Characteristics of evoked potential multiple EEG recordings in patients with chronic pain by means of parallel factor analysis.

This paper presents an alternative method, called as parallel factor analysis (PARAFAC) with a continuous wavelet transform, to analyze of brain activity in patients with chronic pain in the time-frequency-channel domain and quantifies differences between chronic pain patients and controls in these domains. The event related multiple EEG recordings of the chronic pain patients and non-pain controls with somatosensory stimuli (pain, random pain, touch, random touch) are analyzed. Multiple linear regression (MLR) is applied to describe the effects of aging on the frequency response differences between patients and controls. The results show that the somatosensory cortical responses occurred around 250 ms in both groups. In the frequency domain, the neural response frequency in the pain group (around 4 Hz) was less than that in the control group (around 5.5 Hz) under the somatosensory stimuli. In the channel domain, cortical activation was predominant in the frontal region for the chronic pain group and in the central region for controls. The indices of active ratios were statistical significant between the two groups in the frontal and central regions. These findings demonstrate that the PARAFAC is an interesting method to understanding the pathophysiological characteristics of chronic pain.

Practical use of the raw electroencephalogram waveform during general anesthesia: the art and science.

Quantitative electroencephalogram (qEEG) monitors are often used to estimate depth of anesthesia and intraoperative recall during general anesthesia. As with any monitor, the processed numerical output is often misleading and has to be interpreted within a clinical context. For the safe clinical use of these monitors, a clear mental picture of the expected raw electroencephalogram (EEG) patterns, as well as a knowledge of the common EEG artifacts, is absolutely necessary. This has provided the motivation to write this tutorial. We describe, and give examples of, the typical EEG features of adequate general anesthesia, effects of noxious stimulation, and adjunctive drugs. Artifacts are commonly encountered and may be classified as arising from outside the head, from the head but outside the brain (commonly frontal electromyogram), or from within the brain (atypical or pathologic). We include real examples of clinical problem-solving processes. In particular, it is important to realize that an artifactually high qEEG index is relatively common and may result in dangerous anesthetic drug overdose. The anesthesiologist must be certain that the qEEG number is consistent with the apparent state of the patient, the doses of various anesthetic drugs, and the degree of surgical stimulation, and that the qEEG number is consistent with the appearance of the raw EEG signal. Any discrepancy must be a stimulus for the immediate critical examination of the patient's state using all the available information rather than reactive therapy to "treat" a number.

The howling cortex: seizures and general anesthetic drugs.

The true incidence of seizures caused by general anesthetic drugs is unknown. Abnormal movements are common during induction of anesthesia, but they may not be indicative of true seizures. Conversely, epileptiform electrocortical activity is commonly induced by enflurane, etomidate, sevoflurane and, to a lesser extent, propofol, but it rarely progresses to generalized tonic-clonic seizures. Even "nonconvulsant" anesthetic drugs occasionally cause seizures in subjects with preexisting epilepsy. These seizures most commonly occur during induction or emergence from anesthesia, when the anesthetic drug concentration is relatively low. There is no unifying neural mechanism of anesthetic drug-related seizurogenesis. However, there is a growing body of experimental work suggesting that seizures are not caused simply by "too much excitation," but rather by excitation applied to a mass of neurons which are primed to react to the excitation by going into an oscillatory seizure state. Increased gamma-amino-butyric acid (GABA)ergic inhibition can sensitize the cortex so that only a small amount of excitation is required to cause seizures. This has been postulated to occur 1) at the network level by increasing the propensity for reverberation (e.g., by prolongation of the "inhibitory lag"), or 2) via different effects on subpopulations of interneurons ("inhibiting-the-inhibitors") or 3) at the synaptic level by changing the chloride reversal potential ("excitatory GABA"). On the basis of applied neuropharmacology, prevention of anesthetic-drug related seizures would include 1) avoiding sevoflurane and etomidate, 2) considering prophylaxis with adjunctive benzodiazepines (alpha-subunit GABA(A) agonists), or drugs that impair calcium entry into neurons, and 3) using electroencephalogram monitoring to detect early signs of cortical instability and epileptiform activity. Seizures may falsely elevate electroencephalogram indices of depth of anesthesia.