EEG in encephalopathy and coma Flashcards
What % of comatose ICU patients have non-convulsive seizure?
20%
What are predictors of seizures in the ICU setting?
Pre- dictors of seizures on continuous EEG moni- toring in the ICU include coma, age <18 years, history of epilepsy, convulsive seizures prior to monitoring [1], CNS infection, brain tumor, recent neurosurgery, and periodic epileptiform discharges [5].
What are positive predictors on EEG for ICU patients?
For example, EEG reactivity during which there may be a change in EEG amplitude, frequency, or the appearance of other patterns following noxious stimulation, noise or eye opening may indicate a more favorable prognosis. Spontaneous vari- ability along the course of a recording typically suggests a better prognosis than when the EEG is suppressed, monotonous, and unreactive.
IRDA?
IRDA refers to diffuse, synchronous 2–3 Hz sinusoidal waves that are often maximal anteri- orly. It often occurs on a background of delta- or theta-range slowing and can be occasionally asymmetric. As the term “intermittent” implies, it often has an abrupt onset and offset, and is typ- ically a reactive pattern that is blocked by eye opening. In children, it may be maximum in the posterior head regions and termed occipital intermittent rhythmic delta activity, or OIRDA.
What is IRDA associated with?
IRDA was long believed to be a pattern indicative of deep-midline dysfunction originally seen in children with midline tumors and raised intracranial pressure [6], and latter with structural lesions involving both the cortical gray matter and deep nuclei [7]. With time, it came increas- ingly to be seen in the elderly, typically with a frontal predominance (FIRDA), associated with background slowing. It signifies cerebral dys- function, commonly diffuse encephalopathy, although it can be seen with focal lesions. It is seen early in coma, soon after loss of the poste- rior basic rhythm, but is non-specific in terms of pathology. As for all encephalopathic patterns, the prognosis of IRDA depends largely on the underlying pathology.
Building on the work of others, Accolla and colleagues in a prospective study noted that FIRDA occurred with toxic-metabolic disturbances and with structural lesions, but did not correlate with epilepsy [8]. More recently, a large retrospective study found significant sta- tistical correlations with strokes and noted its favorable prognostic significance [9].
While IRDA is not associated with epilepsy, OIRDA in children can have either an encephalopathic or epileptiform significance, as it has been described in association with focal epilepsy and generalized epilepsy, especially absence seizures [10].
Continuous High-Voltage Polymorphic Delta (PDA)
PDA is 1–2 Hz, high-amplitude, arrhythmic slow-wave activity that is generally seen in the later stages of coma than IRDA and triphasic waves, but may still attenuate with stimulation. As the coma deepens, the predominant frequency in PDA becomes slower and loses its reactivity to stimulation.
Figure 9.3 shows bilateral waxing and waning medium-to-high voltage 1–3 Hz delta activity with some interspersed lower voltage theta fre- quencies. There is little alpha or beta activity. The patient had severe head trauma and remains alive but with little functional recovery.
What are triphasic waves associated with?
The cause of triphasic waves has classically been attributed to metabolic encephalopathy such as liver or kidney failure. However, they have also been described in the other toxic and metabolic conditions, including lithium toxicity and hyponatremia, or even with subcortical white matter disease [11]. Interestingly, they may decrease upon administration of benzodiazepines without an improvement in sensorium, making the distinction from epileptiform discharges difficult.
What is PDA associated with?
PDA is believed to be generated in pyramidal neurons in cortical layers II, III, and V. Schaul and colleagues found that this pattern was largely seen in dysfunctions of the subcortical white matter or with lesions which partially deaffer- ented white matter [12, 13]. Further studies revealed that it could be seen with metabolic, toxic, or infectious encephalopathies [14], and less commonly with infratentorial lesions involving the thalamus and rostral brainstem [15, 16]. Occasionally, PDA or more frequently continuous RDA occurs with deep-seated epileptic foci that are remote from the scalp surface, with limbic encephalitis and with limbic status epilepticus.
GPEDs
GPEDs are generalized, usually high-voltage sharp or spike morphologies, occasionally poly- morphic, occurring synchronously and bilater- ally. The discharge frequency typically is 0.5 Hz or slower and occurs in an unreactive coma, sometimes with low-amplitude face or limb myoclonus. There is often little background activity between discharges, but theta and delta may occur. As the coma deepens, amplitude of the inter-GPED activity decreases.
Figure 9.4 shows GPEDs at 1.2 Hz in a patient after cardiac arrest. The record showed little background and no reactivity to stimuli. There were no brainstem reflexes and the patient died.
In what instances are GPEDs commonly seen?
There is a high association of clinical seizures or electrographic seizures before or after the recording of periodic discharges, more so with GPEDs. The most frequent cause is cerebral anoxia after cardiorespiratory arrest. A poor outcome (mortality or vegetative state) is >97%. Severe metabolic disease and overdoses of lithium and baclofen may also cause GPEDs.
The EEG should raise the suspicion of CJD. Patients with later stages of subacute sclerosing encephalitis (SSPE) can have GPEDs with longer inter-GPED interval.
Burst suppression
Burst suppression pattern refers to synchronous bursts of high-voltage, mixed frequency activity, separated by periods of EEG suppression to less than 10 μV (Fig. 9.5). The bursts contain spikes and discharges of almost any other frequency. The duration of the suppression increases with deep- ening coma or anesthetic agent dose. Etiologies that are commonly associated with burst suppres- sion pattern include anoxic encephalopathy, drug
What is burst-suppression associated with?
Etiologies that are commonly associated with burst suppres-sion pattern include anoxic encephalopathy, drug intoxication, anesthetics, and hypothermia. This pattern is generally reversible if induced by hypothermia or anesthetics, including barbiturates or benzodiazepines. However, if it occurs in the
setting of anoxic encephalopathy, it is associated with poor prognosis. Indeed, this pattern occurs shortly before progression to electrocerebral inactivity.
Low-Voltage Slow Non-reactive EEG
Low-voltage records (<20 lV) without variabil- ity or reactivity occur with anoxia or less fre- quently with severe metabolic and ischemic disturbances. Following cardiac arrest, it carries a zero percent prognosis for return to conscious- ness, but care must be taken to exclude signifi- cant hypothermia and sedative or anesthetic agents.
Low-voltage fast patterns conversely may be seen in ~5% of the normal population and with alcoholism and sometimes with benzodi- azepine use, but will also possess normal vari- ability and reactivity.
Electrocerebral inactivity
Electrocerebral inactivity (ECI) (Fig. 9.6) represents an EEG pattern where no activity of cortical origin can be seen. The EEG often shows many
types of artifacts, such as EKG, respiration, and intravenous drips. The record must be run so as to conform to the Guidelines of the American Clin- ical Neurophysiology Society (ACNS) (http:// www.acns.org/pdf/guidelines/Guideline-3.pdf):
– Minimum of 8 scalp electrodes and earlobe references
– Electrode Impedance must be between 100 and 10,000 X
– Interelectrode distance should exceed 10 cm – EEG must be read with sensitivity of
2 lV/mm and a
– s = 0.3–0.4 s
– Integrity of the whole system should be tested – Monitoring techniques (EKG, Ventilator, etc.)
should be kept in mind as sources of artifact
– Reactivity to pain and loud sound must be
checked
– Assessment of adequate core body tempera-
ture is required
–Recording should last for at least 30 min, and done by qualified technologists Electroencephalographers should read the EEG at the bed side, and are advised to repeat the following day if they suspect electrocerebral silence.
Once these criteria are satisfied, and if the presence of anesthetic or suppressant drugs is excluded, the finding of ECI in concert with an appropriate clinical examination (demonstrating the lack of brainstem reflexes) indicates “brain death.” These recordings are usually obtained after cardiorespiratory arrest, severe head trauma, and intractable malignant raised intracranial pressure.
Spindle coma
Spindle coma is a pattern of sleep architecture in which bilateral bursts of fronto-central 9–14 Hz “spindles” are recorded (Fig. 9.7). If the coma deepens, the spindle frequency slows. Often the spindles occur in concert with generalized slow negative waves constituting K-complexes. The spindles may be prolonged and exceed 2 s Typ- ically, the EEG tracing of sleep architecture is unreactive to external stimuli or at least returns to this pattern without a clinical return to consciousness.
Alpha-theta coma
Alpha frequency patterns in coma, and “alpha coma” was first described by Loeb and Poggio in 1953 in a patient with brainstem hemorrhage [19]. Unlike a waking alpha rhythm, it is usually diffusely distributed and often anteriorly domi- nant, and typically invariable and unreactive to external stimuli (Fig. 9.8). The coma pattern is named after the predominant rhythm, which can be in the alpha or theta range. The rhythm is generally diffuse, commonly anterior-maximum, and monomorphic.
Beta coma
Despite the ubiquity and abuse of benzodi- azepines, and previously of barbiturates, this pattern remains infrequent, in contrast to the frequently encountered excessive fast activity in the EEG non-comatose patients receiving ben- zodiazepines or barbiturates. Beta coma or encephalopathy (Fig. 9.9) produces an EEG with high-frequency spindle-like bursts at *20– 25 Hz, often diffusely, but typically involving the fronto-central regions. Waking background is often seen, as is theta activity, and the patient is rarely deeply unresponsive. The beta activity is usually little reactive to external stimuli.
CJD and EEG
CJD is a transmissible prion disease that can be familial, sporadic, or iatrogenic. CJD is the most common of all prion diseases, and 5–15% of the cases are clustered in families. Progressive dementia is the hallmark of the first stage of the disease. In the second stage, rigidity and the myoclonus appear. In the third stage, there is
stupor, coma, worsening rigidity, and progression to death. T
he EEG shows slowing and dis- organization of the background rhythms in the first stage (Fig. 9.10). In the second stage, there are periodic bilaterally synchronous discharges of diphasic or triphasic morphology with volt- ages reaching 300 μV. With more disease pro- gression, multiphasic discharges or polyspikes may appear. Classically, the frequency of these periodic discharges is 1 per second, and they may be associated with myoclonic jerks. These periodic discharges persist into the third stage with gradual increase in the interdischarge interval, gradually evolving into further attenua- tion of the background activity.
