J Nucl Med 1998 Chiu 1711 3 Hipoglikemi

7/23/2019 J Nucl Med 1998 Chiu 1711 3 Hipoglikemi

http://slidepdf.com/reader/full/j-nucl-med-1998-chiu-1711-3-hipoglikemi 1/4

1998;39:1711-1713.J Nucl Med.

Nan-Tsing Chiu, Chao-Ching Huang, Ying-Chao Chang, Chyi-Her Lin, Wei-Jen Yao and Chin-Yin Yu EncephalopathyTechnetium-99m-HMPAO Brain SPECT in Neonates with Hypoglycemic

http://jnm.snmjournals.org/content/39/10/1711This article and updated information are available at:

http://jnm.snmjournals.org/site/subscriptions/online.xhtmlInformation about subscriptions to JNM can be found at:

http://jnm.snmjournals.org/site/misc/permission.xhtmlInformation about reproducing figures, tables, or other portions of this article can be found online at:

(Print ISSN: 0161-5505, Online ISSN: 2159-662X)1850 Samuel Morse Drive, Reston, VA 20190.SNMMI | Society of Nuclear Medicine and Molecular Imaging

is published monthly.The Journal of Nuclear Medicine

© Copyright 1998 SNMMI; all rights reserved.

by Indonesia: J of Nuclear Medicine Sponsored on July 1, 2014. For personal use only. jnm.snmjournals.orgDownloaded from by Indonesia: J of Nuclear Medicine Sponsored on July 1, 2014. For personal use only. jnm.snmjournals.orgDownloaded from

http://jnm.snmjournals.org/content/39/10/1711



http://jnm.snmjournals.org/site/subscriptions/online.xhtml


http://jnm.snmjournals.org/site/misc/permission.xhtml


http://jnm.snmjournals.org/











HMPAOSPECT

Patient n o. F/C P/C 0/COutcomeDelay Epilepsy

TABLE I

HMPAO SPECT RatiosandO utcomesinThree Neonateswith

Hypoglycemic Encephalopa thy

Regio na l b ra in in ju ry in t hr ee n eona te s w ith hypog ly cem ic e nc eph

alo pathy are p resen ted usin g serial @ â€˜T c-h ex am eth yIropylene

am in e oxime HMPAO SPECT and , f or c ompar is on , MRI.Du rin g t h e

a cu te s ta ge , b oth 99@Tc -HMPAOSPECT and MRI r ev ea l a bnorma l

itie s in th e p oste rio r c ere brum . T ec hn etium -9 9m -HMPAO SPECT

rev eals fu rthe r are as o f in su lt, fo r e xam ple th e fro ntal lob es. T he

degree of hypoperfusion correlates w ith the clinical severity of

h ypog ly cem ia dur in g th e n eona ta l p eri od a nd s ub se qu en t n eu ro lo g

ic al s eq ue la e. F ollow-u p w ith HMPAO SPECT s ev era l mo nth s a fte r

in su lt d emons tr ate s p ers is te nt h ypop er fu sio n in s ome a re as , ma in ly

in th e o cc ip ita l a nd p os te rio r p arie ta l re gio ns . MRI c an d ep ic t

morpho lo gic al c ha ng es w ith s up er io r r es olu tio n. Be ca us e mo rpho

logical change general ly fo llows slowly af ter funct ional change,MR I

is l es s s en sit iv e th an HMPAO SPECT in d ete ct in g a nd p re dic tin g th e

extent of hypoglycem ic cerebral injury during the acute phase.

H MP AO S PE CT d urin g t he a cu te s ta ge is a v alu ab le to ol fo r

e valuatin g th e ex ten t an d sev erity o f b rain in ju ry in n eo nates w ith

hypoglycemic encephalopa thy .

K ey W ords: hypoglycem ia; neonate; seizure; H MPA O SPEC T

J N ucl M ed 998; 39 I7 â€” 7 3

Neonatalypoglycemiasacommonisorder1,2)ndan

cause perm anent neurological sequelae 3 . The prognosis of

n eo natal h yp og ly cem ia is p oor if n eu rolog ical sy mp to ms, esp e

cially seizures, occur 2,3 . B ecause the topography and sever

ity of cerebral injuries determ ine subsequent neurological

sequelae 4 , im aging studies m ay provide useful inform ation.

However, to our knowledge there is only one case report

presenting C T and M R im ages of a neonate w ith hypoglycem ic

encephalopathy 5 , and no brain SPECT imaging has been

re po rte d. W e re po rt o n se ria l 9 9mTc@ h ex ameth yl p ro py le ne am

m e oxim e H M PA O brain SPEC T im aging of three neonates

w ith hypoglycem ic encephalopathy and different degrees of

neurol og ic a l s equel ae .

CASE REPORTS

A ll th ree n eo nates w ere full term an d ap prop riate fo r g estatio n

a ge fo r th eir b irth w eig hts . T he p re gn an cie s w ere n ormal, d eliv ery

c ou rse w as smo oth a nd Apg ar s co re s w ere n ormal. T he ir m eta bo lic

s tu die s, in clu din g s erum a nd u rin e, fo r fa tty a cid a nd c arb oh yd ra te

m etabolism s w ere w ithin norm al lim its. N one of them had recur

r en t a tta ck s o f h ypog ly cem ia a fte r t he n eona ta l p er io d. A ll p atie nts

u nd erw en t 9 9m TcH M pA O S PE CT an d M R I d urin g th e acu te sta ge

and follow-up. HMPAO SPECT during the acute stage was

qua ntit ativ ely a na ly ze d u si ng c ir cu la r r eg io ns o f in te re st manu ally

placed on frontal, parietal, occipital and cerebellar areas on the

med io s ag it ta l s li ce , and f ron ta l- to -c er ebe ll um, pa ri et al -t o- ce rebel

lum a nd o cc ip ita l-to -c ere be llum ra tio s w ere c alc ula te d T ab le 1 .

Rec ei ve d Aug. 5 , 1 997; r ev is io n a cc ep te d J an . 1 4, 1 998.

For correspondence or reprin ts contact C hao-C hing H uang, M D, D epartm ent of

P ed iatric s, N atio n@ C hen g K un g U nn ier sfty H os pital, 1 38 S he ng L i R d., T ain an 7 04 28 ,

Taiwan.

1 0.53 0.58 0.51 Severe

2 0.60 0.75 0.96 M ild

3 0.47 0.56 0.59 Severe

F /C = f ron taL /cer ebe ll um; /C = pa ri et aVce rebel lum;0 /C = occi pi ta l/

cerebellum.

P a ti en t 1

A 15-day-old m ale neonate, birth w eight 3,700 g, had several

ep isod es o f tachy pn ea an d cy an osis o ne n ig ht befo re ad missio n.

A fter adm ission, m echanical ventilation w as used because of

frequent generalized tonic clonic seizures, hypotonia, poor re

sponse and pulm onary hem orrhage. B lood glucose level w as 20

mg /d l a nd normaliz ed a fte r in tr av enou s h ig h- do se g lu co se in fu sio n.

A t age 18 days, M RI revealed edem atous change and m ass effect

o ver th e b ilateral parie to -o ccipital a rea F ig . lA . T ech ne tiu m

99m -H MPA O 1 1 1 M Bq SPEC T perform ed 1 w k later dem on

s tra te d h yp op erfu sio n o f th e b ila te ra l c ere bra l h em isp he re s, e sp e

cia lly in th e p osterio r cereb ral areas. T he fron tal areas also w ere

in volve d F ig . lB . A t a ge 5 m o, M R I reve aled en ceph alom alacia

th at w as mo re p romin en t o ve r th e b ila te ra l p arie to -o cc ip ita l lo be s

a nd d if fu se c er eb ra l a tr op hy F ig . IC . T ec hn et ium-99m-HMPAO

SPECT demonst ra ted pe rs is ten t hypoper fu si on i n b il at er al occi pi ta l

and posterior parietal areas and cerebral atrophy Fig. 1D . T he

p atie nt h ad fre qu en t my oc lo nic se iz ure s, m ark ed d ev elo pmen ta l

d elay an d m icro cep haly b elo w th e third p ercen tile at a ge 1 y r 3

mo.

Patient 2

A female neonate, birth weight 3,200 g, had focal clonic

seizu res, p oor activ ity an d leth arg y a t a ge 4 d ay s. B lo od gluco se

level w as 24 m g/dl. S eizures and hypoglycem ia w ere corrected

soo n after in trav en ous g lu co se in fu sio n. H ow ev er, at ag e 5 0 day s,

fo ca l my oc lo nic s eiz ure s d ev elo pe d. T he p atie nt w as tra ns fe rre d to

o ur h osp ital and M R I sh ow ed an ab no rm ality in th e w hite m atte r o f

th e b ila te ra l p os te rio r p arie ta l lo be s F ig . 2A . T ec hn etium-9 9m -

HMPAO I I I MBq SPECT was performed 15 mm after an

ep iso de o f seiz ures F ig . 2B , w hich o ccu rred 4 d ay s after th e M R I

study. R elatively low er cerebral perfusion w as observed in the

fro ntal p arietal areas. In ad dition , a h ype rp erfu sed are a th at w as

considered to be an epileptogenic focus w as noted at the right

o cc ip it al l ob e. S eiz ur es we re c on tr olle d by phe noba rb it al th era py .

Follow -up M RI at age 5 m o revealed a decrease in the extent of

b ila teral p arietal lesio ns F ig . 2 C . T ech ne tiu m-99 m-H M PA O

SPECT a t th is tim e d emo nstra te d m ild white matte r h yp op erfu sio n

that ex ten ded ou tsid e th e p arietal area F ig . 2 D . A t ag e 1 5 m o , th e

p ati en t h ad r el ativ e m i cr oc epha ly 3 rd t o te nth p er ce ntile a nd mi ld

deve lopmen ta l de lay .

+

+

+

H MPA O SP EC T IN N E ON AT ALH YP OG LY CE MIA€¢hiu et al. 1711

Technetium 99m HM PAO Brain SPECT in

N eonates w ith H ypoglycem ic E ncephalopathy

N an-Tsing Chiu, C hao-C hing H uang, Y ing-Chao Chang, Chyi-H er Lin, W ei-Jen Y ao and Chin-Y in Y u

D ep artm en ts o fN uc le ar M ed ic in e P ed ia tr ic s a nd R ad io lo gy Na tio na l C he ng K un g U niv er sity H os pita l T ain an a nd

D e pa rtm e nt o fP ed ia tr ic s C h an g G u ng M e m or ia l H o sp ita l K a oh siu ng Ta iw a n

by Indonesia: J of Nuclear Medicine Sponsored on July 1, 2014. For personal use only. jnm.snmjournals.orgDownloaded from






/

/

â€ ˜ I

/

,

,

0

w@F :

F IGURE1 . Pa t ie n t1. A In i t ia lT2-we igh t edx ia lMRim ag er eve a l shy pe r

intense regionover bilateralparieto-occipitallobes arrows . B Transverse

@Tc-HMPAOSPECT image demonstrates relat ive hypoperfusion in bi lat

eral frontal areas arrowheads and pronounced hypoperfusionin bilateral

occipital and posterior parietal areas arrows . C Follow-upT2-weighted M R

imageshows encephalomalacia arrows withcerebralatrophy. D Techne

tium-99m-HM PAOSPECT imagedemonstratespersistenthypoperlusionin

bilateraloccipitaland posteriorpanetalareas and cerebralatrophy arrows .

Patient 3

A 2960-g male neonate was healthy until 70 hr of age when

cyanosis and seizures developed. The patient was hypotonic, with

poor response and low blood glucose level I0 mg/dl on admis

sion. The patient was treated with a high-dose glucose infusion

followed by hydrocortisone for persistent hypoglycemia and in

tractable clonic seizures. Technetium-99m-HM PAO 1 11 MBq

SPECT at age 2 wk revealed very low perfusion over frontal,

B @

C

,

a

/

FIGURE3. Patient3. A Initial @Tc-HM PA0PECTimagerevealsmarked

hypoperfusionin t@lateralrontal,parletaland occipitalareas arrows . B

T2-weightedaxialM Rimageshows localizedhigh-signal-intensityesionin

right parieto-occipitallobe with loss of normal gray matter arrow . C

Follow-up @T c-HM PA0PECTimagedemonstratesdecreased perfusion

in bilateralpaneto-occipitalregions, especially on rightside arrows . D

T2-weighted axial M R image reveals persistence of right patieto-occipital

lesion arrow accompanied by returnof normalgraymatter in immediately

adjacent areas.

panetal and occipi tal areas Fig. 3A . MRI Fig. 3B performed at

age 1 mo demonstrated an abnormality in the right parieto-occipital

area. Follow-up 99mT cH M pA O SPECT at age 2 mo showed

persistent cerebral hypoperfusion in bilateral parieto-occipital re

gions, especial ly on the right side Fig. 3C . MRI demonstrated

persistence of the right parieto-occipi tal l esion Fig. 3D . The

patient had microcephaly below the third percentile , recurrent

seizures and marked developmental delay at age 8 mo.

DISCUSSION

The human brain consumes glucose as its primary energy

substrate. Severe hypoglycemia can cause cerebral dysfunction

or even neuronal death 6 . A lthough the ini ti al physiological

response to hypoglycemia is increased cerebral blood f low to

compensate for insufficient glucose 7 , delayed hypoperfusion

has been observed after moderate and severe hypoglycemia 8 .

The occurrence of hypoperfusion is important because it is

related to brain injury 9,10 . Therefore, del ineating the degree

and extent of hypoperfusion is crucial. Technetium-99m-

HMPAO brain SPECT is particularly good at detecting perfu

sion changes, and it was used in this study to assess the effects

of hypoperfusion. Using 99mTc@HMPAO brain SPECT to ob

serve cerebral blood f low changes in neonates with hypoglyce

mic encephalopathy, we observed that this technique may

provide valuable information in patient examination.

Previous studies have shown that cerebral perfusion

progresses from the central part of the brain to the cerebel lum,

sensorimotor and then visual cortex of the cerebrum during

maturation in the neonatal period. Cerebral perfusion in the

frontal lobes can be relatively low in neonates and young

infants up to 1â€”2yr of age 11, 12 . T hus, it is important to

recognize cerebral perfusion patterns in the developing brain

and compare them with normal patterns. M easuring the cortical

@ i A

.@

,

D -@

:L@k@

FiGURE2. P a t i en t . A In i t ia l 2 -we igh t e dx i a lMR im ag es ho w sab no rma l

highsignal intensity arrows in whitematter of bilateralparietal lobes. B

Technetium-99m-HM PAOSPECT image revealsrelativehypoperfusionin

frontal and parietal areas arrowheads .Hyperperlusedarea in the right

occipitalarea arrows is seen also. C Follow-upT2-weightedMR image

shows partialresolutionof panetal lesions arrows . D T echnetium-99m-

HM PAOSPECT imagerevealsmildwhitematterhypoperfusion arrows .

1 71 2 T HE JO UR NA LFN UC LE ARM E DIC IN E€¢o l. 3 9 â €¢o . 1 0 â €¢ cto ber 19 98

A

. ,







rati o of H M PA O SPECT duri ng the acute stage by D enays

method 13 ), abnormal cerebral perf usi ons w ere seen i n al l

three pati ents. T he cerebral corti cal regi ons i n Pati ent 3 and

par ietal and occi pi tal ar eas i n Pati ent 1 had obv i ous abnorm al l y

l ow perf usi on, al though onl y rel ati vel y l ow perf usi on w as seen

i n the f rontal area i n Pati ent 1. Pati ent 2 had rel ati vel y l ow

perf usion i n the f rontal and parietal areas, w hereas the hi gh

perf usi on i n the occi pi tal area w as thought to be caused by a

sei zure. T heref ore, the m ani f estati ons of cerebral perf usi on

pat ter ns i n these thr ee pati ents r ef l ect the ef f ects and sev er ity of

hy pogl ycem ia that are not attri butabl e to norm al age-rel ated

patterns.

O ur three pati ents show ed that the degr ee of hy poper fusi on

determi ned by 99mT cH M pA O SPECT at an earl y stage cone

l ated w i th the degree of encephal opathy caused by acute

hy pogl ycemi a and w ith the severi ty of subsequent sequel ae.

D uri ng the acute stage, Pati ents I and 3 had more severe

symptoms and si gns, i ncl udi ng l ow er bl ood gl ucose l evel ,

cy anosi s and i ntr actabl e sei zur es, t han Pati ent 2. Sei zures and

hy pox em ia are associ ated w ith poor outcom es 2,3, 14, 1 5). W e

f ound that Pati ents 1 and 3 had more pronounced cerebral

hy poperf usi on than di d Pati ent 2 and, at f ol low -up, Pati ents 1

and 3 had m ore sev ere neurol ogi cal sequel ae than Pati ent 2. I n

addi ti on, the m ark edl y decreased cerebral perf usi on show n by

99mT cH M pA O SPECT duri ng the acute stage of i nj ury pre

di cted t he per si stence of hy poper fusi on at f ol l ow -up.

C onsi der ing the topogr aphy of br ai n i nj ur y, t he v ul ner abi l it y

of the poster ior cer ebrum to hy pogl y cem ia i n neonates has been

i ndi cated previ ousl y by M RI and pathol ogy 5,16). A l though

normal i nf ants have hi gher regi onal cerebral bl ood f l ow i n the

occi pi tal regi ons 1 7), other f actors, i ncl udi ng ef f ici ency of

cerebral gl ucose usage, m etabol ic requi rem ents and i nf lux of

gl ucose, al so contri bute to v ul nerabi li ty to hy pogl ycem ia 18).

U si ng 99mT c-H M PA O SPECT , w e observed that the areas

i nvol ved i n hypogl ycemi c brai n i nj ury are i n the posteri or

cerebrum and i n other cerebral regi ons, such as the f rontal

l obes. W e bel iev e that the di ff erence betw een thi s stud@ and

previ ous observati ons i s due to the hi gh sensi ti vi ty of mT c

H M PA O SPECT . I n thi s study, w hi ch i ncl uded M RI observa

ti ons f or comparati ve purposes, duri ng the earl y states of

hypogl ycemi a, M RI coul d demonstrate l esi ons onl y i n the

po st er i or cer ebr um , w her eas 9 9m T c@ H M PA O SPE CT i nd icat ed

addi ti onal si tes of dam age. T hi s 99m Tc@H M PA O SPECT f ind

i ng i s of cl i ni cal si gni fi cance. For ex am pl e, i n Pati ent 1, duri ng

the acute stage, 99mT cH M pA O SPECT show ed di ff use hy po

perfusi on of bi l ateral cerebral hemi spheres, w hereas M RI re

v eal ed onl y an abnorm al ity i n the posteri or cerebrum . Sev eral

m onths l ater, how ev er, di ff use cerebral atrophy w as seen w i th

M R I .

T hi s study cl earl y demonstrated that M RI w as not as sensi

ti ve as O9mT cH M pA O SPECT i n detecti ng the extent and

sev eri ty of hy pogl ycemi c i nj ury duri ng the neonatal peri od.

D uri ng the earl y stage of hypogl ycemi a, al though H M PA O

SPECT show ed di ff use bi lateral i nv ol vement of the cerebral

hemi spheres, M RI coul d show onl y sev erel y damaged areas,

namel y the occi pi tal and posteri or pari etal areas. A reas of

addi ti onal i nv ol vem ent coul d be depi cted by M R I onl y sev eral

m onths l ater , af ter m or phol ogi cal changes had occur red.

CONCLUSION

A lthough f urther studi es are needed, the f i ndi ngs f rom

study i ng these three pati ents suggest that cer ebr al hy poper fu

si on m ay be rel ated cl osel y to hy pogl ycem ic encephal opathy i n

neonates and that 99m Tc@H M PA O brai n SPECT i s a v al uabl e

tool i n the detecti on of these cerebral i nsul ts duri ng the acute

phase. T echneti um-99m-H M PA O brai n SPECT proved to be

m or e sensi ti v e t han M R I i n del i neat ing af f ected ar eas dur ing the

neonatal peri od. T he ex tent and sev eri ty of cerebral hy poper

f usi on demonstrated by 99mT cH M pA O brai n SPECT corre

l ated w el l w i th subsequent neurol ogi cal outcom e. Fi nal l y, thi s

l imi ted study agrees w ith prev ious studi es i ndi cati ng that the

occi pi tal and posteri or par iet al regi ons seem m or e v ul ner abl e t o

hy pogl ycem ic i nj ury than other brai n structures i n neonates.

H ow ev er, thi s study i ndi cates that hy pogl ycemi c i nj ury may

occur at addi ti onal si tes, f or ex ampl e, the f rontal l obes. I t w as

observ ed that hypoperf usi on may persi st many months af ter

onset and i s undetectabl e w ith M R I. T heref ore, w e suggest that

99mT cH M pA O brai n SPECT be consi dered duri ng the ev al u

ati on of hypogl ycemi c neonates, especi al ly duri ng the acute

phase.

A C K N O W L E D G M E N T S

Suppor ted i n par t by gr ants f rom the N ati onal Sci ence C ounsel

N SC: 81-04l 2-B 006-28 and 87-22l 8-E006-064 N U), T ai wan.

R E F E R E N C E S

I . S olom on T Felix J M Sa m uel M C t a l. H yp og lycem ia in p ed ia tr ic a dm ission s in

M o za m b iq u e. L a n ce t I 9 94 ;3 43 : 1 49 â € ” 15 0.

2 . K o i v i st o M . B l an co SM , K r au se U . N eo nat al sy m pt om at i c an d asy m pt om at i c h y po

g ly ca em ia : a fo llo w- up s tu d y o f I 5 1 ch ild r en . D ev M e d C h ild N eu r al 1 97 2.1 4: 60 3â €”

614.

3 . H aw o rt h JC , M c R ae K N . T h e n eu ro l og i cal an d d ev el o pm en tal ef f ec ts o f n eo nat al

h yp og ly cem ia : a f ollo w- up o f 2 2 ca se s. C a n M e d A ss oc J 1 96 5: 92 :8 61 â€ ”8 65 .

4 . C h ug an i H T M u lle r R A C h ug an i D C . F u nct io na l b r a in r eo rg an iz at io n in ch ild r en .

Br a i nDe v l 9 9 6; 1 8 : 3 4 7 â€ ” 3 56

5 S p a r JA L e w in e J D O m s o n W W J r N e o na ta l h y po g l yc e m ia :C T a n d M R f in d in g s

AJ NR 9 9 4 : 5 : 4 7 7 â € ” 4 7 8

6. Auer RN. Hypoglycemic brain damage. Stroke 1986: 17: 488â€”496.

7. Pryds0. Greisen G, Fri is-Hansen B. Compensat ory increaseof CBF in pret erm inf ant s

during hypoglycaemia. Acta Paediatr Scand 1988:77:632â€”637.

8 . A b du l-R a hm a n A A ga r dh C D S ies jo B K . L oc al c er e br a l b lo od flo w in t he r a t d u r in g

sev er e hy pogl ycem ia, and i n t he r ecov er y per iod f ol low ing gl ucose i nj ect ion. A ct a

Ph v si o lSc a nd l 9 8 ; 1 9 : 3 7 â €” 3 I 4

9 . A g ar dh C D , K a l i mo H , O l sso n Y . Si esj o B K . H y p og l yc em i c b r ai n i n j ur y . I . M e t ab ol i c

a n d l ig h t m i cr o sc op ic f in d in g s i n r a t c er e b r al c or t ex d u r in g p r o fo u nd i ns u li n- in d u ce d

hy pogl ycem ia and i n t he r ecov er y per iod f ol low i ng gl ucose adm ini st rat ion. A ct a

Ne ur opa t ho lI 9 8 ; 5 : 3â € ” 4 1

1 0. K alim o H . A ga r dh C D O lsson Y S iesj o B K . H yp oglycem ic b ra in in j u ry. I I .

E l ec t r on - m ic r o sc op i c f in d i n gs i n r a t c er e b r a l c or t i ca l n e u r on s d u r i n g p r o f ou n d i n su l in

in d uc ed h yp og ly cem ia a nd in t he r ec ov er y p er io d fo llo win g g lu co se a d min is tr a tio n.

A d a N e ur o pa th ol I 9 8 : 5 : 43 â €” 52

I I . H a d da d J C o ns ta nt in es co A B r un ot B M es ser J . C er eb r al p er fu sio n s tu d ies d u rin g

m at ur at i on u si n g si n gl e p ho to n em i ssi o n c om p ut ed t om og rap hy i n t he n eo nat al p er i od .

Bi o l Ne o na t e I 9 9 4 ; 6 5 : 2 8 1 â €” 2 8 6

1 2. C hi ro n C , R ay nau d C , M az ier e B , C t al . C han ges i n r eg io nal c er eb ral b lo od f l ow d ur in g

b rai n m at ur at io n i n c hi l dr en an d ad ol escen ts. J N uc I M ed l 99 2; 33 :6 96 â€ ” 70 3.

1 3. D en ays R . H am H T on deu r M Piep sz A N oel P . D et ect ion of b ila t er al a n d

s ym m e tr i ca l a n om a li es i n t ec hn e ti um - 99 m -H M P A O b r a in S P E C T s tu d ie s. J N u cl M e d

I992;33:4 85â€”49

14. VolpeJJ. Hypoglycemiaand brain injury. I n: VolpeJJ, ed. Nt urologi of t he newborn,

3 r d e d. P h ila d el ph ia : W B S a un d er s : 1 99 5: 46 7â €” 48 9.

I 5 . H im w ich H E Ber n st ein A O H er lic h H . e t a l. M e ch a nis ms f or t he m a in te na n ce o f lif e

i n t he n ew bo rn d ur in g an ox i a. A m J Ph vsi ol 1 94 2; l3 5: 38 7.

1 6. A n d er s on J M M i ln er R D G S tr i ch S . E f fe ct s o fn eo n at a l h y po gly ce m ia o n t h e n er v ou s

s ys te m : a p a t ho lo gi c s tu d y. J N eu r a l N eu r o su r g P s t c h ia t r t l 96 7; 30 :2 95 â€ ”31 0.

I 7. Y ou nk in D D elivo ria -P ap ad op ou los M . R eivich M . J a ggi J O b rist W . R egion al

variationsin humannewborncerebralbloodf low. J Pediatr 1988:112:104â€” 10

18. L aM anna JC H ar ik SI . Regi onal com par isons of br ai n gl ucose i nf lux . B rai n Res

I985;326:299â€”305.

H M PA O SPECT I N N EON A TA LH Y POGL Y CEM I A€¢hi u et al . 1713





J Nucl Med 1998 Chiu 1711 3 Hipoglikemi

Documents

Transcript of J Nucl Med 1998 Chiu 1711 3 Hipoglikemi