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Liu et al. Anti-NMDAR encephlitis and ADEM-like findings

if it is concurrent with demyelination, there are more consideration. Even if given in the late phase, there
deficits, and more intense immunotherapies are often may still be good effects.
required. Therefore, awareness that anti-NMDAR
[2]
encephalitis and a demyelinating disorder may occur Financial support and sponsorship
in the same patient is important for facilitating timely Nil.
diagnosis and treatment. The pathogenic mechanism
of anti-NMDAR encephalitis and demyelinating Conflicts of interest
disorders coexisting is unknown. Several active There are no conflicts of interest.
immune mechanisms may likely play. One may be
that functional NMDARs are composed of 5 different Patient consent
subunits as GRIN1, GRIN2A, GRIN2B, GRIN2C and Informed consent was obtained from all individual
GRIN2D, and these subunits may be associated with participants included in the study.
demyelinating disorder. Additionally, Lipton’s work
[6]
[7]
showed that oligodendrocytes and myelin contain Ethics approval
NMDAR and that molecular mimicry or immune cross- Data collection in our study involving the patient is
reaction might be involved in pathogenesis. However, consistent with the ethical standards of the institution’s
[8]
the exact relationship between NMDAR antibodies and ethics committee.
myelin dysfunction still needs more study.
REFERENCES
Conventional treatments of anti-NMDAR encephalitis
include corticosteroids, intravenous immunoglobulin 1. Viaccoz A, Desestret V, Ducray F, Picard G, Cavillon G, Rogemond
(IVIG), and plasma exchange (TPE). These three V, Antoine JC, Delattre JY, Honnorat J. Clinical specificities of adult
treatments are considered “first-line” therapies for male patients with NMDA receptor antibodies encephalitis. Neurology
2014;82:556-63.
anti-NMDAR encephalitis. But, in fact, IVIG and TPE 2. Dalmau J, Lancaster E, Martinez-Hernandez E, Rosenfeld MR, Balice-
[9]
are expensive or hard to get in some countries, so Gordon R. Clinical experience and laboratory investigations in patients
hormone therapy is very important. with anti-NMDAR encephalitis. Lancet Neurol 2011;10:63-74.
3. Wandinger KP, Saschenbrecker S, Stoecker W, Dalmau J. Anti-
Our case is notable for the simultaneous occurrence NMDA-receptor encephalitis: a severe, multistage, treatable disorder
of anti-NMDA receptor encephalitis with ADEM-like presenting with psychosis. J Neuroimmunol 2011;231:86-91.
clinical/MR features, where, after given a high dose of 4. Titulaer MJ, Hoftberger R, Iizuka T, Leypoldt F, McCracken L,
Cellucci T, Benson LA, Shu H, Irioka T, Hirano M, Singh G, Cobo
steroid treatment, the patient had a good prognosis. Calvo A, Kaida K, Morales PS, Wirtz PW, Yamamoto T, Reindl M,
The patient’s first signs were symptom of encephalitis: Rosenfeld MR, Graus F, Saiz A, Dalmau J. Overlapping demyelinating
fever, headaches, and mental abnormalities that could syndromes and anti-N-methyl-D-aspartate receptor encephalitis. Ann
not be controlled with DXM 10 mg/day and got worse. Neurol 2014;75:411-28.
Gradually, she developed features of disseminated 5. Lekoubou A, Viaccoz A, Didelot A, Anastasi A, Marignier R, Ducray
encephalomyelitis: confusion, difficulty walking, and F, Rogemond V, Honnorat J. Anti-N-methyl-D-aspartate receptor
urinary and fecal incontinence. With high doses of encephalitis with acute disseminated encephalomyelitis-like MRI
features. Eur J Neurol 2012;19:e16-7.
hormone therapy for two periods, the above symptoms 6. Rossi S SV, Moscatelli A, Motta C, Coghe G, Fenu G, Caillier S,
were improved. Although early and aggressive therapy Buttari F, Mori F, Barbieri F, Castelli M, De Chiara V, Monteleone
had not been given to this patient, a high dose of steroid F, Mancino R, Bernardi G, Baranzini SE, Marrosu MG, Oksenberg
treatment was given in the late phase (1 month after JR, Centonze D. Opposite roles of NMDA receptors in relapsing and
[10]
onset), and had a good therapeutic effect. At 3 months primary progressive multiple sclerosis. PLoS One 2013;8:e67357.
after onset, her motor skills, responsiveness, and 7. Lipton SA. NMDA receptors, glial cells, and clinical medicine.
speech improved rapidly. Neuron 2006;50:9-11.
8. Orengo JP PM, Cree BA. Simultaneous serum aquaporin-4 antibody
and CSF NMDA receptor antibody-positive encephalitis. Neurol
In conclusion, it is very important to recognize that Neuroimmunol Neuroinflamm 2015;2:e101.
patients with anti-NMDAR encephalitis may present 9. DeSena AD, Noland DK, Matevosyan K, King K, Phillips L, Qureshi
as ADEM-like clinical/MRI features, simultaneously SS, Greenberg BM, Graves D. Intravenous methylprednisolone
or sequentially. In addition, anti-NMDAR antibodies versus therapeutic plasma exchange for treatment of anti-n-methyl-d-
should be assessed in patients with encephalitis or aspartate receptor antibody encephalitis: a retrospective review. J Clin
Apher 2015;30:212-6.
psychiatric symptoms, even when the MRI suggests 10. Turkdogan D, Orengul AC, Zaimoglu S, Ekinci G. Anti-N-methyl-
demyelinating disease. Future studies should pay d-aspartate (Anti-NMDA) receptor encephalitis: rapid and sustained
more attention to these associations. In the mean clinical improvement with steroid therapy starting in the late phase. J
time, a high dose of steroid treatment could be the first Child Neurol 2014;29:684-7.

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