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Dipole source localization in a case of epilepsia partialis continua without premyoclonic EEG spikes
316
Electroencephalography and clinical Neurophysiology , 90 (1994) 316 -319 © 1994 Elsevier Science Ireland Ltd. 0013-4694/94/$07.00
E E G 93648
Short communication
Dipole source localization in a case of epilepsia partialis continua without premyoclonic EEG spikes Gastone G. Celesia *, Lucio Parmeggiani and Mitchell Brigell Loyola University o f Chicago, Stritch School o f Medicine, Department o f Neurology, 2160 S. First A l~e., Maywood, IL 60153 (USA) ( A c c e p t e d for p u b l i c a t i o n : 5 J a n u a r y 1994)
Summary A 72-year-old woman with epilepsia partialis continua (EPC) of the right foot is presented. Rhythmic myoclonic jerks were localized to the 1st and 2nd toes of the right foot and persisted for 72 h. E E G / v i d e o monitoring did not show any epileptiform transient in association with myoclonic jerks. M R I and M R A demonstrated an arterio-venous malformation involving the left fronto-parietal parasagittal area. Using the E M G signal from the myoclonic jerk we back-averaged the E E G 640 msec before and after the onset of the twitch. A negative-positive deflection was observed preceding the myoclonic jerks by 128-188 msec. Voltage topographic mapping showed a negative maximum in the left centro-parietal region. A multiple spatio-temporal dipole model was applied to the back-averaged deflection preceding the myoclonus. The patient's MRI was used to determine the center of the best fitting sphere, and the model was corrected accordingly. The best dipole solution consisted of 3 dipoles localized in the parasagittal frontal cortex, in the location of the motor representation for the foot. The utilization of a combined technique of back-averaging from the myoclonus and dipole source localization supported the epileptogenic etiology in this case. Key words: Myoclonus; Epilepsia partialis continua; Brain modelling; Arterio-venous malformation: Back-averaging
The relationship between myoclonic jerks and EEG activity is controversial because the E E G frequently fails to register any abnormal activity preceding a myoclonic jerk (Gastaut and R6mond 1952; Halliday 1967; Hallett et al. 1977, 1979; Halliday and Halliday 1978; Toro et al. 1993). This lack of sensitivity is particularly frequent in cases involving myoclonic jerks of the foot. Back-averaging of E E G time-locked to the myoclonic E M G discharges, a technique introduced by Shibasaki and Kuroiwa (1975), has demonstrated E E G changes associated with myoclonus not previously noted on polygraphic recordings. In epilepsia partialis continua (EPC) there has been considerable argument about the generators of the myoclonic jerks. It has been argued that their origin may be related to subcortical structures (Kristiansen et al. 1971), although the emphasis recently has been on their cortical origin (Schomer 1993). In this case we demonstrate that back-averaging and dipole source modelling may be used to define an epileptogenic source of the myoclonic jerk in EPC even when the generator is located in the mesial surface of the fronto-parietal lobe.
Methods E E G and E M G were simultaneously recorded via a 22-channel polygraphic recorder. Silver cup electrodes were placed on the scalp with collodion in the standard international 10-20 locations. Impedance was below 5000 J2. Recording was carried out from 20 electrodes referred to linked ears. The E M G was recorded from surface silver electrodes placed on the tibialis anterior muscle. All
* Corresponding author. Tel.: (708) 2165328; Fax: (708) 2165617.
SSDI 0 0 1 3 - 4 6 9 4 ( 9 4 ) 0 0 0 1 5 - D
signals were digitized and stored in an optical disk. The digitized sample rate was 200 Hz with a 10-bit A / D converter. The E M G signal was used as a trigger for back-averaging the E E G (Barrett 1992). E M G activity was aligned at the peak of the first positive deflection. Averaging included 640 msec prior and 640 msec following the recorded myoclonic jerk. Dipole source localization was performed using a multiple spatio-temporal dipole model (Scherg and Von Cramon 1985; Scherg 1989). The model assumes multiple generators to be fixed in location and orientation, but to vary in activity during time. An equivalent dipole (ED) is fit using a least squares criterion at a 5 msec interval to the data. Fitting is terminated when the sum-square error could not be decreased by moving the dipole 0.0003 m m in any cardinal direction. A 3-shell spherical model of the head centered on the posterior commissure and having a radius of 85 m m is used. Data are transformed to common average reference prior to modelling. To define the time window over which the E D was fit, we utilized the global field power (GFP). GFP is defined as the sum-squared w)ltage deviation from the mean over the 20 electrode positions at each sampled time point. A high GFP indicates a steep voltage gradient over the surface of the head and therefore could be used as an indicator of high signal-to-noise ratio. We defined the noise level in our data set as the mean GFP plus 2.5 S.D.s, during the first 300 msec of the averaged EEG. EDs were fit over a time window whose beginning and ending points were above noise level. The MRI of the patient's brain was used to locate the ED relative to the patient's brain morphology. The best fitting sphere to a real head is centered at approximately 21 mm posterior to the anterior commissure, 5 m m anterior to the posterior commissure, 6 m m superior to the mammillary bodies and optic chiasm, and 8 m m inferior to the massa intermedia (Towle et al. 1993). We identified these structured in our patients therefore identifying the center of the sphere. The actual center of the patient's head was converted to
EPILEPSIA PARTIALIS CONTINUA
317
Fig. 1. The first image represents the MRI of the patient showing the extensive arterio-venous malformation (AVM) localized primarily in the left parieto-frontal region. The 2nd image shows the MRA of the same patient with the AVM located in the parasagittal area. a percent of the fit sphere radius and the model corrected accordingly.
Results
The patient was a 72-year-old woman in good general health until the day of admission when she developed sudden onset of focal status epilepticus characterized by continuous rhythmic twitching of the foot with rapid march to the leg, trunk and arm. The spreading of the motor twitch spared the face and was always limited to the right side. The focal Jacksonian status lasted for 5 h. The patient was treated with intravenous administration of phenytoin 18 m g / k g without improvement. The focal status was controlled by i.v. phenobarbital total dose of 1200 mg given slowly over 1 h. Although the focal status epilepticus resolved, the patient was left with continuous rhythmic twitching of the toes of the right foot with the greatest involvement in the right big toe. This epilepsia partialis continua lasted for 24 h and was finally brought under control with lorazepam 10 m g / 2 4 h. Magnetic resonance imaging (MRI) and magnetic resonance angiography (MRA) showed that the patient had an arterio-venous malformation localized in the left hemisphere (Fig. 1), with the bulk of the malformation in the left parasagittal frontoparietal area.
from 20 scalp positions showed a maximum negative wave at Cz followed by a maximum positive peak located at C3. A multiple spatio-temporal equivalent dipole model was fit to the data using the least square deviation reiterative algorithm of Scherg (1989). Three generator sources (Fig. 3) were identified and explained the pre-myoclonus potential with a residual variance of less than 10%. The 3 dipoles were located in close proximity to each other in the left prerolandic parasagittal area. The first and third dipole were oriented in a plane tangential to the scalp, whereas the second dipole had a radial orientation. The model was applied to the 8 averages with similar solutions.
Discussion
The present case had a pathological lesion localized in the left hemisphere and a clinical picture that was highly suggestive of an
I
~ c3 ~
~
*
~ i
~...~,~ ,r -z,~
Electrophysiological data The E E G background activity consisted of a mixture of beta and 6-7 Hz theta. Preceding the myoclonic jerk a negative wave of approximately 150-200 msec duration (Fig. 2) was observed over the entire scalp with highest amplitude at Cz, C3 and Fz, its relationship to the myoclonus and its scalp distribution was, however, ambiguous, One hundred and twelve muscle twitches were analyzed. Fourteen single twitches were back-averaged and the process was repeated for 8 different time epochs. The back-averages were then compared to each other for reliability. As shown in Fig. 3 there was a negative positive deflection preceding the muscle jerk in every instance. This deflection was named pre-myoclonus potential (PMP). The excellent superimposition of the 8 averages confirms the reliability and the consistency of the results. The peak of the negative PMP preceded the myoclonic jerk by 117_+ 12 msec while the onset of the PMP preceded the jerk by 192.3 + 15 msec. Myoclonic jerks occurred at a rate of 1 every 2-4 sec. The voltage scalp distribution of the averaged PMP recorded
rpzr4
~
F4C4
~
~
C4 P4
P40Z
f z Cz
Cz Pz PzOz
Fig. 2. Polygraphic recording at the time of epilepsia partialis continua of the right foot. EMG is from the right tibialis anterior. Only 12 of the 22 channels are shown here. Note the ambiguity of the EEG changes preceding the myoclonic jerk. The calibration bar represents 100/xV and the time between vertical lines represents 1 sec.
318
G.G. CELESIA ET AL. -50
r-,,.
czI
fi) 77~ B
-50 -25 0
E
25 50
<
256
512
time
768
1024
(rnsec) 2
2
I
3
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Fig. 3. The upper half of the figure shows back-averaging of myoclonic jerks (EMG) and EEG. The upper tracing shows the superimposition of 8 averaged potentials recorded from Cz. The lower tracings represent 8 averaged EMGs from the right tibialis anterior. Each tracing is the sum of 14 single responses. Note the excellent reproducibility of the tracings. The lower half of the figure shows equivalent dipoles fit to the PMP. On the left is shown the activity profile for each of the dipoles. On the right is shown the location of the dipoles with their vector orientation in the 3 orthogonal planes. The residual variance (RV) in the recordings over the recording sweep is shown below.
epileptogenic focus in the foot area of the left motor cortex (i.e., in the prerolandic parasagittal gyrus). The expected generator or generators of the epilepsia partialis continua were therefore located in an unfavorable location to be identified by EEG recording as they were buried in the mesial surface of the interhemispheric fissure. The case was ideal to test the reliability of back-averaging, voltage amplitude distribution and dipole source localization techniques. Back-averaging was clearly essential in this case to clarify the time features of the pre-myoclonus potential. The ability of the back-averaging method to identifying PMP even when the EEG appears normal has been demonstrated previously (Shibasaki and Kuroiwa 1975; Hallett et al. 1977, 1979; Shibasaki et al. 1991; Barrett 1992). We agree with Barrett (1992) that back-averaging has "earned a place" in determining the origin of the myoclonus in individual patients. However, the PMP generators are not well delineated by simple back-averaging nor by topographic analysis of voltage maps, especially when the presumed generators are located in the mesial surface of cerebral lobes. The voltage amplitude distribution indicated that the maxi-
mum negative PMP was located at the vertex followed by a positive maximum at C3. In the same case, the multiple spatio-temporal constrained inverse problem dipole further localized the PMP. Although there is no unique solution of the inverse problem, knowledge of the pathophysiology in this particular case allowed for the application of appropriate constraints to the model. The resulting solutions were biologically plausible with two dipoles tangentially oriented and one dipole radially oriented. Our results suggest that the PMP was located in an area of the rolandic cortex and was active approximately 150-200 msec before the onset of the myoclonus. The location of the dipoles may be somewhat deeper than one would expect for the location of the foot in the body homunculus of motor cortex. This is not totally unexpected given that dipole modelling of a scalp potential generated by a large superficial cortical generator will result in localization of a point source deeper in the brain (Gloor 1985). This cautionary statement does not exclude the usefulness of dipole modelling if constrained by corroborative anatomic and physiologic information. In our case, the PMP was within the expected time of premovement activity as determined in normal subjects during voluntary movements (Neshige et al. 1988; Toro et al. 1993). A slow negative potential has been recorded from the human sensorimotor area from chronically implanted subdural electrodes (Neshige et al. 1988). The negative potential started 130_+32 msec before the onset of the finger recorded EMG onsel. Our value of 192_+ 15 msec for the onset of the tibialis anterior twitch is therefore within expected physiological boundaries. We conclude that the combined use of back-averaging and dipole modelling techniques clarifies the physiopathology of this patient. Our results suggest that EPC is generated in the cerebral cortex (Andermann 1992; Schomer 1993). In selected clinical cases this technology can be confidently utilized even when polygraphic recordings show ambiguous data. Although errors in the dipole localization cannot be avoided (Snyder 1991; Zhang and Jewett 1993), the parsimonious utilization of the technique with careful attention to the residual variance and the reproducibility of the solution in the same patient over-time assure a reliable solution.
References
Andermann, F. Epilepsia partialis continua and other seizures arising from the precentral gyrus: high incidence in patients with Rasmussen syndrome and neuronal migration disorders. Brain Dev., 1992, 14: 338-339. Barrett, G. Jerk-locked averaging: technique and application. J. Clin. Neurophysiol., 1992, 9: 495-508. Gastaut, H. and R6mond, A. Etude 61ectroenc6phalographique des myoclonies. Rev. Neurol., 1952, 86: 596-609. Gloor, P. Neuronal generators and the problem of localization in electroencephalography: application of volume conductor theory to electroencephalography. J. Clin. Neurophysiol., 1985, 2: 327354. Hallett, M., Chadwick, D., Adam, J. and Marsden, C.D. Reticular reflex myoclonus: a physiological type of human post-hypoxic myoclonus. J. Neurol. Neurosurg. Psychiat., 1977, 40: 253-264. Hallett, M., Chadwick, D. and Marsden, C.D. Cortical reflex myoclonus. Neurology, 1979, 29: 1107-1125. Halliday, A.M. The electrophysiological study of myoclonus in man. Brain, 1967, 90: 241-284. Halliday, A.M. and Halliday, E. Cerebral evoked potentials in myoclonus. In: J.E. Desmedt (Ed.), Somatosensory Evoked Potentials and Their Clinical Uses. Karger, Basel, 1978. Kristiansen, K., Kaada, B.R. and Henriksen, G.F. Epilepsia partialis continua. Epilepsia, 1971, 12: 263-267.
EPILEPSIA PARTIALIS CONTINUA Neshige, R., Liiders, H. and Shibasaki, H. Recording of the movement related potentials from scalp and cortex in man. Brain, 1988, 111: 719-736. Scherg, M. Fundamentals of dipole source potential analysis. In: M. Hoke, F. Grandori and G.L. Romani (Eds.), Auditory Evoked Magnetic Fields and Potentials. Advances in Audiology. Karger, Basel, 1989: 2-30. Scherg, M. and Von Cramon, D. Two bilateral sources of the late AEP as identified by a spatio-temporal dipole model. Electroenceph. clin. Neurophysiol., 1985, 62: 32-44. Schomer, D.L. Focal status epilepticus and epilepsia partialis continua in adults and children. Epilepsia, 1993, 34 (Suppl. 1): $29-$36. Shibasaki, H. and Kuroiwa, Y. Electroencephalographic correlates of myoclonus. Electroenceph. clin. Neurophysiol., 1975, 39: 455-463. Shibasaki, H., Kakigi, R. and Ikeda, A. Scalp topography of giant
319 SEP and pre-myoclonus spike in cortical reflex myoclonus. Electroenceph, clin. Neurophysiol., 1991, 81: 31-37. Snyder, A.Z. Dipole source localization in the study of EP generators: a critique. Electroenceph. clin. Neurophysiol., 199l, 80: 321. Toro, C., Matsumoto, J., Deuschl, G., Roth, B.J. and Hallett, M. Source analysis of scalp-recorded movement-related electrical potentials. Electroenceph. clin. Neurophysiol., 1993, 86: 167-175. Towle, V.L., Bolanos, J.,Suarez, D., Tan, K., Grzeszczuk, R., Levin, D.N., Cakmur, R., Frank, S.A. and Spire, J.P. The spatial location of EEG electrodes: locating the best-fitting sphere relative to cortical anatomy. Electroenceph. clin. Neurophysiol., 1993, 86: 1-6. Zhang, Z. and Jewett, D.L. Insidious errors in dipole localization parameters at a single time-point due to model misspecification of number of shells. Electroenceph. clin. Neurophysiol., 1993, 88: 1-11.
Electroencephalography and clinical Neurophysiology , 90 (1994) 316 -319 © 1994 Elsevier Science Ireland Ltd. 0013-4694/94/$07.00
E E G 93648
Short communication
Dipole source localization in a case of epilepsia partialis continua without premyoclonic EEG spikes Gastone G. Celesia *, Lucio Parmeggiani and Mitchell Brigell Loyola University o f Chicago, Stritch School o f Medicine, Department o f Neurology, 2160 S. First A l~e., Maywood, IL 60153 (USA) ( A c c e p t e d for p u b l i c a t i o n : 5 J a n u a r y 1994)
Summary A 72-year-old woman with epilepsia partialis continua (EPC) of the right foot is presented. Rhythmic myoclonic jerks were localized to the 1st and 2nd toes of the right foot and persisted for 72 h. E E G / v i d e o monitoring did not show any epileptiform transient in association with myoclonic jerks. M R I and M R A demonstrated an arterio-venous malformation involving the left fronto-parietal parasagittal area. Using the E M G signal from the myoclonic jerk we back-averaged the E E G 640 msec before and after the onset of the twitch. A negative-positive deflection was observed preceding the myoclonic jerks by 128-188 msec. Voltage topographic mapping showed a negative maximum in the left centro-parietal region. A multiple spatio-temporal dipole model was applied to the back-averaged deflection preceding the myoclonus. The patient's MRI was used to determine the center of the best fitting sphere, and the model was corrected accordingly. The best dipole solution consisted of 3 dipoles localized in the parasagittal frontal cortex, in the location of the motor representation for the foot. The utilization of a combined technique of back-averaging from the myoclonus and dipole source localization supported the epileptogenic etiology in this case. Key words: Myoclonus; Epilepsia partialis continua; Brain modelling; Arterio-venous malformation: Back-averaging
The relationship between myoclonic jerks and EEG activity is controversial because the E E G frequently fails to register any abnormal activity preceding a myoclonic jerk (Gastaut and R6mond 1952; Halliday 1967; Hallett et al. 1977, 1979; Halliday and Halliday 1978; Toro et al. 1993). This lack of sensitivity is particularly frequent in cases involving myoclonic jerks of the foot. Back-averaging of E E G time-locked to the myoclonic E M G discharges, a technique introduced by Shibasaki and Kuroiwa (1975), has demonstrated E E G changes associated with myoclonus not previously noted on polygraphic recordings. In epilepsia partialis continua (EPC) there has been considerable argument about the generators of the myoclonic jerks. It has been argued that their origin may be related to subcortical structures (Kristiansen et al. 1971), although the emphasis recently has been on their cortical origin (Schomer 1993). In this case we demonstrate that back-averaging and dipole source modelling may be used to define an epileptogenic source of the myoclonic jerk in EPC even when the generator is located in the mesial surface of the fronto-parietal lobe.
Methods E E G and E M G were simultaneously recorded via a 22-channel polygraphic recorder. Silver cup electrodes were placed on the scalp with collodion in the standard international 10-20 locations. Impedance was below 5000 J2. Recording was carried out from 20 electrodes referred to linked ears. The E M G was recorded from surface silver electrodes placed on the tibialis anterior muscle. All
* Corresponding author. Tel.: (708) 2165328; Fax: (708) 2165617.
SSDI 0 0 1 3 - 4 6 9 4 ( 9 4 ) 0 0 0 1 5 - D
signals were digitized and stored in an optical disk. The digitized sample rate was 200 Hz with a 10-bit A / D converter. The E M G signal was used as a trigger for back-averaging the E E G (Barrett 1992). E M G activity was aligned at the peak of the first positive deflection. Averaging included 640 msec prior and 640 msec following the recorded myoclonic jerk. Dipole source localization was performed using a multiple spatio-temporal dipole model (Scherg and Von Cramon 1985; Scherg 1989). The model assumes multiple generators to be fixed in location and orientation, but to vary in activity during time. An equivalent dipole (ED) is fit using a least squares criterion at a 5 msec interval to the data. Fitting is terminated when the sum-square error could not be decreased by moving the dipole 0.0003 m m in any cardinal direction. A 3-shell spherical model of the head centered on the posterior commissure and having a radius of 85 m m is used. Data are transformed to common average reference prior to modelling. To define the time window over which the E D was fit, we utilized the global field power (GFP). GFP is defined as the sum-squared w)ltage deviation from the mean over the 20 electrode positions at each sampled time point. A high GFP indicates a steep voltage gradient over the surface of the head and therefore could be used as an indicator of high signal-to-noise ratio. We defined the noise level in our data set as the mean GFP plus 2.5 S.D.s, during the first 300 msec of the averaged EEG. EDs were fit over a time window whose beginning and ending points were above noise level. The MRI of the patient's brain was used to locate the ED relative to the patient's brain morphology. The best fitting sphere to a real head is centered at approximately 21 mm posterior to the anterior commissure, 5 m m anterior to the posterior commissure, 6 m m superior to the mammillary bodies and optic chiasm, and 8 m m inferior to the massa intermedia (Towle et al. 1993). We identified these structured in our patients therefore identifying the center of the sphere. The actual center of the patient's head was converted to
EPILEPSIA PARTIALIS CONTINUA
317
Fig. 1. The first image represents the MRI of the patient showing the extensive arterio-venous malformation (AVM) localized primarily in the left parieto-frontal region. The 2nd image shows the MRA of the same patient with the AVM located in the parasagittal area. a percent of the fit sphere radius and the model corrected accordingly.
Results
The patient was a 72-year-old woman in good general health until the day of admission when she developed sudden onset of focal status epilepticus characterized by continuous rhythmic twitching of the foot with rapid march to the leg, trunk and arm. The spreading of the motor twitch spared the face and was always limited to the right side. The focal Jacksonian status lasted for 5 h. The patient was treated with intravenous administration of phenytoin 18 m g / k g without improvement. The focal status was controlled by i.v. phenobarbital total dose of 1200 mg given slowly over 1 h. Although the focal status epilepticus resolved, the patient was left with continuous rhythmic twitching of the toes of the right foot with the greatest involvement in the right big toe. This epilepsia partialis continua lasted for 24 h and was finally brought under control with lorazepam 10 m g / 2 4 h. Magnetic resonance imaging (MRI) and magnetic resonance angiography (MRA) showed that the patient had an arterio-venous malformation localized in the left hemisphere (Fig. 1), with the bulk of the malformation in the left parasagittal frontoparietal area.
from 20 scalp positions showed a maximum negative wave at Cz followed by a maximum positive peak located at C3. A multiple spatio-temporal equivalent dipole model was fit to the data using the least square deviation reiterative algorithm of Scherg (1989). Three generator sources (Fig. 3) were identified and explained the pre-myoclonus potential with a residual variance of less than 10%. The 3 dipoles were located in close proximity to each other in the left prerolandic parasagittal area. The first and third dipole were oriented in a plane tangential to the scalp, whereas the second dipole had a radial orientation. The model was applied to the 8 averages with similar solutions.
Discussion
The present case had a pathological lesion localized in the left hemisphere and a clinical picture that was highly suggestive of an
I
~ c3 ~
~
*
~ i
~...~,~ ,r -z,~
Electrophysiological data The E E G background activity consisted of a mixture of beta and 6-7 Hz theta. Preceding the myoclonic jerk a negative wave of approximately 150-200 msec duration (Fig. 2) was observed over the entire scalp with highest amplitude at Cz, C3 and Fz, its relationship to the myoclonus and its scalp distribution was, however, ambiguous, One hundred and twelve muscle twitches were analyzed. Fourteen single twitches were back-averaged and the process was repeated for 8 different time epochs. The back-averages were then compared to each other for reliability. As shown in Fig. 3 there was a negative positive deflection preceding the muscle jerk in every instance. This deflection was named pre-myoclonus potential (PMP). The excellent superimposition of the 8 averages confirms the reliability and the consistency of the results. The peak of the negative PMP preceded the myoclonic jerk by 117_+ 12 msec while the onset of the PMP preceded the jerk by 192.3 + 15 msec. Myoclonic jerks occurred at a rate of 1 every 2-4 sec. The voltage scalp distribution of the averaged PMP recorded
rpzr4
~
F4C4
~
~
C4 P4
P40Z
f z Cz
Cz Pz PzOz
Fig. 2. Polygraphic recording at the time of epilepsia partialis continua of the right foot. EMG is from the right tibialis anterior. Only 12 of the 22 channels are shown here. Note the ambiguity of the EEG changes preceding the myoclonic jerk. The calibration bar represents 100/xV and the time between vertical lines represents 1 sec.
318
G.G. CELESIA ET AL. -50
r-,,.
czI
fi) 77~ B
-50 -25 0
E
25 50
<
256
512
time
768
1024
(rnsec) 2
2
I
3
--588
msl pUeff
Fig. 3. The upper half of the figure shows back-averaging of myoclonic jerks (EMG) and EEG. The upper tracing shows the superimposition of 8 averaged potentials recorded from Cz. The lower tracings represent 8 averaged EMGs from the right tibialis anterior. Each tracing is the sum of 14 single responses. Note the excellent reproducibility of the tracings. The lower half of the figure shows equivalent dipoles fit to the PMP. On the left is shown the activity profile for each of the dipoles. On the right is shown the location of the dipoles with their vector orientation in the 3 orthogonal planes. The residual variance (RV) in the recordings over the recording sweep is shown below.
epileptogenic focus in the foot area of the left motor cortex (i.e., in the prerolandic parasagittal gyrus). The expected generator or generators of the epilepsia partialis continua were therefore located in an unfavorable location to be identified by EEG recording as they were buried in the mesial surface of the interhemispheric fissure. The case was ideal to test the reliability of back-averaging, voltage amplitude distribution and dipole source localization techniques. Back-averaging was clearly essential in this case to clarify the time features of the pre-myoclonus potential. The ability of the back-averaging method to identifying PMP even when the EEG appears normal has been demonstrated previously (Shibasaki and Kuroiwa 1975; Hallett et al. 1977, 1979; Shibasaki et al. 1991; Barrett 1992). We agree with Barrett (1992) that back-averaging has "earned a place" in determining the origin of the myoclonus in individual patients. However, the PMP generators are not well delineated by simple back-averaging nor by topographic analysis of voltage maps, especially when the presumed generators are located in the mesial surface of cerebral lobes. The voltage amplitude distribution indicated that the maxi-
mum negative PMP was located at the vertex followed by a positive maximum at C3. In the same case, the multiple spatio-temporal constrained inverse problem dipole further localized the PMP. Although there is no unique solution of the inverse problem, knowledge of the pathophysiology in this particular case allowed for the application of appropriate constraints to the model. The resulting solutions were biologically plausible with two dipoles tangentially oriented and one dipole radially oriented. Our results suggest that the PMP was located in an area of the rolandic cortex and was active approximately 150-200 msec before the onset of the myoclonus. The location of the dipoles may be somewhat deeper than one would expect for the location of the foot in the body homunculus of motor cortex. This is not totally unexpected given that dipole modelling of a scalp potential generated by a large superficial cortical generator will result in localization of a point source deeper in the brain (Gloor 1985). This cautionary statement does not exclude the usefulness of dipole modelling if constrained by corroborative anatomic and physiologic information. In our case, the PMP was within the expected time of premovement activity as determined in normal subjects during voluntary movements (Neshige et al. 1988; Toro et al. 1993). A slow negative potential has been recorded from the human sensorimotor area from chronically implanted subdural electrodes (Neshige et al. 1988). The negative potential started 130_+32 msec before the onset of the finger recorded EMG onsel. Our value of 192_+ 15 msec for the onset of the tibialis anterior twitch is therefore within expected physiological boundaries. We conclude that the combined use of back-averaging and dipole modelling techniques clarifies the physiopathology of this patient. Our results suggest that EPC is generated in the cerebral cortex (Andermann 1992; Schomer 1993). In selected clinical cases this technology can be confidently utilized even when polygraphic recordings show ambiguous data. Although errors in the dipole localization cannot be avoided (Snyder 1991; Zhang and Jewett 1993), the parsimonious utilization of the technique with careful attention to the residual variance and the reproducibility of the solution in the same patient over-time assure a reliable solution.
References
Andermann, F. Epilepsia partialis continua and other seizures arising from the precentral gyrus: high incidence in patients with Rasmussen syndrome and neuronal migration disorders. Brain Dev., 1992, 14: 338-339. Barrett, G. Jerk-locked averaging: technique and application. J. Clin. Neurophysiol., 1992, 9: 495-508. Gastaut, H. and R6mond, A. Etude 61ectroenc6phalographique des myoclonies. Rev. Neurol., 1952, 86: 596-609. Gloor, P. Neuronal generators and the problem of localization in electroencephalography: application of volume conductor theory to electroencephalography. J. Clin. Neurophysiol., 1985, 2: 327354. Hallett, M., Chadwick, D., Adam, J. and Marsden, C.D. Reticular reflex myoclonus: a physiological type of human post-hypoxic myoclonus. J. Neurol. Neurosurg. Psychiat., 1977, 40: 253-264. Hallett, M., Chadwick, D. and Marsden, C.D. Cortical reflex myoclonus. Neurology, 1979, 29: 1107-1125. Halliday, A.M. The electrophysiological study of myoclonus in man. Brain, 1967, 90: 241-284. Halliday, A.M. and Halliday, E. Cerebral evoked potentials in myoclonus. In: J.E. Desmedt (Ed.), Somatosensory Evoked Potentials and Their Clinical Uses. Karger, Basel, 1978. Kristiansen, K., Kaada, B.R. and Henriksen, G.F. Epilepsia partialis continua. Epilepsia, 1971, 12: 263-267.
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