89Copyrights © 2013 The Korean Society of Radiology

INTRODUCTION

Postictal neurologic deficit is a well-known complication of focal or generalized seizures mimicking clinical manifestation of a stroke; however, it can be misdiagnosed as a stroke (1-3). Thus, in an acute setting, imaging studies are the most useful means for making the correct diagnosis (3). To our knowledge, there were a few reports of cortical hyperperfusion during postictal motor deficit in the literature. We report a patient who was pre-sented with postictal right hemiparesis accompanied by perfu-sion and diffusion abnormalities in the left parietal cortical ar-eas. Our case suggests that Todd’s paralysis may reveal transient perfusion and diffusion abnormalities; this report can be helpful for making an accurate diagnosis in patients with acute neuro-logic deficits.

CASE REPORT

A 72-year-old male was presented with sudden-onset right

extremity weakness after clonic seizure. He had a history of na-sopharyngeal cancer and his overall health condition was poor. He was alert and was able to follow commands. At initial neuro-logic examination, motor grade was III in the extremity of the right limb.

He underwent brain CT angiography (CTA), perfusion CT and magnetic resonance (MR) imaging including diffusion-weighted image (DWI) immediately after admission. On MR imaging (3T system, Achieva; Philips Medical Systems, Best, the Netherlands), an axial DWI showed subtle cortical hyperintensi-ty in the left parietal lobe with restricted diffusion on an appar-ent diffusion coefficient (ADC) map (Fig. 1A, B). However, no abnormal finding was observed on other MR sequences. A per-fusion CT (Somatom Definition AS+, Siemens Medical Solu-tions, Forchheim, Germany) demonstrated a dramatic increase in cerebral blood flow (CBF) and cerebral blood volume (CBV) involving mainly the cortical areas of the left parietal lobe with sparing white matter. Mean transition time (MTT), a sensitive indicator of acute cerebral ischemia, was relatively symmetric in

Case ReportpISSN 1738-2637 / eISSN 2288-2928J Korean Soc Radiol 2013;69(2):89-92http://dx.doi.org/10.3348/jksr.2013.69.2.89

Received March 18, 2013; Accepted June 14, 2013Corresponding author: Hye Jin Baek, MDDepartment of Radiology, Inje University College of Medicine, Haeundae Paik Hospital, 875 Haeundae-ro, Haeundae-gu, Busan 612-896, Korea.Tel. 82-51-797-0364 Fax. 82-51-797-0379E-mail: sartre81@gmail.com

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0) which permits unrestricted non-commercial use, distri-bution, and reproduction in any medium, provided the original work is properly cited.

Postictal neurologic deficit is a well-known complication mimicking the manifesta-tion of a stroke. We present a case of a patient with clinical evidence of Todd’s pa-ralysis correlating with reversible postictal parenchymal changes on perfusion CT and magnetic resonance (MR) imaging. In this case, perfusion CT and MR imaging were helpful in the differential diagnosis of stroke-mimicking conditions.

Index termsPostictalTodd’s ParalysisPerfusion CT, MR

Regional Cortical Hyperperfusion on Perfusion CT during Postictal Motor Deficit: A Case Report 발작 후 운동 결손 환자에서 관찰된 관류 영상에서의 국소적 피질 과다관류: 증례 보고 Hye Jin Baek, MDDepartment of Radiology, Haeundae Paik Hospital, Inje University College of Medicine, Busan, Korea

Regional Cortical Hyperperfusion on Perfusion CT during Postictal Motor Deficit

90 jksronline.orgJ Korean Soc Radiol 2013;69(2):89-92

further neuroimaging was performed.

DISCUSSION

It is estimated that between 5 to 30% of cases identified as “brain attacks” are, in fact, due to stroke-mimicking conditions (3, 4). Stroke mimics include diagnosis such as complex mi-graine, infectious condition, metabolic disorder, intracranial tu-mor, epilepsy, Todd’s paralysis and psychiatric illness, such as conversion disorder (3, 4). Despite the fact that Todd’s paralysis is a well-known entity for postictal motor deficit, the physiologic explanation for it has not been established yet (2). Many mecha-nisms may account for the postictal state, including neurotrans-mitter depletion, neuronal desensitization, altered local cerebral blood flow and various forms of active inhibition, for which the utility of various imaging modalities have been investigated in

configuration (Fig. 1C-E). CTA source images demonstrated slightly abundant vessels in the corresponding region with nor-mal-appearing major intracranial arteries (Fig. 1F, G). Such findings suggested that acute neurologic deficit in this patient was unlikely to have been secondary to a vascular occlusive event. An electroencephalography was performed on the next day, and it demonstrated a diffuse left-hemispheric dysfunction without a definite epileptiform discharge.

However, a follow-up MR imaging on the same day revealed the disappearance of the preexisting diffusion abnormality (Fig. 1H). In addition, perfusion CT demonstrated normalization of CBF and CBV in the left parietal lobe (Fig. 1I, J).

The patient had no further seizures, and symptoms of the right hemiparesis gradually improved from grade III to IV over the next several days. Then, he was transferred to the medical department in order to treat acute gangrenous cholecystitis; no

Fig. 1. A 72-year-old male with acute onset aphasia and right extremity weakness. A. Axial DWI shows subtle cortical hyperintensity in the left parietal lobe. B. ADC reveals mild diffusion restriction. C-E. Perfusion CT images demonstrate increased CBF (C) and CBV (D) in the left parietal cortices, but relatively normal configuration of MTT (E). F, G. Axial CTA source images demonstrates mild increased vascular pattern. H. Follow-up DWI on the next day shows no diffusion abnormality. I, J. Follow-up perfusion CT at one week shows complete normalization of the preexisting hyperperfusion on CBF (I) and CBV (J) maps.Note.-ADC = apparent diffusion coefficient, CBF = cerebral blood flow, CBV = cerebral blood volume, CTA = CT angiography, DWI = diffusion-weighted image, MTT = mean transition time

F

A

G

B

H

C

I

D

J

E

Regional Cortical Hyperperfusion on Perfusion CT during Postictal Motor Deficit Hye Jin Baek

91jksronline.org J Korean Soc Radiol 2013;69(2):89-92

REFERENCES

1.DavisDP,RobertsonT, ImbesiSG.Diffusion-weighted

magneticresonanceimagingversuscomputedtomogra-

phy inthediagnosisofacute ischemicstroke.JEmerg

Med2006;31:269-277

2.MathewsMS,SmithWS,WintermarkM,DillonWP,Binder

DK.LocalcorticalhypoperfusionimagedwithCTperfusion

duringpostictalTodd’sparesis.Neuroradiology2008;50:

397-401

3.MastersonK,VargasMI,DelavelleJ.Postictaldeficitmim-

ickingstroke:roleofperfusionCT.JNeuroradiol2009;36:

48-51

4.HemmenTM,MeyerBC,McCleanTL,LydenPD.Identifica-

tionofnonischemicstrokemimicsamong411codestrokes

attheUniversityofCalifornia,SanDiego,StrokeCenter.J

StrokeCerebrovascDis2008;17:23-25

5.WeinandME,CarterLP,el-SaadanyWF,SioutosPJ,Labiner

DM,OommenKJ.Cerebralbloodflowandtemporallobe

epileptogenicity.JNeurosurg1997;86:226-232

6.MoritaniT,SmokerWR,SatoY,NumaguchiY,Westesson

PL.Diffusion-weightedimagingofacuteexcitotoxicbrain

injury.AJNRAmJNeuroradiol2005;26:216-228

7.WarachS,LevinJM,SchomerDL,HolmanBL,EdelmanRR.

HyperperfusionofictalseizurefocusdemonstratedbyMR

perfusionimaging.AJNRAmJNeuroradiol1994;15:965-968

8.ChanS,ChinSS,KarthaK,NordliDR,GoodmanRR,Pedley

TA,etal.Reversiblesignalabnormalitiesinthehippocam-

pusandneocortexafterprolongedseizures.AJNRAmJ

Neuroradiol1996;17:1725-1731

9.WiestR,vonBredowF,SchindlerK,SchaubleB,Slotboom

J,BrekenfeldC,etal.Detectionofregionalbloodperfu-

sionchangesinepilepticseizureswithdynamicbrainper-

fusionCT--apilotstudy.EpilepsyRes2006;72:102-110

10.SzaboK,PoepelA,Pohlmann-EdenB,HirschJ,BackT,

SedlaczekO,etal.Diffusion-weightedandperfusionMRI

demonstratesparenchymalchanges incomplexpartial

statusepilepticus.Brain2005;128(Pt6):1369-1376

the previous studies (2, 3, 5-8). However, the results of the previ-ous studies regarding postictal perfusion findings are still con-troversial. Recently, Mathews et al. (2) demonstrated postictal regional hypoperfusion on perfusion CT caused by postictal ex-haustion or inhibition, whereas Masterson et al. (3) reported re-gional hyperperfusion with postictal neurologic deficit due to the spread of a residual ictal discharge.

In this case, our patient’s clinical and neuroimaging findings were consistent with those of the postictal state. We observed re-gional cortical hyperperfusion showing an increase in CBF and CBV with a relative preservation of MTT on the perfusion CT. According to previous studies, it is generally accepted that an in-crease in CBF and CBV is found in the seizure-onset zone as well as in the cortical areas affected by the spread of ictal discharges during the course of seizure, and the presence of a cortical hy-perperfusion can be a valid indicator of ongoing seizure activity (3, 7, 9, 10). Further, there was increased vascularity in the cor-responding region similar to the previous study with MR angi-ography (10). In addition, subtle cortical hyperintensity with lower ADC value on DWI showing normalization in the follow-up can be explained as a reversible excitotoxic brain injury me-diated by prolonged seizure activity. The neuronal seizure activi-ty increases the release of glutamate from the presynaptic terminals of neuronal axons, and excessive glutamate crosses the synaptic cleft in order to bind to the N-methyl-D-aspartate (NMDA) and non-NMDA receptors. This mechanism causes cytotoxic edema in neurons and adjacent glial cells, leading to apoptosis or selective neuronal necrosis. In this process, astro-cytic response to excessive glutamate release plays an important role in tissue repair by dampening its excitotoxic effects. There-fore, cytotoxic edema in the acute phase of reactive astrocytosis is presumed to be responsible for reversible signal intensity ab-normalities (6, 8).

In summary, our case provides a temporal and spatial correla-tion of regional cortical hyperperfusion in patients with postic-tal motor deficits. The transient nature of this clinical deficit cor-relates with the reversibility of cortical perfusion and diffusion abnormalities, and such findings can be helpful in diagnosing stroke-mimicking conditions.

Regional Cortical Hyperperfusion on Perfusion CT during Postictal Motor Deficit

92 jksronline.orgJ Korean Soc Radiol 2013;69(2):89-92

발작 후 운동 결손 환자에서 관찰된 관류 영상에서의 국소적 피질 과다관류: 증례 보고

백혜진

발작 후 신경학적 결손은 뇌졸중으로 오인할 수 있는 잘 알려진 합병증이다. 저자는 토드씨 마비의 임상적 근거를 가진 환

자에서 발견된 관류 컴퓨터단층촬영과 뇌 자기공명영상상의 발작 후 뇌실질의 변화가 경과 관찰 중 가역적인 변화를 보인

증례를 경험하였다. 본 증례를 통해 저자는 관류 컴퓨터단층촬영과 뇌 자기공명영상이 뇌졸중과 유사한 임상질환을 감별

하는 데 도움이 될 수 있음을 보고하고자 한다.

인제대학교 의과대학 해운대백병원 영상의학과