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Pediatric anti-NMDA receptor encephalitis is seasonal.

Adang LA, Lynch DR, Panzer JA - Ann Clin Transl Neurol (2014)

Bottom Line: We aimed to characterize this poorly understood population, investigating epidemiological factors potentially related to disease etiology, particularly season of onset.In this retrospective case review study, we analyzed data from the 29 pediatric subjects with anti-NMDAR antibodies and found that symptoms were first reported in the warm months of April-September in 78% of non-tumor-related NMDARe (NT-NMDARe) cases.These findings support further investigation into a possible seasonal trigger of NT-NMDARe.

View Article: PubMed Central - PubMed

Affiliation: Departments of Pediatrics and Neurology, University of Pennsylvania Philadelphia, Pennsylvania, 19104.

ABSTRACT
In the majority of pediatric anti-N-methyl-d-aspartate receptor encephalitis (NMDARe) cases, the underlying cause of antibody production and subsequent disease remains unknown. We aimed to characterize this poorly understood population, investigating epidemiological factors potentially related to disease etiology, particularly season of onset. In this retrospective case review study, we analyzed data from the 29 pediatric subjects with anti-NMDAR antibodies and found that symptoms were first reported in the warm months of April-September in 78% of non-tumor-related NMDARe (NT-NMDARe) cases. These findings support further investigation into a possible seasonal trigger of NT-NMDARe.

No MeSH data available.


Related in: MedlinePlus

Laboratory testing of serum or CSF from patients with NMDARe upon presentation. Bars are divided as follows: dark grey bars = NT-NMDARe positive results, light grey = NT-NMDARe negative/normal results, white bars = T-NMDARe positive results, and black = T-NMDARe negative/normal results. Three of the 13 tested had evidence of prior EBV infection (IgM-IgG+), 2/10 mycoplasma IgM-IgG+ (PCR negative), 1/3 parvovirus B19 IgM-IgG+ (PCR negative), and 1/7 Adenovirus PCR+ of respiratory sample (negative CSF PCR). RPR, rapid plasma reagin (for syphilis); CEV, California encephalitis virus; CMV, cytomegalovirus; EEEV, Eastern equine encephalitis virus; EBV, Epstein–Barr virus; HHV-6, human herpesvirus-6; HIV, human immunodeficiency virus; HSV, herpes simplex virus; St. Louis EV, St. Louis encephalitis virus; RRP, rapid respiratory panel (respiratory syncytial virus, influenza A and B, parainfluenza viruses 1, 2, and 3, adenovirus, rhinovirus, and human metapneumovirus by sputum sample PCR), VZV, varicella zoster virus; WNV, West Nile virus; WEEV, Western equine encephalitis virus; ANA, antinuclear antibody; ASO, antistreptolysin antibodies; OCB, oligoclonal bands. NMDARe, N-methyl-d-aspartate receptor encephalitis.
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fig02: Laboratory testing of serum or CSF from patients with NMDARe upon presentation. Bars are divided as follows: dark grey bars = NT-NMDARe positive results, light grey = NT-NMDARe negative/normal results, white bars = T-NMDARe positive results, and black = T-NMDARe negative/normal results. Three of the 13 tested had evidence of prior EBV infection (IgM-IgG+), 2/10 mycoplasma IgM-IgG+ (PCR negative), 1/3 parvovirus B19 IgM-IgG+ (PCR negative), and 1/7 Adenovirus PCR+ of respiratory sample (negative CSF PCR). RPR, rapid plasma reagin (for syphilis); CEV, California encephalitis virus; CMV, cytomegalovirus; EEEV, Eastern equine encephalitis virus; EBV, Epstein–Barr virus; HHV-6, human herpesvirus-6; HIV, human immunodeficiency virus; HSV, herpes simplex virus; St. Louis EV, St. Louis encephalitis virus; RRP, rapid respiratory panel (respiratory syncytial virus, influenza A and B, parainfluenza viruses 1, 2, and 3, adenovirus, rhinovirus, and human metapneumovirus by sputum sample PCR), VZV, varicella zoster virus; WNV, West Nile virus; WEEV, Western equine encephalitis virus; ANA, antinuclear antibody; ASO, antistreptolysin antibodies; OCB, oligoclonal bands. NMDARe, N-methyl-d-aspartate receptor encephalitis.

Mentions: Analysis of prior infectious exposure was limited by the heterogeneity of testing, but the rates of prior infectious exposure (IgM−IgG+) were within that previously described for the general pediatric population; three of the 13 tested (23%) had evidence of prior Epstein–Barr virus (EBV) infection, two of 10 (20%) were positive for mycoplasma IgG (PCR negative), one of three (33%) was positive for parvovirus B19 antibodies (PCR negative; IgG), and one of seven was positive for Adenovirus by PCR of respiratory sample (14%) (negative CSF PCR) (Fig. 2).9–11 No patients within the T-NMDARe population were positive for infectious studies.


Pediatric anti-NMDA receptor encephalitis is seasonal.

Adang LA, Lynch DR, Panzer JA - Ann Clin Transl Neurol (2014)

Laboratory testing of serum or CSF from patients with NMDARe upon presentation. Bars are divided as follows: dark grey bars = NT-NMDARe positive results, light grey = NT-NMDARe negative/normal results, white bars = T-NMDARe positive results, and black = T-NMDARe negative/normal results. Three of the 13 tested had evidence of prior EBV infection (IgM-IgG+), 2/10 mycoplasma IgM-IgG+ (PCR negative), 1/3 parvovirus B19 IgM-IgG+ (PCR negative), and 1/7 Adenovirus PCR+ of respiratory sample (negative CSF PCR). RPR, rapid plasma reagin (for syphilis); CEV, California encephalitis virus; CMV, cytomegalovirus; EEEV, Eastern equine encephalitis virus; EBV, Epstein–Barr virus; HHV-6, human herpesvirus-6; HIV, human immunodeficiency virus; HSV, herpes simplex virus; St. Louis EV, St. Louis encephalitis virus; RRP, rapid respiratory panel (respiratory syncytial virus, influenza A and B, parainfluenza viruses 1, 2, and 3, adenovirus, rhinovirus, and human metapneumovirus by sputum sample PCR), VZV, varicella zoster virus; WNV, West Nile virus; WEEV, Western equine encephalitis virus; ANA, antinuclear antibody; ASO, antistreptolysin antibodies; OCB, oligoclonal bands. NMDARe, N-methyl-d-aspartate receptor encephalitis.
© Copyright Policy - open-access
Related In: Results  -  Collection

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Show All Figures
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fig02: Laboratory testing of serum or CSF from patients with NMDARe upon presentation. Bars are divided as follows: dark grey bars = NT-NMDARe positive results, light grey = NT-NMDARe negative/normal results, white bars = T-NMDARe positive results, and black = T-NMDARe negative/normal results. Three of the 13 tested had evidence of prior EBV infection (IgM-IgG+), 2/10 mycoplasma IgM-IgG+ (PCR negative), 1/3 parvovirus B19 IgM-IgG+ (PCR negative), and 1/7 Adenovirus PCR+ of respiratory sample (negative CSF PCR). RPR, rapid plasma reagin (for syphilis); CEV, California encephalitis virus; CMV, cytomegalovirus; EEEV, Eastern equine encephalitis virus; EBV, Epstein–Barr virus; HHV-6, human herpesvirus-6; HIV, human immunodeficiency virus; HSV, herpes simplex virus; St. Louis EV, St. Louis encephalitis virus; RRP, rapid respiratory panel (respiratory syncytial virus, influenza A and B, parainfluenza viruses 1, 2, and 3, adenovirus, rhinovirus, and human metapneumovirus by sputum sample PCR), VZV, varicella zoster virus; WNV, West Nile virus; WEEV, Western equine encephalitis virus; ANA, antinuclear antibody; ASO, antistreptolysin antibodies; OCB, oligoclonal bands. NMDARe, N-methyl-d-aspartate receptor encephalitis.
Mentions: Analysis of prior infectious exposure was limited by the heterogeneity of testing, but the rates of prior infectious exposure (IgM−IgG+) were within that previously described for the general pediatric population; three of the 13 tested (23%) had evidence of prior Epstein–Barr virus (EBV) infection, two of 10 (20%) were positive for mycoplasma IgG (PCR negative), one of three (33%) was positive for parvovirus B19 antibodies (PCR negative; IgG), and one of seven was positive for Adenovirus by PCR of respiratory sample (14%) (negative CSF PCR) (Fig. 2).9–11 No patients within the T-NMDARe population were positive for infectious studies.

Bottom Line: We aimed to characterize this poorly understood population, investigating epidemiological factors potentially related to disease etiology, particularly season of onset.In this retrospective case review study, we analyzed data from the 29 pediatric subjects with anti-NMDAR antibodies and found that symptoms were first reported in the warm months of April-September in 78% of non-tumor-related NMDARe (NT-NMDARe) cases.These findings support further investigation into a possible seasonal trigger of NT-NMDARe.

View Article: PubMed Central - PubMed

Affiliation: Departments of Pediatrics and Neurology, University of Pennsylvania Philadelphia, Pennsylvania, 19104.

ABSTRACT
In the majority of pediatric anti-N-methyl-d-aspartate receptor encephalitis (NMDARe) cases, the underlying cause of antibody production and subsequent disease remains unknown. We aimed to characterize this poorly understood population, investigating epidemiological factors potentially related to disease etiology, particularly season of onset. In this retrospective case review study, we analyzed data from the 29 pediatric subjects with anti-NMDAR antibodies and found that symptoms were first reported in the warm months of April-September in 78% of non-tumor-related NMDARe (NT-NMDARe) cases. These findings support further investigation into a possible seasonal trigger of NT-NMDARe.

No MeSH data available.


Related in: MedlinePlus