Indian J Pediatr
DOI 10.1007/s12098-015-1988-8
ORIGINAL ARTICLE
Childhood Anti-NMDA Receptor Encephalitis
Renu Suthar 1 & Arushi Gahlot Saini 1 & Naveen Sankhyan 1 & Jitendra Kumar Sahu 1 &
Pratibha Singhi 1
Received: 19 September 2015 / Accepted: 9 December 2015
# Dr. K C Chaudhuri Foundation 2016
Abstract
Objectives To study the clinical profile, and outcome of chil-
dren with anti-N-methyl-D-aspartate receptor (NMDAR)
encephalitis.
Methods This is a retrospective case series of children <12 y of
age, diagnosed with anti-NMDAR encephalitis at a tertiary care
institute during the period, May 2013 through June 2015.
Results Twenty patients were tested for suspected anti-
NMDAR encephalitis over this 2 y period. Of these, six chil-
dren were positive for anti-NMDAR antibodies. Four of these
six children had completed treatment and two are currently
receiving immunotherapy. Behavioral changes, psychosis,
seizures and oro-lingual-facial dyskinesia were the presenting
features. Extreme irritability, insomnia and mutism were noted
in all the children. The symptoms were persistent, and the
course was progressive over 48 wk duration. Neuroimaging
and electroencephalography were non-specific. Intravenous
pulse methylprednisolone and immunoglobulins were used
as first-line therapeutic agents. Only one patient responded
to first line immunotherapy; five out of six children required
second-line immunotherapy. One patient recovered following
rituximab, and two patients showed a good response to cyclo-
phosphamide pulse therapy; two patients are currently under
Part of this study was presented at IJP Senior Resident Grand Rounds
held on 7th September 2014 at AIIMS, New Delhi and was adjudged to
be the best by the expert committee.
* Pratibha Singhi
doctorpratibhasinghi@gmail.com
1
Unit of Pediatric Neurology and Neurodevelopment, Department of
Pediatrics, Advanced Pediatrics Centre, Post Graduate Institute of
Medical Education and Research, Chandigarh 160012, India
treatment with second line immunotherapeutic agents. Tumor
screen was negative in all children.
Conclusions Anti-NMDAR encephalitis is rare but a potential-
ly treatable condition. Timely recognition is essential because
treatment is entirely different from other viral encephalitis. Ag-
gressive immunotherapy is the key to a favourable outcome.
Keywords Autoimmune encephalitis . Encephalopathy .
Neuropsychiatric . Neuroimmunology
Introduction
Anti N-methyl-D-aspartate receptor (NMDAR) encephalitis is
a recently described potentially treatable immune mediated en-
cephalitis [1]. Anti-NMDAR encephalitis has been recognized
as the most frequent autoimmune encephalitis in children after
acute demyelinating encephalomyelitis [24]. The frequency of
anti-NMDAR encephalitis has surpassed any of the viral en-
cephalitides in patients with encephalitis of unknown etiology
as reported by the California Encephalitis Project [4]. The syn-
drome has characteristic progression with several stages of ill-
ness and recovery [2, 5]. However, due to the variable clinical
presentation, the paucity of specific findings on standard labo-
ratory and radiological investigations, and limitations in clini-
cians knowledge, anti-NMDAR encephalitis remains under-
recognized. Only a few cases have been reported from India
[6, 7]. The authors discuss this rare encephalitis along with their
clinical experience in managing six children with this disorder.
Material and Methods
This study is a retrospective review of children diagnosed as
anti-NMDAR encephalitis from May 2013 through June 2015.

The authors institute is a tertiary care centre receiving referrals
from hospitals and covering more than 85 million population of
North India. During the study period, all children with acute-
subacute febrile encephalopathy were admitted in the pediatric
emergency for immediate management. All these children were
also seen by a Pediatric Neurologist. Children without a clear
cause of encephalitis, especially with normal or non-specific
imaging findings were evaluated for NMDAR encephalitis.
On suspicion, the cerebrospinal fluid (CSF) and serum sample
were tested for the presence of anti-NMDAR antibodies. Pos-
itive results were further confirmed by sending CSF and serum
samples to a reference laboratory (Dr Dalmau, Barcelona).
These children were treated and followed up in neurology
follow-up clinic. Most of these children required repeated hospi-
tal admissions for the institution of immunosuppressive drugs.
Retrospective records of children with anti-NMDAR encephali-
tis were retrieved and reviewed in detail. Clinical details, inves-
tigations and management, were recorded from hospital admis-
sion files and follow-up files. For the sake of this report, all these
children were re-examined for assessment of outcome.
Results
During the study period, a total of 22,573 children were ad-
mitted to the pediatric emergency of authors department.
Twenty children were suspected to have autoimmune enceph-
alitis. Among these, six children were confirmed to have anti-
NMDAR encephalitis, an overall prevalence of 26 per 100,
000 pediatric emergency admissions. Out of the six, four have
completed treatment and have recovered; another two patients
are currently receiving immunotherapy. Table 1 describes the
investigations, clinical, and management details of these six
children. All children presented with alteration in the sleep
wake cycle, behavior and cognitive functions. The MRI was
either normal or had non-specific abnormalities in all except
one child (case 6), who had bilateral basal ganglia hyper-
intensities on T2W,FLAIR-MRI. CSF showed mild lympho-
cytic pleocytosis. The NMDAR antibodies were positive in all
in CSF. Tumor screening was done in girls by MRI abdomen
and pelvis and USG abdomen and scrotum in boys. Screening
for tumors was negative in all.
Immuno-modulation was done in all children with variable
drug choice and duration (Table 1). Intravenous methylpred-
nisolone (30 mg/kg/d, maximum 1000 mg/d, for 5 d) followed
by oral steroids (Prednisolone 2 mg/kg/d for 46 wk) and
intravenous immunoglobulins (IVIG, 2 g/kg) were used as
first line agents. Rituximab [375 mg/m2 body surface area
(BSA); four doses] was used as second line immunomodula-
tory agent in four children. Only one child responded to first
line immunotherapy (Case 3). One of the four children treated
with rituximab showed a significant response (Case 4). Two
children (Case 1, 2) showed a remarkable response to
Indian J Pediatr
cyclophosphamide pulse therapy, despite 69 mo of persistent
symptoms. One child (Case 5) has partly responded to cyclo-
phosphamide pulse therapy and is ongoing treatment. One
child (Case 6) is currently receiving second line immunother-
apeutic agents. Four children recovered completely and
returned to premorbid state. Only one child (Case 1) has epi-
lepsy as a persistent morbidity. Long term immunosuppres-
sion with oral azathioprine has been started after substantial
recovery in all the children.
Discussion
First recognized in 2005, anti-NMDAR encephalitis has been
increasingly identified as a significant cause of autoimmune
and paraneoplastic encephalitis [3]. It has been reported across
all age groups but most commonly affected are children and
young adults; and 80 % patients are females [2, 8, 9]. Anti-
NMDAR encephalitis is a syndrome that has characteristic
evolution in several stages [10]. A prodrome consisting of
fever, malaise, nausea, vomiting, diarrhea, or upper
respiratory-tract symptoms is present in about 70 % patients
[2]. Subsequently, within two weeks, patients develop psy-
chotic and seizure phase characterized by behavioral and emo-
tional disturbances such as fear, apathy and psychotic symp-
toms (delusions, hallucinations and mania). In children, the
initial features can be subtle such as temper tantrums, hyper-
activity, irritability and marked agitation. In children, neuro-
logical presentation with seizures, status epilepticus, dystonia,
verbal reduction or mutism is more common [7, 8, 1113].
Intractable insomnia and rapid fluctuations in sensorium
(Blight switch mental status^) have been described as salient
and early feature of anti-NMDAR encephalitis in children
[14]. All six of the index patients had a prominent neurolog-
ical presentation with characteristic movement disorder and
seizures (Table 1). Marked irritability, intractable insomnia
and mutism are very characteristic and were present in all
children. Subsequently, patients developed hyperkinetic phase
with extrapyramidal signs, stereotypic motor automatisms and
autonomic instability [2, 9]. The movement disorder in anti-
NMDAR encephalitis is distinctive and characterized by lip-
smacking, sustained jaw movements, clenching of teeth,
grimacing and oculogyric crises, opisthotonus, and dystonic
limb posturing [15].
Autonomic manifestations include marked and rapid fluc-
tuation of heart rate, blood pressure and respiration and uri-
nary incontinence [2]. Generalized tonic clonic, complex par-
tial seizures and status epilepticus can occur in the early stage
of illness, sometimes the complex movement disorder can be
mistaken for seizures and children may be on multiple antiep-
ileptic drugs (AEDs) including midazolam infusion. Milder
and incomplete forms include isolated seizures, psychiatric
symptoms or dystonia, however mono-symptomatic
Table 1 Clinical features, investigations and treatment details in children with anti-NMDAR encephalitis

Case 1 Case 2 Case 3 Case 4 Case 5 Case 6

Age, sex 4.5 y, F 8 y, M 8 y, F 3 y, M 9 y, F 5 y, M

Indian J Pediatr

Fever Brief at onset Brief at onset None None Brief at onset None
Behavioral problems Severe at onset, agitation, Agitation, confusion Aggression, hyperactive, Irritability Irritability, agitation, Irritability, restlessness,
irritability irritability restlessness agitation
Movement disorder Oro-lingual-facial dyskinesia, Axial and appendicular Oro-lingual-facial Dystonia starting from Focal onset followed Choreo-athetoid
Choreo-athetoid movements dystonia dyskinesia, fast right foot, followed by by generalized movements, facial,
choreo-athetotic generalized dystonia, dystonia, oro-lingual oro-lingual dyskinesia
movements oro-lingual dyskinesia facial dyskinesia
Sleep disturbances Marked insomnia Insomnia Complete insomnia Insomnia Insomnia Insomnia
Autonomic disturbances Tachycardia, hypertension None Hypertension, tachycardia None None None
Cognitive alteration Severe, totally unaware Impaired awareness Severely impaired Global neuro regression Severe, marked impairment Partially preserved
cognition and awareness in awareness awareness
Seizures Repetitive generalized Repeated seizures and Right focal seizures None None None
status epilepticus
Speech alteration Mutism Mutism Mutism Speech regression Reduced speech output Reduced speech,
slurring of speech
Focal deficits Nil Nil Right hemiparesis None None None
Duration of symptoms 8 wk 4 wk 4 wk 8 wk 3 wk 4.5 mo
before presentation
Investigations
MRI brain Mild cortical atrophy Normal study Normal study Normal study Right cerebellar Basal ganglia
hyperintensities hyperintensities
CSF cells 25 cells (L) No cells 30 cells (L) No cells No cells No cells
CSF protein 18.6 mg/dl, 14 mg/dl 68 mg/dl 94 mg/dl 40 mg/dl 48 mg/dl
CSF glucose 58 mg/dl 83 mg/dl 56 mg/dl 68 mg/dl 55 mg/dl 62 mg/dl
CSF culture Sterile Sterile Sterile Sterile Sterile Sterile
EEG/VEEG Diffuse rhythmic delta theta Diffuse delta waves, Diffuse delta waves, Diffuse delta waves, Diffuse delta waves, Not done
waves, absence of sleep absence of sleep absence of sleep reduced sleep markers, absence of sleep
markers VEEG-No ictal markers markers left fronto-central markers
correlate of movements spike and slow waves
Treatment lag for 2 mo 1 mo 1 mo 2 mo 1 mo 4.5 mo
definitive
immunotherapy
Treatment MP, IVIG, CyP, Azp MP, IVIG, Rtx, CyP, Azp MP, IVIG MP, IVIG, Rtx, Azp MP, IVIG, CyP, currently MP, IVIG, Rtx, currently
under treatment under treatment
Tumor screen MRI abdomen and USG abdomen and MRI abdomen and USG abdomen and MRI abdomen and USG abdomen and
pelvis: normal scrotum: normal, MRI pelvis: normal scrotum: normal pelvis: normal scrotum: normal
abdomen: normal
Duration of follow 24 mo, attending school, 15 mo, attending school 18 mo, attending 8 mo, attained Marked improvement Still in intensive
up and outcome on LEV for epilepsy school premorbid state with CyP therapy phase of therapy

MP Methylprednisolone; IVIG Intravenous immunoglobulins; Rtx Rituximab; CyP Cyclophosphamide; Azp Azathioprine; LEV Levetiracetam; CSF Cerebrospinal fluid; EEG Electroencephalogram;
VEEG Video electroencephalogram; USG Ultrasonography; MRI Magnetic resonance imaging

presentations are rare (<5 %) [2, 16]. Recently anti-NMDAR
encephalitis has been reported in association with herpes virus
encephalitis, immunization, mycoplasma infection and demy-
elinating disorders [1719].
NMDA receptors are ligand gated cation channels involved
in synaptic glutaminergic transmission [20]. Glutaminergic
transmission plays a key role in functions involving synaptic
plasticity such as memory, learning, behavior and cognition
[21]. Anti-NMDAR encephalitis is associated with antibodies
in serum and cerebrospinal fluid (CSF) against the NRI1 sub-
unit of NMDA receptors. By capping and internalization,
these antibodies cause selective and reversible dose-
dependent reduction in synaptic NMDA receptors [2, 22].
Glutaminergic excitotoxicity and inactivation of GABAergic
neurons lead to a state of excitatory-inhibitory imbalance; re-
sponsible for characteristic clinical manifestations [2].
The disease can closely mimic various infective and autoim-
mune central nervous system (CNS) conditions. Viral encepha-
litis such as herpes and Japanese B encephalitis are close differ-
ential diagnosis. Neurometabolic disorders such as organic
acidemia, mitochondrial disorders, and other autoimmune syn-
aptic receptor encephalitis (against Hu, Ma2, CV2 and
amphiphysin) and poorly understood epileptic encephalopathies
such as febrile infections related epilepsy syndrome (FIRES) are
other differential diagnosis in children [5]. Anti-NMDAR en-
cephalitis should be suspected in any child or teenager, who
develops a rapid change of behavior or psychosis, abnormal
postures or movements (mostly oro-lingual-facial and limb dys-
kinesia), seizures, and variable signs of autonomic instability.
Magnetic resonance imaging (MRI) changes are non-spe-
cific. In 50 % patients T2 and fluid-attenuated inversion re-
covery (FLAIR) hyperintensities can be seen in the hippocam-
pus, cerebellar or cerebral cortex, frontobasal, insular regions,
basal ganglia and brainstem. Findings are mild and transient;
subtle contrast enhancement might be seen in the affected
areas. MRI brain was normal in four children; reversible mild
brain atrophy was seen in one patient with frequent seizures
(Case 1). One child (Case 6) had bilateral basal ganglia hyper-
intensities on T2W, FLAIR MRI. Rarely, MRI lesions can
mimic demyelinating disorders [17].
Electroencephalogram (EEG) changes are also non-specific.
EEG showed slowing and disorganised background activity in
all children. Generalized rhythmic delta activity and
superimposed high-frequency beta activity (1440 Hz), named
as extreme delta brushes have been described as specific finding
for anti-NMDAR encephalitis in adult patients [23, 24]. Video-
EEG monitoring might be essential in few cases for differenti-
ating seizures and abnormal movements. CSF abnormalities are
commonly seen such as moderate lymphocytic pleocytosis,
normal or mildly elevated protein and positive oligoclonal
bands (in 60 %) [2]. Diffusion tensor imaging shows alteration
of functional connectivity of both right and left hippocampi and
extensive white matter tract changes in cingulate gyrus [25].
Indian J Pediatr
FDG-PET may show cortical hypometabolism predominantly
affecting the temporal areas [26].
Definitive diagnosis is based on demonstration of anti-
NMDAR antibodies in CSF or serum. Though presence of
antibodies in serum confirms the diagnosis; CSF titres are
more sensitive (sensitivity CSF 100 % vs. serum 98.5 %)
and correlates well with disease severity [27]. CSF testing is
especially important in patients receiving immunotherapy
[27]. Anti-NMDAR antibodies can be detected by indirect
immunofluorescence (IF) on rat hippocampus or cerebellar
neurons with specific staining patterns [2]. Human embryonic
kidney (HEK) cells transfected with complementary DNA
containing specific NR1 subunits have been used [10]. In all
of the index patients, the diagnosis was confirmed with IF at a
local laboratory and samples were also sent to the reference
laboratory (See acknowledgement).
Anti-NMDAR encephalitis can occur with or without a
tumor, about 40 % patients are paraneoplastic [8]. The pres-
ence of tumor depends upon the age, sex and ethnicity [2].
Female sex, black race and older age patients have the higher
incidence of paraneoplastic anti-NMDAR encephalitis [2]. In
the largest series by Titulaer et al., ovarian teratomas were the
commonest tumor (94 %) and only <6 % patients below 12 y
of age had tumor [8]. So younger the patient, less likely a
tumor will be detected. Tumor screening was negative in all
of the index patients, and yearly tumor surveillance is being
done during follow-up visits. Rarely, viral encephalitis partic-
ularly herpes encephalitis may act as a precipitating event
[19]. Non-specific viral encephalitis may be a more common
association in children than in adults. Larger studies in chil-
dren may be helpful in identifying the associations in this
tumor-negative young population.
Management includes symptomatic treatment, definitive im-
munotherapy, and tumor surveillance. Symptomatic treatment
consists of antiepileptic agents for seizure control; antipsy-
chotics like haloperidol, risperidone for behavior control;
pacitane and tetrabenazine for extrapyramidal movements and
dystonic storms; and benzodiazepines like midazolam, loraze-
pam and zolpidem for insomnia, agitation and behavioral prob-
lems [28]. Supportive care in intensive care unit might be need-
ed in these patients because of status epilepticus, status
dystonicus, autonomic instability, and cardiac decompensation.
Guidelines for definitive treatment in adult patients have
been proposed by Dalmau et al. [2]. Sequential immunother-
apy and tumor removal are the mainstay of treatment. Step-
wise immunotherapies with combined methylprednisolone
and intravenous immunoglobulins have been used as first line
agents. In refractory patients, plasmapheresis, rituximab and
cyclophosphamide have been used as second line immuno-
modulators [2]. However, experience in children is limited,
and treatment is empirical. The authors have used methylpred-
nisolone and IVIG as first line agents in all children. Rituxi-
mab has been used as second line therapeutic agent.
Indian J Pediatr
Immediate and remarkable response to cyclophosphamide
was seen in three children, who remained refractory to first
and second line agents. Successful use of cyclophosphamide
is increasingly reported in children with anti-NMDAR en-
cephalitis [7, 29]. Use of plasma-exchange has been limited
in children because of autonomic instability, poor patient co-
operation and technical difficulties.
Treatment is discontinued once patients have had substan-
tial clinical recovery, which is usually accompanied by a de-
crease in CSF and serum antibody titers [27]. Relapse can
occur in about 1225 % patients, so continued immunosup-
pression with azathioprine or mycophenolate mofetil has been
recommended for at least two years along with continuous
tumor surveillance [2, 8]. No long-term follow-up data is cur-
rently available in the literature to recommend further immu-
nosuppression in children without underlying tumor. Hence,
extrapolating from the available adult data and recommenda-
tions, the authors have also planned oral maintenance immu-
nosuppressive therapy atleast for two years. The outcome is
favourable with early and aggressive immunotherapy; about
50 % patient respond to first-line agents, and 80 % patients
show substantial recovery [8]. All patients should be exam-
ined for the presence of an underlying tumor, particularly an
ovarian teratoma or testicular germ cell tumor. Periodic
screening for two years is recommended even after encepha-
litis has subsided [2].
Conclusions
Anti-NMDAR encephalitis should be included in the differen-
tial diagnosis of all children presenting with findings of Bviral
encephalitis^ especially if symptoms are persistent, and CSF
and MRI studies are inconclusive. The diagnosis is clinical, and
confirmation is easy with a demonstration of antibodies in se-
rum and CSF. Further, all patients with suspected anti-NMDAR
encephalitis should be thoroughly investigated for the presence
of a tumor. Early diagnosis and aggressive immunotherapy are
imperative. However, it is Bnever too late^ for diagnosing and
treating this entity.
Acknowledgments The authors wish to thank Dr. Josep Dalmau,
(ICREA Senior Investigator, InstitutdInvestigacionsBiomdiques Au-
gust Pi iSunyer (IDIBAPS), Hospital Clinic, University of Barcelona,
Spain) for his support in testing the samples.
Contributions RS, AGS: Patient management, draft of manuscript and
review of literature; JKS: Patient management, critical review of manu-
script for important intellectual content and final approval of the version
to be published; NS: Patient management, critical review of manuscript
for important intellectual content and final approval of the version to be
published; PS: Clinician-in-charge, concept and design of the study, crit-
ical review of manuscript for important intellectual content and final
approval of the version to be published. She will act as guarantor for
the paper.
Compliance with Ethical Standards
Conflict of Interest None.
Source of Funding None.
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