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Self-regulation of Slow Cortical Potentials in Normal Subjects and Patients with Frontal Lobe Lesions*
Self-regulation of Slow Cortical Potentials in Normal Subjects and Patients with Frontal Lobe Lesions* W. LUTZENBERGER, N. BIRBAUMER, T. ELBERT, B. ROCKSTROH, W. BIPPUS and R. BREIDT Instilute of Psychology, University of Tiibingen, Tiibingen, and Versorgungskrankenhaus, Tiibingen (F.R.G.)
Results from our laboratory demonstrated that normal human subjects ( S s ) are able to control their slow cortical potentials (SCPs) by means of a biofeedback procedure (Elbert et al., 1979, 1980). Ss acquire differential self-control of cortical negativity and positivity within one session; they are able to sustain the learned control in trials without feedback after about 80 trials with visual feedback of the SCP. Learned control of SCP has an influence on response speed and signal detection rate (Lutzenberger et al., 1979; Rockstroh et al., this volume). Reported changes of CNV in patients with frontal lobe lesions are inconsistent. Most of the studies (McCallum et al., 1970; McCallum and Cummins, 1973; Zappoli et al., 1976) reported smaller CNV compared to normals, a result which seems to be not restricted to frontal lesions but which was found also after lesions in other parts of the cortical surface. Research on CNV with ISIs longer than 2sec indicated two components: a first negativity after stimulus onset and a second component before presentation of the second imperative stimulus. The first component seems to be part of a decision process, the second motor responding. The first component was located toward the frontal brain, the second component more toward the central area (Rohrbaugh et al., 1976). We assume that patients with frontal lobe lesions are unable to control the first component of their SCP leaving the second component relatively unaffected. METHOD Subjects
Seventeen healthy male Ss (age 20-24) constituted the control group. Eight patients (male, age 20-40) with lesions of the frontal lobe only of traumatic origin constituted the experimental group. Time interval between the accident and the present experiment was longer than half a year. All patients were able to follow instructions, none was aphasic. Five patients were bilateral prefrontal, two left and one right prefrontal. Three patients (two with the left lesion, one with a bilateral lesion) had verified basal destructions in addition to the prefrontal lesion. The extension of the lesion was verified by computer tomography (2) or surgery (4). *This study was supported by the Deutsche Forschungsgemeinschaft (Grant Bi 195).
428 Design
The feedback stimulus was an outline of a small rocket ship which moved from the left to the right of a TV screen within 6 sec. Subjects were instructed to direct the rucket into one of two goals marked on the right side of the screen depending on the pitch of a signal tone. Rocket’s height was a linear function of the integral of the EEG from the onset of the signal tone: flying into one goal represented a change towards more cortical negativity, flying into the other a change towards less negativity or positivity. Ocular influences prevented successful control of rocket’s flight into the desired goal. Each feedback interval (6 sec) was followed by a reinforcement interval ( 5 sec) during which win and loss points informed about successful trials and failures (for details see Elbert et al., 1979, 1980). The experimental session consisted of 100 trials of 11 sec each with randomly varying intertrial intervals. Forty feedback trials alternated with 10 test trials without feedback during which subjects only heard the signal tones but neither saw the rocket nor the score on the TV screen. The EEG was recorded from vertex (C,) with the right earlobe as reference. Vertical eye movements (VEMs), electrocardiogram and skin conductance responses (SCRs) were recorded as in Elbert et al. (1979). Data reduction and analysis
For the analysis of the EEG a parametric model was developed, which assumed that the EEG is composed of a two-component model of SCP, an ocular influence, a serial dependency which can be described by an autoregressive filter of the 5th order and white noise. Parameters were fit to every single trial (see Lutzenberger et al., 1980). The first component is described by a linear increase within 1 sec and a linear decrease to the end of the feedback interval, the second component by a linear increase until the end of the feedback interval. The minimum of the autocorrection function of the EEG within a lag of 40 and 60msec was used as a measure of the EEG alpha. Mean heart rate and maximum heart rate changes within each feedback interval were measured. Skin conductance response (SCR) was described by the maximum change of skin conductance during the feedback interval referred to baseline. The effects were confirmed by an ANOVA with the factors group (G, normals vs. patients), polarity (P, trials with required negativity vs. trials with required positivity), series (S) and feedback (F, feedback trials vs. trials without feedback). RESULTS While there were no significant differences between groups in the second component of the SCP (due to large variance in the patient group) the ANOVA of the first component resulted in significant interactions G x P (F=6.68, P < 0.05), G x F x P (F=8.51, PeO.Ol), G x S x P (F=4.86, P e 0 . 0 5 ) and G x S x F x P (F=4.38, PtO.05, df= 1, 23): During feedback trials there was no difference between groups, but during test trials without feedback normals showed the best differentiation in SCP, especially in the second test, while patients were unable to produce the required differences without feedback (Fig. 1). In the second test without feedback, in which normals showed the
429 Patents
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Fig. 1. Mean first component of the SCP during feedback trials (F1 and F2) and trials without feedback (TI and T2). The hatched beams represents the trials with required cortical positivity.
largest differences, all patients performed more than 2 S.D.s poorer than the normals (PO.9). During trials without feedback normals had smaller SCRs and more alpha than during feedback trials, while patients had the inverse pattern (F=4.29, P < 0.05 for SCR, F= 13.14, P
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Analysis of the first 20 feedback trials and heart rate changes might be interpreted as effort of normal Ss to suppress the negative shift during trials with required positivity in contrast to the patient group, which seemed to have more difficulties in producing cortical negativity. REFERENCES Elbert, T., Birbaumer, N., Lutzenberger, W. and Rockstroh, B. (1979) Biofeedback of slow cortical potentials: self-regulation of central-autonomic patterns. In Biofeedback and Self-Regulation, N. Birbaumer and H. D. Kimmel (Eds.), Erlbaum, Hillsdale, N.J., pp. 321-337. Elbert, T., Rockstroh, B., Lutzenberger, W. and Birbaumer, N. (1980) Biofeedback of slow cortical potentials, I. Electroenceph. din. Neurophysiol., 48: 293-301. Hecaen, H. and Albert, M. L. (1978) Human Neuropsychology. Wiley and Sons, New York. Lutzenberger, W., Elbert, T., Rockstroh, B. and Birbaumer, N. (1979) The effects of self-regulation of slow cortical potentials on performance in a signal detection task. Inr. J . Neurosci., 9: 175-183. Lutzenberger, W., Elbert, T., Rockstroh, B. and Birbaumer, N. (1980) Biofeedback of slow cortical potentials. 11. Analysis of single event-related slow potentials by time series analysis. Electroenceph. din. Neurophysiol., 48: 302-31 1. McCallum, W. C. and Cummins, B. (1973) The effects of brain lesions on the contingent negative variation in neurosurgical patients. Electroenceph. elin. Neurophysiol., 35: 449456. McCallum, W. C., Walter, W. G., Winter, A., Scotton, L. and Cummins, B. (1970) The contingent negative variation in cases of known brain lesions. Electroenceph. din. Neurophysiol., 28: 120. Rohrbaugh, J. W., Syndulko, K. and Lindsley, D. B. (1976) Brain wave components of the contingent negative variation in humans. Science, 191: 1055-1057. Zappoli, R., Papini, M., Briani, S., Benvenuti, P. and Pasquinelli, A. (1976) CNV in patients with frontal-lobe lesions and mental disturbances. In The Responsive Brain, W. C. McCallum and J. R. Knott (Eds.), Wright and Sons, Bristol, pp. 158-163.
Results from our laboratory demonstrated that normal human subjects ( S s ) are able to control their slow cortical potentials (SCPs) by means of a biofeedback procedure (Elbert et al., 1979, 1980). Ss acquire differential self-control of cortical negativity and positivity within one session; they are able to sustain the learned control in trials without feedback after about 80 trials with visual feedback of the SCP. Learned control of SCP has an influence on response speed and signal detection rate (Lutzenberger et al., 1979; Rockstroh et al., this volume). Reported changes of CNV in patients with frontal lobe lesions are inconsistent. Most of the studies (McCallum et al., 1970; McCallum and Cummins, 1973; Zappoli et al., 1976) reported smaller CNV compared to normals, a result which seems to be not restricted to frontal lesions but which was found also after lesions in other parts of the cortical surface. Research on CNV with ISIs longer than 2sec indicated two components: a first negativity after stimulus onset and a second component before presentation of the second imperative stimulus. The first component seems to be part of a decision process, the second motor responding. The first component was located toward the frontal brain, the second component more toward the central area (Rohrbaugh et al., 1976). We assume that patients with frontal lobe lesions are unable to control the first component of their SCP leaving the second component relatively unaffected. METHOD Subjects
Seventeen healthy male Ss (age 20-24) constituted the control group. Eight patients (male, age 20-40) with lesions of the frontal lobe only of traumatic origin constituted the experimental group. Time interval between the accident and the present experiment was longer than half a year. All patients were able to follow instructions, none was aphasic. Five patients were bilateral prefrontal, two left and one right prefrontal. Three patients (two with the left lesion, one with a bilateral lesion) had verified basal destructions in addition to the prefrontal lesion. The extension of the lesion was verified by computer tomography (2) or surgery (4). *This study was supported by the Deutsche Forschungsgemeinschaft (Grant Bi 195).
428 Design
The feedback stimulus was an outline of a small rocket ship which moved from the left to the right of a TV screen within 6 sec. Subjects were instructed to direct the rucket into one of two goals marked on the right side of the screen depending on the pitch of a signal tone. Rocket’s height was a linear function of the integral of the EEG from the onset of the signal tone: flying into one goal represented a change towards more cortical negativity, flying into the other a change towards less negativity or positivity. Ocular influences prevented successful control of rocket’s flight into the desired goal. Each feedback interval (6 sec) was followed by a reinforcement interval ( 5 sec) during which win and loss points informed about successful trials and failures (for details see Elbert et al., 1979, 1980). The experimental session consisted of 100 trials of 11 sec each with randomly varying intertrial intervals. Forty feedback trials alternated with 10 test trials without feedback during which subjects only heard the signal tones but neither saw the rocket nor the score on the TV screen. The EEG was recorded from vertex (C,) with the right earlobe as reference. Vertical eye movements (VEMs), electrocardiogram and skin conductance responses (SCRs) were recorded as in Elbert et al. (1979). Data reduction and analysis
For the analysis of the EEG a parametric model was developed, which assumed that the EEG is composed of a two-component model of SCP, an ocular influence, a serial dependency which can be described by an autoregressive filter of the 5th order and white noise. Parameters were fit to every single trial (see Lutzenberger et al., 1980). The first component is described by a linear increase within 1 sec and a linear decrease to the end of the feedback interval, the second component by a linear increase until the end of the feedback interval. The minimum of the autocorrection function of the EEG within a lag of 40 and 60msec was used as a measure of the EEG alpha. Mean heart rate and maximum heart rate changes within each feedback interval were measured. Skin conductance response (SCR) was described by the maximum change of skin conductance during the feedback interval referred to baseline. The effects were confirmed by an ANOVA with the factors group (G, normals vs. patients), polarity (P, trials with required negativity vs. trials with required positivity), series (S) and feedback (F, feedback trials vs. trials without feedback). RESULTS While there were no significant differences between groups in the second component of the SCP (due to large variance in the patient group) the ANOVA of the first component resulted in significant interactions G x P (F=6.68, P < 0.05), G x F x P (F=8.51, PeO.Ol), G x S x P (F=4.86, P e 0 . 0 5 ) and G x S x F x P (F=4.38, PtO.05, df= 1, 23): During feedback trials there was no difference between groups, but during test trials without feedback normals showed the best differentiation in SCP, especially in the second test, while patients were unable to produce the required differences without feedback (Fig. 1). In the second test without feedback, in which normals showed the
429 Patents
T1
F2
T2
F1
T1
F2
T2
Fig. 1. Mean first component of the SCP during feedback trials (F1 and F2) and trials without feedback (TI and T2). The hatched beams represents the trials with required cortical positivity.
largest differences, all patients performed more than 2 S.D.s poorer than the normals (P
430
Analysis of the first 20 feedback trials and heart rate changes might be interpreted as effort of normal Ss to suppress the negative shift during trials with required positivity in contrast to the patient group, which seemed to have more difficulties in producing cortical negativity. REFERENCES Elbert, T., Birbaumer, N., Lutzenberger, W. and Rockstroh, B. (1979) Biofeedback of slow cortical potentials: self-regulation of central-autonomic patterns. In Biofeedback and Self-Regulation, N. Birbaumer and H. D. Kimmel (Eds.), Erlbaum, Hillsdale, N.J., pp. 321-337. Elbert, T., Rockstroh, B., Lutzenberger, W. and Birbaumer, N. (1980) Biofeedback of slow cortical potentials, I. Electroenceph. din. Neurophysiol., 48: 293-301. Hecaen, H. and Albert, M. L. (1978) Human Neuropsychology. Wiley and Sons, New York. Lutzenberger, W., Elbert, T., Rockstroh, B. and Birbaumer, N. (1979) The effects of self-regulation of slow cortical potentials on performance in a signal detection task. Inr. J . Neurosci., 9: 175-183. Lutzenberger, W., Elbert, T., Rockstroh, B. and Birbaumer, N. (1980) Biofeedback of slow cortical potentials. 11. Analysis of single event-related slow potentials by time series analysis. Electroenceph. din. Neurophysiol., 48: 302-31 1. McCallum, W. C. and Cummins, B. (1973) The effects of brain lesions on the contingent negative variation in neurosurgical patients. Electroenceph. elin. Neurophysiol., 35: 449456. McCallum, W. C., Walter, W. G., Winter, A., Scotton, L. and Cummins, B. (1970) The contingent negative variation in cases of known brain lesions. Electroenceph. din. Neurophysiol., 28: 120. Rohrbaugh, J. W., Syndulko, K. and Lindsley, D. B. (1976) Brain wave components of the contingent negative variation in humans. Science, 191: 1055-1057. Zappoli, R., Papini, M., Briani, S., Benvenuti, P. and Pasquinelli, A. (1976) CNV in patients with frontal-lobe lesions and mental disturbances. In The Responsive Brain, W. C. McCallum and J. R. Knott (Eds.), Wright and Sons, Bristol, pp. 158-163.