![]() 13 However, the waveform distortion and amplitude attenuation of SPCs obtained even with this lower filter limit degrades the signal-to-noise ratio and precludes recording of the true cortical DC potential.Ī few studies have now highlighted that it is possible to make unfiltered, full-band recordings with DC-coupled amplifiers from platinum electrodes in patients. AC-coupled ECoG with a lower limit of 0.02 Hz is therefore currently considered the minimum standard for clinical SD monitoring. Thus, detection of SPCs overcomes the problem of false negatives encountered with recordings of only higher (0.5–70 Hz) frequency bands by distinguishing between different causes of depressed activity in individual recording channels and allowing identification of SDs in electrically silent tissue. 12 That is, filtering at 0.02 Hz distorts the waveform and substantially attenuates the amplitude of the negative DC potential shift, but the resulting SPC signals its occurrence. 10, 11 With a lower limit of 0.02 Hz, the slow roll-off of the attenuation curve of the filter allows for detection of slow potential changes (SPCs) that reflect the negative DC potential shifts of SDs. The limitations of traditional AC-coupled techniques for SD monitoring have been partially overcome by the use of amplifiers with higher time constants, i.e. ![]() In these cases especially, recording of the DC shift is essential for identification of SD. isoelectricity) precludes the possibility for spreading depression. 3 This frequency band alone, however, does not reliably identify all SDs, since (1) a depolarization wavefront propagating perpendicular to the axis of an electrode strip will result in near-simultaneous depression along the strip, making it indistinguishable from other causes of synchronous depression (2) determination of spread is uncertain when depolarizations propagate to only one or two electrode locations and (3) depolarizations can occur in injured tissue where baseline suppression of cortical activity (i.e. identified spreading depression episodes in five of 14 patients with acute brain injury. These activities occur at frequencies up to 200 Hz or more and are recorded with AC-coupled amplifiers which, due to capacitive coupling in the amplifier, filter slow (0.5 Hz) recordings, Strong et al. 4 Such preoperative recordings evaluate cortical activity in the frequency range of local field potentials that reflect functional activity, as well as pathologic activity including seizures and fast ripples. In such patients, ECoG recordings from surgically placed electrode grids and strips are evaluated to determine the seizure focus for resection and define the borders of eloquent regions of cerebral cortex to maximize functional sparing from the procedure. The electrocorticographic (ECoG) technique originally adopted by Strong et al., 3 using linear subdural electrode strips, was borrowed from methods to evaluate patients with refractory epilepsy who were candidates for surgical treatment. Monitoring of spreading depolarizations (SD) for research and, increasingly, as a potential target and guide for neurointensive care in patients with stroke and traumatic brain injury 1, 2 poses unique methodological challenges in clinical neurophysiology. We conclude that intracranial monitoring of slow potentials can be achieved with platinum electrodes and that unfiltered, direct current-coupled recordings are advantageous for identifying and assessing the impact of spreading depolarizations. Following a standardized training session, novice scorers achieved a high degree of accuracy and interobserver reliability in identifying depolarizations, suggesting that direct current-coupled recordings can facilitate bedside diagnosis for future trials or clinical decision-making. Transient negative direct current shifts of spreading depolarizations were easily recognized and in 306/551 (56%) cases had stereotyped, measurable characteristics. While large baseline direct current offsets developed, loss of data due to amplifier saturation was minimal and rates of baseline drift throughout recordings were generally low. To determine the feasibility of monitoring the full signal bandwidth of spreading depolarizations in patients, we performed subdural electrocorticography using platinum electrode strips and direct current-coupled amplifiers in 27 patients with acute brain injury at two neurosurgical centers. ![]() The negative direct current shift (<0.05 Hz) is an important identifier of cortical depolarization and its duration is a measure of potential tissue injury associated with longer lasting depolarizations. Spreading depolarizations cause cortical electrical potential changes over a wide spectral range that includes slow potentials approaching the direct current (or 0 Hz) level.
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