EEG in Connection with Coma 53 – 7
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Feature Neurophysiology REVIEW ARTICLE Feature Neurophysiology Review article EEG in connection with coma 53 – 7 BACKGROUND Coma is a dynamic condition that may have various causes. Important chan- John A. Wilson ges may take place rapidly, often with implications for treatment. The purpose of this article [email protected] Section for Clinical Neurophysiology is to provide a brief overview of EEG patterns for comas with various causes, and indicate how EEG can contribute to an assessment of the prognosis for coma patients. Helge J. Nordal Department of Neurology METHOD The article is based on many years of clinical and research experience with EEG Oslo University Hospital in connection with coma states. A self-built reference database was supplemented with searches in PubMed for relevant articles. RESULTS EEG reveals immediate changes in coma, and can provide early information on cause and prognosis. It is the only diagnostic tool for detecting non-convulsive epileptic MAIN POINTS status. Locked-in syndrome may be overlooked without EEG. Repeated EEG recordings EEG holds a central place in the assessment increase diagnostic certainty and make it possible to monitor coma developments. and treatment of coma INTERPRETATION EEG reflects brain function continuously and therefore holds a key place Repeated EEG recordings may be useful in in the assessment and treatment of coma. connection with coma irrespective of cause Some causes and complications of coma The word «coma» stems from Greek, and standing of electroencephalography (EEG), can only be diagnosed with the aid of EEG means deep sleep. The term is first found in with an outline of the basic physiology and the works of Hippocrates (ca. 460–370 BC) some simple pathophysiological observa- and subsequently of Galen (129–199 AD) tions. We will also present an overview of (1). The term is used again by Thomas Willis EEG findings with known prognostic value (1621–1675). He localised the state of for coma states and an overview of findings lethargy (Gr. lethe = forgetfulness) and argos that have implications for treatment. (Gr. = lazy) in the cortex and that of coma beneath the cortex (i.e. subcortically) (1). Method With von Economo’s (1876– 1931) finding The overview is based on the authors’ exten- of lesions in the hypothalamus of patients sive clinical and research-related experience who died of encephalitis lethargica (2) and of EEG in comatose patients and a discre- the subsequent finding of the ascending reti- tionary selection of relevant articles on EEG cular activating system (3), it became clear in connection with coma. The articles were that coma could be caused by affection of all selected from a self-built literature database these structures (see illustration). and supplemented by searches for relevant Damage to the cortex can affect integration articles in PubMed. The search was conclu- of information, resulting in confusion, hallu- ded in October 2011. cinations or memory problems, without the degree of wakefulness necessarily being af- What does a scalp EEG measure? fected. However, a diffuse cortical affection An electrocardiogram that is recorded by may cause reduced consciousness, depending means of electrodes attached to the skin of on how much of the cortex is affected. An the head is called a scalp EEG. The excita- injury that affects the activating systems in tory pyramidal cells of the cerebral cortex the brain stem, midbrain or thalamus may be are organised in functional columns at right small, but may cause a deep coma. angles to the surface. The electrical activity Today the word coma means a patho- in these cells generates field potentials logical state of suspended consciousness and through interaction with inhibitory interneu- unresponsiveness to external or internal sti- rons. The potentials are an expression of the muli (4). The state can last for anything from total synaptic activity (6). Inhibition and hours to weeks and change to the regaining of excitation in the neurons and the neuronal consciousness with or without sequelae, to networks cause the field potentials to syn- death or to a permanent state where the pati- chronise and oscillate at different frequen- ent may be «awake», but without (or with a cies and voltages (7). The fewer the neurons minimal amount of) awareness, known as a oscillating in small networks, the higher the chronic vegetative state (4). frequency and the lower the voltage. It is An overview of clinical diagnosis, grada- this activity which is measured in an EEG. tion and causes of coma is beyond the scope Some of the activity can be registered by of this review. For this we recommend a very means of electrodes attached to the scalp, good review by Young (5). In the present but intracranial electrodes are required to article we seek to provide a principle under- register the smallest, most rapid oscillations. Tidsskr Nor Legeforen nr. 1, 2013; 133: 53 – 7 53 REVIEW ARTICLE Feature Neurophysiology The top right shows an anatomical illustration of the ascending reticular activating system, which consists of two parts: the ventral part, which goes through the hypo- thalamus, and the dorsal, which goes through the thalamus. There are five EEG printouts: A) EEG for normal sleep. The uppermost blue panel shows the frequency spec- trogram (predominant frequencies along the Y-axis and time along the X-axis) through the recording, in this case throughout a 24-hour period. The last half shows the sleep period, with seven REM/NREM cycles. The EEG sequence shows 12 seconds of NREM sleep, with spindles and delta waves. Red is from the left and blue from the right side of the head. B) EEG from patient with acute demyelinising encephalomyelitis in the upper brain stem. EEG shows persistent deep sleep with preserved cortico- thalamic interaction (compare with printout A), but without reactivity. No alternation is seen between NREM and REM sleep (see uppermost panel with 3.5-hour spectro- gram) because the REM-NREM alternation is regulated by the upper brain stem. C) EEG with status myoclonicus from patient who had been resuscitated after cardiac arrest. D) EEG from another patient who had been resuscitated after cardiac arrest. EEG shows low voltage with burst-suppression. E) EEG from patient who had been resuscitated after cardiac arrest. Periodic activity and nonconvulsive status epilepticus are seen here. The spectrogram shows a period of 18 minutes of periodic activity preceded and followed by two shorter sequences of continuous epileptic activity (marked with red). Illustration © Illumedic 54 Tidsskr Nor Legeforen nr. 1, 2013; 133 Feature Neurophysiology REVIEW ARTICLE During sleep, the interaction of the cortex, also reduce consciousness by affecting the polyradiculitis (Guillain-Barré syndrome) thalamus, hypothalamus and brain stem activating systems in the upper brain stem and critical illness myopathy/neuropathy generates slow oscillations that may involve and midbrain (14). Repeated EEG recor- may also cause a similar condition (21). all the neurons in large networks (8–10). dings may reveal such a development. It is very important clinically that locked- This is of relevance to coma diagnosis. in syndrome is not mistaken for alpha coma. In a scalp EEG recorded in relaxed, awake Thalamus, hypothalamus, EEG is thus essential for distinguishing condition and with closed eyes, activity with mesencephalon and brain stem between these two states. a frequency of 8–13 cycles per second (alpha The corticothalamic system is involved in a activity) predominates over the posterior continuous interaction, which varies over a Ischaemic coma areas of the head. Rapid activity with a fre- 24-hour period, with the mesencephalic and With ischaemic coma, a wide range of chan- quency of 13–30 cycles per second and low hypothalamic sleep regulation systems, with ges can be seen in EEGs (22, 23). The voltage predominates over the anterior areas the frontobasal activating system and with brain’s cortical pyramid cell system is most of the head (beta activity). During light sleep, the reticular activating system (15). The cor- vulnerable to ischaemia, but there may be slower activity of 4–7 cycles per second tical activity is in constant interaction with large individual variations. Hypoxia may predominates (theta activity). During deeper the thalamus (16). This is visible in the EEG have developed rapidly, as with cardiac sleep (non-rapid eye movement sleep, as characteristic patterns during sleep. The arrest, or more slowly, as with respiratory NREM) spindle-shaped sequences of 10–16 patterns can provide an indication of which arrest, with initially preserved cerebral per- cycles per second predominate (sigma or systems are affected. fusion. Different medicines may also affect spindle activity) and slow activity of 1–4 Extensive damage to the upper brain stem the brain’s susceptability to ischaemia. Body cycles per second (delta activity) with higher may appear in the EEG almost like deep phy- temperature may be an important factor, as voltages. Both are modulated by slow back- siological sleep. However, with damage of with drowning accidents or other forms of ground oscillation of 0.2–1 cycle per second. this nature the whole corticothalamic system hypothermia. Some areas of the brain may NREM sleep alternates with REM sleep in and the frontobasal activating system in the also be more susceptible due to arterioscle- periods of about 70–80 minutes (illustration, hypothalamus will be deafferentated. The rosis with reduced perfusion. EEG printout A). sleep-physiological corticothalamic interac- In an EEG this may result in different tion may nonetheless be preserved. The EEG degrees of diffuse cortical functional im- Cortical dysfunction of such a coma does not differ from physiolo- pairment without excitatory elements. Hy- Diffuse cortical dysfunction can reduce gical sleep, but the patient cannot be woken perexcitability, or disinhibition, is also com- synaptic activity, damage networks and (illustration, EEG printout B).