Journal of Neurology, Neurosurgery, and Psychiatry 1985;48:866-869

Appearing and disappearing CT scan abnormalitiesand seizuresPK SETHI, BR KUMAR, VS MADAN, V MOHAN

From the Neurological Centre, Army Hospital, Delhi, India

SUMMARtY A group of patients presenting with seizures (focal or generalised) and abnormal CTscans who, on follow up, showed complete resolution of the CT scan changes, without any

treatment other than anticonvulsants, are described.

Seizures may be due to idiopathic epilepsy or besymptomatic of an underlying disorder which maybe revealed by computed tomography (CT). Poss-ible scan abnormalities include: congenital disorder(birth injury and infarction), trauma, tumour, infec-tion (abscess, encephalitis, tuberculosis, toxoplas-mosis, cysticercosis), vascular disease and degenera-tive disorders.' These CT abnormalities areexpected to persist, increase or leave some evidenceof the original lesion in follow up scans unless somespecific treatment is given in treatable cases. Wereport patients presenting with seizures in whichinitial CT scans were abnormal, but on follow up CTscans these abnormalities had disappeared with nospecific treatment except anticonvulsants.

Materials and methods

Eleven cases, seen in the epilepsy clinic of our neurologicalcentre in the past year had initial CT scan abnormalitiesthat completely disappeared over the next 6 to 24 weekswith no treatment except anticonvulsants.

Case reports

The table summarises the clinical data from eleven cases.In the following three cases the sequence of events sur-rounding the seizure and the follow up are described.

Case 1A 14-year-old boy, product of term delivery with a historysuggestive of slight hypoxia at birth, was well till the morn-ing of 26 June 1983, when he had clonic movements of theright toes with JacksQnian extension on the right side, later

Address for reprint requests: Lt Col PK Sethi VSM, Army Hospi-tal, Delhi Cantt 110010, India.

Received 25 September 1984 and in revised form 14 December1984.

Accepted 24 December 1984

Fig 1 Enhanced Scans. (a) There is a small area oJincreased attenuation value in left parietal parasagittalregion with significant perifocal oedema. (b) Follow up CTshowed complete disappearance of the lesion.becoming generalised with loss of consciousness. On 10August, he had three similar episodes of focal seizuresstarting on the right side but with no generalisation or lossof consciousness. On 26 August he had another suchepisode following which he had weakness of right foot.There was a partial right foot drop, and the right knee jerkwas brisk. Fundi were normal. Blood count, urinalysis,skull, chest and thigh radiographs, blood chemistry andawake EEG were all normal. CT scan on 26 August 1983showed a small area of increased attenuation value in theleft perasagittal region with significant perifocal oedema(fig la). He was given phenobarbitone 30 mgm morningand 60 mgm at night. The weakness of the right foot andleg completely disappeared over the next two weeks and heremained seizure free. A repeat CT scan on 1 February1984 was normal (fig lb).

Case 2A 41/2 year-old boy, a product of a normal term deliverywas well till the evening of 7 September 1983 when he hadclonic motor seizures involving the left arm. He had six orseven seizures in one hour and developed mild postictalweakness of the left arm. Temperature was 99-8°F andfundi were normal. Blood count, urinalysis, blood chemis-try, skull radiography and CSF examination were normal.

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Appearing and disappearing CT scan abnormalities and seizures

able Summary ofclinical findingwe No Age (yr) Sex Clinical presentation EEG CT scan abnormality Follow up

14 M Rt Jacksonian seizures starting from NAD Small attenuation left parasagittal Asymptomatic(Rt) toe, postictal Rt foot drop. region with perifocal oedema. CT abnormalityFirst seizure 26 June 83. Last (CT 26 Aug 83). clearedseizure 26 Aug 83 at time (01 Feb 84).of CT scan.

4½/2 M Repeated Lt focal motor seizures Generalised burst Low attenuation lesion Lt fronto- Asymptomatic CTPostictal Lt side weakness. First of spike/slow parietal region. (CT 14 Sept 83). clearedseizure 7 Sept 83. discharges. (12 Feb 84).

K. 34 F Generalised seizures with headache Slowing Lt sided High attenuating lesion with perifocal Asymptomatic CTand vomiting prolonged postictal leads monopolar oedema in (Lt) post-temporal abnormalityconfusion and (Rt) hand weakness. run with spikes. region. (CT 28 Oct 83). clearedFirst seizure 16 Oct 83, repeat (27 Apr 84).18 Oct 83.

I.* 14 F Rt focal seizures with speech arrest Generalised burst Decrease attenuation in left parietal Asymptomatic CTand later generalisation. Birth of spike/slow region. (CT 6 Aug 83). repeatedhistory prolonged labour, hypoxia wave discharges. 17 Oct 83. Noat birth. First seizure 3 Aug 83. abnormality.

i. 33 F Lt Focal motor seizures 6 episodes, Brief episodes of Small high attenuation lesion with Asymptomatic.no postictal weakness. First generalised perifocal oedema. Left temporal Repeated CTseizure 11 Sept 83, later five bursts of slow region. (CT 17 Dec 83). (3 Mar 84)more. Last episode 27 Nov 83. waves 4-5 Hz. clear.

i. 30 M Focal seizure in form of speech Left temporal High attenuating lesion with perifocal Asymptomatic.difficulties with turning of head lobe epilepto- oedema left temporal region CT clearneck to right. Solitary seizure genic activity. (CT 22 July 83). (27 Sep 83).09 July 83.

7. 50 M Generalised tonic/clonic convulsions Left fronto- Low attenuation in post temporal Asymptomatic CT3 episode in one month. First temporal region. (CT 31 Jan 83). clearseizure 11 Dec 82 and last dysrhythmia. (18 Mar 83).14 Jan 83.

3. 6 F Focal motor seizure starting from Normal EEG. Right parietal high attenuated Asymptomatic.Lt hand with generalisation 3 shadow surrounded with low Repeat CTepisode 25 Mar 83 and last attenuation area. (CT 25 Apr 83). clear25 Apr 83. (23 June 83).).*39 M Two transient episodes fecling left Normal EEG/ Decrease attenuation Rt parietal Asymptomatichand larger followed by episode angiogram region (CT 19 Mar 83). Repeat CTof blankness. First episode 5 Mar 83 normal. clearand last 6 Mar 83. (3 May 83).

)t 58 M Episode of vacant look followed by Rt fronto- Decrease attenuation lesion in right Asymptomaticgeneralised with head and neck parietal slowing frontal region with ring like Repeat CTturning to left-2 episodes. All with enhancement. (CT 22 Jan 83). 9 Mar, 22 Mar,episodes on 18 Jan 83. dysrhythmia. 6 Apr 83.

Gradedclearance.

11 M Episode starting Lt hand clonic Not done. Increased area of attenuation Asymptomatic.convulsion; later generalised surrounded by low attenuation. Repeat CTtonic/clonic convulsions 5 to 6. (CT 31 Jan 84). clear.Postictal Lt arm weakness l/2 hr (30 Apr 84).temp 99°F. First epidose 22 Jan 84and last 24 Jan 84.

_SF done -NAD[ndividual declined admission but had follow up scans in an another hospital. Repeat Ct scan 16 Apr 83. Complete clearance.

EEG showed generalised bursts of spike/slow wave dis-charges bilaterally. CT scan on 14 September 1983 showeda low attenuation lesion in the right fronto-parietal region.The child was given phenobarbitone 30 mgm twice a dayand has remained asymptomatic. A repeat CT scan after20 weeks showed complete disappearance of the earlierCT findings (fig 2 ab).Case 3A 34-year-old female presented with generalised seizureson 16 October 1983 with postictal prolonged confusionand postictal weakness of the right hand which recoveredin the next four hours. She had another generalised seizureon 18 October 1983 with postictal prolonged confusionand vomiting. She continued to have left sided headacheand projectile vomiting. Examination was normal exceptthat she looked apprehensive, depressed and had repeated

yawning. Fundi were normal. A diagnosis of late onsetseizures with Todd's paresis on the right side was made andan intracranial space occupying lesion was suspected. Shewas put on phenobarbitone 30 mgm morning and 60 mgmat night. Blood count, urinalysis, skull thigh and chestradiographs were normal. EEG showed slowing in the leftsided leads (monopolar run) with occasional spikes. CTscan showed a high attenuation lesion with perifocaloedema in the left posterior temporal region. Herheadache and vomiting subsided in a week and she becameasymptomatic. In view of vomiting and headache, anintracranial space occupying lesion was strongly suspectedand she was given steroids initially for a week. She becameasymptomatic and repeat scan eight weeks later showedgradual clearance of the lesion, so it was decided to followthe patient with repeat CT scans. CT scan 24 weeks latershowed complete clearance of the lesion (fig 3 ab).

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Fig 2 (a) Showing low attenuating lesion in right parietalregion. (b) Showing complete disappearance of this lesionon follow up CT.

._ _

Fig 3 Enhanced Scans. (a) High attenuating lesion withperifocal oedema in left post-temporal region laterallyplaced. (b) Repeat scan showing complete clearance oflesion.

Fig 4 (Case No 11) Enhanced Scans. (a) Disc area ofincreased attenuation surrounded by low attenuation area inright parietal region. (b) Shows complete disappearance ofthis lesion in follow up scans.

Discussion

Over one year we encountered 11 cases with CTabnormalities (both low attenuation and mixed)

Sethi, Kumar, Madan, Mohanafter seizures, which subsequently disappeared.What are the clinico-CT scan correlates of theseattenuations, what is their pathology and what doestheir disappearance imply?

It is their disappearance without any specifictherapy (except anticonvulsants) which is intriguing.It can be concluded that whatever the underlyingpathology or pathophysiological -changes respons-ible for the appearance of these lesions, the processis ultimately reversible. Therefore, congenital disor-ders, tumours, and degenarative disease are unlikelycauses. Trauma also can be excluded as there was nohistory of head injury. The clinical setting andresults of investigations and follow up also stronglyargue against trauma, vascular diseases and infec-tion.

Several studies2` are available dealing with CTscans in patients with various type of seizures. Gas-taut and Gastaut,2 reported findings of CT in 401 of500 consecutive patients with epilepsy. 90% hadnormal CT and were classed under primary general-ised epilepsy, while the rest had abnormal CT scansso were classed as secondary epilepsy. With organiclesions, (tumour, trauma, ischaemia and infection,etc.) CT was considered to have markedly increasedthe ability to establish the aetiology. In anotherseries,7 150 patients with seizure disorder wereanalysed in detail. Of these 60 patients had abnor-mal scans. These abnormalities included atrophy(focal 13, diffuse 20), porencephaly (4), hyd-rocephalus (5), vascular abnormalities (6), infarct(6), and neoplasm (6). In these series2 8 not a singlecase of seizures with disappearing CT scan attenua-tion was reported.

Theoretically some of the cases of the presentseries may be due to infarction or rupture of a smallangioma. Gastaut et a19 emphasised that Jacksonianseizures may herald Sylvian infarctions, as revealedby computed tomography. Out of a population of942 adult epileptics examined with CT they foundSylvian infarction in 17 patients without any priorhistory of cerebrovascular accident. In most of thesecases vascular occlusion was confirmed by carotidangiography. In the majority, however, there waspost-ictal neurological abnormality for hours or daysand in one third of the cases there was persistence ofneurological deficit and/or Jacksonian seizures. Innone of our cases except one with focal deficit pres-ent, and this subsequently disappeared. Further, inall Gastaut's cases there was CT scan evidence oflow attenuation in areas corresponding with Sylvianinfarction. In the present series the involved areawas not necessarily Sylvian and in some cases therewas increased as well as low attenuation. Further,the complete disappearance of the CT abnormalitiesin our patients differs from the CT scan changes due

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Appearing and disappearing CT scan abnormalities and seizures

to infarction, which would persist and do not disap-pear totally.The possibility of cryptic malformation must be

considered.'0 These are commonly present withintracranial haemorrhage which was not present inour cases. Further, although CT scan may not revealthese cryptic vascular malformations (micro-angioma), the resultant haematoma points out to theunderlying pathology.The disappearance of CT scan attenuations with-

out any specific therapy excludes most forms ofinfective pathology. Cysticercosis or tuberculoma asa cause of seizures is not so uncommon in this geo-graphical region, but neither is likely to be the causeof the CT scan abnormalities discussed here,because the latter disappeared without specifictherapy. Bhargava and Tandon," studied in CNStuberculosis in 55 cases and described a specialgroup of 17 cases. This group of 17 patients, mostlychildren and young adults, presented with focalseizures with or without generalisation or associatedpostictal deficit but without evidence of raisedintracranial pressure. On CT scan they had smalldisc or ring lesions. Antituberculous treatmentappeared to clear the lesion on the CT scanpromptly.

In view of the above discussion one wonderswhether the responsible pathological lesion may notbe structural but functional. Seizures may producecerebral oedema. Meera, Goulatia and Bhargava'2in CT analysis of 525 patients reported 20 cases ofseizures of late onset with or without papilloedemabut with no focal neurological deficit, which werereported to have diffuse white matter oedema vary-ing in absorption values from 5-15 HU and withsmall midline ventricles. Focal low attenuation areasseen in CT scan in our cases corresponded very wellwith the focal seizures and may be explained bypostictal oedema akin to postictal EEG slowing.Their disappearance after appropriate anti-convulsant therapy with control of seizure may alsosupport this hypothesis of postictal oedema. Buthow does one explain high attenuating lesion sur-rounded by low attenuated area in some of thesecases? Moreover, we have encountered patients pre-senting with a status epilepticus with CT scans whichare normal. Several reports2-7 have not describedany CT scan changes in seizures per se.

Accordingly, the changes we have described maynot simply be the result of focal seizures. Prior to CTscanning, such focal seizures might be attributed tomissed tuberculoma or cysticercosis, which couldhave escaped detection using cerebral angiographyor pneumoencephalography. The CT scan findings,

and the subsequent recovery, do not suggest suchdiagnoses. Alternatively, the changes describedcould be a form of focal encephalitis, perhapspeculiar to this region.

In conclusion, if a patient presents with seizuresand the sort of CT scan findings discussed here,without signs of raised intracranial pressure or CTscan evidence of mass effect, it appears wise to waitand repeat the CT scan instead of starting prolongedantituberculous therapy or subjecting him to inva-sive procedures and surgery.

We are grateful to Maj Gen JM Grover, AVSM, theCommandant, Army Hospital, for constant encour-agement and the Director General, Armed ForcesMedical Services for permission to publish thisarticle.

References

'Valentine AR, Pullicino P, Bannan E. A Practical Intro-duction to Cranial CT. London: William Heinemann.Medical Booke Ltd, 1981:137.

2 Gastaut H, Gastaut JL. Computerized transverse axialtomography in epilepsy. Epilepsia 1976; 17:325-36.

3Bauor G, Mayr U, Pallua A. Computerized axial tomo-graphy in chronic partial epilepsies. Epilepsia 1980;21:227-33.

4Bordanoff BM, Stafford CR, Green L, et al. Computer-ized transaxial tomography in the evaluation ofpatient with focal epilepsy. Neurology (Minneap)1975;25: 1013-7.

5 Gall MV, Becker H, Hacker H. Computerized trans-verse axial tomography in epilepsy. Epilepsia1976; 17:340-1.

6 Scollo-Lavizzari G, Eichhom K, Wuthrich R. Computer-ized transverse axial tomography in the diagnosis ofepilepsy. Eur Neurol 1977; 15:5-8.

7McGahan JP, Dublin AB, Hill RP. The evaluation ofseizure disorders by computerized tomography. JNeurosurg 1979;50:328-32.

8 Russo LS, Goldstein KH. The diagnostic assessment ofsingle seizures. Arch Neurol 1983;40:744-6.

9 Gastaut H, Boudouresques G, Gastaut JL, et al. Jackso-nian epileptic seizures as inaugural manifestations ofsylvian infarction revealed by computerized axialtomography. In: du Boulay GH, Moseley IF, eds. TheFirst European Seminar on Computerized AxialTomography in clinical practice. New York:Springer-Verlag, 1977:237-242.

'° Prakash B, Beohar PC, Misra RC. Low flow (cryptic)arteriovenous malformation and spontaneoushaematoma. Acta Neurochir (Wein) 1983; 69:61-67.

"Bhargava S, Tandon PN. CNS Tuberculosis-Lessonslearnt from CT studies. Neurology India1980;28:207-12.

12 Meera RI, Goulatia RK, Bhargava S. CT anaylsis of first525 patients. Neurology India 1980; 17:86-94.

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doi: 10.1136/jnnp.48.9.866 1985 48: 866-869J Neurol Neurosurg Psychiatry

 P K Sethi, B R Kumar, V S Madan, et al. seizures.scan abnormalities and Appearing and disappearing CT

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