Journal of Neurology, Neurosurgery, and Psychiatry 1992;55:63-64

SHORT REPORT

Clinical features of Todd's post-epileptic paralysis

Loren A Rolak, Paul Rutecki, Tetsuo Ashizawa, Yadollah Harati

AbstractTwo hundred and twenty nine patientswith generalised tonic-clonic seizureswere prospectively evaluated. Fourteenwere identified who had transient focalneurological deficits thought to be Todd'spost-epileptic paralysis (PEP). Eight ofthese 14 patients had underlying focalbrain lesions associated with the postictaldeficits. All patients with PEP were weak,but there was wide variation in the pat-tern (any combination of face, arm, leg),severity (plegia to mild), tone (spastic,flaccid, or normal), and reflexes(increased, decreased, or normal). Sig-nificant sensory loss occurred in only onepatient. The only other signs ofPEP wereaphasia (in five patients all with under-lying lesions) and gaze palsy (in fourpatients). Post-epileptic paralysis persis-ted from halfan hour to 36 hours (mean of15 hours). Post-epileptic paralysis mayoccur with the first seizure or after manyyears of seizures and does not appearafter every seizure. The clinical featuresofPEP are thus heterogeneous.

Houston VeteransAffairs Medical Centerand Baylor College ofMedicine, Houston,Texas, USAL A RolakP RuteckiT AshizawaY Harati

Correspondence to:Dr Rolak, Department ofNeurology, Baylor College ofMedicine, 6501 Fannin,NB302, Houston, Texas77030, USA

Received 18 February 1991.Accepted 2 May 1991

Bravais in 1827 first noted that paralysis mayfollow a unilateral seizure, a condition hetermed hemiplegia epileptique.' Todd used thesame term (epileptic hemiplegia), apparentlyarrived at independently, in his 1854 descrip-tion.2 He noted that paralysis may occur ononly one side even when both sides had beenconvulsed and that in contrast to the spasticityexpected from a central nervous system lesion,the limbs were flaccid. By 1890, HughlingsJackson had extended these observations anddescribed post-epileptic aphasia, sensory loss,stupor, and mania.3 Since then post-epilepticparalysis (PEP) has become a well acceptedsyndrome, and numerous post-epileptic symp-toms have been reported, including hemia-nopsia,4 complete blindness,5 weakness,&-Iunilateral pupillary dilatation,"2 aphasia,'3bulimia,'4 and prolonged confusion.'5 Thesedescriptions, however, are all in the form ofcase reports, and there has never been a pros-pective, systematic analysis ofPEP to describeits fundamental clinical features, such asincidence, physical findings, duration, and rela-tion to underlying pathology. Focal findings areespecially vexing after generalised (as opposedto partial) seizures because there is often nostructural (focal) brain lesion to account forthem. We studied the clinical characteristics ofPEP after generalised tonic-clonic seizures.

Patients and methodsWe prospectively evaluated all patients admit-ted to one hospital during a one year periodwith generalised tonic-clonic seizures, definedas the sudden onset of bilateral symmetrical;tonic and clonic convulsive activity with loss ofconsciousness. Some patients could have had avery brief unwitnessed focal onset to theirseizure (partial seizure with secondary general-isation), but every effort was made to exclude allpatients with any focality in the beginning orsubsequent course of their seizure. All patientshad a thorough neurological exam-inationimmediately after the seizure and at about twohour intervals until all neurological deficitsreturned to baseline. All patients also had brainimaging with contrast CT scanning or MRI,EEG, and other appropriate diagnostic tests.

ResultsTwo hundred and twenty nine patients (allmen, mean age 46 years) presented with gen-eralised tonic-clonic seizures, of whom 14(mean age 47 years) had transient focal post-ictal deficits (PEP). Their clinical features aresummarised in the table. Eight of the 14patients with PEP had an underlying structurallesion, which in each case was a pre-existingischaemic stroke in the hemisphere con-tralateral to the paralysis. All strokes were inthe middle cerebral artery territory, affectingthe frontal or temporal lobe. Only 51 ofthe 215patients without PEP had structural lesions (X2769, p < 0-01). Altogether, 69 of the 229 hadstructural lesions and eight had PEP. Allpatients with PEP had weakness, but it variedfrom very mild paresis to complete plegia. Theweakness involved any combination of face orarm or leg. The tone could be flaccid, normal, orspastic, and the reflexes decreased, normal, orincreased. Very miniimal sensory deficitsoccurred in eight patients but only one com-plained of noticeable numbness. Five patients,all with pre-existing left hemisphere strokes,developeui aphasia, which was fluent in one andnon-fluent in four. The only other neurologicaldeficit seen in PEP was gaze palsy, in fourpatients.

Post-epileptic paralysis persisted from halfan hour to 36 hours, with a mean of 15 hours.The nature, duration, and severity ofPEP wereunrelated to the duration or severity of theseizures, the presence or absence of underlyinglesions, or any changes on the EEG. Weaknessalways persisted longer than other symptoms.Post-epileptic paralysis occurred sporadically

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Rolak, Rutecki, Ashizawa, Harati

Table Clinicalfeatures ofpatients with post-epileptic paralysis (PEP)Weakness

Age Duration of Cause of Duration ofPatient (years) epilepsy (years) seizures EEG Severity Pattern Tone Reflexes Extensor plantar Other signs PEP (hours)

1 50 10 Alcohol NL 0/5 F, A, L l Yes Gaze palsy 8withdrawal

2 28 1st seizure Idiopathic NL 4+/5 A NL NL No None 363 25 15 Idiopathic NL 4/5 A, L NL T No Numbness 44 31 1 Idiopathic NL 4/5 F, A, L NL NL No None 245 36 3 Idiopathic NL 4+/5 A, L NL T No None 246 28 5 Idiopathic NL 3/5 A, L I I No None 187 51 1st seizure Stroke Focal 4/5 A, L t t No Gaze palsy 6

theta8 54 1st seizure Stroke Focal 0/5 A, L l No Gaze palsy + 12

spikes aphasia+ delta

9 48 1 Stroke Focal 4+ /5 A NL NL No Aphasia 24spikes+ delta

10 61 10 Stroke NL 4/5 F, A T t No Aphasia 3611 63 8 Stroke Focal 4/5 L NL NL No Aphasia 8

theta12 70 6 Stroke Focal 0/5 F, A, L 1 No Gaze palsy 6

spikes+ delta

13 47 8 Stroke Focal 4/5 A, L NL NL No None 0 5spikes+ theta

14 66 24 Stroke NL 4/5 A, L t T Yes Aphasia 8F = face, A = arm, L = leg, t = increased, I = decreased, NL = normal.

and did not follow every seizure. Some patientshad suffered recurrent seizures for years beforetheir first episode of PEP, and most had sub-sequent seizures without associated PEP.There was no apparent reason why someseizures resulted in PEP and others did not. Sixpatients with PEP had a baseline abnormalEEG (see table), which in each case showed aslow wave (theta or delta) focus in the con-tralateral frontal or temporal lobe, correspond-ing to an underlying ischaemic stroke. Four ofthe tracings also had epileptiform spike activityaccompanying the focal slowing. Only onepatient (number 2, with idiopathic seizures)had an EEG recorded during his PEP, and itshowed no abnormality.

DiscussionTransient focal neurological deficits after anepileptic seizure are often called Todd'sparalysis in recognition of their description bythe British neurologist Robert Todd.2 Sincethen, research has focused primarily on possi-ble mechanisms of post-epileptic paralysis,"6but its clinical features have never been sys-tematically studied, and there is almost noinformation about the nature, duration, oraetiology of the deficits that occur after aseizure. Our conclusions about PEP are limitedby the population studied (adult male veterans)and the restriction to generalised tonic-clonicseizures without ictal focality. In this group,PEP was a heterogeneous syndrome encompas-sing a variety of neurological signs includingaphasia, gaze palsy, weakness, and (rarely)numbness. The motor deficits were highlyvariable, from mild to severe, flaccid to spastic,focal to hemiparetic. Abnormalities neverpersisted beyond 36 hours. Most patients withPEP had an underlying structural lesion but,interestingly, in many (43%) no cause was

found. The aetiology ofPEP is not clear. It maybe due to neuronal exhaustion from hypoxia orsubstrate depletion because a localised regionof the brain is already damaged or is moreseverely affected by the seizure, or because someunderlying condition, such as vascular disease,predisposes to insufficient metabolism.6 Alter-natively, it may result from inhibitory neuronaldischarges,7 arterial venous shunting,8 9 orrelease of endogenous inhibitory (possiblyopioid) substances."6 Our study, though notintended to address the aetiology of PEP,demonstrates its great clinical diversity andthus suggests that it may have multiple causes.

1 Bravais LF. Recherches sur les symptomes et le traitement del'epilepsie hemiplegique. Paris: Faculte de Medecine deParis, 1827.

2 Todd RB. Clinical lectures on paralysis, certain diseases of thebrain, and other affections of the nervous system. London:John Churchill, 1854;284-307.

3 Jackson JH. The Lumleian lectures on convulsive seizures.Br Med J 1890;1:821-7.

4 Salmon JH. Transient postictal hemianopsia. Arch Ophthal-mol 1968;79:523-5.

5 Kosnik E, Paulson GW, Laguna JF. Postictal blindness.Neurology 1976;26:248-50.

6 Meyer JS, Portnoy HD. Post-epileptic paralysis. A clinicaland experimental study. Brain 1959;82:162-85.

7 Efron R. Post-epileptic paralysis: Theoretical critique andreport of a case. Brain 1961;84:381-94.

8 Yarnell PR, Burdick D, Sanders B, Stears J. Focal seizures,early veins, and increased flow. Neurology 1974;24:512-6.

9 Yarnell PR. Todd's paralysis: a cerebrovascularphenomenon? Stroke 1975;6:301-3.

10 Collier HW, Engelking K. Todd's paralysis following aninterscalene block. Anesthesiol 1984;61:342-3.

11 Youkey JR, Clagett GP, Jaffin JH, et al. Focal motor seizurescomplicating carotid endarterectomy. Arch Surg 1984;119:1080-4.

12 Gadoth N, Margalith D, Bechar M. Unilateral pupillarydilitation during focal seizures. JNeurol 1981;225:227-30.

13 Koemer M, Laxer KD. Ictal speech, postictal languagedysfunction, and seizure lateralization. Neurology 1988;38:634-6.

14 Remick RA, Jones MW, Campos PE. Postictal bulimia. JClin Psychiatry 1980;41:256.

15 Biton V, Gates JR, Sussman LD. Prolonged postictalencephalopathy. Neurology 1990;40:963-6.

16 Tortella FC, Long JB. Endogenous anticonvulsant sub-stance in rat cerebrospinal fluid after a generalized seizure.Science 1985;228:1 106-8.

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paralysis.Clinical features of Todd's post-epileptic

L A Rolak, P Rutecki, T Ashizawa and Y Harati

doi: 10.1136/jnnp.55.1.631992 55: 63-64 J Neurol Neurosurg Psychiatry

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