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Correlation of tibial nerve SEPs with the development of seizures in patients with supratentorial cerebral infarcts
Electr~encephalography and clinical Neurophysiology, 1990, 7 7 : 3 4 7 - 3 5 2 Elsevier Scientific Publishers Ireland, Ltd.
347
EVOPOT 89522
Correlation of tibiai nerve S E P s with the d e v e l o p m e n t of seizures in patients with supratentorial cerebral infarcts T. Kovala a, U. Tolonen a and J. Pyhtinen b Departments of a Clinical Neurophysiology and b Radiology, Oulu Unioersity Central Hospital, Oulu (Finland) (Accepted for publication: 22 November 1989)
Summary In 40 patients with supratentorial non-haemorrhagic cerebral infarct, the findings in the tibial nerve SEPs recorded during the acute stage correlated significantly with the development of seizures during a 1 year follow-up period. Abnormality in the side-to-side difference of the P40-N48 amplitude was the finding with the highest correlation with the development of seizures: 87.5% of the patients were classified correctly as to the risk of seizures. Key words: Epilepsy; Somatosensory evoked potentials; Cerebral infarction; Cerebral ischaemia; Posterior tibial nerve
A substantial proportion of patients with supratentorial cerebral infarct will suffer from later epileptic attacks (Richardson and Dodge 1954; Olsen et al. 1987). The involvement of the cortical structures has been shown to have a particular importance in the pathogenesis of epilepsy after stroke. Persistence of the paresis also seems to increase the risk of epilepsy (Olsen et al. 1987). In contrast, the EEG does not predict the risk of developing epilepsy (Olsen et al. 1987). The present study was conducted to evaluate whether tibial nerve SEPs might give some information about the risk of developing seizures after supratentorial cerebral infarct.
Patients and methods
The patient group consisted of 40 patients with supratentorial cerebral infarct treated in the Department of Neurology of Oulu University Central
Correspondence to: Tero Kovala, Department of Clinical Neurophysiology, Oulu University Central Hospital, 90220 Oulu (Finland).
Hospital during the period from August 1985 to August 1987. For all patients the diagnosis was based on a careful clinical neurological examination and ancillary investigations, e.g., cerebral computed tomography (CT). The control group consisted of 25 healthy volunteers from the staff of the hospital. The mean age in the patient group was 51.7 years (S.D. 12.6), and in the control group 43.3 years (S.D. ll.3). The mean height in the patient group was 172 cm (S.D. 7.7), and in the control group 166 cm (S.D. 8.8). The ratio males/females was 29/11 (males 72.5%, females 27.5%) in the patient group, and 10/15 (males 40%, females 60%) in the control group. The development of seizures was assessed twice during the follow-up period. Clinical neurological examinations and interviews of the patients were performed in the Department of Neurology about 2 3 months (56--99 days) and about 11.5-13 months (347 392 days) after the stroke. Seizures occurring within 2 weeks after the stroke were not taken into account. None of the patients was epileptic before the stroke. CT was performed at least once during the acute stage in all patients (days 1 21, mean 5.1, S.D. 5.3) and was abnormal in 32 patients (80%).
0168-5597/90/$03.50 ~ 1990 Elsevier Scientific Publishers Ireland, Ltd.
348 Eight patients (20%) had normal findings in the CT; for them the diagnosis was based on a history and a clinical neurological examination. During the acute stage (days 4-15, mean 8.5, S.D. 3.7), clinical neurological examination was carried out using a form specially designed for this study. Neurological deficits were observed in all patients except one. One year after the stroke, 8 out of 35 patients had neither neurological signs nor symptoms, and they returned to their previous way of living; 19 patients had neurological defects but were independent in the activities of daily living (ADL); 8 patients needed help in ADL. The tibial nerve SEPs were recorded 3 times: 4 - 1 9 days (mean 9.8 days), 56-100 days (mean 69 days) and 348-393 days (mean 370 days) after the onset of the symptoms. The posterior tibial nerves were stimulated with surface electrodes at the ankles on each side separately. The stimulation frequency was 3 Hz. The bandpass was 2 H z - 2 kHz in both channels. Analysis time was 200 msec. Each average consisted of 1500 trials, and this procedure was performed twice on both sides. The response in the peripheral nerve was recorded in the ipsilateral popliteal fossa. The latencies to peaks P40, N48, P57 and N75, and peak-to-peak amplitudes N32-P40, P40-N48 and P57-N75 were measured from an electrode situated in the midline 2 cm behind the C z position, using linked ears reference. The means of the latencies and amplitudes from both averages on each side were calculated. The interpeak latencies (IPLs) and side-toside differences were calculated from these means. Amplitudes were transformed to logarithms and side-to-side differences in the amplitudes were transformed to decibels by the formula: 1 0 . l o g ( a m p l a f f / a m p l n o n ) , where amplaff = amplitude on the affected side (in microvolts), amplno n = amplitude on the non-affected side (in microvolts). After these transformations the distributions of the amplitude parameters in the control group did not deviate significantly from the normal (i.e., gaussian) distribution (the Shapiro-Wilk test for normality). In the tibial nerve SEPs the following variables were used as criteria of normality: the P40-N75 IPL on the affected side, the side-to-side differences of P40, N48, P57 and N75 peak latencies,
T. KOVALA ET AL. the N32-P40, P40-N48 and P57-N75 peak-to-peak amplitudes on the affected side, and the side-toside differences of N32-P40, P40-N48 and P57N75 amplitudes. The limits of normality were: mean + 3 S.D. in the interpeak latencies, mean - 3 S.D. in the amplitudes (after logarithmic transformation), zero _+ 3 S.D. in the side-to-side differences (where the values were distributed symmetrically around zero) calculated from the control group. The absence of a peak was classified as amplitude abnormality. The correlations of the later occurrence of seizures with the findings in the CT, in the neurological examination and in the tibial nerve SEPs were tested with Fishers's exact test. Results Seizures occurred during the 1 year follow-up period in 10 (25%) of the 40 patients; 6 patients (15%) had 1 seizure, 4 patients (10%) had 2 or more seizures. The seizures were classified according to the classification of Dreifuss et al. (1981) accepted by the International League Against Epilepsy. Six patients had one or several partial seizures, 3 of them had one or several elementary seizures with motor symptoms, but preserved consciousness, and 3 of them had one or several partial seizures evolving to secondarily generalized seizures. In 4 patients the type of seizure could not be classified exactly because the beginning of the seizure was not seen by anyone, 2 of them had either partial seizures secondarily generalized or generalized tonic-clonic seizure; 1 patient had motor jerking during his seizures, and 1 patient had an unclassified epileptic seizure. N o n e of these 10 patients had had any attacks before the stroke. The seizures occurred in 9 patients during the period between 2 and 12 months after the stroke, and in 1 patient 25 days after the stroke. The findings in the tibial nerve SEPs recorded during the acute stage correlated clearly with the later development of seizures (Table I and Fig. 1), but no significant associations were found between the development of seizures and the following factors assessed during the acute stage: patient's age and gender, the level of vigilance, sensory and motor signs in the neurological ex-
SEPs AND SEIZURES AFTER STROKE
349
TABLE I The risk of secondary epileptic attacks in relation to the findings in the tibial nerve SEPs recorded during the acute stage. Significance levels were tested with Fisher's exact test (2-tailed). NS = P > 0.05. Tibial nerve SEPs
N 40
Amplitudes Abnormal Normal
13 27
katencies Abnormal Normal
15 25
Epileptic attacks Yes
No
(10 patients)
(30 patients)
8 2
5 25
5 5
P
Odds ratio
(95% confidence interval)
0.0006
20.0
(3.23 124)
2.0
(0.47 8.6)
0.003
13.5
(2.37 76.8)
0.0002
26.0
(3.99-169)
3.9
(0.64- 23.4)
0.001
21.0
(3.46- 127)
0.00008
36.0
(5.09- 254)
0.003
13.5
(2.37-76.8)
10 20 NS
Arnplitudes on the affected side
N32-P40 Abnormal Normal
9 31
P40-N48 Abnormal Normal
12 28
P57-N75 Abnormal Normal
6 34
6 4
8 2
3 7
3 27
4 26
3 27 NS
Side-to-side differences
N32-P40 Abnormal Normal
10 30
P40-N48 Abnormal Normal
11 29
P57-N75 Abnormal Normal
9 31
7 3
8 2
6 4
3 27
3 27
3 27
a m i n a t i o n , e v i d e n c e of m a s s d i s p l a c e m e n t in the C T a n d i n v o l v e m e n t o f t h e c o r t i c a l g r a y m a t t e r in
(47%) w i t h i n v o l v e m e n t o f b o t h t h e c o r t i c a l g r a y m a t t e r a n d the subcortical white m a t t e r of the
the CT. A slight trend
rolandic region had seizures during the follow-up in t h e c o r r e l a t i o n
p e r i o d , w h e r e a s o n l y 2 o u t o f 13 p a t i e n t s (15%)
b e t w e e n t h e f i n d i n g s in t h e C T a n d t h e d e v e l o p -
with involvement of only the subcortical white
m e n t o f s e i z u r e s . A s m a n y as 7 o u t o f 15 p a t i e n t s
matter of the rolandic region had
was
noted
seizures (the
350 Right
T. K O V A L A ET AL, Left
foot
first
85
first
foot
average
average
~PV
1.25 pv
48
Q
20
ms
20 ms
39./*
60
60
econd
7
average
~
47
20
v
econd
average
]l . z s p v
ms
20 ms
38.6
60
59 Fig. 1. The tibial nerve SEPs of a 30-year-old male (code 14) recorded from C" with A1A2 reference. This patient had several partial seizures with secondary generalization during the follow-up period. The responses to stimulation of the right foot are on the left and to stimulation of the left foot on the right. The first average on each side is above and the second average below. The P40-N75 IPL, and the side-to-side differences in peak latencies were normal. The P40-N48 peak-to-peak amplitude was abnormal when the left foot was stimulated (both the absolute value and the side-to-side difference were abnormal). The P57-N75 amplitude was normal.
odds ratio was 4.81, 95% confidence limits: 0.7829.6, P = 0.114 with Fisher's exact test). The development of seizures correlated significantly with abnormalities of amplitude of the tibial nerve SEPs recorded during the acute stage, but not with abnormalities of latency and IPLs (Table I). The development of seizures also correlated significantly with amplitude abnormalities in the second SEPs recorded 56-100 days after the stroke ( P = 0.006 with Fisher's exact test, the odds ratio was 9.33, the 95% confidence limits were 1.8447.2), but no significant association was found with amplitude abnormalities in the third SEPs recorded 348-393 days after the stroke. The abnormal side-to-side difference (absence or attenuation in relation to the non-affected side)
in the P40-N48 peak-to-peak amplitude was the finding with the highest correlation with the development of seizures (Table I and Fig. 2). As m a n y as 8 out of 11 patients (72.7%) with an absent P40 wave or abnormal side-to-side difference in the P40-N48 amplitude had one or more seizures during the follow-up period, whereas only 2 out of 29 patients (6.9%) with normal side-to-side difference in this component developed seizures. By using this variable as m a n y as 35 (8 + 27) patients (87.5%) could have been classified correctly; only 2 patients (5.0%) had false negative results, and only 3 patients (7.5%) had false positive results. N o false positive result was observed in the control group. In addition, this variable was abnormal in all the 4 patients who had recurrent epileptic
351
SEPs AND SEIZURES AFTER STROKE P40-N48 side-by-side difference ( a f f e c t e d s i d e / n o n . a f f , side) * 100%
odds ratio was 4.9, the 95% confidence limits were 1.08-22.6).
400.0%
Discussion 200.0%
100.0%
50.0%
25.0%
12.5%
6.25%
absent
***
no
l
(30 patients)
******
yes
I
(10 p a t i e n t s )
SEIZURES
Fig. 2. The scatter in the side-to-sidedifferences of the P40-N48 peak-to-peak amplitudes in the group of 30 patients with no seizures during the follow-up period, and in the group of 10 patients with one or more se;~ures during the follow-upperiod. * 1 patient.
attacks during the follow-up period. The association between the development of seizures and abnormality in the P40-N48 side-to-side difference in the second SEPs (56-100 days after the stroke) was still significant ( P = 0.003 with Fisher's exact test, the odds ratio was 13.5, the 95% confidence limits were 2.37-76.8), and in the third tibial nerve SEPs (348-393 days after the stroke) nearly significant ( P = 0.052 with Fisher's exact test, the
In the present study the development of one or more seizures during the first year after a supratentorial infarct could have been predicted by tibial nerve SEPs recorded during the acute stage in a majority of the cases (87.5%). Olsen et al. (1987) previously found that 50% of stroke patients with persisting paresis and cortical involvement developed seizures. Thus the predictability of this parameter combination was lower than that of the tibial nerve SEP alone in our study. The involvement of cortical structures is associated with a risk of epilepsy. Olsen et al. (1987) found that 26% of thr, patients with infarcts involving cortical stn,~:tures developed epilepsy, compared with only 2% of the patients with subcortical infarcts. In our series 47% of patients with involvement of the cortex developed seizures, compared with 15% of patients with subcortical infarcts. The abnormalities in the P40-N48 peak-to-peak amplitude (attenuation and absence) were better predictors of a seizure than abnormalities of the middle latency component P57-N75 and of the latencies and the IPL. It is widely agreed that the source of the P40 peak is probably a cortical generator located in the interhemispheric fissure (Cruse et al. 1982; Beri~ and Prevec 1983; Seyal et al. 1983; Desmedt and Bourguet 1985; Lesser et al. 1987). Thus, the P40 peak provides information concerning the function of the somatosensory cortex, possibly explaining why the SEPs had a better predictive value for the occurrence of seizures than the computed tomography, in which distinction between cortical and subcortical damage is difficult. In the present study the high correlation of the tibial nerve SEPs with the development of seizures after cerebral infarct suggests a possible clinical application of tibial nerve SEPs in this context. However, further study with a larger group of patients is needed before clinical usage can be recommended.
352
References Beri6, A. and Prevec, T.S. Distribution of scalp somatosensory potentials evoked by stimulation of the tibial nerve in man. J. Neurol. Sci., 1983, 59: 205-214. Cruse, R., Klem, G., Lesser, R.P. and Liiders, H. Paradoxical lateralization of cortical potentials evoked by stimulation of posterior tibial nerve. Arch. Neurol., 1982, 39: 222-225. Desmedt, J.E. and Bourguet, M. Color imaging of parietal and frontal somatosensory potential fields evoked by stimulation of median or posterior tibial nerve in man. Electroenceph. clin. Neurophysiol., 1985, 62: 1-17. Dreifuss, F.E., Bancaud, J., Henriksen, O., Rubio-Donnadieu, F., Penry, J.K. and Seino, M. Proposal for revised clinical
T. KOVALA ,ET AL. and electroencephalographic classification of epileptic seizures. Epilepsia, 1981, 22: 489-501. Lesser, R.P., Liiders, H., Dinner, D.S., Hahn, J., Morris, H., Wyllie, E. and Resor, S. The source of 'paradoxical lateralization' of cortical evoked potentials to posterior tibial nerve stimulation. Neurology, 1987, 37: 82-88. Olsen, T.S., H~genhaven, H. and Thage, O. Epilepsy after stroke. Neurology, 1987, 37: 1209-1211. Richardson, E.P. and Dodge, P.R. Epilepsy in cerebral vascular disease. Epilepsia, 1954, 3: 49-74. Seyal, M., Emerson, R.G. and Pedley, T.A. Spinal and early scalp-recorded components of the somatosensory evoked potential following stimulation of the posterior tibial nerve. Electroenceph. clin. Neurophysiol., 1983, 55: 320-330.
347
EVOPOT 89522
Correlation of tibiai nerve S E P s with the d e v e l o p m e n t of seizures in patients with supratentorial cerebral infarcts T. Kovala a, U. Tolonen a and J. Pyhtinen b Departments of a Clinical Neurophysiology and b Radiology, Oulu Unioersity Central Hospital, Oulu (Finland) (Accepted for publication: 22 November 1989)
Summary In 40 patients with supratentorial non-haemorrhagic cerebral infarct, the findings in the tibial nerve SEPs recorded during the acute stage correlated significantly with the development of seizures during a 1 year follow-up period. Abnormality in the side-to-side difference of the P40-N48 amplitude was the finding with the highest correlation with the development of seizures: 87.5% of the patients were classified correctly as to the risk of seizures. Key words: Epilepsy; Somatosensory evoked potentials; Cerebral infarction; Cerebral ischaemia; Posterior tibial nerve
A substantial proportion of patients with supratentorial cerebral infarct will suffer from later epileptic attacks (Richardson and Dodge 1954; Olsen et al. 1987). The involvement of the cortical structures has been shown to have a particular importance in the pathogenesis of epilepsy after stroke. Persistence of the paresis also seems to increase the risk of epilepsy (Olsen et al. 1987). In contrast, the EEG does not predict the risk of developing epilepsy (Olsen et al. 1987). The present study was conducted to evaluate whether tibial nerve SEPs might give some information about the risk of developing seizures after supratentorial cerebral infarct.
Patients and methods
The patient group consisted of 40 patients with supratentorial cerebral infarct treated in the Department of Neurology of Oulu University Central
Correspondence to: Tero Kovala, Department of Clinical Neurophysiology, Oulu University Central Hospital, 90220 Oulu (Finland).
Hospital during the period from August 1985 to August 1987. For all patients the diagnosis was based on a careful clinical neurological examination and ancillary investigations, e.g., cerebral computed tomography (CT). The control group consisted of 25 healthy volunteers from the staff of the hospital. The mean age in the patient group was 51.7 years (S.D. 12.6), and in the control group 43.3 years (S.D. ll.3). The mean height in the patient group was 172 cm (S.D. 7.7), and in the control group 166 cm (S.D. 8.8). The ratio males/females was 29/11 (males 72.5%, females 27.5%) in the patient group, and 10/15 (males 40%, females 60%) in the control group. The development of seizures was assessed twice during the follow-up period. Clinical neurological examinations and interviews of the patients were performed in the Department of Neurology about 2 3 months (56--99 days) and about 11.5-13 months (347 392 days) after the stroke. Seizures occurring within 2 weeks after the stroke were not taken into account. None of the patients was epileptic before the stroke. CT was performed at least once during the acute stage in all patients (days 1 21, mean 5.1, S.D. 5.3) and was abnormal in 32 patients (80%).
0168-5597/90/$03.50 ~ 1990 Elsevier Scientific Publishers Ireland, Ltd.
348 Eight patients (20%) had normal findings in the CT; for them the diagnosis was based on a history and a clinical neurological examination. During the acute stage (days 4-15, mean 8.5, S.D. 3.7), clinical neurological examination was carried out using a form specially designed for this study. Neurological deficits were observed in all patients except one. One year after the stroke, 8 out of 35 patients had neither neurological signs nor symptoms, and they returned to their previous way of living; 19 patients had neurological defects but were independent in the activities of daily living (ADL); 8 patients needed help in ADL. The tibial nerve SEPs were recorded 3 times: 4 - 1 9 days (mean 9.8 days), 56-100 days (mean 69 days) and 348-393 days (mean 370 days) after the onset of the symptoms. The posterior tibial nerves were stimulated with surface electrodes at the ankles on each side separately. The stimulation frequency was 3 Hz. The bandpass was 2 H z - 2 kHz in both channels. Analysis time was 200 msec. Each average consisted of 1500 trials, and this procedure was performed twice on both sides. The response in the peripheral nerve was recorded in the ipsilateral popliteal fossa. The latencies to peaks P40, N48, P57 and N75, and peak-to-peak amplitudes N32-P40, P40-N48 and P57-N75 were measured from an electrode situated in the midline 2 cm behind the C z position, using linked ears reference. The means of the latencies and amplitudes from both averages on each side were calculated. The interpeak latencies (IPLs) and side-toside differences were calculated from these means. Amplitudes were transformed to logarithms and side-to-side differences in the amplitudes were transformed to decibels by the formula: 1 0 . l o g ( a m p l a f f / a m p l n o n ) , where amplaff = amplitude on the affected side (in microvolts), amplno n = amplitude on the non-affected side (in microvolts). After these transformations the distributions of the amplitude parameters in the control group did not deviate significantly from the normal (i.e., gaussian) distribution (the Shapiro-Wilk test for normality). In the tibial nerve SEPs the following variables were used as criteria of normality: the P40-N75 IPL on the affected side, the side-to-side differences of P40, N48, P57 and N75 peak latencies,
T. KOVALA ET AL. the N32-P40, P40-N48 and P57-N75 peak-to-peak amplitudes on the affected side, and the side-toside differences of N32-P40, P40-N48 and P57N75 amplitudes. The limits of normality were: mean + 3 S.D. in the interpeak latencies, mean - 3 S.D. in the amplitudes (after logarithmic transformation), zero _+ 3 S.D. in the side-to-side differences (where the values were distributed symmetrically around zero) calculated from the control group. The absence of a peak was classified as amplitude abnormality. The correlations of the later occurrence of seizures with the findings in the CT, in the neurological examination and in the tibial nerve SEPs were tested with Fishers's exact test. Results Seizures occurred during the 1 year follow-up period in 10 (25%) of the 40 patients; 6 patients (15%) had 1 seizure, 4 patients (10%) had 2 or more seizures. The seizures were classified according to the classification of Dreifuss et al. (1981) accepted by the International League Against Epilepsy. Six patients had one or several partial seizures, 3 of them had one or several elementary seizures with motor symptoms, but preserved consciousness, and 3 of them had one or several partial seizures evolving to secondarily generalized seizures. In 4 patients the type of seizure could not be classified exactly because the beginning of the seizure was not seen by anyone, 2 of them had either partial seizures secondarily generalized or generalized tonic-clonic seizure; 1 patient had motor jerking during his seizures, and 1 patient had an unclassified epileptic seizure. N o n e of these 10 patients had had any attacks before the stroke. The seizures occurred in 9 patients during the period between 2 and 12 months after the stroke, and in 1 patient 25 days after the stroke. The findings in the tibial nerve SEPs recorded during the acute stage correlated clearly with the later development of seizures (Table I and Fig. 1), but no significant associations were found between the development of seizures and the following factors assessed during the acute stage: patient's age and gender, the level of vigilance, sensory and motor signs in the neurological ex-
SEPs AND SEIZURES AFTER STROKE
349
TABLE I The risk of secondary epileptic attacks in relation to the findings in the tibial nerve SEPs recorded during the acute stage. Significance levels were tested with Fisher's exact test (2-tailed). NS = P > 0.05. Tibial nerve SEPs
N 40
Amplitudes Abnormal Normal
13 27
katencies Abnormal Normal
15 25
Epileptic attacks Yes
No
(10 patients)
(30 patients)
8 2
5 25
5 5
P
Odds ratio
(95% confidence interval)
0.0006
20.0
(3.23 124)
2.0
(0.47 8.6)
0.003
13.5
(2.37 76.8)
0.0002
26.0
(3.99-169)
3.9
(0.64- 23.4)
0.001
21.0
(3.46- 127)
0.00008
36.0
(5.09- 254)
0.003
13.5
(2.37-76.8)
10 20 NS
Arnplitudes on the affected side
N32-P40 Abnormal Normal
9 31
P40-N48 Abnormal Normal
12 28
P57-N75 Abnormal Normal
6 34
6 4
8 2
3 7
3 27
4 26
3 27 NS
Side-to-side differences
N32-P40 Abnormal Normal
10 30
P40-N48 Abnormal Normal
11 29
P57-N75 Abnormal Normal
9 31
7 3
8 2
6 4
3 27
3 27
3 27
a m i n a t i o n , e v i d e n c e of m a s s d i s p l a c e m e n t in the C T a n d i n v o l v e m e n t o f t h e c o r t i c a l g r a y m a t t e r in
(47%) w i t h i n v o l v e m e n t o f b o t h t h e c o r t i c a l g r a y m a t t e r a n d the subcortical white m a t t e r of the
the CT. A slight trend
rolandic region had seizures during the follow-up in t h e c o r r e l a t i o n
p e r i o d , w h e r e a s o n l y 2 o u t o f 13 p a t i e n t s (15%)
b e t w e e n t h e f i n d i n g s in t h e C T a n d t h e d e v e l o p -
with involvement of only the subcortical white
m e n t o f s e i z u r e s . A s m a n y as 7 o u t o f 15 p a t i e n t s
matter of the rolandic region had
was
noted
seizures (the
350 Right
T. K O V A L A ET AL, Left
foot
first
85
first
foot
average
average
~PV
1.25 pv
48
Q
20
ms
20 ms
39./*
60
60
econd
7
average
~
47
20
v
econd
average
]l . z s p v
ms
20 ms
38.6
60
59 Fig. 1. The tibial nerve SEPs of a 30-year-old male (code 14) recorded from C" with A1A2 reference. This patient had several partial seizures with secondary generalization during the follow-up period. The responses to stimulation of the right foot are on the left and to stimulation of the left foot on the right. The first average on each side is above and the second average below. The P40-N75 IPL, and the side-to-side differences in peak latencies were normal. The P40-N48 peak-to-peak amplitude was abnormal when the left foot was stimulated (both the absolute value and the side-to-side difference were abnormal). The P57-N75 amplitude was normal.
odds ratio was 4.81, 95% confidence limits: 0.7829.6, P = 0.114 with Fisher's exact test). The development of seizures correlated significantly with abnormalities of amplitude of the tibial nerve SEPs recorded during the acute stage, but not with abnormalities of latency and IPLs (Table I). The development of seizures also correlated significantly with amplitude abnormalities in the second SEPs recorded 56-100 days after the stroke ( P = 0.006 with Fisher's exact test, the odds ratio was 9.33, the 95% confidence limits were 1.8447.2), but no significant association was found with amplitude abnormalities in the third SEPs recorded 348-393 days after the stroke. The abnormal side-to-side difference (absence or attenuation in relation to the non-affected side)
in the P40-N48 peak-to-peak amplitude was the finding with the highest correlation with the development of seizures (Table I and Fig. 2). As m a n y as 8 out of 11 patients (72.7%) with an absent P40 wave or abnormal side-to-side difference in the P40-N48 amplitude had one or more seizures during the follow-up period, whereas only 2 out of 29 patients (6.9%) with normal side-to-side difference in this component developed seizures. By using this variable as m a n y as 35 (8 + 27) patients (87.5%) could have been classified correctly; only 2 patients (5.0%) had false negative results, and only 3 patients (7.5%) had false positive results. N o false positive result was observed in the control group. In addition, this variable was abnormal in all the 4 patients who had recurrent epileptic
351
SEPs AND SEIZURES AFTER STROKE P40-N48 side-by-side difference ( a f f e c t e d s i d e / n o n . a f f , side) * 100%
odds ratio was 4.9, the 95% confidence limits were 1.08-22.6).
400.0%
Discussion 200.0%
100.0%
50.0%
25.0%
12.5%
6.25%
absent
***
no
l
(30 patients)
******
yes
I
(10 p a t i e n t s )
SEIZURES
Fig. 2. The scatter in the side-to-sidedifferences of the P40-N48 peak-to-peak amplitudes in the group of 30 patients with no seizures during the follow-up period, and in the group of 10 patients with one or more se;~ures during the follow-upperiod. * 1 patient.
attacks during the follow-up period. The association between the development of seizures and abnormality in the P40-N48 side-to-side difference in the second SEPs (56-100 days after the stroke) was still significant ( P = 0.003 with Fisher's exact test, the odds ratio was 13.5, the 95% confidence limits were 2.37-76.8), and in the third tibial nerve SEPs (348-393 days after the stroke) nearly significant ( P = 0.052 with Fisher's exact test, the
In the present study the development of one or more seizures during the first year after a supratentorial infarct could have been predicted by tibial nerve SEPs recorded during the acute stage in a majority of the cases (87.5%). Olsen et al. (1987) previously found that 50% of stroke patients with persisting paresis and cortical involvement developed seizures. Thus the predictability of this parameter combination was lower than that of the tibial nerve SEP alone in our study. The involvement of cortical structures is associated with a risk of epilepsy. Olsen et al. (1987) found that 26% of thr, patients with infarcts involving cortical stn,~:tures developed epilepsy, compared with only 2% of the patients with subcortical infarcts. In our series 47% of patients with involvement of the cortex developed seizures, compared with 15% of patients with subcortical infarcts. The abnormalities in the P40-N48 peak-to-peak amplitude (attenuation and absence) were better predictors of a seizure than abnormalities of the middle latency component P57-N75 and of the latencies and the IPL. It is widely agreed that the source of the P40 peak is probably a cortical generator located in the interhemispheric fissure (Cruse et al. 1982; Beri~ and Prevec 1983; Seyal et al. 1983; Desmedt and Bourguet 1985; Lesser et al. 1987). Thus, the P40 peak provides information concerning the function of the somatosensory cortex, possibly explaining why the SEPs had a better predictive value for the occurrence of seizures than the computed tomography, in which distinction between cortical and subcortical damage is difficult. In the present study the high correlation of the tibial nerve SEPs with the development of seizures after cerebral infarct suggests a possible clinical application of tibial nerve SEPs in this context. However, further study with a larger group of patients is needed before clinical usage can be recommended.
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References Beri6, A. and Prevec, T.S. Distribution of scalp somatosensory potentials evoked by stimulation of the tibial nerve in man. J. Neurol. Sci., 1983, 59: 205-214. Cruse, R., Klem, G., Lesser, R.P. and Liiders, H. Paradoxical lateralization of cortical potentials evoked by stimulation of posterior tibial nerve. Arch. Neurol., 1982, 39: 222-225. Desmedt, J.E. and Bourguet, M. Color imaging of parietal and frontal somatosensory potential fields evoked by stimulation of median or posterior tibial nerve in man. Electroenceph. clin. Neurophysiol., 1985, 62: 1-17. Dreifuss, F.E., Bancaud, J., Henriksen, O., Rubio-Donnadieu, F., Penry, J.K. and Seino, M. Proposal for revised clinical
T. KOVALA ,ET AL. and electroencephalographic classification of epileptic seizures. Epilepsia, 1981, 22: 489-501. Lesser, R.P., Liiders, H., Dinner, D.S., Hahn, J., Morris, H., Wyllie, E. and Resor, S. The source of 'paradoxical lateralization' of cortical evoked potentials to posterior tibial nerve stimulation. Neurology, 1987, 37: 82-88. Olsen, T.S., H~genhaven, H. and Thage, O. Epilepsy after stroke. Neurology, 1987, 37: 1209-1211. Richardson, E.P. and Dodge, P.R. Epilepsy in cerebral vascular disease. Epilepsia, 1954, 3: 49-74. Seyal, M., Emerson, R.G. and Pedley, T.A. Spinal and early scalp-recorded components of the somatosensory evoked potential following stimulation of the posterior tibial nerve. Electroenceph. clin. Neurophysiol., 1983, 55: 320-330.