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The EEG in Coma Journal of Clinical Neurophysiology 17(5):473–485, Lippincott Williams & Wilkins, Inc., Philadelphia © 2000 American Clinical Neurophysiology Society The EEG in Coma G. Bryan Young Department of Clinical Neurological Sciences, The University of Western Ontario, London, Ontario, Canada Summary: The EEG allows insight into thalamocortical function in comatose patients when this is inaccessible clinically. A single EEG can help with broad diagnostic categorization whereas continuous or serial EEG provides monitoring for unstable and potentially treatable conditions and for monitoring the effects of therapy. The EEG plays a supplemental role in establishing the prognosis in disease states that are capable of causing neuronal death. The most prevalent and problematic of these conditions involves survivors of cardiac arrest who are initially in coma with intact brainstem reflexes. In such patients single EEGs are of 100% specificity for no possibility of recovery of consciousness only for essentially complete generalized suppression (Ͻ10 ␮V) after the first day of the arrest. Several other generalized patterns, including less marked suppression, burst–suppression, epileptiform activity, periodic complexes, and ␣–⌰ coma patterns, usually but not invariably indicate a poor outcome. Serial EEGs, continuous raw and automated “trending,” testing of reactivity, and the inclusion of multiple variables hold promise for an improved role in the prognostic determination in these patients. Key Words: EEG—Coma—Prognosis—Anoxic-ischemic encepha- lopathy. The EEG is underused in coma. Although thalamocor- or drug-induced coma). When the etiology of the coma is tical function cannot be adequately assessed clinically in known, the EEG can be very useful in determining the the comatose patient, EEG allows for an immediate prognosis in some conditions, especially when combined examination of cortical or cortical–subcortical dysfunc- with the neurologic examination (Sharbrough, 1981). tion in an inexpensive, safe, and readily available manner The EEG is usually dynamic: If variation does not occur in the intensive care unit. Although patients may show within a given recording, it usually will over time. The the same clinical features, especially when brainstem variety and complexity of possible rhythms is inversely functions are clinically intact, the EEG can reveal a wide related to the severity of the dysfunction (Rumpl, 1987). spectrum of abnormalities. EEG is especially sensitive to Absolutely invariant EEGs usually indicate a severe the graded severity of brain dysfunction and the direction encephalopathy and often a poor prognosis (Cant and of the process if serial tracings or continuous recordings Shaw, 1984; Karnaze et al., 1982). are used (Chiappa and Ropper, 1984). Although rarely The clinical importance of various EEG patterns in specific for the etiology of coma, the EEG may help coma must take into consideration the clinical picture, determine the class or general category of disease pro- age, etiology, acuity, and the integrity of brainstem cess (e.g., the differentiation of seizures from metabolic reflexes. Most EEG patterns are nonspecific, but some findings lead to productive intervention (Jordan, 1993). EEG allows for the recognition and monitoring of treat- Presented at the 1999 annual meeting of the American Neurophys- ment of seizures. In patients with vasospasm, the EEG iology Society; St. Louis, MO; October 29–November 1, 1999. can be used to note the response to adjustment of perfu- Address correspondence and reprint requests to Dr. G. B. Young, Department of Clinical Neurological Sciences, London Health Sciences sion pressure. Certain “metabolic patterns” (e.g., tripha- Centre, 375 South Street, London, Ontario, Canada N6A 4G5. sic waves or intermittent rhythmic ␦-waves with an 473 474 G. B. YOUNG abnormal background) may trigger searches for systemic epilepticus, recurring seizures, and conditions in which disorders or exogenous toxins. Lateralized abnormalities intracranial pressure is elevated or cerebral perfusion is prompt a scan to detect a treatable structural lesion variable (e.g., various neurosurgical conditions including (Jordan, 1993). post-traumatic coma, subarachnoid hemorrhage, tumor, It is valuable to assess reactivity or EEG change after postoperative cases, and hydrocephalus). Changes in sensory stimulation in states of decreased consciousness frequency and amplitude, new focal features, or epilep- (Fishgold and Mathis, 1959). In general, reactivity is a tiform activity have diagnostic and therapeutic implica- feature of lighter stages of coma, but it is inconsistently tions that can influence management and outcome (Jor- associated with clinical arousability. Reactivity may ex- dan, 1990, 1992). Continuous EEG monitoring is the best ist in a variety of forms: an increase in amplitude, method of monitoring the depth of anesthesia achieved frequency, or even slowing (often as bisynchronous with barbiturates used in the treatment of status epilep- rhythmic ␦-activity), or a decrease in amplitude of back- ticus, or even of monitoring the depth of sedation in other ground rhythms. In general, EEG responsiveness is as- patients (Van Ness, 1990). This technology may be sociated with a greater chance of recovery than the lack valuable in monitoring those with central nervous system of reactivity (Fishgold and Mathis, 1959; Young et al., disease who cannot be assessed clinically, especially 1999). Reactivity should be tested in all comatose pa- patients on neuromuscular blocking agents. tients, unless contraindicated because of concerns re- Although this review is restricted to EEG, comprehen- garding raised intracranial pressure. We usually test for sive neurophysiologic monitoring includes sensory auditory reactivity by clapping or shouting in the pa- evoked potentials (Chiappa and Hoch, 1993). These and, tient’s ears. Somatosensory stimulation should be tested potentially, motor evoked responses, add new dimen- by applying pressure to the nail bed of each hand and to sions to the examination of integrity of the anatomic– the supraorbital nerve above the medial third of the physiologic subcortical pathways and primary sensory eyebrow. Passive eye opening is recommended in sus- and motor cortices. The early components are not af- pected ␣-coma (no change in ␣) as well as a stimulus for fected substantially by drugs or reversible metabolic reactivity. Because some patients may respond to only abnormalities, whereas EEGs are. These techniques al- one of these stimuli, all should be tried. low for the assessment of prognosis in a more robust way There are several scoring systems for grading the than has been possible with EEG alone (Chiappa and severity of EEG abnormalities: for anoxic, see Hockaday Hoch, 1993; Goldie et al., 1981; Rothstein et al., 1991). et al. (1965); traumatic, Rae–Grant et al. (1991); or both Any review of EEG in coma is hampered by the varied anoxic and traumatic, Hughes et al. (1976), Synek causes of coma, the concomitant use of sedative medi- (1988), and Young et al. (1997); septic encephalopathy, cations, the small number of patients in each study, the Young et al. (1990a); and Reye’s syndrome, Aoki and paucity of prospective studies, the nonuniform criteria Lombroso (1973). In attempting to determine a progno- for coma, the different EEG classification systems, and sis, however, it is best to relate the EEG to the entire the absence of validation (insufficient survival times, clinical picture and to consider whether potentially re- lack of follow-up studies or postmortem correlation). versible factors may be operative (Hansotia et al., 1981). With these caveats in mind, the EEG in several disease The less ambiguous the categories, the better the inter- categories is reviewed, with emphasis on anoxic–isch- and intrarater reliability (Rae–Grant et al., 1991; Young emic encephalopathy. et al., 1999). Quantitative EEG, notably power spectral analysis, STRUCTURAL LESIONS allows for trending over longer periods of time. This is useful in examining variability objectively, in charting The role of the EEG as a primary diagnostic test for the course of encephalopathies, and in detecting sudden structural brain lesions has been greatly modified by the changes such as those produced by seizures (Nuwer, widespread use of computed tomography and MRI. 1988a, 1988b). Purely quantitative studies may miss However, focal EEG abnormalities should raise the sus- major morphologic phenomena in EEG (e.g., triphasic picion of structural cerebral lesions. Furthermore, the waves, some seizures). Hence, the “raw EEG” should EEG reveals the functional disturbance caused by the always be available along with the spectral plot or brain structural abnormality and thus plays a complementary map. role to imaging tests. Continuous EEG monitoring might best be applied to Single structural lesions in the supratentorial compart- cases in which the patient is in coma with an unstable but ment produce coma mainly by compression or displace- potentially treatable condition. Examples include status ment of the diencephalon or mid-brain tegmentum. EEG J Clin Neurophysiol, Vol. 17, No. 5, 2000 EEG IN COMA 475 manifestations may be diffuse by the time the patient is rhage into the brain substance or subarachnoid, subdural, in coma, but one should suspect a supratentorial lesion if or epidural space; ischemic infarction (e.g., from vascu- there is a marked and consistent asymmetry of voltage lar injury, arterial spasm, or decreased
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