ENCEPHALITIS: ORIGIN, DIAGNOSIS AND TREATMENT

ENCEPHALITIS: ORIGIN, DIAGNOSIS AND TREATMENT Debayan Chakraborty* West Bengal-713301. E.mail: [email protected] IN TRO D U CTIO N Encephalitisisa vectorborne disease caused by a group ofB arbovirus(Flavivirus)and transm itted by culicine m osquitoes, notably C .tritaeniorhynchus , C.vishnui, C.gelidus and along w ith som e anophelines. Itisnow w ell-established thata substantial proportion ofencephalitidesare associated w ith auto-antibodiesdirected againstthe extracellulardom ainsofcell-surface proteins w hich are criticalin the regulation ofneuronal excitability. These include LG I 1 , CA SPR 2 , contactin-2 (V G K C -com plex antibodies), and the N M D A, A M PA , and G A BA B receptors. H ISTO RY O F EN CEPH A LITIS 1800s-recognized in Japan. 1924-Japan epidem ic.6125cases,3797deaths 1935-virusisolated in brain Japanese patientw ho died ofencephalitis 1938-virusisolated from Culex m osquito in japan 1948-Japan outbreak 1949-korea outbreak Today-extream ely prevalentin South EastA sia 30,000-50,000 casesreported year2014. CAUSES OF ENCEPHALOPATHY H ypoxic/ischaem ic M etabolic (liverand renalfailure, diabetes) Toxic (alcohol, drugs) V ascular(vasculitis, SLE, SA H , SD H , stroke, B ehcet’s) Epileptic (non-convulsive status) N utritionaldeficiency System ic infections(m alaria) Traum atic brain injury M alignanthypertension M itochondrialcytopathy (Reye’sand M ELAS syndrom es) H ashim oto’sencephalopathy Paraneoplastic lim bic encephalitis N euroleptic m alignantsyndrom e… … .. (and m ore!) PRO G N O SIS IN H SE M ortality > 70% ifuntreated (20% w ith Rx) Poorprognostic factors -A ge > 60 yrs -G CS < 7 -D elay in starting acyclovir(esp > 2days) 2/3 rdsptshave neuropsychiatric sequelae -69% m em ory im pairm ent -45% personality/behaviorchange -41% dysphasia -25% epilepsy CONCLUSION Som e cases of encephalitis m ay be associated w ith autoantibodies to cellsurface proteins.These syndrom es have characteristic clinical features and often a good response to im m unotherapies. A s m ore antibody assays are developed, the spectrum of im m unotherapy- responsive phenotypesw illcontinue to expand. REFERENCE W H O -recom m ended standardsforsurveillance of selected vaccine-preventable diseases [http://w w w .w ho.int/vaccines docum ents/D ocsPD F06/843.pdf] D avison K L, Crow croftN S, Ram say M E,Brow n DW , A ndrew sN J:V iralencephalitisin England, 1989–1998:w hatdid w e m iss?Em erg InfectD is2003, 9:234:240.

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Transcript of ENCEPHALITIS: ORIGIN, DIAGNOSIS AND TREATMENT

ENCEPHALITIS: ORIGIN, DIAGNOSIS AND TREATMENT

Debayan Chakraborty*

West Bengal-713301.

E.mail: [email protected]

INTRODUCTION

Encephalitis is a vector borne disease caused by a group of B arbovirus (Flavivirus) and transmitted by culicine mosquitoes, notably C.tritaeniorhynchus, C.vishnui, C.gelidus and along with some anophelines.

It is now well-established that a substantial proportion of encephalitides are associated with auto-antibodies directed against the extracellular domains of cell-surface proteins which are critical in the regulation of neuronal excitability. These include LGI1, CASPR2, contactin-2 (VGKC-complex antibodies), and the NMDA, AMPA, and GABAB receptors.

HISTORY OF ENCEPHALITIS 1800s- recognized in Japan. 1924- Japan epidemic.6125cases,3797deaths 1935- virus isolated in brain Japanese patient who

died of encephalitis 1938- virus isolated from Culex mosquito in japan 1948- Japan outbreak 1949- korea outbreak Today- extreamely prevalent in South East Asia

30,000-50,000 cases reported year 2014.

CAUSES OF ENCEPHALOPATHY Hypoxic/ischaemic Metabolic (liver and renal failure, diabetes) Toxic (alcohol, drugs) Vascular (vasculitis, SLE, SAH, SDH, stroke,

Behcet’s) Epileptic (non-convulsive status) Nutritional deficiency Systemic infections (malaria) Traumatic brain injury Malignant hypertension Mitochondrial cytopathy (Reye’s and MELAS

syndromes) Hashimoto’s encephalopathy Paraneoplastic limbic encephalitis Neuroleptic malignant syndrome…….. (and more!)

PROGNOSIS IN HSE Mortality > 70% if untreated (20% with Rx) Poor prognostic factors

-Age > 60 yrs -GCS < 7 -Delay in starting acyclovir (esp > 2days)

2/3 rds pts have neuropsychiatric sequelae -69% memory impairment -45% personality/behavior change -41% dysphasia -25% epilepsy

CONCLUSION Some cases of encephalitis may be associated with autoantibodies to cell surface proteins. These syndromes have characteristic clinical features and often a good response to immunotherapies. As more antibody assays are developed, the spectrum of immunotherapy-responsive phenotypes will continue to expand.

REFERENCE

WHO-recommended standards for surveillance of selected vaccine-preventable diseases [http://www.who.int/vaccines

documents/DocsPDF06/843.pdf]

Davison KL, Crowcroft NS, Ramsay ME, Brown DW, Andrews NJ:Viral encephalitis in England,

1989–1998:what did we miss?Emerg Infect Dis2003, 9:234:240.