Somatosensory evoked potentials: Variability analysis in unilateral hemispheric disease

266

Electroencephalograp,~v and clinical Neurophysiology,, 1982, 54:266-274 Elsevier Scientific Publishers Ireland, Ltd.

S O M A T O S E N S O R Y EVOKED POTENTIALS: VARIABILITY ANALYSIS IN UNILATERAL HEMISPHERIC DISEASE P.K.H. WONG I C.T. LOMBROSO and Y. MATSUMIYA

Seizure Unit and Division of Neurophysiologv, Department of Neurology', Children's Hospital Medical Center, and the Department of Neurology', Harvard Medical School, Boston, Mass. 02115 (U.S.A.) (Accepted for publication: May 7, 1982)

Evoked potentials (EP) play an important role in clinical neurophysiology. Somatosensory spinal cord and brain stem evoked potentials may reveal pathology of peripheral nerve. Supratentorial lesions are more elusive and require particular care and effort (Starr 1978). Whereas peak latency and amplitude measures are usually adequate in testing sensory pathway conduction, there is often the need to study data from multielectrode sites before a meaningful diagnosis can be reached with cerebral lesions (Rrmond and Lesrvre 1965; Halliday et al. 1967; Goff et al. 1977). Our discussion will be confined to the longerlatency components of the somatosensory evoked potential (SEP). Cracco et al. (1979) have expressed doubts about the clinical value of such components, citing not only large inter- and intra-subject variations even in normals, but also the fact that the generators for these potentials are ill-understood. Lesions in the cerebral hemispheres cause changes in cortical somatosensory evoked potentials (SEP) depending on many factors: structures involved (locus), extent and type of deficit, and the time interval between the lesion and EP recording. Giblin (1964), Larson et al. (1966) and Shibasaki et al. (1977) studied such patients with cerebral lesions and obtained good correlation between clinical sensory deficit and SEP changes, with some Department of Paediatrics, University of British Columbia, Vancouver, B.C., Canada. Address reprint requests to P.K.H. Wong, EEG Dept., 4480 Oak St., Vancouver, B.C. V6H 3V4, Canada.

exceptions noted. Although he found good agreement in 34 of 42 cases, Giblin (1964) noted normal SEP in 7 patients with moderate to severe cortical sensory loss including unilateral extinction. Larson et al. (1966) noted that in stroke patients, SEP correlated well with clinical deficits in the acute phase, but not in the recovery phase. Williamson et al. (1970) studied 17 patients with unilateral cerebral lesions. They concluded that the degree of alteration of the SEP followed the extent of clinical sensory loss in 15 cases, but 2 patients had cerebral lesions and relatively normal SEP. Shibasaki et al. (1977) detected early SEP wave abnormalities over the diseased hemisphere in 82% of his cases. In our experience, we likewise encountered similar problems. In cases of mild deficits, by and large the commonest group, the SEP alone was usually insufficient to implicate which hemisphere was diseased. Hence it is clear that for the SEP to be clinically useful, we need some analytical methods with greater sensitivity. From a pilot study (Wong et al. 1981) we observed that the SEP recorded over the normal hemisphere seemed to be more reproducible from trial to trial than that recorded over the diseased hemisphere (Fig. 1). The next logical step was to quantify this phenomenon. For this we made use of the signal-to-noise estimation technique of Wong and Bickford (1980, see also Appendix). A systematic study of such EP 'variability' in 17 patients yielded encouraging results. We now present data illustrating the use of such analysis in 35 patients with unilateral supratentorial lesions.

SEPs: VARIABILITY ANALYSIS

267

STIMULATED L

LEFT

.A

/N

PAR I E T A L

~V k"~

RIGHT

# / '\,

MEDIAN

R

_

''~'"

NERVE L

R

/~' %/",-

\'t

',./

f,

PARIETAL

"'''~

i~ ~J

]5uV

200

RESPONSES

AVERAGED

50

RESPONSES

AVERAGED

200 msec.

X 4

Fig. 1. Data from case 26 showing a greater variability on the diseased right hemisphere.

Methods

(.4) Population The study was retrospective and was carried out in 2 stages. The first group consisted of 17 cerebral palsy patients with unilateral hemiparesis (Wong et al. 1981). The age ranged from 4 to 21 years (mean 11.8). Twelve had purely unilateral deficits, while 5 had predominantly unilateral deficits. Two were classed as 'minimal,' 9 'mild,' 4 'moderate' and 2 'severe.' These 17 and an additional 18 patients constitute our study group. Thus, 35 patients with ages between 3 days and 81 years (mean 12.1 years) were retrospectively selected for focal or unilateral supratentorial lesions. Patients with diffuse lesions were excluded, as were those with additional infratentorial, spinal cord or peripheral nerve involvement. The EP data were retrieved from the original FM tape. Obvious technical flaws as can be seen by the presence of artifacts constitute further reason for omission. A chart review was done on all patients to classify as best as possible the location, severity and extent of the lesion.

All 35 of our patients had motor deficits, with 12 showing some reported sensory involvement. Seizures, focal or otherwise, occurred in 17 cases. Most of our patients suffered the lesion prior to or at birth (22 cases). Other causes include arteriovenous malformation (3), stroke (3), porencephalic cyst (3), tumor (1), cerebral malformation (1), cerebral demyelination (1) and meningitis (1). The neurological findings of sensory and motor deficits were compiled using the following grades: (1) minimal = minimal neurological findings only, including equivocal unilateral reflex changes, impaired fine motor performance or arm drift but no sensory loss (pain, light touch, proprioception, 2 point discrimination, etc.), weakness nor spasticity; (2) m i l d = m i l d l y significant findings including weakness of 4 + power (scale used: 5 + = normal; 0 = hemiplegia) in one or both limbs, or face, mild tone and reflex increases, a n d / o r mild sensory loss; (3) m o d e r a t e = moderate weakness (2 + or 3 + out of 5), a n d / o r moderate sensory loss; (4) severe = severe weakness (0 or 1 + out of 5), a n d / o r sensory loss including hemi-anesthesia or hemi-neglect.

268 Our population is thus biased towards motor and away from sensory involvement (23 patients had no reported sensory findings). Part of the reason for this may be due to the younger age group (mean age 12.1 years). As sensory examination is often unreliable in younger patients, it is likely that more of the population studied had also some undisclosed sensory involvements,

(B) Evoked potential testing Usually 200 responses were averaged for each trial from either median or ulnar nerve stimulation. Informed consent was obtained from all patients or their parents. No experimental or nonstandard procedures were included. Electrode positions p~, P4, and occasionally C 3, C4, were used, with linked ears as reference. The stimulus intensity was adjusted to be 3 mA above motor threshold. The usual care was taken to maintain good artifact-free conditions and to ensure the same conscious state of the patient. Most of the trials were split as follows: 50 stimuli were delivered to first one side (random choice), then 100 were delivered to the other side, then the remaining 50 delivered to the first side. This controlled to a degree any gradual change in patient recording condition. Interstimulus intervals were usually 2 - 4 sec. Data analysis was done via a microcomputer using 8 bits of analog-to-digital precision. Playback of the raw data was monitored by an oscilloscope, allowing manual rejection of suspect data. Analog filters (3dB points: 1-100 Hz, 24 dB roll-off) were used with a 500 Hz sampling rate for a 512 msec epoch with 256 data points. Such a low cut-off frequency was used because it is adequate for the slow long-latency components. As stated, we were not interested in resolving the earlier fast components which would require much higher bandwidth and sampling rate. Automatic on-line artifact rejection by voltage overload sensing was also done. Averaged data consisting of the EP and its noise estimate were viewed on a video graphics display, the P ratios calculated, and all data saved onto floppy diskettes. The on-line results from computer averaging yield 2 tracings: the traditional EP and a noise estimate (or + / average, for details and exam-

P.K.H. WONG ET AL. ples refer to Appendix and Wong and Bickford 1980). It has been shown that the ratio, P, of the power of the EP curve to that of the noise curve is correlated with the degree of reproducibility of the EP. In other words, if repeated trials of EPs were done, the ones with a high P ratio would have low variability and could be superimposed very well in the manner used in Fig. 1. Those with P ratios in between have been shown to exhibit subtle differences in peak latencies and amplitudes. Finally, EPs with a low P ratio have gross and unpredictable errors in morpology, peak latency and amplitude. Any of these can lead to erroneous conclusions.

Results

Firstly, the data from the initial group of 17 patients will be analyzed. Component analysis was carried out by measuring the peak latencies and amplitudes of the first 4 major peaks (N20, P100, N140, P220). For ease of comparison, a simple semi-quantitative method was applied. Each EP carried 8 measures (4 peaks, each with a latency and an amplitude measure). Corresponding peaks of the EPs from both sides were compared: the side with greater latency or lower amplitude was assigned to be abnormal. Thus, 8 such assignments were obtained for an individual patient, Each assignment was then marked as correct or incorrect. If correct, a 'Y' (yes) score was applied, and if not, an ' N ' (no) given. Thus, we end up with 8 such 'Y' or ' N ' scores per patient. Table Ia summarizes the results. Ideally, a perfect diagnostic accuracy would occur if all scores were 'Y.' While this might occur with severe clinical deficits accompanying massive lesions, mild or minimal cases would be expected to have a lower yield. Such a trend is suggested by Table Ia: the 'minimal' and 'mild' groups were correct only 29 out of 57 times (51%), while the figure was 15 out of 21 (71%) for the 'moderate' and 'severe' groups. Overall, the prediction accuracy was only 56%. This low yield had also to be considered in the light of another major difficulty: that at times, the peak latency a n d / o r amplitude could not be measured. In this case we omit the missing values from

269

SEPs: VARIABILITY ANALYSIS

f u r t h e r c o m p i l a t i o n . Also, l o c a l i z a t i o n o f t e n differed b e t w e e n m e a s u r e s o b t a i n e d f r o m d i f f e r e n t p e a k s in the s a m e p a t i e n t . F o r e x a m p l e , the N 2 0 a n d N 1 4 0 , say, m i g h t p o i n t to o n e side as a b n o r m a l , w h i l e P100 a n d P200 m i g h t i m p l i c a t e the o t h e r side. S u c h a m b i g u i t i e s are a s i g n i f i c a n t p r o b l e m for c o m p o n e n t analysis a n d r e m a i n s unsolved. L i k e l y this c a n be r e s o l v e d o n l y w i t h detailed k n o w l e d g e of the n a t u r e a n d i d e n t i t y of the respective neuronal generators. T u r n i n g n o w to v a r i a b i l i t y analysis on the s a m e 17 p a t i e n t s , t h e r e are 2 m e a s u r e s f r o m e a c h patient: the P ratios of the S E P s f r o m each side. U s i n g the s a m e s c o r i n g t e c h n i q u e , a ' Y ' was ass i g n e d if the P r a t i o was l o w e r o n the a b n o r m a l side. If not, an ' N ' was assigned. T h i s p r o c e d u r e was similar to d o i n g a sign test o n the data. Fig. 2 p r e s e n t s r e p r e s e n t a t i v e tracings: A a n d B w e r e from one patient, C and D from another. A and C

TABLE I Combined amplitude + latenc) scores for 1st 4 peaks. Score

Severity

Total

Min. + mild

Mod. + severe

(a) Component analysis 'Y" 'N'

29 28

"Y' +'N"

57

17 cases 15 6

~

21

(b) Variability analysis 'Y' "N'

.....

I

5 I

11

!

78 (100%)

- -

17 cases

7 4

'Y'+'N'

44 (56%) 34 (44%)

+

I

12 (70%) 5 (30%)

6

-

17(100%)

I

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65.7 !

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Fig. 2. Examples of 2 cases with EP (top tracing), noise estimate (lower tracing) and P ratio. A and B are from 1 patient, and C, D from another. Both A and C are over the diseased hemisphere with the lower P ratios. The first case is clinically more severe than the second. Note the lack of obvious asymmetry in the second case, and that there is subtle difference in the P ratios.

P.K.H. W O N G ET AL.

270 TABLE 11 Variability analysis - - 35 cases. No.

Age

C.C. b

Side

Grade

Lesion DX ,I

P ratio c

PPV

Y/N ~

Minimal 1 a 2 a 3 a

Mild 4 5 6 7 8 9 ~,

10 ~ 11 ~ 12 a 13 a 14 d 15 ~

2 1:6 10: 6:10

1,2 2 2

R L L

1+ I+ 1+

CP CP CP

14.4/6.8 3.4/16.9 17.0/48.6

2.12 4.97 2.86

N N N

3d (3: 16: 8: 4: 16 : 7:6 9: 17: 4: 14: 10: 6:

? R R R R L L L L L R R>L R>L

9 2+ 2+ 2+ 2+ 2+ 2+ 2+ 2+ 2+ 2+ 2+/1+ 2+/1 +

PERI.INS CP) PREN.VIR IUGR CP 1UGR CP, I U G R CVA CP CP CP MEN PERI.INS

0.99/3.67

3.71

Y

1 2 2,3 1,2 1,2,3 1,2 2 1,2 2 1,2,3 1,2 5

9.13/21.7 31.9/46.1 2.25/6.23 30.7/14.1 83.2/23.1 28.7/19.5 46.9/21.0 25.0/13.1 25.9/16.8 3.7/1.1 3.4/7.6

2.38 1.45 2.77 2.18 3.6 1.47 2.23 1.91 1.54 3.36 2.24

Y Y Y Y Y Y Y Y N N Y

19:6 2,3 +4d 13: 81: 2 9: 2 12:8 1,2 : 10 1,2 :9 1,2 1 1 1,2,3 14 2,3 10 1,2,4 15 1,2,3 1 10 1,2 :9 1,5 10: 3,5 15: 1,5 18: 2,3 (post L hemispherectomy:

R R L R R R L L R R R R R L>R R>L R>L L

3+ 2+ 3+ 3+ 3+ 3+ 3+ 3+ 3+ 3+ 3+ 3+ 3+ 2+/3+ 3+/1 + 3+/2+ 3+ 4+

?MS

22.0,/79.3 64.5/97.0 23.1/2.81 1.36/9.49 1.35/39.3 3,46/6.29 3.35/1.89 3.36/1.48 0.331 / 1.963 6.8/28.7 2.1/3.0 2.4/21.0 0.03/0.16 2.54/0.25 4.6/12.2 5.2/4.4 6.7/4.97 20.1/2.44

3.6 1.50 8.22 6.98 29.1 1.82 1.77 2.27 5.93 4.22 1.43 8.75 5.33 10.2 2.65 1.18 1.35 8.25)

Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y N Y

13 : 13:6 17 : 5:

L R R L

4+ 4+ 4+ 4+

53.1/3.3 1.8/21.9 18.2/74.5 6.94/0.70

16,1 12.2 4.09 9.91

Y Y Y Y

Moderate

16 17 18 19 20 21 22 23 24 a 25 ~ 26 a 27 28 29 ;' 30 ~ 31

POR CY CVA POR CY PREN.VIR AVM HYPOX AVM CP MALFOR CP POR CY IVH, CP CP CP PERI.1NS

Set, ere

32 33 a 34 a 35

1,2 2,3 1,2,4 1,2,3

CVA CVA Thai.tumor AVM

~' Denotes 1st group of 17 patients. b Code for Chief Complaints: 1 = seizure, 2 = hemiparesis, 3 = sensory loss, 4 = hemiatrophy, 5 = asymmetric quadriparesis. " P ratio always given right/left; P A I R E D P VALUES (PPV) always a r r a n g e d > 1. d DX. code: CP = cerebral palsy; I U G R = intrauterine growth retardation; PREN.VIR = prenatal viral infection; PERI.INS = perinatal hypoxic insult; C V A = c e r e b r a l vascular accident; POR C Y = p o r e n c e p h a l i c cyst; A V M = a r t e r i o v e n o u s malformation; M E N . = meningitis; HYPOX = hypoxic injury; M A L F O R = cerebral malformation; IVH = intraventricular hemorrhage. Y--correct prediction of disease side; N =incorrect.

SEPs: VARIABILIT Y ANALYSIS

271

were recorded over the diseased hemisphere. The first case was from the 'moderate' group, showing large noise components and a 'noisy' EP. The PPV (see below) was 5 . 1 - 1.8= 2.83 and correctly pointed to the diseased side. The other case was from the 'mild' group, the EPs being almost identical and with little noise. The PPV was 65.7 + 49.2 = 1.34, again correctly lateralized. The fact that C and D were so similar underscores the difficulty we alluded to in using traditional component analysis. The P ratio which we are testing as an alternate measure has the advantage of being at least unambiguous. Table Ib summarizes the data. The 'minimal' and 'mild' groups yielded 7,/11 (or 64%) accuracy, while the 'moderate' and 'severe' group showed 5 / 6 (or 83%) accuracy. Overall, the P ratio method yielded a 70% accuracy. Table II presents the data for the entire group of 35 patients. One patient was tested twice, thus there are 36 results presented. The presenting symptoms and signs, side of lesions (established beyond doubt on clinical or CT grounds), severity and the P ratios are listed. Further, the P ratios were arranged with the greater value as numerator, and a paired P value calculated. The result is a single value always greater than or equal to 1. If equal to 1, it indicates equal variabilities bilaterally. The last column indicated whether the lower P ratio was on the diseased side. Overall, there were 30 'Y' (83%) and 6 ' N ' (17%). The breakdown for 'Y' according to severity is as follows: 'minimal' - - 0 / 3 (0%), 'mild' - - 10/12 (83%), 'moderate' - 16/17 (94%), and 'severe' - - 4 / 4 (100%). The increased overall yield of 83% as compared to 70%

TABLE III Variability analysis - - 35 cases. Statistical analysis of results from Table lI. Grade

Severity

Total

Min. + mild

Mod. + severe

'Y' 'N'

10 5

19 1

29 6

'Y+N'

15

20

35

Fisher's P =

29!x6!x 15!x20! =0.037 ( P <0.05). 3 5 ! x 1 0 ! x 1 9 ! × 5 ! x 1!

for the first 17 patients (marked with *) probably reflects a greater number of 'moderate' and 'severe' cases. Finally, the entire group of 35 patients could be viewed as a 2 X 2 contingency table (Table III) and analyzed for statistical significance by Fisher's Exact Test. This non-parametric procedure determines the probability of obtaining such an extreme distribution (favoring a high prediction ability of the EP test). The null hypothesis is that Table III was a random process, i.e., that the distribution of 'Y' and ' N ' occurred by chance. Fisher's Exact Test gave a probability of that hypothesis being true as P = 0.037, thus satisfying a confidence level of P less than 0.05. In other words, the result in Table III was not likely chance occurrence, despite any problems associated with it as discussed. This lends weight to the approach of using the pair P values in the way we have described.

Discussion The use of such a simple comparison test of the P values to assign correct or incorrect predictions of lesion side obviously has short-comings. An improvement would be to determine the statistical range of variation of the P ratio in a control group, establish a value for a given level of probability significance, and then apply such a value to determine whether a particular test prediction was correct or not. Although the control data for such a varied group (large age range) would be difficult to get, it nevertheless has clear statistical merit. It is worth mentioning that the P ratio is independent of the absolute EEG amplitude of either hemisphere. That is, it is irrelevant whether the average amplitude of the EP from the good side is different from that of the diseased side. This is because the amplitudes cancel out during the ratio calculation. Thus, there is no merit to the argument that changes in the P ratios may be due to a higher background E E G on the diseased side (or the good side for that matter). The overall diagnostic accuracy (83%) obtained by variability analysis is encouraging, particularly since it is an entirely objective procedure,with no

272 observer bias. A critical comparison with traditional analysis is not easy: our attempt to compare these two methods using 17 patients was adopted for its operational ease, and is not an in-depth analysis. The problems as mentioned were missing peaks and intra-subject inconsistencies. Missing peaks were encountered on both normal and diseased sides. Due to the retrospective nature of the study, we had little choice but to omit these measures from our compilation. Intrasubject inconsistencies present more of a problem: in any one patient, one or more of the components analyzed might indicate disease on one side, while the rest of the components might point to the opposite hemisphere. In lesions of peripheral and spinal pathways, there is justification to put greater emphasis on the earlier components. Williamson et al. (1970) discussed the issue of 'lemniscal' versus 'extralemniscal' pathways, thought to separately account for early ( < 80 msec) and later components. They presented data refuting such a hypothesis in their patients with unilateral cerebral lesions. As little is known about the generators of the later components, and there are even controversies among the small amount of existing data (e.g., Hazemann et al. 1969; G o f f et al. 1980), it is not justified to arbitrarily assign weighting factors or omit components. We thus viewed such intrasubject inconsistencies as 'scatter' in the data and perhaps reflecting our lack of understanding. Case 4 in Table II presents a provocative thought. He was studied at 3 days of age after perinatal hypoxic insult. Clinical examination did not show lateralizing findings. At 3 years of age, he exhibited persistent left-sided epileptic seizures with right focal discharges seen on EEG. This agreed with the neonatal SEP data which showed a greater variability on the right side (paired P value 3.71). We did not have the opportunity to retest him. Another patient, case 16, was studied twice 4 days apart. She had an undiagnosed right subcortical lesion which spontaneously improved prior to retesting. Her first SEP had P ratios R / L = 22.0/79.3, the paired P value being thus 79.3 + 22.0 = 3.60. This indicates a greater variability on the diseased (R) side. The repeat study during the recovery phase showed correctly lateralized P ratios but decreased paired P value of 1.50. It is tempting

P.K.H. WONG ET AL. to ascribe this drop in variability of the diseased hemisphere to recovery of the involved neuronal structures. Case 31 offers another point for discussion. He had left, cerebral atrophy secondary to birth trauma. A left hemispherectomy was performed for intractable seizures. The paired P value ( R / L ) before surgery was low at 1.35 but correctly lateralized. Also, the SEP from the left was abnormal in morphology as compared to the right. After hemispherectomy, no discernible SEP was seen on the left. The paired P ( R / L ) value increased to 8.25, reflecting a much decreased signal from the now missing left hemisphere. These particular examples, and the good overall prediction accuracy, suggest that variability may be a useful parameter for EP studies, despite operational difficulties mentioned above. Care has to be exercised during testing. Patient state changes can influence the results dramatically. Movements and other artifacts are also important. Such 'extrinsic' factors will cause increased variability and may well overshadow the 'intrinsic' neuronal variability that we are looking for. Ideally, randomly alternating right- and leftsided stimulation would be best. Also, simultaneous bilateral stimulation might prove useful. Such procedures will negate any changes in patient state and might yield more unbiased data. We have controlled for such factors to an extent by supplying n / 4 stimuli to first one side, then the other for n / 2 times, then finally back to the first side for n / 4 stimuli. As in the case of Williamson et al. (1970), we used the known normal side of each patient for comparison, thus skirting the issue of inter-subject variations. With greater number of patients and normal subjects, we hope to establish guidelines and confidence limits for the P ratio data. In all likelihood, it is hoped that variability measure may complement traditional EP analysis and routine E E G studies, and refine the ability to localize dysfunctional regions. An important point worth emphasizing is that the P ratio by itself is just a statistic: it cannot indicate the presence or absence of valid EP components. When used in conjunction with knowledge of normal EP morphology and skepticism

SEPs: VARIABILITYAN£LYSIS about possible artifacts, it can be of help. A high P ratio may be caused purely by large myogenic reflex components. Conversely, a low P ratio may reflect possible problems, starting from the stimulating equipment, peripheral nerve, spinal pathways, brain stem, thalamus, etc., all the way to the cortex. A lesion in the peripheral pathways may yield the same P values as one affecting the hemisphere. The P ratio can be seen as a reasonably suitable measure of EP variability in our present patient data. To try to explain the reason for the difference in variability, we make the following hypothesis: when stimulated, normal neurons generate stable and reproducible scalp potential changes (EP). Diseased neurons may not, thus giving a more variable response. This in turn can be seen as an increase in 'randomness' or 'noise' of the EP, causing the P ratio to fall. Extrinsic causes of variability must be controlled for. These include patient states, artifacts and other sources of noise. An important source of error is the presence of myogenic components in the EP. By nature of their also being time-locked to the stimulus, they are treated as 'signal' and thus artificially increase the P ratio. To guard against this error, all EPs should be inspected prior to calculation of P ratios.

Summary A new method to study SEP using signalto-noise estimate was applied to 35 patients (age 3 days-81 years, mean 12.1 years) with unilateral supratentorial cerebral lesions. The patients were grouped according to severity of deficits: minimal, mild, moderate and severe. Based on the observation that the SEPs were much more variable over the diseased hemisphere, we proposed the following hypothesis: normal neurons when stimulated generate a series of wave forms which are stable and reproducible. These are seen as stable and 'clean' scalp EPs. Diseased neurons on the other hand are malfunctioning and may tend to depolarize erratically. This can be seen as variable, 'noisy' and poorly reproducible EPs.

273 To test this hypothesis, we measured the degree of variability of the SEPs on both the normal and affected sides, using the technique of Wong and Bickford (1980). Overall, 30 of the 36 SEPs (83%) had a greater variability on the diseased side. The prediction accuracy was greatest with the severely affected cases and least in the minimally affected cases. There are minor suggestions that the variability parameter may be useful for long-term follow-up. Clearly, if used with care, the amount of 'noise' in an EP can be a useful parameter.

R6sum6 Potentiels bvoquOs somesthbsiques: btude de leur variabilitb lors de lbsions cbrbbrales unilatbrales Une nouvelle m6thode d'6tude des potentiels 6voqu6s somesth6siques (PES) bas6e sur l'estimation du signal par rapport au bruit a 6t~ appliqu6e 35 patients (ag6 de 3 jours h 81 ans, moyenne: 12,1 arts) avec 16sion c6r6brale supratentoriale unilat6rale. Ces patients 6taient regroup6s selon l'importance de leur d6ficit: minimal, b6nin, mod6r6 ou s6v6re. Nous proposons l'hypothbse suivante, bas6e sur l'observation d'une bien plus grande variabilit6 des PES sur l'h6misph6re atteint: des neurones sains r6pondent ~t une stimulation par une s6rie d'ondes stables et reproductibles; celles-ci forment des PE de scalp stables et 'nets'; par opposition, des neurones anormaux ne fonctionnent pas correctement et peuvent se d6polariser de faqon erratique entrainant des PE variables, 'bruyants' et peu r6productibles. Pour tester cette hypoth6se, nous avons mesur6 le degr6 de variabilit6 des PES du c6t6 sain et du c6t6 malade, en utilisant la m6thode de Wong et Bickford (1980). Parmi 36 PES, 30 (83%) avaient une variabilit6 du c6t6 malade. La pr6cision de la pr6diction 6tait plus grande dans les cas de d6ficit s6v6re et plus faible darts les cas de d6ficit minimal. Ces r6sultats sugg6rent que le param6tre de variabilit6 peut &re utile dans les cas suivis sur une longue p6riode, la quantit6 de 'bruit' dans l'6tude des PE peut &re un param6tre utile.

274

P.K.H. WONG ET AL.

Appendix The post-stimulus EEG can be represented by E ( t ) -- s ( t ) + n ( t ) where s(t)= signal component (time-locked); n(t) = n o i s e (i.e., all n o n - s i g n a l c o m p o n e n t s ) . T h e a v e r a g e d E P a f t e r N s t i m u l i is: An(t)=

s(t) +n(t),

t-- 1-256

A n i n d e p e n d e n t e s t i m a t e o f a v e r a g e n o i s e is:

A; (t)= ~i=l

toN,

Neven

i.e., a ' + / - ' a v e r a g e . A ratio, P , c a n b e c a l c u l a t e d : p:

Var(A • ) Var(A~)

P c a n b e s h o w n to e s t i m a t e t h e s i g n a l - t o - n o i s e r a t i o o f t h e o r i g i n a l d a t a set, t h e EP.

References Cracco, R.O., Cracco, J.B. and Anziska, B.J. Somatosensory evoked potentials in man: cerebral, subcortical, spinal and peripheral nerve potentials. Amer. J. EEG Technol., 1979, 19: 59-81. Giblin. D.R. Somatosensory evoked potentials in healthy subjects and in patients with lesions of the nervous system. Ann. N.Y. Acad. Sci., 1964, 112: 93-142.

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