Control of cortical excitability in epilepsy.
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Biomedical subjects
Publications and source records attributed to N Birbaumer.
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It is well known that the Stroop effect is subject to influence by same-modality primes, but the possibility of cross-modal priming effects is unclear. Smell is a fundamental sensory system that is assumed to have potent cross-modality priming effects. We might expect the presence of a specific odor to interfere with performance on Stroop cards containing odor-congruent words. Forty participants, half of whom were primed with an unpleasant odor and half with a pleasant odor, were examined with modified Stroop cards containing pleasant and unpleasant descriptive words. A significant Stroop card by odor group interaction was found, indicating that the presence of an odor interferes with the performance on an odor-congruent Stroop card. These findings demonstrate cross-modality priming between olfaction and vision.
The study was intended to answer the question whether self-regulation of brain activity can be operantly learnt when the brain is disconnected from motor periphery. Two neurological patients with nearly complete motor paralysis learned bi-directional control of their slow cortical potentials (SCP) at vertex. After 4-6 weeks training both patients could reliably differentiate between SCP shifts in a negative versus positive direction. With one patient, training has been continued for a subsequent 4 months, which resulted in precise self-control, i.e. the patient was able to produce positive SCP shifts on command with an accuracy of about 95%. This indicates that self-regulation of cortical excitability (as manifested in the SCP) does not require feedback loops from the periphery. Although we cannot rule out that healthy subjects may employ behavioral strategies such as muscle contractions or changes in breathing, obviously humans can also control their SCP without using these strategies.
Functional magnetic resonance imaging was used to determine the activation of the amygdala while seven social phobics and five healthy controls were exposed to slides of neutral faces as well as aversive odor stimuli. The amygdala was selectively activated in the social phobics during presentation of the face stimuli. The data show for the first time that the amygdala is active in human phobics when they are exposed to potentially fear-relevant stimuli. Further research is needed to determine the extent to which overactivation of the amygdala precedes or is a consequence of phobia.
The role of hypochondriasis in the attentional control of pain perception was investigated in 28 in-patients (12 women and 16 men) at a hospital for psychosomatic disorders, who had been classified into high- and low-hypochondriacal categories by means of the Illness Attitude Scales (IAS). The two groups did not differ in their basic pain sensitivity based on their heat pain thresholds. Attentional control was manipulated by a mental arithmetic task, resulting in one experimental condition with distraction and one without distraction. In both of the conditions, subjects rated the intensity and the unpleasantness of nonpainful and painful heat stimuli on visual analog scales (VAS). Distraction significantly reduced the perceived intensity and unpleasantness of the stimuli at painful levels but not at nonpainful levels. Contrary to our expectation, the individual level of hypochondriasis did not influence this result. Although distraction seemed to have a strong influence on pain perception, hypochondriasis as a symptom or a trait did not contribute to this effect.
A biofeedback procedure was used to influence participants' cortical polarity before the presentation of single digit multiplication problems. To ensure that participants could solve the problems by direct memory retrieval of arithmetic facts, only nine different multiplication problems were used, and participants received extensive pre-experimental practice on these problems. After biofeedback training, cortical positivity before problem presentation was associated with faster response initiation times, a measure of mental calculation time, for correctly solved problems and with more multiplication errors than cortical negativity. Response execution time, a measure of motor speed, was not affected by cortical polarity. The shift in positivity from the amplitude of the slow cortical potential (SCP) before problem presentation to the amplitude of the positive slow wave (pSW) after problem presentation was less in positivity-required compared to negativity-required trials, mainly because of the manipulation of SCP starting points by biofeedback. We assume that cortical positivity is associated with direct retrieval of arithmetic facts, more precisely with the inhibition of incorrect answers. Cortical positivity before task presentation results in a reduced positive shift, a sign of less inhibition before answer production. The effect of less inhibition during positivity-required trials is to produce faster responses and more errors. The opposite might to be true of cortical negativity.
Behavioral psychophysiological treatment entailing Slow Cortical Potential (SCP) biofeedback training and behavioral self-control training was conducted with a 27-year-old male epileptic patient (seizures for 23 years) with Wechsler IQ 64 who underwent callosotomy. The patient had 12/week secondary generalized tonic-clonic seizures. The treatment, consisting of 43 SCP training sessions and 22 behavioral control sessions, yielded a highly significant reduction of seizure frequency to about 7.5/week; such a decrease had never been observed after administration of new anticonvulsant drugs, nor after the callosotomy. During SCP feedback training, the patient was able to produce highly-significant cortical differentiation of SCPs of about 4 microV. In addition, he developed several new behaviors indicating growing ability of self-perception and self-regulation. These findings suggest that a combination of SCP biofeedback with behavioral treatment of epilepsy can be used even in mentally retarded patients with organic brain disorders.
The extent of the cortical somatotopic map and its relationship to phantom phenomena was tested in five subjects with congenital absence of an upper limb, four traumatic amputees with phantom limb pain and five healthy controls. Cortical maps of the first and fifth digit of the intact hand, the lower lip and the first toe (bilaterally) were obtained using neuroelectric source imaging. The subjects with congenital upper limb atrophy showed symmetric positions of the left and right side of the lower lip and the first toe, whereas the traumatic amputees with pain showed a significant shift (about 2.4 cm) of the cortical representation of the lower lip towards the hand region contralateral to the amputation side but no shift for the toe representation. In healthy controls, no significant hemispheric differences between the cortical representation of the digits, lower lip or first toe were found. Phantom phenomena were absent in the congenital but extensive in the traumatic amputees. These data confirm the assumption that congenital absence of a limb does not lead to cortical reorganization or phantom limbs whereas traumatic amputations that are accompanied by phantom limb pain show shifts of the cortical areas adjacent to the amputation zone towards the representation of the deafferented body part.
The causes underlying phantom limb pain are still unknown. Recent studies on the consequences of nervous system damage in animals and humans reported substantial reorganization of primary somatosensory cortex subsequent to amputation, and one study showed that cortical reorganization is positively correlated with phantom limb pain. This paper examined the hypothesis of a functional relationship between cortical reorganization and phantom limb pain. Neuroelectric source imaging was used to determine changes in cortical reorganization in somatosensory cortex after anesthesia of an amputation stump produced by brachial plexus blockade in six phantom limb pain patients and four pain-free amputees. Three of six phantom limb subjects experienced a virtual elimination of current phantom pain attributable to anesthesia (mean change: 3.8 on an 11-point scale; Z = -1.83; p < 0.05) that was mirrored by a very rapid elimination of cortical reorganization in somatosensory cortex (change = 19.8 mm; t(2) = 5.60; p < 0.05). Cortical reorganization remained unchanged (mean change = 1.6 mm) in three phantom limb pain amputees whose pain was not reduced by brachial plexus blockade and in the phantom pain-free amputation controls. These findings suggest that cortical reorganization and phantom limb pain might have a causal relationship. Methods designed to alter cortical reorganization should be examined for their efficacy in the treatment of phantom limb pain.
Biofeedback-supported self-regulation of slow cortical potentials (SCP) is increasingly being used for treatment of intractable epilepsy. However, it is unknown whether the acquired ability to regulate one's own cortical potentials remains stable over time. In this study, 18 patients with drug-resistant partial epilepsy performed 35 training sessions in which they learned to generate slow cortical potential shifts in either positive or negative direction. At the end of training, they differentiated significantly between required cortical positivity and required cortical negativity. Six months after this point, they still demonstrated an unchanged between-condition differentiation. The performance in the booster session was particularly good in trials without continuous SCP feedback. The ability to generate positive SCP shifts was related to decrease of seizure frequency during the 6 months follow-up period compared with the 3 month baseline period. This data indicate that the acquired ability of humans to regulate their cortical potentials did not decrease over a 6 month period but rather, tended to consolidate.
Associative connections between cortical cell assemblies representing pain-related memories should be stronger and more extensive in subjects with chronic pain. To test this hypothesis, the dimensional complexity of the electroencephalograph (EEG) was examined during the actual experience as well as during memory for pain. Nine chronic pain patients and nine matched healthy controls participated in the study. During acute pain induction, acute pain recall, personal stress and pain recall, the EEG was recorded from 15 scalp sites. Non-linear analysis, based on the theory of deterministic chaos, revealed higher and more widespread EEG complexity in the patients compared to the healthy controls only during the recall of the personal pain scene. The personal stress scene was rated equally aversive but did not induce more EEG complexity. These more extensive and more readily accessible pain memories may be instrumental for the persistence of chronic pain.
Fractal dimensions has been proposed as a useful measure for the characterisation of electrophysiological time series. But one of the problems of this approach, is the difficulty to record time series long enough of determine the 'real' fractal dimension. Nevertheless it is possible to calculate fractal dimensions for very short data-segments. Using time series of different length it is possible to show, that there is a monotoneous relation between fractal dimension and the number of data-points. This relation could be further interpreted with the help of an extrapolation scheme. In addition this effect is also seen with surrogate data, generated from that signal. We conclude that it is feasible to use fractal dimension as a tool to characterise the complexity for short electroencephalographic (EEG) time series, but it is not possible to decide whether the brain is a chaotic system or not.
The hypothesis of reorganization of the primary somatosensory cortex in states of chronic pain was assessed in 10 low back pain patients and nine matched healthy controls. Intracutaneous electric stimuli were applied to the left back and index finger at a standard, a non-painful and a painful intensity. Magnetic fields were recorded by a 37-channel BTi biomagnetometer from the hemisphere contralateral to the site of stimulation. The power of the early evoked magnetic field (< 100 ms) elicited by painful stimulation of the painful back in very chronic patients was elevated relative to that elicited by painful back stimulation of healthy controls and showed a linear increase with chronicity (r = 0.74). The maximum activity elicited in primary somatosensory cortex was shifted more medially in the very chronic back pain subjects. These data suggest that chronic pain is accompanied by cortical reorganization and may serve an important function in the persistence of the pain experience.
Sixteen subjects naive to biofeedback learned lateralised interhemispheric control of slow cortical potentials (SCPs) across electrode sites F3-F4 during three sessions of visual electroencephalograph (EEG) biofeedback. Subjects were required to generate slow negativity shifts either towards the left or the right hemisphere in sixty pseudorandomly ordered trials per session. Group 1 (n = 8) were told to use emotional strategies in the task (positive emotions for left hemisphere activation, negative emotion for right hemisphere activation), group 2 received no guidance. Both groups received feedback in the form of an on-screen rocket-ship, initially centrally placed, which rose to indicate an increase in left hemisphere negativity (relative to the right hemisphere) and fell to indicate an increase in right hemisphere negativity (relative to the left hemisphere). A 2 x 3 x 3 x 2 ANOVA (group x session x block x trial) showed no performance differences between the strategy and no strategy groups. Both groups learned to produce correct direction shifts in the final third of each session during both trial types (P < 0.001). The no strategy group showed a particularly strong within session learning effect (P < 0.0037) with poor performance in the early part of the sessions, and strong shifts at the end. Subjects high on withdrawal showed stronger rightward shifts in keeping with right hemisphere involvement in behavioural withdrawal. This is the first demonstration of self regulation of interhemispheric frontal asymmetry.
In a controlled clinical study, we investigated the effects of behavioral treatment on postural and gait initiation problems idiopathic Parkinson's disease (PD). Comparable groups of patients received therapy (experimental group, n = 15) and nonspecific psychological treatment (control group, n = 14) for 10 weeks. We monitored various variables reflecting properties of posture and gait initiation by using an optoelectronic motion analyzer (electronic movement analysis system, ELITE). A clinician blind to group membership of the patients assessed PD severity with the United Parkinson's Disease Rating Scale (UPDRS) before and after the treatment period. ELITE measures of postural stability and movement initiation revealed treatment-specific effects. In addition, UPDRS motor scores showed significant improvement only after behavioral treatment. We conclude that behavioral treatment in Parkinson's disease may improve motor disabilities in moderately advanced PD patients.
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Sixteen patients with partial epilepsy learned to produce positive or negative slow cortical potential shifts in a biofeedback condition during 20 consecutive training sessions. Visual ERPs to the presentation of the feedback and the discriminative stimulus were recorded at vertex. Regardless of the subjects' task (positivity versus negativity), amplitudes of the P2 (mean peak latency about 225 ms) and P3a (322 ms) components decreased across sessions, resulting in appearance and subsequent enhancement of a negative wave N2 (298 ms) between P2 and P3a. As N2 grew the P2 latency decreased and the P3a latency increased. Additionally, the P3b (472 ms) decreased with repetition, however, it did so slower than P2 and P3a. A comparison between the present data, on the one hand, and those obtained in the ERP habituation paradigm within one session, on the other hand, indicates that some repetition effects cannot be explained by habituation.
Nineteen chronic low back pain patients (aged 19-63) and 17 controls (aged 20-41) received electrical pain stimuli during manipulation of their carotid baroreceptors. The non-invasive mechanical manipulation of baroreceptors, using the PRES technique (Phase Related External Suction), simulates the end-effects of phasic blood pressure changes. This technique was developed to assess pain responses induced by changes in blood pressure without the typical shortcomings of pharmacological manipulation or lack of a control condition. During maximum baroreceptor activity, there was an unexpected increase in the amplitude of the somatosensory evoked potentials (SEPs) elicited by the electrical pain stimuli condition (N150-P260 peak-to-peak). In most other studies the opposite effect was found, with decreased pain responses during maximum baroreceptor activity. The chronic pain group reported greater pain during highest baroreceptor activation than did the controls. In addition, the chronic pain group showed lower diastolic blood pressure. To determine whether pain and baroreceptor responses observed in the chronic pain group depended on lower blood pressure levels, a second experiment with a non-clinical sample was performed. Results showed that lower tonic blood pressures are associated with greater baroreceptor activity amplifying pain, while higher blood pressure is associated with pain dampening during high baroreceptor activity. Data suggested that the differences in pain responses found in low back pain patients were associated with their lower tonic blood pressure levels. It is proposed that in general, lower blood pressures may be associated with greater pain during baroreceptor activation.