CME Lateralizing value of Todd’s palsyin patients with epilepsy

Christoph Kellinghaus, MD; and Prakash Kotagal, MD

Abstract—The authors retrospectively investigated the value of Todd’s palsy (TP) in lateralizing the hemisphere ofseizure onset in patients admitted for video-EEG monitoring in a tertiary epilepsy center. In 29 patients, a postictalhemiparesis was observed. TP always occurred contralateral to the epileptogenic hemisphere in 27 patients (93%). In theremaining two patients, the seizure onset could not be lateralized. In some patients, TP occurred after a seizure withoutfocal motor features or secondary generalization.

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It has been shown that information about the hemi-sphere of seizure onset in focal epilepsy can be reli-ably derived from careful analysis of the seizuresemiology. In combination with EEG data and imag-ing findings, semiology may allow the evaluation ofpossible resective surgery without the need of inva-sive monitoring, or it may help guide the placementof subdural or intracerebral electrodes. In a numberof ictal phenomena, the lateralizing value has beenassessed.1,2 Comparable studies regarding postictalphenomena, in particular Todd’s palsy (TP), arescarce.3 In two small studies of patients with refrac-tory focal epilepsy undergoing presurgical video-EEGmonitoring, the seizure onset was always contralat-eral to the observed postictal weakness.4,5 However,these studies were performed in highly selective pa-tient groups. Moreover, the occurrence of postictalweakness may have influenced the decision to oper-ate, thus preventing patients with ipsilateral seizureonset from inclusion into the study group.4 There-fore, the results are of limited value when the later-alization of the seizure onset has not yet beenestablished. In addition, it is not clear whether TPalso occurs in other epilepsies, besides focal epilepsy.We performed a retrospective analysis of all patients(regardless of the epilepsy classification) who haveundergone long-term video-EEG monitoring in a ter-tiary referral epilepsy center.

Methods. Medical records of approximately 4,500 consecutivepatients who underwent long-term (i.e., �24 hours) video-EEGmonitoring at the Cleveland Clinic between 1990 and 2002 andwho had undergone cranial MRI were screened for the documen-tation of transient lateralized postictal weakness during the eval-uation. The patient population consisted of approximately 75%with focal epilepsy, 5% with generalized epilepsy or multifocalepilepsy, and 20% with nonepileptic seizures. During the monitor-ing, scalp electrodes were placed according to the 10–20 Interna-tional System. The charts of the patients and, if possible, theiroriginal video, EEG, and imaging data were reviewed. The dura-

tion and distribution of the postictal lateralized weakness weredocumented. Seizure types were classified according to the semio-logic seizure classification.6 Lateralizing signs (focal motor sei-zure, focal somatosensory or lateralized visual aura, ictal speech,dystonic hand posturing, forced head version, postictal aphasia)were also documented. The side of the epileptogenic zone wasdetermined based on all available clinical, neurophysiologic, andimaging data. Data processing was performed using commercialsoftware (SPSS for Windows 11.0; SPSS, Chicago, IL).

Results. Lateralized postictal weakness was documentedduring video-EEG monitoring in 29 patients (table 1). Thelateralization of the epileptogenic zone was confirmed onthe basis of seizure freedom after epilepsy surgery in 6(20%) of the 29 patients. In 15 patients (52%), the epilepto-genic zone was determined by interictal/ictal EEG find-ings, seizure semiology, and a structural lesion on MRI. Infour patients (14%), the MRI was normal, but functionalimaging (fluorodeoxyglucose PET, ictal SPECT) showed anabnormality in concordance with EEG findings and seizuresemiology. In another two patients (7%) with normal MRIfindings, the lateralization of the epileptic zone was basedon EEG and seizure semiology alone. In the remaining twopatients (7%), the epileptogenic zone could not belateralized.

TP always occurred contralateral to the epileptogeniczone in 27 patients (93%) (table 2). In one patient (3.5%)with seizure onset in both hemispheres, the EEG onset ofthe seizure type resulting in postictal weakness was al-ways contralateral to the involved body side. In the re-maining patient (3.5%), the epileptogenic zone could not bedetermined.

In 20 (69%) of the patients, TP was confined to the armand face. In seven patients, it lasted �10 minutes, and�12 hours in only one patient.

The seizure preceding TP started with an aura in 15patients, 6 of whom had a somatosensory aura in the bodyparts involved in the TP (table 3). In 15 patients, TP waspreceded by a focal clonic or tonic seizure involving thebody part that became paretic. A bilateral asymmetrictonic seizure occurred in 10 patients, whereas a general-

From the Departments of Neurology, The Cleveland Clinic Foundation (Drs. Kellinghaus and Kotagal), Cleveland, OH; and University of Münster (Dr.Kellinghaus), Germany.Supported by Innovative Medizinische Forschung, University of Münster, Germany (KE 620201; C.K.).Received May 16, 2003. Accepted in final form September 17, 2003.Address correspondence and reprint requests to Dr. Christoph Kellinghaus, Department of Neurology, University of Munster, Albert-Schweitzer-Str. 33,48129 Munster, Germany; e-mail: kelling@uni-muenster.de

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ized tonic-clonic seizure occurred in 12 patients prior to aTP. An automotor seizure with dystonic hand posturingipsilateral to TP was observed in five patients. In five

patients, TP occurred after a complex motor seizure thatwas not preceded or followed by a simple motor seizure. Inone patient, TP was observed following a seizure withoutsignificant motor symptoms.

Discussion. In 29 of approximately 3,600 patients(0.8%) undergoing long-term video-EEG monitoringin a tertiary epilepsy center, lateralized postictalweakness could be documented during the evalua-tion. This incidence is comparable with the data ofanother study investigating TP in a heterogeneouspatient cohort.7 In contrast, TP was found in 22(14%) of 160 patients with refractory focal epilepsywhose seizure videotapes were systematically re-viewed for postictal symptoms.5 However, in ourstudy, the patients were identified by the descriptionof postictal weakness in their chart data. Therefore,patients with subtle signs of postictal weakness thatmay have been overlooked during the evaluationcould not have been identified in our study. In addi-tion, their patient group consisted only of patientswith refractory focal (predominantly temporal) epi-lepsy,5 whereas our patients were recruited from aheterogeneous group admitted for diagnostic evalua-tion of spells with recent onset as well as epilepsysurgery candidates. The only study prospectively an-alyzing the occurrence of TP in a mixed patient pop-ulation8 found an incidence of 6%. However, onlypatients presenting with generalized motor seizureswere included in this study. Therefore, as of yet,there are no valid data about the incidence of TP in arepresentative group of epilepsy patients.

Table 2 Lateralization of the epileptogenic zone

Epileptogenic zone determined byTP observed duringevaluation, n � 29

Seizure freedom �1 y after epilepsy surgery 6 (20)

EEG/semiology and structural imaging 15 (52)

EEG/semiology and functional imaging,structural imaging normal

4 (14)

EEG/semiology only 2 (7)

Could not be determined 2 (7)

Postictal weakness compared withhemisphere of epileptogenic zone

Always contralateral 27 (93)

Epileptogenic zone could not bedetermined or both hemispheresepileptogenic

2 (7)

Values are no. (%).

TP � Todd’s palsy.

Table 1 Characteristics of the patients

Variable

TP observed duringevaluation,

n � 29

Age at admission, y; median (range) 17 (2–59)

Duration of disease, y; median (range) 12 (0.3–52)

Gender, no. (%) female 9 (31)

Handedness, no. (%)

Right 27 (93)

Ambidextrous/unknown 2 (7)

Diagnosis, no. (%)

Focal epilepsy 29 (100)

Temporal lobe 4 (14)

Frontal lobe 10 (34)

Perirolandic area 5 (18)

Parietal lobe 4 (14)

Occipital lobe 1 (3)

Only lateralizable 3 (10)

Not lateralizable and not localizable 2 (7)

Etiology of epilepsy, no. (%)

Vascular 3 (10)

Neoplasm 0

Trauma 2 (7)

Inflammatory 4 (14)

Congenital malformation 7 (24)

Hippocampal sclerosis 0

Other 1 (3)

Unknown 12 (42)

TP � Todd’s palsy.

Table 3 Clinical features of the seizures preceding the postictalweakness

FeaturesTP observed duringevaluation, n � 29

Aura 15 (52)

Somatosensory aura 6 (21)

Simple motor activity (focal orgeneralized)

23 (79)

Focal clonic or tonic seizure 15 (52)

Bilateral asymmetric tonic seizure 10 (34)

Versive seizure 4 (14)

Generalized tonic or tonic-clonicseizure

12 (41)

Complex motor activity* 10 (34)

Without preceding or followingsimple motor activity

5 (17)

With dystonic posturing of one arm/hand

5 (17)

No motor seizure† 1 (3.5)

Percentages do not add up because more than one feature couldbe seen in a patient. Values are no. (%).* Including automotor and hypermotor seizures.† Loss of consciousness without motor features.

TP � Todd’s palsy.

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Theoretically, false lateralization of the epilepto-genic zone could have occurred in some of our pa-tients. However, most of the unsuccessful surgeriesin our series were among patients with epilepsy aris-ing from the posterior frontal lobe near the primarymotor cortex, precluding complete resection of thelesion. In some patients, the surgical or pathologicreport explicitly mentioned that not all anatomicallyor neurophysiologically abnormal tissue could be re-sected. This may explain the relatively low rate ofseizure freedom despite unequivocal determinationof the epileptogenic zone. Only two patients had noabnormalities on neuroimaging, but each had EEGand semiologic findings clearly indicating the hemi-sphere of seizure onset. Therefore, false lateraliza-tion of the epileptogenic zone is highly unlikely.

All 27 patients in whom the epileptogenic zonecould be lateralized to one hemisphere had TP in thecontralateral side of the body, regardless of the lobeof seizure onset. Two studies evaluating focal epi-lepsy had similar findings without any patients hav-ing TP on the side of the body ipsilateral to theepileptogenic zone.4,5 Other semiologic features, likeforced head deviation, dystonic limb posturing, andpostictal nose wiping, were found to lateralize cor-rectly in only 85 to 95% of cases.2 Therefore, TPseems to have a strong and consistent value withoutany reports of paradoxical lateralization in patientswith a clearly defined epileptogenic zone. Owing tothe obvious limitations of retrospective studies, ourdata should be confirmed by a prospective study,including a wide variety of different epilepsies.

Three-quarters of the patients had a seizure withtonic or clonic movements preceding TP, the majorityof which (at least in the beginning) were restricted tothe limb or side affected by TP. This underscores thecrucial role of the cortical motor centers in the gene-

sis of TP. However, in some patients, only bilateralmotor activity was seen, and one patient did nothave significant motor symptoms in the seizure pre-ceding TP. Other authors also have observed postic-tal weakness after sensory auras and in unaffectedlimbs.9 In those patients, epileptic activation of thecontralateral primary motor cortex alone may not bereaching the threshold of motor activity and still re-sult in TP. In addition, the epileptic activation ofsubcortical structures, in particular the basal gan-glia,10 may contribute to TP. However, definite ex-perimental or clinical evidence illuminating thepathophysiology of TP is still lacking.

AcknowledgmentThe authors thank Dr. Kevin Chapman for help in preparing themanuscript.

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