Lateralizing value of Todd’s palsy in 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 of seizure onset in patients admitted for video-EEG monitoring in a tertiary epilepsy center. In 29 patients, a postictal hemiparesis was observed. TP always occurred contralateral to the epileptogenic hemisphere in 27 patients (93%). In the remaining two patients, the seizure onset could not be lateralized. In some patients, TP occurred after a seizure without focal motor features or secondary generalization.
NEUROLOGY 2004;62:289 –291

It has been shown that information about the hemisphere of seizure onset in focal epilepsy can be reliably derived from careful analysis of the seizure semiology. In combination with EEG data and imaging findings, semiology may allow the evaluation of possible resective surgery without the need of invasive monitoring, or it may help guide the placement of subdural or intracerebral electrodes. In a number of ictal phenomena, the lateralizing value has been assessed.1,2 Comparable studies regarding postictal phenomena, in particular Todd’s palsy (TP), are scarce.3 In two small studies of patients with refractory focal epilepsy undergoing presurgical video-EEG monitoring, the seizure onset was always contralateral to the observed postictal weakness.4,5 However, these studies were performed in highly selective patient groups. Moreover, the occurrence of postictal weakness may have influenced the decision to operate, thus preventing patients with ipsilateral seizure onset from inclusion into the study group.4 Therefore, the results are of limited value when the lateralization of the seizure onset has not yet been established. In addition, it is not clear whether TP also occurs in other epilepsies, besides focal epilepsy. We performed a retrospective analysis of all patients (regardless of the epilepsy classification) who have undergone long-term video-EEG monitoring in a tertiary referral epilepsy center.
Methods. Medical records of approximately 4,500 consecutive patients who underwent long-term (i.e., 24 hours) video-EEG monitoring at the Cleveland Clinic between 1990 and 2002 and who had undergone cranial MRI were screened for the documentation of transient lateralized postictal weakness during the evaluation. The patient population consisted of approximately 75% with focal epilepsy, 5% with generalized epilepsy or multifocal epilepsy, and 20% with nonepileptic seizures. During the monitoring, scalp electrodes were placed according to the 10 –20 International System. The charts of the patients and, if possible, their original video, EEG, and imaging data were reviewed. The dura-

tion and distribution of the postictal lateralized weakness were documented. Seizure types were classified according to the semiologic seizure classification.6 Lateralizing signs (focal motor seizure, 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 was determined based on all available clinical, neurophysiologic, and imaging data. Data processing was performed using commercial software (SPSS for Windows 11.0; SPSS, Chicago, IL).

Results. Lateralized postictal weakness was documented during video-EEG monitoring in 29 patients (table 1). The lateralization of the epileptogenic zone was confirmed on the basis of seizure freedom after epilepsy surgery in 6 (20%) of the 29 patients. In 15 patients (52%), the epileptogenic zone was determined by interictal/ictal EEG findings, seizure semiology, and a structural lesion on MRI. In four patients (14%), the MRI was normal, but functional imaging (fluorodeoxyglucose PET, ictal SPECT) showed an abnormality in concordance with EEG findings and seizure semiology. In another two patients (7%) with normal MRI findings, the lateralization of the epileptic zone was based on EEG and seizure semiology alone. In the remaining two patients (7%), the epileptogenic zone could not be lateralized. TP always occurred contralateral to the epileptogenic zone in 27 patients (93%) (table 2). In one patient (3.5%) with seizure onset in both hemispheres, the EEG onset of the seizure type resulting in postictal weakness was always contralateral to the involved body side. In the remaining patient (3.5%), the epileptogenic zone could not be determined. In 20 (69%) of the patients, TP was confined to the arm and face. In seven patients, it lasted 10 minutes, and 12 hours in only one patient. The seizure preceding TP started with an aura in 15 patients, 6 of whom had a somatosensory aura in the body parts involved in the TP (table 3). In 15 patients, TP was preceded by a focal clonic or tonic seizure involving the body part that became paretic. A bilateral asymmetric tonic 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: ¨ Copyright © 2004 by AAN Enterprises, Inc. 289

Table 1 Characteristics of the patients TP observed during evaluation, n 29 17 (2–59) 12 (0.3–52) 9 (31)

Table 3 Clinical features of the seizures preceding the postictal weakness TP observed during evaluation, n 29 15 (52) 6 (21) 23 (79) 15 (52) 10 (34) 4 (14) 12 (41) 10 (34) 5 (17) 5 (17) 1 (3.5)

Variable Age at admission, y; median (range) Duration of disease, y; median (range) Gender, no. (%) female Handedness, no. (%) Right Ambidextrous/unknown Diagnosis, no. (%) Focal epilepsy Temporal lobe Frontal lobe Perirolandic area Parietal lobe Occipital lobe Only lateralizable Not lateralizable and not localizable Etiology of epilepsy, no. (%) Vascular Neoplasm Trauma Inflammatory Congenital malformation Hippocampal sclerosis Other Unknown TP Todd’s palsy.

Features Aura Somatosensory aura Simple motor activity (focal or generalized) Focal clonic or tonic seizure Bilateral asymmetric tonic seizure Versive seizure

27 (93) 2 (7)

29 (100) 4 (14) 10 (34) 5 (18) 4 (14) 1 (3) 3 (10) 2 (7)

Generalized tonic or tonic-clonic seizure Complex motor activity* Without preceding or following simple motor activity With dystonic posturing of one arm/ hand No motor seizure†

3 (10) 0 2 (7) 4 (14) 7 (24) 0 1 (3) 12 (42)

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

patients, TP occurred after a complex motor seizure that was not preceded or followed by a simple motor seizure. In one patient, TP was observed following a seizure without significant motor symptoms.

ized tonic-clonic seizure occurred in 12 patients prior to a TP. An automotor seizure with dystonic hand posturing ipsilateral to TP was observed in five patients. In five
Table 2 Lateralization of the epileptogenic zone TP observed during evaluation, n 29 6 (20) 15 (52) 4 (14) 2 (7) 2 (7)

Epileptogenic zone determined by Seizure freedom 1 y after epilepsy surgery

EEG/semiology and structural imaging EEG/semiology and functional imaging, structural imaging normal EEG/semiology only Could not be determined Postictal weakness compared with hemisphere of epileptogenic zone Always contralateral Epileptogenic zone could not be determined or both hemispheres epileptogenic Values are no. (%). TP

27 (93) 2 (7)

Todd’s palsy.
NEUROLOGY 62 January (2 of 2) 2004

Discussion. In 29 of approximately 3,600 patients (0.8%) undergoing long-term video-EEG monitoring in a tertiary epilepsy center, lateralized postictal weakness could be documented during the evaluation. This incidence is comparable with the data of another study investigating TP in a heterogeneous patient cohort.7 In contrast, TP was found in 22 (14%) of 160 patients with refractory focal epilepsy whose seizure videotapes were systematically reviewed for postictal symptoms.5 However, in our study, the patients were identified by the description of postictal weakness in their chart data. Therefore, patients with subtle signs of postictal weakness that may have been overlooked during the evaluation could not have been identified in our study. In addition, their patient group consisted only of patients with refractory focal (predominantly temporal) epilepsy,5 whereas our patients were recruited from a heterogeneous group admitted for diagnostic evaluation of spells with recent onset as well as epilepsy surgery candidates. The only study prospectively analyzing the occurrence of TP in a mixed patient population8 found an incidence of 6%. However, only patients presenting with generalized motor seizures were included in this study. Therefore, as of yet, there are no valid data about the incidence of TP in a representative group of epilepsy patients.

Theoretically, false lateralization of the epileptogenic zone could have occurred in some of our patients. However, most of the unsuccessful surgeries in our series were among patients with epilepsy arising from the posterior frontal lobe near the primary motor cortex, precluding complete resection of the lesion. In some patients, the surgical or pathologic report explicitly mentioned that not all anatomically or neurophysiologically abnormal tissue could be resected. This may explain the relatively low rate of seizure freedom despite unequivocal determination of the epileptogenic zone. Only two patients had no abnormalities on neuroimaging, but each had EEG and semiologic findings clearly indicating the hemisphere of seizure onset. Therefore, false lateralization of the epileptogenic zone is highly unlikely. All 27 patients in whom the epileptogenic zone could be lateralized to one hemisphere had TP in the contralateral side of the body, regardless of the lobe of seizure onset. Two studies evaluating focal epilepsy had similar findings without any patients having TP on the side of the body ipsilateral to the epileptogenic zone.4,5 Other semiologic features, like forced head deviation, dystonic limb posturing, and postictal nose wiping, were found to lateralize correctly in only 85 to 95% of cases.2 Therefore, TP seems to have a strong and consistent value without any reports of paradoxical lateralization in patients with a clearly defined epileptogenic zone. Owing to the obvious limitations of retrospective studies, our data should be confirmed by a prospective study, including a wide variety of different epilepsies. Three-quarters of the patients had a seizure with tonic or clonic movements preceding TP, the majority of which (at least in the beginning) were restricted to the limb or side affected by TP. This underscores the crucial role of the cortical motor centers in the gene-

sis of TP. However, in some patients, only bilateral motor activity was seen, and one patient did not have significant motor symptoms in the seizure preceding TP. Other authors also have observed postictal weakness after sensory auras and in unaffected limbs.9 In those patients, epileptic activation of the contralateral primary motor cortex alone may not be reaching the threshold of motor activity and still result in TP. In addition, the epileptic activation of subcortical structures, in particular the basal ganglia,10 may contribute to TP. However, definite experimental or clinical evidence illuminating the pathophysiology of TP is still lacking.
The authors thank Dr. Kevin Chapman for help in preparing the manuscript.

1. Bleasel A, Kotagal P, Kankirawatana P, Rybicki L. Lateralizing value and semiology of ictal limb posturing and version in temporal lobe and extratemporal epilepsy. Epilepsia 1997;38:168 –174. 2. Chee MW, Kotagal P, Van Ness PC, Gragg L, Murphy D, Lüders HO. Lateralizing signs in intractable partial epilepsy: blinded multipleobserver analysis. Neurology 1993;43:2519 –2525. 3. Leutmezer F, Baumgartner C. Postictal signs of lateralizing and localizing significance. Epileptic Disord 2002;4:43– 48. 4. Adam C, Adam C, Rouleau I, Saint-Hilaire JM. Postictal aphasia and paresis: a clinical and intracerebral EEG study. Can J Neurol Sci 2000; 27:49 –54. 5. Leutmezer F, Serles W, Pataraia E, et al. [The postictal state. A clinically oriented observation of patients with epilepsy]. Wien Klin Wochenschr 1998;110:401– 407. 6. Lüders H, Acharya J, Baumgartner C, et al. Semiological seizure classification. Epilepsia 1998;39:1006 –1013. 7. Urrestarazu E, Iriarte J, Alegre M, et al. [Postictal paralysis during video-EEG monitoring studies]. Rev Neurol 2002;35:404 – 407. 8. Rolak LA, Rutecki P, Ashizawa T, Harati Y. Clinical features of Todd’s post-epileptic paralysis. J Neurol Neurosurg Psychiatry 1992;55:63– 64. 9. Efron R. Post-epileptic paralysis: theoretical critique and report of a case. Brain 1961;84:381–396. 10. Rektor I, Kuba R, Brazdil M. Interictal and ictal EEG activity in the basal ganglia: an SEEG study in patients with temporal lobe epilepsy. Epilepsia 2002;43:253–262.

January (2 of 2) 2004



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