Acute Necrotizing Encephalopathy In Korean Infants And .
Acute Necrotizing Encephalopathy inKorean Infants and Children: ImagingFindings and Diverse Clinical OutcomeJi Hye Kim, MD1In-One Kim, MD2Myung Kwan Lim, MD3Man Soo Park, MD4Choong Gon Choi, MD5Hye Won Kim, MD6Jee Eun Kim, MD6Soo Jin Choi, MD6Young Hwan Koh, MD6Dal Mo Yang, MD6Sung Wook Choo, MD1Myung Jin Chung, MD1Hye-Kyung Yoon, MD1Hyun Woo Goo, MD5Munhyang Lee, MD7Index terms :Brain, encephalopathyInfants and children, diseaseBrain, MRKorean J Radiol 2004;5:171-177Received February 23, 2004; acceptedafter revision September 8, 2004.Department of Radiology and Center forImaging Science, Samsung MedicalCenter, Sungkyunkwan University Schoolof Medicine; 2Department of Radiology,Seoul National University College ofMedicine; 3Department of Radiology,Incheon Medical Center, College ofMedicine, Inha University; 4Department ofRadiology, Asan Kang Nung Hospital;5Department of Radiology, Asan MedicalCenter, University of Ulsan College ofMedicine; 6Department of Radiology,Gachon Medical School, Ghil MedicalCenter; 7Department of Pediatrics,Samsung Medical Center, SungkyunkwanUniversity School of Medicine1Address reprint requests to:Ji Hye Kim, MD, Department ofRadiology and Center for ImagingScience, Samsung Medical Center,Sungkyunkwan University School ofMedicine, 50 Ilwon-dong, Kangnam-gu,Seoul 135-710, Korea.Tel. (822) 3410-0511Fax. (822) 3410-0084e-mail: jhkate.kim@samsung.comKorean J Radiol 5(3), September 2004Objective: The purpose of our study was to describe acute necrotizingencephalopathy in Korean infants and children, and we sought to evaluate theprognostic factors.Materials and Methods: Acute necrotizing encephalopathy was diagnosed in14 Korean infants and children. We retrospectively analyzed the neuroimagingfindings including the follow-up changes. The clinical course of the disease wasgraded, and we evaluated prognostic factors including age, serum level of theaminotransferase, hemorrhage, and localized atrophy of the brain.Results: This encephalopathy predominantly affected the bilateral thalami(n 14), pons (n 12), and midbrain (n 10) in a symmetrical pattern.Hemorrhage was observed in eight patients (57%). On the follow-up images(n 12), the brain lesions were reduced in extent for all patients, and generalizedatrophy was seen in six patients. Localized tissue loss was observed in fivepatients and a complete resolution occurred for one patient. All the patients survived and two recovered completely; mild (n 6) to severe (n 6) neurologicaldeficits persisted in the remaining 12 patients. The significant prognostic factorsidentified in this study were the presence of hemorrhage (p 0.009) and localized atrophy (p 0.015).Conclusion: Acute necrotizing encephalopathy in Korean patients showed thecharacteristic patterns of the post-infectious encephalopathy as described in theliterature. The high survival rate and the relatively favorable clinical courseobserved for the present study suggest a more diverse spectrum of diseaseseverity than was previously described. The presence of hemorrhage and localized tissue loss on MR images may suggest a poor prognosis.cute necrotizing encephalopathy (ANE) represents a peculiar type ofencephalopathy characterized by bilateral symmetrical lesions that arepredominantly observed in the thalami and brain stem of infants andchildren. It has been described by Japanese pediatricians, and it is regarded as a noveldisease entity based on clinico-pathological data (1, 2). Although there is someargument on specific terminology (3), the term acute necrotizing encephalopathy hasbeen widely accepted since it was first proposed by Mizuguchi et al. (1). ANE occursfollowing a systemic viral infection, and death or irreversible neurological sequelaehave been described as the typical result of this disease. However, the etiology andpathogenesis of the disease remain mostly unknown. ANE has been predominantlyreported in Japan and Taiwan in the Far East, and although Korea is geographicallyclose to these countries, only three Korean cases have been reported (4, 5). Thus, wehave conducted the first large series study on ANE in Korea.A171
Kim et al.The purpose of this multi-institutional study was todescribe the radiological findings and the clinical course ofANE in Korean infants and children, and we sought toevaluate the clinico-radiological prognostic factors relatedto this disease.MATERIALS AND METHODSFourteen infants and children with ANE that wasdiagnosed in six Korean institutions over the past 10 yearswere the study subjects. The diagnoses were based on thecriteria proposed by Mizuguchi et al. (6) (Table 1). The agesof the 14 patients ranged from 5 months to 12 years with amedian age of 26 months, and there were 8 boys and 6girls. The clinical findings during their hospital admissionare summarized in Table 2. Presenting symptoms includedfever and seizure followed by impairment of consciousness;this was often precipitated by seizures in all patients exceptfor one (patient 3) who stayed alert throughout the clinicalcourse. All of the patients had experienced precedingsymptoms, and they all had signs of upper respiratory tractinfection (n 11) or acute viral gastroenteritis (n 3). TheTable 1. Diagnostic Criteria of Acute Necrotizing Encephalopathy Proposed by Mizuguzi (modified from reference 11)1. Acute encephalopathy following viral disease, with seizure and deterioration of consciousness.2. Absence of CSF pleocytosis. CSF protein is commonly increased.3. Neuroimaging findings of symmetric, multifocal brain lesions involving the bilateral thalmi, upper brain stem tegmentum, periventricular white matter, internal capsule, putamen and cerebellum.4. Elevation of serum aminotransferase level to a variable degree. No increase in blood ammonia.5. Exclusion of any resembling disease.A. Clinical differential diagnosis; toxic shock syndrome, hemolytic uremic syndrome, Reye syndrome, hemorrhagic shock andencephalopathy syndrome, and heat stroke.B. Radiological (or pathological) differential diagnosis; Leigh encephalopathy, glutaric acidemia, methyl malronic aciduria, infantilebilateral strial necrosis, Wernicke encephalopathy, carbon monoxide poisoning, acute disseminated encephalomyelitis, acutehemorrhagic leukoencephalitis, arterial or venous infarct, severer hypoxic or traumatic injury.Table 2. Summary of the Clinical Findings of 14 PatientsCase Age/Viral InfectionNo Gender010203Presentation ofEncephalopathyS-AST/ALT(IU/L)CSF Profile5 Mo/M5 Yr/M5 Mo/FURI, 3DAURI, 4DAURI, 7DASeizure, stuporousSeizure, comatoseSeizure89/45242/100088/43WNLWNLWNL04 10 Mo/F05 5 Mo/M06 6 Yr/M07 19 Mo/MURI, 15DAURI, 14DAAGE, 7DAURI, 10DASeizure, stuporousSeizure, drowsySeizure, comatoseSeizure, lethargic80/2836/35159/21688/17408094 Yr/F10 Yr/MURI, 10DAURI, 14 DASeizure, stuporousStuporous to drowsy68/4566/21WNLWNLWNLProtein,240 mg/dlWNLWNL10 28 Mo/MURI, 10DA38/103WNL1112AGE, 13DAURI, 4DASeizure, lethargic,deviated left eyeSeizure, comatoseSeizure, drowsy12 Yr/F3 Yr/F13 10 Mo/M146 Mo/FAntiviralAntibody/PCROutcomeNDSpastic quadriplegia, rigidityNDStuporous, rigidityNegative for HSV,RecoveredTORCHNDSpastic quadriplegiaNDRecoveredNDComaNegative for Coxackie,Increased DTR,JBV, HSV1, Echovirusankle clonusNDLeft motor weaknessNDDrowsy to alert,increased DTRNegative for HSVAlert, eye deviation62/15 Protein, 61 mg/dlND153/162Protein,Positive for179 mg/dlInfluenza AAGE, 2DASeizure, drowsy,102/42 Increased protein Negative for HSV,decerebrated rigidityenterovirusURI, 4DA Seizure, mental change, 54/21 Increased protein Negative for HSV,rigidity of extremityenterovirusStuporDrowsy to alert, eyeblinking, left arm clonusSevere motor deficitAlert, less rigidextremityNote. URI upper respiratory infection, AGE acute viral gastroenteritis, S-AST/ALT serum level of aspartate/alanine aminotransferase,WNL within normal limit, JBV Japanese B encephalitis virus, HSV herpes simplex virus, Mo months, Yr years, DA days ago,ND Not performed, DTR deep tendon reflex172Korean J Radiol 5(3), September 2004
Imaging and Clinical Findings of Acute Necrotizing Encephalopathy in Korean Infants and Childrentime interval between the most recent viral infection andthe onset of encephalopathy varied from 3 to 15 days witha mean period of 8 days. None of the patients had beenrecently immunized.The serum levels of the aspartate aminotransferase andalanine aminotransferase were found to be elevated tovariable extents in 13 patients. The serum ammoniumlevels were not elevated in any of the 10 patients tested.Cerebrospinal fluid (CSF) analysis was done for 12 patientsand none of them exhibited pleocytosis. A mild increase inthe protein level of the CSF was noted in 5 patients. Serumanti-viral antibody and polimerase chain reaction (PCR)analysis for viral DNA were performed for 6 patients; allof them were negative except for one in whom inflenza Avirus was cultured from the CSF and nasal secretions(patient 12). Stains and cultures for bacteria in the CSFwere all negative.ACKorean J Radiol 5(3), September 2004BAll the patients underwent an MR examination betweenone and seven days from the encephalopathy onset, and atotal of 28 MRIs and 3 CT scans were obtained. Becausethe cases were collected from multiple institutes, MRimaging were performed on various equipment, including1.5-T, 1.0-T and 0.5-T superconducting systems (SiemensAG, Erlangen, Germany/ General Electric Medical Systems,Milwaukee, U.S.A.), and the images included spin echo T1-,T2-weighted images and fluid attenuated inversionrecovery sequences having combinations of axial, sagittaland coronal image planes. Post-contrast enhancementimages were obtained for eight patients. The slice thicknessused was usually 5 mm.The neuroimaging findings were analyzed in terms of thedistribution and pattern of the lesions, the presence ofhemorrhage and temporal evolution. We classified thepatients into favorable and severe sequelae groups accord-Fig. 1. MRIs of a 10-month-old girl(patient 4) who was left with severesequelae.A, B. Initial MR images obtained on theday following the hospital admission. T2weighted axial images (A, B) showincreased signal intensity in the thalami,the posterior internal capsule, putamen,periventricular white matter and thetegmen of the pons (arrows).C, D. Follow-up MR images obtainedafter one month of initial study. The T1weighted image (C) shows shrunkenthalami, localized low signal intensity thatwas similar to the cerebrospinal fluid inthe periventricular white matter, andgeneralized atrophy of the cerebralhemispheres. The patches of brightsignal intensity in the bilateral thalami(open arrows) suggest a subacute stageof hemorrhage. The localized brightsignal intensity in the periventricularwhite matter and in the right thalamus onT2 weighted images (D) suggest thecystic evolution.D173
Kim et al.ing to the clinical outcome, where the favorable groupincluded those patients who recovered completely or hadonly mild sequelae. Mild sequelae were defined as arestored gait and speech abilities in spite of the residualneurological deficits (6). The remaining subjects wereincluded in the severe sequelae group. Several prognosticfactors were evaluated with respect to the patientoutcome: 1) age 2 years, 2) elevated serum levels ofaspartate aminotransferase or alanine aminotransferase of 100 IU/liter, 3) presence of hemorrhage, and 4) localizedtissue loss on follow-up MR images. Statistical analysis wasperformed using Fisher’s exact test in a 2 2 table. A pvalue of 0.05 was regarded as statistically significant.RESULTSNeuroimaging findingsThe neuroimaging findings are summarized in Table 3.ABThe major involved sites were the thalami (n 14), pons(n 12), midbrain (n 10), and internal capsule (n 7) in abilateral symmetrical pattern (Figs. 1, 2). The brainsteminvolvement was predominantly tegmental (Figs. 1B, 3B)in eight patients, and both the ventral and dorsalbrainstems were involved for four patients. The temporallobe (n 4), external capsule (n 4), cerebral deep whitematter (n 3), cerebellum (n 2), putamen (n 2), frontallobe (n 1), and caudate nuclei (n 1) were also involvedin some patients. The observed lesions were initiallyedematous with T1 and T2 prolongation. There werehyperintense thalamic lesions noted on the T1-weightedimages in eight patients on the initial images (n 5) or onthe follow-up images (n 3, Fig. 1D); this suggested thatthere was a subacute stage of hemorrhage, which was alsoseen in the pons in one patient. These hemorrhagic lesionsshowed variable T2 signal intensity. Contrast enhancementwas performed for eight patients and enhancementCFig. 2. MRIs of a 5-month-old boy(patient 5) who recovered completely.A, B. The initial T2-weighted imagesreveal the bilateral thalamic swelling. Theposterior limb of the internal(arrowheads) capsule, external capsule(arrows), and the pons (arrow, B) arealso involved.C, D. Follow-up images obtained 18 dayslater show the thalamic swelling hassubsided and disappeared as comparedto the abnormal signal intensity noted onprior MR images.E. Generalized cerebrospinal fluid spacewidening is seen 6 months after the initialMR scan.D174EKorean J Radiol 5(3), September 2004
Imaging and Clinical Findings of Acute Necrotizing Encephalopathy in Korean Infants and Childrenoccurred in four of them, usually on the follow-up images(n 3).Follow up images were obtained for 12 patients fromday 7 to day 180 after the first MR scan. The lesionswelling had subsided and the extent of the abnormalsignal intensity decreased in all the patients (Figs. 1, 2). Forpatient 5, along with the clinical recovery, the brain lesionshaving abnormal signal intensity disappeared on thefollow-up MR images obtained 18 days after the firstimages were taken, and the last MR imaging taken 6months after the initial scan revealed a generalized CSFspace widening (Fig. 2). Shrunken thalami (n 3) orlocalized cystic encephalomalacia (n 2, Figs. 1C, D) werenoted on the relatively long-term follow-up images.Generalized CSF space widening was noted for 6 patients(Figs. 1C, D, 2E), and it was considered to be atrophy.Patient outcomeAll the patients survived and two of them (14%)completely recovered. Mild neurological deficit remainedTable 3. Summary of Radiological Findings of 14 PatientsNo. Scan timeDistribution of the LesionsHemorrhage015DBilat. thalami, IC, CNThalami024DThalami, pons03041D1DBilat. thalami, pons, midbrain,IC, ECBilat. thalami, ponsBilat. thalami, pons, midbrain, IC,PVWM, temporal lobe051DNone063D072D0809105D6D4D117DBilat. thalami, pons, midbrain, IC,EC, frontal & temporal lobesBilat. thalami, pons, midbrain, IC,putamen, PVWM, cerebellumBilat. thalami, pons, midbrain, IC,EC, temporal lobe, cerebellumBilat. thalami, pons, midbrainBilat. thalami, pons, midbrainBilat. thalami, pons, midbrain, IC,PVWM, temporal lobeBilat. thalami, pons, midbrain121D13142D4DBilat. thalami, putamen,pons, midbrainBilat. thalami, pons, PVWMBilat. thalami, ECTemporal EvolutionInterval of ScansNoneDecreased extent, residual hemorrhage,localized tissue loss & generalized atrophyDecreased extent, strong enhancement,generalized atrophyDecreased swelling & extentDecreased extent, new thalamichemorrhage, mild enhancement,localized & generalized atrophyResolved lesions & generalized CSFspace wideningDecreased extent, mild enhancement,localized tissue loss & generalized atrophyNANoneNoneNoneDecreased extent, generalized atrophyNADecreased extent3 MoNA13 DDecreased extent, new thalamic hemorrhage,dense enhancement, localized atrophyResidual lesion, hemorrhage23 DResidual atrophy of lesions and hemorrhageImproved lesion3 Mo1WNoneThalami(delayed )ThalamiThalami(delayed )Thalami(delayed )ThalamiThalami4 D, 5 Mo4, 25 D9D28 D18 D, 6 Mo1, 3 MoNA23 DNote.Scan time time interval between scan time and onset of the neurological symptoms.delayed hemorrhage was first appeared on follow-up MR images.D days, Mo months, W week, NA Not applicable, Bilat. bilateral, IC internal capsule, EC external capsule, PVWM periventricular whitematter, CN caudate nucleiTable 4. Significance of Prognostic FactorsPatient OutcomePrognostic Factorsp ValueFavorable Severe SequelaeAge 2 yearsElevated aspartate /alanine aminotransferasePresence of hemorrhageLocal tissue loss4320Korean J Radiol 5(3), September 20043365Table 5. Outcome of the Patients with Acute NecrotizingEncephalopathy Described in the Literature and ThisStudy110.0090.015Survival with e Cases(6 25)Cases inThis Study32 (35%)37 (40%)23 (25%)092 (100%)8 (57%)6 (43%)0 (0%)014 (100%)175
Kim et al.in six patients (43%) and moderate to severe neurologicaldeficits or mental alterations persisted in six patients(43%). For the prognostic factors that we tested, we foundthat hemorrhage (p 0.009) and localized tissue loss (p 0.015) were associated with a poor prognosis.DISCUSSIONANE has been recently established as a disease entityand it predominantly affects infants and young children inJapan and Taiwan. Despite the fact that these countriesand Korea are in close geographical proximity, the firstcase in Korea was reported as recently as 2003 (4).However, we were able to identify another 12 patients insix institutions over the last 10 years, and this suggests thatmost ANE patients have remained unreported in Korea.Nevertheless, it is not known whether the cause of thisracial or geographic predilection is related to genetic orenvironmental factors. Having considered the recent casesfrom outside the Far East (7, 8 14), it appears that thegeographic distribution of this malady could be wider thanwas previously thought.The outcome of ANE is generally grave, although theprognosis has improved recently. We reviewed theoutcomes of the 92 reported cases in the literature (6 26)that occurred in countries other than Korea, and we foundthat 65% of the patients died or were left with severeneurological sequelae. In contrast to the literature cases, allof the patients in our study survived and 57% completelyrecovered or were left with only mild deficits (Table 5).There are several other reported cases with good outcomesin the literatures (10, 14, 18, 26, 27). Those patients withgood outcomes, including several cases in the presentstudy, could be categorized as having a “mild” form ofANE, as has been described by Yoshigawa et al. (26). Thepathologic process of ANE is presumed to be reversible inthe less severely affected patients who proceed on to acomplete clinical recovery and disease resolution, as wasdemonstrated by the MRI findings.It is interesting that all our patients with severe neurological sequelae had hemorrhagic lesions on the MR images(Fig. 1), and the presence of localized atrophy or cysticencephalomacia seemed to be related to the severesequelae. In addition, it is known that older patients, nonJapanese children and those patients with low values ofserum aminotranferase, and also those patients withoutbrainstem lesions tended to recover well (6). However, thepatients’ age and serum aminotranferase levels were notfound to be significantly correlated with the clinicaloutcome in the present study. This was possibly due to therelatively small number of cases, which undoubtedly is a176limitation of this study.The distributions of lesions detected on CT or MRI scansin the present study were typical of ANE as described inthe literature; the locations included thalami, upperbrainstem tegmentum, cerebral white matter, internalcapsule, putamen and the cerebellar medulla. Hemorrhageusually occurred in the thalami, and it was occasionallyaccompanied by brainstem hemorrhage. The cerebralwhite matter may be involved, although hemorrhage wasseldom seen. The involved brain was often initiallyedematous, and it subsequently became atrophic. Thetemporal evolution of brain lesions on the MR imagesranged from cystic encephalomalacia (n 2, Fig. 1) tocomplete resolution (n 1, Fig. 2), and this could indicate amore diverse spectrum of this disease’s severity.In clinical practice, ANE should be differentiated fromviral encephalitis and the other types of parainfectiousencephalopathies. Viral encephalitis may have a specificsite of symmetrical brain involvement including thethalami, hypothalami, basal ganglia, or brainstem, andprobably this is the result of a specific route of infection orfrom a molecular interaction between a viral protein and areceptor on the host cells (28). Of these, Japaneseencephalitis virus involves the bilateral thalami; thisdisease is an endemic encephalitis spread by mosquitoesand it occurs only during a specific season. Unlike ANE,the thalamic lesions in Japanese encephalitis are notnecessarily symmetrical, and brainstem involvement isrelatively uncommon. Moreover, other brain areas such asthe hippocampus, basal ganglia, substantia nigra, cerebellum, cerebral cortex and white matter are the frequentlyinvolved areas (29, 30).Radiological findings are very helpful for differentiatingthe other types of postinfectious encephalopathies such asReye syndrome or acute disseminated encephalomyelopathy (ADEM). However, the ANE having a favorableoutcome may not be easily differentiated from ADEM withbilateral thalamic involvement (31, 32), although theinvolvement of other sites and the response to steroidtherapy for patients with ADEM may be helpful. It’s alsointeresting that the high apparent diffusion coefficient(ADC) of ADEM and the decreases in the ADC value inANE on the diffusion-weighted images have been reportedto suggest the different nature of the edema (20). Theother radiological differential diagnoses that must beconsidered before arriving at a final diagnosis of ANE are;the acute form of infantile bilateral striatal necrosis,thrombosis of the internal and great cerebral vein, centralpontine/extrapontine myelinolysis, Wernike encephalopathy, urea encephalopathy and Leigh encephalopathy. Theother brain disorders that should be clinically excluded areKorean J Radiol 5(3), September 2004
Imaging and Clinical Findings of Acute Necrotizing Encephalopathy in Korean Infants and Childrenlisted in Table 1.In summary, ANE in Korean patients was found to be apost-infectious brain disorder predominantly involving thebilateral thalami and the brainstem, the disease willoccasionally be accompanied by hemorrhage. The highsurvival rate with a relatively favorable clinical course andthe various neuroimaging evolution patterns observed inthe present study also suggest that there is a mild form ofANE and a more diverse spectrum of disease severity. Thepresence of hemorrhage and localized tissue loss on MRimages may suggest a poor prognosis.References1. Mizuguchi M, Abe J, Mikkaichi K, et al. Acute necrotisingencephalopathy of childhood: a new syndrome presenting withmultifocal, symmetric brain lesions. J Neurol NeurosurgPsychiatry 1995;58:555-5612. Yagishita A, Nakano I, Ushioda T, Otsuki N, Hasegawa A.Acute encenphalopathy with bilateral thalamotegmentalinvolvement in infants and children: imaging and pathologyfindings. AJNR Am J Neuroradiol 1995;16:439-4473. Kato T. The similarity and homogeneity in acute necrotizingencephalopathy: acute cerebral necrotizing syndrome. BrainDev 1999;21:138-1394. Goo HW, Choi CG, Yoon CH, Ko TS. Acute necrotizingencephalopathy: diffusion MR imaging and localized proton MRspectroscopic findings in two infants. Korean J Radiol 2003;4:61-655. Kim TK, Eun BL, Cha SH, et al. Moyamoya disease in a childwith previous acute necrotizing encephalopathy. Pediatr Radiol2003;33:644-647 (Epub 2003 Jun 12)6. Mizuguchi M. Acute necrotizing encephalopathy of childhood: anovel form of acute encephalopathy prevalent in Japan andTaiwan. Brain Dev 1997;19:81-927. Campistol J, Gassio R, Pineda M, Fernandez-Alvarez E. Acutenecrotizing encephalopathy of childhood (infantile bilateralthalamic necrosis): two non-Japanese cases. Dev Med ChildNeurol 1998;40:771-7748. Porto L, Lanferman H, Moller-Hartmann W, Jacobi G, ZanellaF. Acute necrotising encephalopathy of childhood afterexanthema subitum outside Japan or Taiwan. Neuroradiology1999;41:732-7349. Voudris KA, Skaardoutsou A, Haronitis I, Vagiakou EA, ZeisPM. Brain MRI findings in influenza A-associated acutenecrotizing encephalopathy of childhood. Europ J PaediatrNeurol 2001;5:199-20210. Ravid S, Topper L, Eviatar L. Acute necrotizing encephalopathypresenting as a basal ganglia syndrome. J Child Neurol2001;16:461-46211. Macieira L, Carvalho L, Fagundes F, Borges L, Neves F. Acutenecrotizing encephalopathy due to influenza A. Rev Neurol2000;30:798-79912. Mastroyianni SD, Voudris KA, Katsarou E, et al. Acutenecrotizing encephalopathy associated with parainfluenza virusin a Caucasian child. J Child Neurol 2003;18:570-57213. Weitkamp JH, Spring MD, Brogan T, Moses H, Bloch KC,Wright PF. Influenza A virus-associated acute necrotizingKorean J Radiol 5(3), September 2004encephalopathy in the United States. Pediatr Infect Dis J2004;23:259-26314. Protheroe SM, Mellor DH. Imaging in influenza A encephalitis.Arch Dis Child 1991;66:702-70515. Matsushita E, Takita K, Shimada A. Suspected acuteencephalopathy with symmetrical abnormal signal areas in thebasal ganglia, thalamus, midbrain and pons diagnosed bymagnetic resonance imaging. Acta Paediatr Jpn 1997;39:45445816. Sugaya N. Influenza-associated encephalopathy in Japan:pathogenesis and treatment. Pediatr Int 2000;42:215-21817. Wang HS, Huang SC. Acute necrotizing encephalopathy ofchildhood. Chang Gung Med J 2001;24:1-1018. Tran TD, Kubota M, Takeshita K, Yanagisawa M, Sakakihara Y.Varicella-associated acute necrotizing encephalopathy with agood prognosis. Brain Dev 2001;23:54-5719. Fujimoto Y, Shibata M, Tsuyuki M, Okada M, Tsuzuki K.Influenza A virus encephalopathy with symmetrical thalamiclesions. Eur J Pediatr 2000;159:319-32120. Harada M, Hisaoka S, Mori K, Yoneda K, Noda S, Nishitani H.Differences in water diffusion and lactate production in twodifferent types of postinfectious encephalopathy. J Magn ResonImaging 2000;11:559-56321. Huang SM, Chen CC, Chiu PC, Cheng MF, Lai PH, Hsieh KS.Acute necrotizing encephalopathy of childhood associated withinfluenza type B virus infection in a 3-year-old girl. J ChildNeurol 2004;19:64-6722. Albayram S, Bilgi Z, Selcuk H, et al. Diffusion-weighted MRimaging findings of acute necrotizing encephalopathy. AJNRAm J Neuroradiol 2004;25:792-79723. Sazgar M, Robinson JL, Chan AK, Sinclair DB. Influenza Bacute necrotizing encephalopathy: a case report and literaturereview. Pediatr Neurol 2003;28:396-39924. Mizuguchi M, Hayashi M, Nakano I, et al. Concentric structureof thalamic lesions in acute necrotizing encephalopathy.Neuroradiology 2002;44:489-493 (Epub 2002 Apr 04)25. Bassuk AG, Burrowes DM, McRae W. Acute necrotizingencephalopathy of childhood with radiographic progressionover 10 hours. Neurology 2003;60:1552-155326. Yoshikawa H, Watanabe T, Abe T, Oda Y. Clinical diversity inacute necrotizing encephalopathy. J Child Neurol 1999;14:24925527. Cusmai R, Bertini E, Capua MD, et al. Bilateral, reversible,selective thalamic involvement demonstrated by brain MR andacute severe neurological dysfuction with favorable outcome.Neuropediatrics 1994;25:44-4728. Barkovich AJ. Infections of the nervous system. In: Pediatricneuroimaging, 3rd ed. Philadelphia: Lippincott Willams &Wilkins, 2000:744-74629. Kumar S, Misra UK, Kalita J, Salwani V, Gupta RK, Gujral R.MRI in Japanese encephalitis. Neuroradiology 1997;39:180-18430. Abe T, Kojima K, Shoji H, et al. Japanese encephalitis. JMRI1998;8:755-76131. Anezaki T, Aida I, Takagi M, Inuzuka T, Tsuji S. An early-onsetcase of acute disseminated encephalomyelitis with bilateralthalamic lesions on MRI. Rinsho Shinkeigaku 1999;39:821-82432. Baum PA, Barkovich AJ, Koch TK, Berg BO. Deep gray matterinvolvement in children with acute disseminatedencephalomyelitis. AJNR Am J Neuroradiol 1994;15:1275-1283177
TORCH 04 10 Mo/F URI, 15DA Seizure, stuporous 80/28 WNL ND Spastic quadriplegia 05 5 Mo/M URI, 14DA Seizure, drowsy 36/35 WNL ND Recovered . 14 DA Stuporous to drowsy 66/21 WNL ND Drowsy to alert, increased DTR 10 28 Mo/M URI, 10DA Seizure, lethargic, 38/103 WNL Negative for HSV Alert, eye deviation . (arrows). C, D. Follow-up MR images .
and G92, Toxic encephalopathy, for toxic metabolic encephalopathy due to acute on chronic hepatic encephalopathy. Code G92 is assigned separately to specifically capture the toxic metabolic encephalopathy. All three codes are needed to capture the patient's diagnoses. Hepatic encephalopathy is a result of liver disease.
to intermediate and advanced Korean lessons. Before you go, here is a bit of history of 한글 (Hangeul, the Korean alphabet): Korean is the official language of Korea, both North and South. There are around 78 million people who speak Korean around the world. [1] 한글 (the Korean alphabet) was invented by Sejong the Great in the 15th century.File Size: 903KB
Intermediate Korean: Read Less [-] KOREAN 10AX Intermediate Korean for Heritage Speakers 5 Units Terms offered: Fall 2019, Fall 2018, Fall 2017 This is an intermediate course for students whose Korean proficiency level is higher in speaking than in reading or writing due to Korean-herita
Tsu, Mie- , Japan Correspondence should be addressed to Susumu Saigusa; saigusa@wakabahsp.jp . NF can also occur in young, otherwise healthy patients with none of these predisposing factors [ , , ]. We report a case of necrotizing fasciitis a er . C.-H. Wong and Y.-S. Wang, e diagnosis of necrotizing
ARAMARK Dietetic Internship CHRISTUS Santa Rosa Hospital April 24, 2013 Case Report Nutritional Management of Necrotizing Pancreatitis . Necrotizing Pancreatitis
alcohol Coding –ICD-10-CM Index to Diseases Encephalopathy (acute) G93.40-due to--drugs --see also Table of Drugs and Chemicals G92-metabolic G93.41--drug induced G92--toxic G92-toxic G92--metabolic G92 Jamaican-neuropathy G92 Leukoencephalopathy -see also Encephalopathy
Delirium - Manifestation Encephalopathy - Underlying Cause Delirium -Acute change or fluctuation in mental status and inattention, accompanied by either disorganized thinking or an altered level of consciousness Encephalopathy -Global brain dysfunction resulting in an altered mental status Dr. Kennedy's opinion -If the .
The Korean language in historical perspective (6 credits) KORE3032. Directed readings in Korean Studies (6 credits) KORE3034. Korean Studies internship (6 credits) KORE3035. Korean Studies field trip (6 credits) KORE3036. Crime, passion, love: Korean popular culture before K-pop (6 credits) Fine Arts FINE2097. Arts of Korea (6 credits) FINE2098. History of Korean paintings (6 credits) Japanese .
