Clinical EEG (electroencephalography)最新文献

Two issues concerning sensorimotor EEG operant conditioning, or biofeedback, as a therapeutic modality for the treatment of seizure disorders are the focus of this review. The first relates to the question of whether relevant physiological changes are associated with this procedure. This question is addressed through review of an extensive neurophysiological literature that is likely unfamiliar to many clinicians but that documents both immediate and sustained functional changes that are consistent with elevation of seizure thresholds. The second focuses on the clinical efficacy of this method and whether it should carry the designation of "experimental". This designation is challenged through an assessment of over 25 years of peer-reviewed research demonstrating impressive EEG and clinical results achieved with the most difficult subset of seizure patients.

Significant public health concerns exist regarding our current level of success in treating ADHD. Medication management is very helpful in 60-70% of patients. Side effects, lack of compliance and the fact that stimulant medications cannot be given late in the day limit the benefits largely to school hours. While stimulants improve behavior and attention, less of an effect has been noted on academic and social performance. Continuing concerns exist about long-term safety, and studies on long-term cardiovascular and neurophysiological effects have not been carried out. Neurotherapy for ADHD offers an effective alternate for patients whose treatment is limited by side effects, poor medication response and in cases in which the patients and/or their parents refuse to consider medications. Studies indicate clinical improvement is largely related to measurable improvements in the EEG signature, evidenced by declining theta/beta ratios over frontal/central cortex and/or reduced theta/alpha band amplitudes.

Contrary to the belief that schizophrenic patients will be unable to learn self control of electrocortical activity due to attentional and motivational deficits, the two studies which have investigated this, both involving operant conditioning of slow cortical potentials, have demonstrated that self regulation can take place. This was particularly true of a study of interhemispheric control. Learning difficulties were found to be more to do with sustaining motivation towards the end of sessions or training programs, rather than in initial learning. Schizotypical features in the normal population have in the case of anhedonia been associated with slower learning, while withdrawn introversion has been associated with faster learning. In view of the affirmative evidence and advances in understanding the functional significance of electroencephalographic (EEG) rhythms, the undertaking of therepeutic regimens with electrocortical operant conditioning is warranted in the schizophrenia spectrum.

A review is presented of the currently sparse literature about EEG operant conditioning or biofeedback as a treatment to reduce symptomology and patient complaints following a traumatic brain injury. The paper also evaluates the general use of quantitative EEG (QEEG) to assess traumatic brain injury and to facilitate EEG biofeedback treatment. The use of an age matched reference normative QEEG database and QEEG discriminant function are presented as a method to evaluate the nature or neurological basis of a patient's complaints as well as to individualize an efficient and optimal feedback protocol and to help evaluate the efficacy of the biofeedback therapy. Univariate and multivariate statistical issues are discussed, different classes of experimental designs are described and then a "double blind" research study is proposed in an effort to encourage future research in the area of EEG biofeedback for the treatment and rehabilitation of traumatic brain injury.

QEEG was studied in a population of chronic male PSUD/ADHD (psychoactive substance use disorder/attention deficit hyperactivity disorder) subjects vs. a matched sample of non-ADHD subjects with PSUD. Our first interest in conducting this study was to determine if the Thatcher University of Maryland database and complex demodulation method could replicate the specific QEEG findings reported for cocaine and cannabis using the John-NYU database and Fourier Transform method. The effects of cannabis and stimulants were also studied both separately and together to see if there were interactions and to see if the QEEG changes associated with chronic stimulant dependence were predicted by childhood ADHD status. Eyes-closed QEEGs were obtained and two independent artifacted 60 second samples were compared for reliability. The Thatcher database was used to analyze QEEG data from 56 subjects with mixed substance use disorder. Results showed that the Thatcher database replicates the John database for chronic stimulant dependence findings. Because of confounding variables of alcohol and polysubstance abuse, the findings related to cannabis and stimulant interaction were difficult to assess. Cannabis and stimulant dependence together produced more QEEG changes than either alone. More right temporal abnormalities were observed with stimulant dependence. In the absence of stimulant use, the QEEG effects of cannabis were relatively small; however, sample selection and methods used precluded comparison to previous studies. The persistent QEEG abnormalities associated with chronic stimulant dependence were independent of ADHD status in this sample using the methods of this study. Further research is needed to clarify the relationship of stimulant dependence with QEEG changes and ADHD status, and to clarify the interactions of chronic stimulant and cannabis abuse on QEEG.

This study examined the course of EEG recovery in an animal model of hypoxic-ischemic injury. The model used periods of hypoxia, room air and asphyxia to induce cardiac arrest. One-week-old piglets (n = 16) were exposed to a period of hypoxia, room air and complete asphyxia for 7 minutes. After cardiac arrest and resuscitation, two EEG features were evaluated as prognostic indicators of behavioral outcome as assessed by a neuroscore at 24 hours after insult. A prominent EEG feature was the number and duration of bursts evident during recovery. Episodes of bursting were detected through the thresholds on sustained periods of elevated power. After the animal was resuscitated, the EEG was monitored continuously for 4 hours. To assess outcome in the recovering animal, a behavioral testing scale was used to test the animal's neurological capabilities. Trends of EEG burst counts were measured through thresholds on sustained power changes. Bursts are energy transients in the EEG record. High degrees of bursting were characteristic of animals having good neurological condition whereas piglets having low burst counts had poor 24 hr neuroscores. At 100 min the average burst rate of the good neuroscore outcome group was more than 8 per min and was significantly different from the poor outcome group's level of 2.7 (p < or = 0.05). When these counts were weighted by their total duration, differences between groups increased (p < or = 0.02). This study showed that the QEEG measure of burst counts and duration together provided a strong prognostic indication of the 24 hour outcome after asphyxic injury in a neonatal animal model. The critical determinant of the bursting character was the time when bursting occurred. Bursting occurring early in recovery was a good gauge of outcome. We conclude that quantitative EEG analysis and interpretation can be an important tool for the outcome determination during recovery from cerebral injury states.

A new formulation of death proposed in this study is based on the basic physiopathological mechanisms of consciousness generation in human beings. Two physiological components control conscious behavior: arousal and awareness (content of consciousness). We cannot simply differentiate and locate arousal as a function of the ascending reticular activating system and awareness as a function of the cerebral cortex. Substantial interconnections among the brainstem, subcortical structures and the neocortex, are essential for subserving and integrating both components of human consciousness. Therefore, consciousness does not bear a simple one-to-one relationship with higher or lower brain structures, because the physical substratum for consciousness is based on anatomy and physiology throughout the brain. This new account of human death is based on the irreversible loss of consciousness because it provides the key human attributes and the highest level of control in the hierarchy of integrating functions within the organism. The notion of consciousness as the ultimate integrative function is more consistent with the biologically-based systems than the more philosophically-based notions of personhood.