Epilepsia, 33(6): 1101-1 105, 1992 Raven Press, Ltd., New York
0 International League Against Epilepsy
Bilateral Todd’s Paralysis After Focal Seizures Donna C. Bergen, Lea Rayman, and *Peter Heydemann Departments of Neurological Sciences and *Pediatrics, Rush Medical College, Chicago, Illinois, U.S.A.
Summary: Transient postictal hemiparesis or monoparesis is not uncommon after partial (focal) seizures. We report 2 patients who complained of severe bilateral limb weakness after generalized tonic-clonic seizures (GTCS) beginning focally. Bilateral Todd’s paralysis was verified
and documented in both patients. EEG and clinical evidence indicate the supplementary motor cortex as the most likely source of the seizures in both cases. Key Words: Seizures-Epilepsy-Weakness-Paralysis.
Transient, focal neurologic deficits after focal seizures are common. Aphasia, visual loss, and somatosensory deficits may occur after seizures arising in or near Broca’s area, visual cortex, and primary sensory cortex, respectively (Ajmone-Marsan and Ralston, 1957; Efron, 1961). One of the most obvious postictal symptoms is unilateral muscle weakness, known as Todd’s paralysis (Todd, 1854). Although originally observed as a hemiparesis, both monoparesis and/or facial weakness may also occur (Ajmone-Marsan and Ralston, 1957). We recently witnessed and recorded bilateral Todd’s paralysis in 2 young women with epilepsy and report the details.
right temporal and right posterofrontal areas. An interictal EEG showed spikes at and just to the right of the vertex, as well as independent right midtemporal spikes (Fig. 1). Patient 2, a 9-year-old girl, had onset at age 6 years of seizures consisting of tonic posturing of the right hand with mild clonic movements, without postictal symptoms or signs. A left parasagittal parietal ganglioglioma was removed with postoperative right hemiparesis, worse in the leg than in the arm. Subsequent seizures consisted of a feeling of right arm heaviness, followed by tonic posturing of the right arm behind the back, and extension of the left arm and both legs, with postictal fatigue and weakness of both arms. Birth, development, and medical history were unremarkable. An MRI scan with gadolinium 3 years after tumor removal showed an area of hypodensity without enhancement in the left parietal area near the midline. An interictal EEG showed frequent bilateral epileptiform discharges with phase reversals near the vertex and near Pz (Fig. 2). Because complaints of bilateral postictal paresis after full recovery of consciousness were unusual and puzzling, both patients underwent diagnostic video/EEG (VEEG) monitoring to clarify the clinical diagnoses. EEG recordings were made on 2 1-channel NihonKodon 4300 electroencephalographs using gold cup electrodes attached with collodion and the 10-20 system of application. The EEG was recorded both on paper and on simultaneous videotape, with the picture displayed on a split-screen format along with the videotape of the patient. Several seizures were recorded from each patient. Postictal physical
PATIENTS AND METHODS
Patient 1, a 17-year-old right-handed woman, had onset at age 8 years of seizures consisting of a motionless stare followed by several minutes of disorientation. At age 12 years, she had a first generalized tonic-clonic seizure (GTCS) which began with clonic left leg jerking. Postictally, she reported fatigue, headache, and generalized weakness, particularly in the arms. Birth, development, and medical history were unremarkable. Computed tomography (CT) and magnetic resonance imaging (MRI) scans of the head were normal. Single-photon emission CT (SPECT) scan showed relatively reduced blood flow in the Received November 1991; revision accepted March 1992. Address correspondence and reprint requests to Dr. Donna C. Bergen at Department of Neurological Sciences, Rush Medical College, 1725 W. Harrison, Chicago, IL 60612, U.S.A. This paper was presented at the annual meeting of the American Epilepsy Society, December 1989, in Boston, Massachusetts and published in abstract form in Epilepsia 1989;30:650.
1101
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D . C . BERGEN ET AL.
FIG. 1. lnterictal EEG of patient 1 showing sharp waves with phase reversals near the midline. Time constant 0.3 s, low-pass filter 70 Hz, 15 kV/mm.
examinations were performed after some of the seizures.
RESULTS The GTCS of patient 1 were unusual in that they were prolonged (+ F , - Tp ~
FIG. 4. lctal EEG of patient 2 showing ictal onset across a wide field in the parasagittal region, with phase reversals between central and parietal electrodes on anteroposterior chains and between C3 and C4 on a transverse
Epilepsia, Vol. 33, No, 6, 1992
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D . C . BERGEN ET AL.
not the most common, is Todd’s paralysis. Other focal postictal deficits may well be more common but may be missed in the more dramatic postictal confusion and lethargy. Ajmone-Marsan and Ralston (1957), for example, carefully examined patients after various types of focal seizures and noted postictal aphasia in 62% of attacks beginning in the language-dominant hemisphere. Even more complex postictal phenomena have also been likened to Todd’s paralysis. Savard et al. (1987) reported nine cases of postictal psychosis lasting 3 h to months after bouts of complex partial seizures in patients who were otherwise psychiatrically stable. Morrell drew the same analogy from the reversible memory impairment observed after bilateral hippocampal seizure discharges in a patient with implanted cerebral electrodes (Morrell, 1980). Efron (1961) summarized the major pathophysiologic theories about Todd’s paralysis. The major opposing views were originally championed by Hughlings Jackson and Henry Gowers. Jackson (1880) accepted Todd’s original hypothesis of postictal neuronal exhaustion, relying on his clinical experience that postictal dysfunction was always “in the parts first and most convulsed.” He even thought it reasonable to consider generalized postictal inactivity or confusion to be postictal “universal or widespread paralysis,” a sort of paralysis of higher functions and voluntary motor powers. In this scheme, postictal agitation or irrationality was ascribed to temporary exhaustion or paralysis of higher centers of control or intellect. Jackson himself, however, reported the curious case of a man with focal motor seizures who often aborted an attack by vigorously rubbing his thigh (Jackson, 1868). If this maneuver succeeded, he had a Todd’s paresis of the leg; if it did not, he had no postictal weakness despite a longer, more severe seizure. Such cases led Gowers to reject the neuronal exhaustion theory in favor of the hypothesis that the inhibitory cortical activity which stopped a seizure also produced Todd’s paralysis (Gowers, 1881). As further evidence, he cited cases in which short seizures were associated with surprisingly prolonged Todd’s paralysis. Dissociations between the length and EEG extent of a seizure and the subsequent EEG depression or slowing have since been reported and are commonly observed, lending some credence to Gowers’ view (Kaibara and Blume, 1988). Modern speculations on the pathophysiology of postictal depression have centered around ictal accumulation of extracellular potassium (Matsumoto and Ajmone-Marsan, 1964). Whatever the mechanism, the type of postictal Epilepsia, Vol. 33, No. 6, 1992
focal deficit in each patient apparently depends on the cortical region in which the seizure begins or which it invades. In our patients, the initial EEG ictal activity was observed near the vertex, and interictal vertex spikes were also present. Patient 2 had a biopsy-proven ganglioglioma in the centroparietal area, with its edge abutting the midline. Clinically, the seizures of patient 1 were remarkable for ending with a prolonged series of slow, bilateral jerks of both arms, suggesting unusually intense ictal recruitment of bilateral motor systems. In both patients, the supplementary cortex, located on the mesial surface of the posterofrontal lobe, appears to be the likely focus of seizure origin. The seizures of patient 2 invariably began with tonic posturing of the right arm behind the back. Penfield and Jasper (1954) reported tonic postures of the arm, especially external rotation and adduction of the shoulder and flexion of the elbow, to be common results of electrical stimulation of the supplementary motor cortex. Others investigators have observed more complex tonic posturing, often bilateral, mainly involving proximal limb muscles as in our patient (Van Buren and Fedio, 1976; Morris et al., 1988). “Postural, focal tonic” motor phenomena are also part of the latest proposal for classification of supplementary motor seizures by the International League Against Epilepsy (Commission, 1989). In addition, the supplementary motor cortex is known to have strong bilateral motor projections to primary motor cortex (Williams et al., 1989). The rarity of bilateral Todd’s paralysis is puzzling. Perhaps it is sometimes missed in the global postictal confusion and lethargy that follow the frequently generalized seizures originating from this area, or perhaps it simply recovers along with consciousness in most cases. Ictal foci in the mesial frontal area are not particularly common, possibly because it is an area neither particularly susceptible to injury nor highly epileptogenic. This may be one of the clinical findings about which we never ask a patient, or look for or see for ourselves, because it is “not supposed to happen.” Indeed, patient I was monitored partly because the patient’s own claim of postictal inability to move her limbs raised the diagnostic possibility of pseudoseizures. This report may well trigger other observations of this phenomenon. Acknowledgment:We thank Jean Stewart for help in the manuscript preparation.
REFERENCES Ajmone-Marsan C, Ralston B . The epileptic seizure. Springfield, 11, Charles C Thomas, 1957.
1105
BILATERAL TODD’S PARALYSIS Commission for Classification and Terminology of the International League Against Epilepsy. Proposal for revised classification of epilepsies and epileptic syndromes. Epilepsia 1989;30:389-99. Efron R. Post-epileptic paralysis: theoretical critique and report of a case. Brain 1961;84:381-4. Gowers WR. Epilepsy and other chronic convulsive diseases. London, Churchill, 1881. Jackson H. Lancet 1868;1:618. Jackson H. On temporary paralysis after epileptiform and epileptic seizures; a contribution to the study of dissolution of the nervous system. Brain 1880;3:433-51. Kaibara M, Blume W. The postictal electroencephalogram. Electroencephalogr Clin Neurophysiol 1988;70:99-104. Matsumoto H, Ajmone-Marsan C. Cortical cellular phenomena in experimental epilepsy: ictal manifestations. Neurology 1964;9:305-26. Morrell F. Memory loss as a Todd’s paralysis. Epilepsia 1980; 21:185. Morris HH, Dinner DS, Luders H, Wylie E, Kramer R. Supplementary motor seizures: clinical and electroencephalographic findings. Neurology 1988;38:1075-82. Penfield W, Jasper H. Epilepsy and the functional anatomy of the human brain. Boston: Little Brown, 1954. Savard G, Andermann F , Remillard GM, Oliver A. Post-ictal psychosis following partial complex seizures is analogous to Todd’s paralysis. In: Wolf P, et al., eds. Advances in epileptology. XVZth Epilepsy International Symposium, vol. 16. New York: Raven, 1987:603-5. Todd RB. Clinical lectures on paralysis, disease of the brain and other uffections of the nervous system. London: Churchill, 1854.
Van Buren JM, Fedio P. Functional representation of the medial aspect of the frontal lobes in man. J Neurosurg 1976;44:27589. Williams PL, Warwick R, Dyson M, Bannister LH, eds. Gray’s anatomy. Edinburgh: Churchill Livingstone, 1989.
FU%UME Une htmiparksie ou une monopartsie post-critique est assez souvent constatte apres les crises partielles. Les auteurs rapportent deux patients qui se plaignaient d’une importante faiblesse bilattrale des membres apres des crises genkralistes tonicocloniques B dtbut focal. Une paralysie de TODD bilaterale a t t t vtrifiCe et documentte chez deux patients. Les arguments tlectroencephalographiques et cliniques sugggerent que l’aire motrice suppltmentaire est la source la plus probable des crises dans les deux cas. (P. Genton, Marseille)
ZUSAMMENFASSUNG Eine vorubergehende postiktale Hemi- oder Monoparese ist nach partiellen (fokalen) Anfallen nicht ungewohnlich. Wir berichten uber 2 Patienten, die uber eine starke bilaterale GliedmaBenschwache nach generalisierten, tonisch-klonischen Anfallen mit fokalem Beginn klagten. Eine bilaterale Todd’sche Paralyse wurde bei beiden Patienten verifiziert und dokumentiert. Der elektroenzephalographische und klinische Befund lassen in beiden Fallen den supplementar-motorischen Kortex als wahrscheinlichsten Entstehungsort der Anfalle vermuten. (C. K. Benninger, Heidelberg)
Epilepsia, Vol. 33, No. 6, 1992
0 International League Against Epilepsy
Bilateral Todd’s Paralysis After Focal Seizures Donna C. Bergen, Lea Rayman, and *Peter Heydemann Departments of Neurological Sciences and *Pediatrics, Rush Medical College, Chicago, Illinois, U.S.A.
Summary: Transient postictal hemiparesis or monoparesis is not uncommon after partial (focal) seizures. We report 2 patients who complained of severe bilateral limb weakness after generalized tonic-clonic seizures (GTCS) beginning focally. Bilateral Todd’s paralysis was verified
and documented in both patients. EEG and clinical evidence indicate the supplementary motor cortex as the most likely source of the seizures in both cases. Key Words: Seizures-Epilepsy-Weakness-Paralysis.
Transient, focal neurologic deficits after focal seizures are common. Aphasia, visual loss, and somatosensory deficits may occur after seizures arising in or near Broca’s area, visual cortex, and primary sensory cortex, respectively (Ajmone-Marsan and Ralston, 1957; Efron, 1961). One of the most obvious postictal symptoms is unilateral muscle weakness, known as Todd’s paralysis (Todd, 1854). Although originally observed as a hemiparesis, both monoparesis and/or facial weakness may also occur (Ajmone-Marsan and Ralston, 1957). We recently witnessed and recorded bilateral Todd’s paralysis in 2 young women with epilepsy and report the details.
right temporal and right posterofrontal areas. An interictal EEG showed spikes at and just to the right of the vertex, as well as independent right midtemporal spikes (Fig. 1). Patient 2, a 9-year-old girl, had onset at age 6 years of seizures consisting of tonic posturing of the right hand with mild clonic movements, without postictal symptoms or signs. A left parasagittal parietal ganglioglioma was removed with postoperative right hemiparesis, worse in the leg than in the arm. Subsequent seizures consisted of a feeling of right arm heaviness, followed by tonic posturing of the right arm behind the back, and extension of the left arm and both legs, with postictal fatigue and weakness of both arms. Birth, development, and medical history were unremarkable. An MRI scan with gadolinium 3 years after tumor removal showed an area of hypodensity without enhancement in the left parietal area near the midline. An interictal EEG showed frequent bilateral epileptiform discharges with phase reversals near the vertex and near Pz (Fig. 2). Because complaints of bilateral postictal paresis after full recovery of consciousness were unusual and puzzling, both patients underwent diagnostic video/EEG (VEEG) monitoring to clarify the clinical diagnoses. EEG recordings were made on 2 1-channel NihonKodon 4300 electroencephalographs using gold cup electrodes attached with collodion and the 10-20 system of application. The EEG was recorded both on paper and on simultaneous videotape, with the picture displayed on a split-screen format along with the videotape of the patient. Several seizures were recorded from each patient. Postictal physical
PATIENTS AND METHODS
Patient 1, a 17-year-old right-handed woman, had onset at age 8 years of seizures consisting of a motionless stare followed by several minutes of disorientation. At age 12 years, she had a first generalized tonic-clonic seizure (GTCS) which began with clonic left leg jerking. Postictally, she reported fatigue, headache, and generalized weakness, particularly in the arms. Birth, development, and medical history were unremarkable. Computed tomography (CT) and magnetic resonance imaging (MRI) scans of the head were normal. Single-photon emission CT (SPECT) scan showed relatively reduced blood flow in the Received November 1991; revision accepted March 1992. Address correspondence and reprint requests to Dr. Donna C. Bergen at Department of Neurological Sciences, Rush Medical College, 1725 W. Harrison, Chicago, IL 60612, U.S.A. This paper was presented at the annual meeting of the American Epilepsy Society, December 1989, in Boston, Massachusetts and published in abstract form in Epilepsia 1989;30:650.
1101
1102
D . C . BERGEN ET AL.
FIG. 1. lnterictal EEG of patient 1 showing sharp waves with phase reversals near the midline. Time constant 0.3 s, low-pass filter 70 Hz, 15 kV/mm.
examinations were performed after some of the seizures.
RESULTS The GTCS of patient 1 were unusual in that they were prolonged (+ F , - Tp ~
FIG. 4. lctal EEG of patient 2 showing ictal onset across a wide field in the parasagittal region, with phase reversals between central and parietal electrodes on anteroposterior chains and between C3 and C4 on a transverse
Epilepsia, Vol. 33, No, 6, 1992
1104
D . C . BERGEN ET AL.
not the most common, is Todd’s paralysis. Other focal postictal deficits may well be more common but may be missed in the more dramatic postictal confusion and lethargy. Ajmone-Marsan and Ralston (1957), for example, carefully examined patients after various types of focal seizures and noted postictal aphasia in 62% of attacks beginning in the language-dominant hemisphere. Even more complex postictal phenomena have also been likened to Todd’s paralysis. Savard et al. (1987) reported nine cases of postictal psychosis lasting 3 h to months after bouts of complex partial seizures in patients who were otherwise psychiatrically stable. Morrell drew the same analogy from the reversible memory impairment observed after bilateral hippocampal seizure discharges in a patient with implanted cerebral electrodes (Morrell, 1980). Efron (1961) summarized the major pathophysiologic theories about Todd’s paralysis. The major opposing views were originally championed by Hughlings Jackson and Henry Gowers. Jackson (1880) accepted Todd’s original hypothesis of postictal neuronal exhaustion, relying on his clinical experience that postictal dysfunction was always “in the parts first and most convulsed.” He even thought it reasonable to consider generalized postictal inactivity or confusion to be postictal “universal or widespread paralysis,” a sort of paralysis of higher functions and voluntary motor powers. In this scheme, postictal agitation or irrationality was ascribed to temporary exhaustion or paralysis of higher centers of control or intellect. Jackson himself, however, reported the curious case of a man with focal motor seizures who often aborted an attack by vigorously rubbing his thigh (Jackson, 1868). If this maneuver succeeded, he had a Todd’s paresis of the leg; if it did not, he had no postictal weakness despite a longer, more severe seizure. Such cases led Gowers to reject the neuronal exhaustion theory in favor of the hypothesis that the inhibitory cortical activity which stopped a seizure also produced Todd’s paralysis (Gowers, 1881). As further evidence, he cited cases in which short seizures were associated with surprisingly prolonged Todd’s paralysis. Dissociations between the length and EEG extent of a seizure and the subsequent EEG depression or slowing have since been reported and are commonly observed, lending some credence to Gowers’ view (Kaibara and Blume, 1988). Modern speculations on the pathophysiology of postictal depression have centered around ictal accumulation of extracellular potassium (Matsumoto and Ajmone-Marsan, 1964). Whatever the mechanism, the type of postictal Epilepsia, Vol. 33, No. 6, 1992
focal deficit in each patient apparently depends on the cortical region in which the seizure begins or which it invades. In our patients, the initial EEG ictal activity was observed near the vertex, and interictal vertex spikes were also present. Patient 2 had a biopsy-proven ganglioglioma in the centroparietal area, with its edge abutting the midline. Clinically, the seizures of patient 1 were remarkable for ending with a prolonged series of slow, bilateral jerks of both arms, suggesting unusually intense ictal recruitment of bilateral motor systems. In both patients, the supplementary cortex, located on the mesial surface of the posterofrontal lobe, appears to be the likely focus of seizure origin. The seizures of patient 2 invariably began with tonic posturing of the right arm behind the back. Penfield and Jasper (1954) reported tonic postures of the arm, especially external rotation and adduction of the shoulder and flexion of the elbow, to be common results of electrical stimulation of the supplementary motor cortex. Others investigators have observed more complex tonic posturing, often bilateral, mainly involving proximal limb muscles as in our patient (Van Buren and Fedio, 1976; Morris et al., 1988). “Postural, focal tonic” motor phenomena are also part of the latest proposal for classification of supplementary motor seizures by the International League Against Epilepsy (Commission, 1989). In addition, the supplementary motor cortex is known to have strong bilateral motor projections to primary motor cortex (Williams et al., 1989). The rarity of bilateral Todd’s paralysis is puzzling. Perhaps it is sometimes missed in the global postictal confusion and lethargy that follow the frequently generalized seizures originating from this area, or perhaps it simply recovers along with consciousness in most cases. Ictal foci in the mesial frontal area are not particularly common, possibly because it is an area neither particularly susceptible to injury nor highly epileptogenic. This may be one of the clinical findings about which we never ask a patient, or look for or see for ourselves, because it is “not supposed to happen.” Indeed, patient I was monitored partly because the patient’s own claim of postictal inability to move her limbs raised the diagnostic possibility of pseudoseizures. This report may well trigger other observations of this phenomenon. Acknowledgment:We thank Jean Stewart for help in the manuscript preparation.
REFERENCES Ajmone-Marsan C, Ralston B . The epileptic seizure. Springfield, 11, Charles C Thomas, 1957.
1105
BILATERAL TODD’S PARALYSIS Commission for Classification and Terminology of the International League Against Epilepsy. Proposal for revised classification of epilepsies and epileptic syndromes. Epilepsia 1989;30:389-99. Efron R. Post-epileptic paralysis: theoretical critique and report of a case. Brain 1961;84:381-4. Gowers WR. Epilepsy and other chronic convulsive diseases. London, Churchill, 1881. Jackson H. Lancet 1868;1:618. Jackson H. On temporary paralysis after epileptiform and epileptic seizures; a contribution to the study of dissolution of the nervous system. Brain 1880;3:433-51. Kaibara M, Blume W. The postictal electroencephalogram. Electroencephalogr Clin Neurophysiol 1988;70:99-104. Matsumoto H, Ajmone-Marsan C. Cortical cellular phenomena in experimental epilepsy: ictal manifestations. Neurology 1964;9:305-26. Morrell F. Memory loss as a Todd’s paralysis. Epilepsia 1980; 21:185. Morris HH, Dinner DS, Luders H, Wylie E, Kramer R. Supplementary motor seizures: clinical and electroencephalographic findings. Neurology 1988;38:1075-82. Penfield W, Jasper H. Epilepsy and the functional anatomy of the human brain. Boston: Little Brown, 1954. Savard G, Andermann F , Remillard GM, Oliver A. Post-ictal psychosis following partial complex seizures is analogous to Todd’s paralysis. In: Wolf P, et al., eds. Advances in epileptology. XVZth Epilepsy International Symposium, vol. 16. New York: Raven, 1987:603-5. Todd RB. Clinical lectures on paralysis, disease of the brain and other uffections of the nervous system. London: Churchill, 1854.
Van Buren JM, Fedio P. Functional representation of the medial aspect of the frontal lobes in man. J Neurosurg 1976;44:27589. Williams PL, Warwick R, Dyson M, Bannister LH, eds. Gray’s anatomy. Edinburgh: Churchill Livingstone, 1989.
FU%UME Une htmiparksie ou une monopartsie post-critique est assez souvent constatte apres les crises partielles. Les auteurs rapportent deux patients qui se plaignaient d’une importante faiblesse bilattrale des membres apres des crises genkralistes tonicocloniques B dtbut focal. Une paralysie de TODD bilaterale a t t t vtrifiCe et documentte chez deux patients. Les arguments tlectroencephalographiques et cliniques sugggerent que l’aire motrice suppltmentaire est la source la plus probable des crises dans les deux cas. (P. Genton, Marseille)
ZUSAMMENFASSUNG Eine vorubergehende postiktale Hemi- oder Monoparese ist nach partiellen (fokalen) Anfallen nicht ungewohnlich. Wir berichten uber 2 Patienten, die uber eine starke bilaterale GliedmaBenschwache nach generalisierten, tonisch-klonischen Anfallen mit fokalem Beginn klagten. Eine bilaterale Todd’sche Paralyse wurde bei beiden Patienten verifiziert und dokumentiert. Der elektroenzephalographische und klinische Befund lassen in beiden Fallen den supplementar-motorischen Kortex als wahrscheinlichsten Entstehungsort der Anfalle vermuten. (C. K. Benninger, Heidelberg)
Epilepsia, Vol. 33, No. 6, 1992
