalization’ seen at 1 year, followed by
changes in white matter microstructure and apparent
increases in the coherence of the remaining white matter
structure by 9 years post-FSE. One possible speculation
about these findings is an adaptive change to maximize
efficient organization after disruption of normal white mat-
ter maturation. The fact that the functional cognitive and
memory outcomes 9 years post-FSE are within the average
range of population norms lends some support to this
speculation.
Recurrence and mortality
The recurrence risk of short febrile seizures is between
15% and 70% within 2 years of an initial febrile seizure,
particularly if the initial event occurred under the age of
18 months. One-year recurrence of FSE after first-ever

Review 1247

FSE is 16% (95% CI 10–24).23 Case fatality during hospi-
talization for the acute episode of FSE and at 8 years 6
months post-FSE is 0%.23,24
Psychiatric comorbidities
In a retrospective population-based study, Danish investi-
gators recently found that the 30-year risk of epilepsy in
children who had three or more febrile seizures was 15%,
compared to 2% in those without febrile seizures.3 It is
likely that children with short febrile seizures and those
with FSE were included as the registry did not reliably
distinguish these states. In addition, the risk of mental ill-
ness was 30% in those with febrile seizures compared to
17% in unaffected individuals.3 This figure (17%) was
obtained by the authors looking at admissions for psychi-
atric disorders over that timescale. It is notable that there
is a stepwise increase in risk of epilepsy and of psychiatric
disease with each additional febrile seizure. Children with
a single febrile seizure had a sevenfold increased risk of
an epilepsy diagnosis before 5 years of age (hazard ratio
7.11), while three or more febrile seizures elevated this
risk 42-fold (hazard ratio 42.06).3 Dreier et al. also found
an increased mortality in children with recurrent febrile
seizures.3 However, this association disappeared after
adjusting for epilepsy, suggesting that the increased
mortality is to do with the subsequent development of
epilepsy.
There are at least two possible interpretations of these
data. The first is that each febrile seizure is causing brain
injury and that this injury is cumulative. If true, then this
would imply that prevention of febrile seizures would be
critical to minimize these adverse outcomes. The only
strategies shown to effectively prevent febrile seizures are
regular antiseizure medications,25 as managing fever early
and aggressively has been shown to have limited effect.25
Given that the former is associated with side effects that
could impair quality of life, these need factoring in when
considered as a therapeutic option.
The second interpretation of the findings from the
Dreier et al. study could be due to genetic susceptibility
to febrile seizure.3 Family and twin studies confirm a
strong genetic susceptibility to fever-induced seizure.
Genome-wide association studies have identified several
genetic loci, confirming that genetic susceptibility to feb-
rile seizure is heterogeneous. A priori it is possible that a
genetic susceptibility to febrile seizures could also be a
genetic susceptibility to psychiatric disorders. In this con-
textual frame, prevention of febrile seizures is unlikely to
have a significant impact on psychiatric outcomes. It is
also not clear given the retrospective nature of this study
whether all the children were developmentally and neuro-
logically typical at the time of their febrile seizures. This
definition issue could be relevant as a predictor to out-
comes. As such there is no strong argument to alter ther-
apeutic guidelines for febrile seizures based on this study,
until further evidence to clarify this issue becomes avail-
able. As for acute treatment of prolonged febrile seizure
1248 Developmental Medicine & Child Neurology 2020, 62: 1245–1249
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and FSE, this follows the same treatment algorithm as
that of status epilepticus (afebrile), such as use of buccal
midazolam as first-line treatment, followed by second-
and third-line medications which can vary according to
local or national guidelines.25
Mortality
A recent retrospective study assessed the potential role of
febrile seizure in SUDC.4 The authors reviewed 622 con-
secutive child death cases from 2001 to 2017, aged 1 to
17 years from 18 countries.4 The findings were of a sig-
nificantly higher prevalence of febrile seizures of 28.8%
(95% CI 23.3–34.2%) among cases of SUDC and also in
sudden explained death in childhood of 22.1% (95% CI
14.8–29.3%), in contrast to a general population preva-
lence of febrile seizures of 2% to 5%. However, febrile
seizures in this study was defined broadly and is likely to
have included children with other significant neurological
impairments (e.g. 10% of the children were receiving
early cognitive interventions). The odds of death during
sleep was 4.6-fold higher in the SUDC cohort than in
the sudden explained death in childhood cohort. It is also
interesting to note that many of the deaths occurred at
ages above 3 years, with four SUDC deaths being in
adults older than 30 years. Siblings of SUDC cases did
not die prematurely during a follow-up for 3144 life-
years, suggesting a higher vulnerability to sudden death
in children with febrile seizures. It is unlikely that the
febrile seizure per se is responsible for this outcome given
the benign nature of febrile seizure in every other evalu-
ated domain. However, it is possible that there is an
underlying genetic predisposition to both febrile seizures
and SUDC. Although possible, this does not explain why
febrile seizure would predispose to higher sudden
explained death in childhood rates. It is critical to note
that the authors recognize that this observation could be
a result of bias and should really be considered to be
hypothesis generating. Given the implication of the
results, it is essential that these findings are corroborated
in further studies that define the epidemiology and spec-
trum of risk factors. Once completed, such studies could
have an important impact on current understanding and
treatment approaches to febrile seizures.
Reflection: the role of aetiology?
A brain that responds to fever and relatively trivial viral
illnesses during a defined developmental window with a
seizure (be it a simple, complex, or FSE) in only a small
proportion of children raises the question of why only
those children had a seizure and not all the others. The
most parsimonious explanation is that there is a constitu-
tive difference in the brain of those who have seizures
compared to those that do not. In the majority of chil-
dren with febrile seizures the underlying aetiology appears
to be benign with no major implication for outcome. Just
as there are many different aetiologies for epileptic ence-
phalopathies, it is likely that there are many aetiologies of

febrile seizures. In some children the aetiology of febrile
seizures is also the aetiology of subsequent afebrile sei-
zures and/or psychiatric and other associated morbidities.
These observations suggest that it is time to review
whether febrile seizures are a single entity. Further stud-
ies with emphasis on predictors of adverse outcomes that
are not necessarily seizure-related could be important for
reclassification of febrile seizure, similar to the process
used to reclassify childhood wheeze.26 We should aim to
distinguish phenotypes of febrile seizure considering pre-
existing conditions, clinical presentation, detailed investi-
gation results, and long-term outcomes. Until such stud-
ies are completed it is important that therapeutic
14698749, 2020, 11, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/dmcn.14642 by Nat Prov Indonesia, Wiley Online Library on [13/12/2023]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License
strategies remain unchanged, including recommendations
for the acute treatment of FSE.
CONCLUSION
Febrile seizures (simple, complex, or prolonged) are to be
viewed as markers of an underlying aberrant brain process,
likely developmentally regulated, as febrile seizures often
resolve when the child reaches 5 to 6 years old. In light of
recent research looking at long-term outcomes, additional
longitudinal data are needed to further scrutinize whether
adverse comorbidities can be predicted at the time a child
presents with febrile seizures and to clarify the nature of
any link or association.

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