EEG importance is well recognized for epilepsy diagnostic evaluation; nevertheless, sometimes this is wrongfully considered the unique clinical EEG indication. In our country, EEG meets other applications: at the neurologist office, and checkup for risky professions evaluation, always keeping in mind that EEG represents no substitute for clinical neurological evaluation.
EEG for hospitalized (mostly ICU) patients may be considered an area of greater clinical importance, helping acute or subacute pathologies diagnosis. Concerning brain anatomy the image tests are superior to EEG, whose information rests basically on 22 electrodes. EEG major advantage is time-based, with data updated every second, occupying a present and future place, provided difficulties and advantages are fully discussed.
Difficulties may arise from tentative to anatomize EEG waves, eventually following the mirage of pathognomonic aspects. Do they really exist? Are cerebral rhythms accompanied by rather simplistic EEG formats? Wave designation has changed over time, an example provided by physiological vertex waves (ancient vertex “sharp” waves – “sharp” abandoned to avoid confusion). Fortunately, only on few occasion it is not simple to distinguish normal vertex waves from abnormal vertex sharp waves.1
EEG activities are distinguished by their frequency range, while EEG rhythms definition must include topography and reactivity, such as alpha rhythm. Conversely, alpha coma (alpha as the dominant activity, not a rhythm) is different; however, reactivity has sometimes been described during alpha coma, and also some variability may occur. EEG clinical correlation is fundamental, since alpha rhythm may be present during light states of altered consciousness, but not in coma.2,3 Another example occurs during clinical partial seizures recording, frequently showing repetitive theta (or any other frequency activity), no typical wave seizure signature.
A recent (2015) discussion on the relevance of typical and atypical triphasic waves by Kaplan and Sutter4 leaves open questions on their clinical significance and their cryptic origins. In our experience triphasic waves are frequently seen in older patients presenting with different pathologies, not characterizing hepatic insufficiency, and atypical triphasic waves continues to pose diagnostic challenges.
EEG changes during metabolic disorders or pharmacological agents responses are generally stereotyped, showing either a progressive (graded) slowing of background activity with increasing amplitude till burst-suppression and death, or an otherwise improvement of the EEG, sequentially presenting higher frequencies, perhaps reflecting and accompanying successful treatment. EEG interpretation should occur in close correlation to clinical context, studying controllable sources of variation to establish the cause of observed changes. Lack of EEG change may be as important as its presence.5
Is burst suppression a drug induced pattern or a sign of severe brain post-anoxic lesion? Asymmetrical burst suppression occurs more frequently after anoxia, with brain lesions varying in intensity and location. Otherwise, central acting drug induced patterns are usually symmetrical, involving all the brain. What happens when drugs act on a previously lesioned brain? An asymmetrical burst suppression.6
EEG waves evaluation pretending to determine which post-anoxic patients are able to survive or will present a better prognosis is doomed to failure, since brain anoxia is enormously complex due to multifactorial events such as anoxia duration, type, efficiency of cardiopulmonary resuscitation, occurrence of secondary brain lesions, use of hypothermia and its level, presence of hyperthermia, seizures and other complicating factors.7
Continuous EEG monitoring is important for many ICU patients, and efforts towards terminology standardization to face research in this area were developed by the American Clinical Neurophysiology Society (ACNS), trying to eliminate terms with clinical connotations regarding difficulties that involve finer definition of ongoing neuronal lesion. Wisely, the abandonment of prior terms were not suggested, since its use continues to be important to allow the clinical neurophysiologist to properly “translate” the EEG findings to ICU staff, and participate in case discussion.8
These few examples favor the hypothesis that brain waves are rather simple, not pathognomonic. EEG waveform analysis continues to be very important, pending on the proper correlation with clinical aspects, when the clinical neurophysiologist may help decisions concerning treatment and patient monitoring. This objective will many times only be attained if the clinical neurophysiologist accompanies the recording and sees the patient, especially when acute and subacute evolving pathologies are focused.
Hospitalized patients proper care demand the coordinate participation of several teams, such as ICU staff, with whom the clinical neurophysiology team must positively interact. EEG recording of hospitalized patients is highly dependent on well trained technologists, with three to four years training program (accordingly to international recommendations), followed by further educational development programs. Regrettably, this objective may be limited or not well accomplished in many regions. It must be kept in mind that clinical neurophysiology is also team dependent, represented by the working capacity and interaction of their components (physicians, technologists, and biomedicals). We have developed a good experience with biomedicals, provided continuous educational activities are developed through panel discussion, reviews, and meetings, always considering the learning curve importance.
Technologists and intensive care staff lack clinical neurology competence to perform the EEG correlation, role that the clinical neurophysiologist must perform, avoiding isolation in the laboratory to analyze only the recorded EEG. It is important to state that critical care demands immediate verbal information to ICU staff; the written EEG report has a lesser degree of clinical relevance, taking a longer time to write and print, representing a second step,
EEG many times is a small and undervalued piece of the diagnostic “patchwork” in the ICU. However, properly executed with adequate clinical observation and correlation, may have an important contributory value:
- Clinical observation and EEG recordings help seizures and pseudo-seizures diagnosis; besides, EEG may also help involuntary movements, tremors, and myoclonus evaluation. Example: 55 yo patient seen with abnormal involuntary movements was suspected of status epilepticus; both clinical observation and some isolated EEG slow waves were not suggestive of epileptic seizures; leucoencephalopathy was demonstrated by MRI.
- Some ICU older patients with altered level of consciousness present frequent epochs of drowsiness followed by snoring and alternating short wakefulness periods, highly suggestive of obstructive sleep apnea syndrome, hypotheses advanced by applying oronasal electrode thermistor. Clear improvement occurs after specialist consultation and CPAP installation.
- Sometimes EEG clinical importance is characterized by negative values. Example: EEG few slow waves were not correlated to frequent syncope episodes in 86 yo patient with retrograde vertebral artery flux during transcranial Doppler; a suggestion of subclavian steal syndrome was later confirmed. Normal EEG during delirium may be suggestive of psychogenic pathology.
- During orthopedic surgery a 30 yo patient presented some jerks; next day she was comatose, and it was suspected NCSE, but the EEG revealed generalized depression, characteristic of severe brain lesion; hypotheses of fat embolism was later confirmed.
These few examples illustrate clinical neurophysiologist participation, not limited to EEG reporting, and reinforcing the importance of patient observation. It must be remembered that clinical neurophysiology is many times undervaluated during medical residence training, limiting EEG valoration and neurologist atuation in ICU patients, scenario that deserves reversion.
- Ernst Niedermeyer – Sleep and EEG. in Electroencephalography. Basic Principles, Clinical Applications, and Related Fields. Ernst Niedermeyer & Fernando Lopes da Silva ed., 4th edition, Lippincott Williams & Wilkins, Philadelphia, 1998, p. 174-188.
- Frank W. Sharbrough – Nonspecific Abnormal EEG Patterns. in Electroencephalography. Basic Principles, Clinical Applications, and Related Fields. Ernst Niedermeyer & Fernando Lopes da Silva ed., 4th edition, Lippincott Williams & Wilkins, Philadelphia, 1998, p. 215-234.
- Barbara F. Westmoreland, Donald W. Klass, Frank W. Sharbrough & Thomas J Reagan – Alpha-Coma. Arch Neurol, 1975, 32:713-718.
- Peter W. Kaplan & Raoul Sutter – Affair With Triphasic Waves – Their Striking Presence, Mysterious Significance, and Cryptic Origins: What Are They? J Clin Neurophysiol 2015;32:401-405.
- C.D. Binnie – Computer Applications in Monitoring. Chapter 2. Handbook of Electroencephalography and Clinical Neurophysiology. Revised Series. Volume 2. Clinical Applications of Computer Analysis of EEG and other Neurophysiological Signals. Edited by F.H. Lopes da Silva, W. Storm van Leeuwen & A. Rémond. Elsevier. Amsterdan. 1986, p. 67-91.
- E.F.M. Wijdicks, A. Hijdra, G.B. Young, C.L. Bassetti & S. Wiebe – Practice Parameter: Prediction of outcome in comatose survivors after cardiopulmonary resuscitation (an evidence-based review). Report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology 2006; 67:203-210.
- Elsa Juan, Peter W. Kaplan, Mauro Oddo, Andrea O. Rossetti – EEG as an Indicator of Cerebral Functioning in Postanoxic Coma. J Clin Neurophysiol 2015; 32(6): 465-471.
- Lawrence J. Hirsch, Richard P. Brenner, Frank W. Drislane, Elson So, Peter W. Kaplan, Kenneth G. Jordan, Susan T. Herman, Suzette M. LaRoche, Bryan Young, Thomas P. Bleck, Mark L. Scheuer & Ronald G. Emerson – The ACNS Subcommittee on Research Terminology for Continuous EEG Monitoring: Proposed Standardized Terminology for Rhythmic and Periodic EEG Patterns Encountered in Critically Ill Patients. Journal of Clinical Neurophysiology, 2005, 22(2): 128-135.