Generalized Slowing

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In discussing generalized slowing of the EEG, several qualifiers must be mentioned. Is the slowing intermittent or continuous? Is it rhythmic-monomorphic or arrhythmic-polymorphic? In what context does it occur? For example, a buildup of generalized slowing during hyperventilation is a normal finding in children, adolescents, and young adults. Finally, some special examples will be considered.

Intermittent rhythmic delta activity (IRDA) tends to be monomorphic and is a commonly observed EEG abnormality. It is usually diffuse, bisynchronous, monomorphic, and reactive to eye opening. Hyperventilation may activate the pattern and sleep may attenuate it. Commonly, there is bianterior predominance to the slowing, hence, the term frontal IRDA (FIRDA) (Fig. 2). Note that children and adolescents often show a biposterior predominant IRDA and, thus, the term occipital IRDA activity has been applied.

IRDA is thought to be a projected rhythm and may reflect diffuse gray matter dysfunction, either cortical or subcortical. Acute or subacute disturbances are more likely to produce this pattern than chronic encephalopathies. FIRDA suggests a changing or evolving underlying disturbance—an encephalopathy that is either worsening or improving. Toxic-metabolic encephalopathies or electrolyte disturbances are typical underlying etiologies. Rarely, this pattern may accompany a postictal state. Eye blink or glossokinetic artifact should be excluded because they are common FIRDA imitators.

Continuous generalized slowing (Fig. 3) is an extremely common pattern, distinct from the intermittent rhythmic pattern described in the preceding paragraphs, although they may frequently appear together within the same tracing. Continuous slow patterns may refer solely to slowing of the posterior waking background rhythm. This observation usually implies a type of diffuse encephalopathy. In adults, a commonly used lower limit of normal for the waking background rhythm is 8 Hz. Varying degrees of background slowing may be encountered, including delta and theta frequencies. The degree of slowing of the posterior waking background rhythm is thought to correlate with the degree of clinical cerebral disturbance. As the encephalopathy deepens, other features may accrue in addition to progressive slowing of the posterior background rhythm. These include slowing of anterior rhythms; the normal frontal beta activity may slow to reveal varying degrees of frontal alpha or theta frequencies. In addition, the overall rhyth-micity of the tracing wanes in conjunction with progressive deepening of encephalopathy states. In more marked encephalopathies, the entire tracing may become dominated by polymorphic slow forms, particularly delta activities, with much less of the reactivity and organization observed in the normal tracing. Owing to its fidelity as a surrogate marker of current CNS function, serial EEGs may be valuable to monitor the course of an acute or subacute encephalopathy.

Despite the helpful correlation between the degree of EEG slowing and the degree of cerebral dysfunction, there is no specificity to the observation of continuous slowing. It may be observed equally in static encephalopathies or in those of acute or subacute natures. Continuous diffuse slowing may arise in the setting of any diffuse CNS insult, including head trauma, hypoxic-ischemic injury, toxic or metabolic derangement, diffuse CNS infectious or

Rhythmic Delta Activity
Fig. 2. Frontal intermittent rhythmic delta activity. This tracing is from an 83-yr-old woman with dementia, normal pressure hydrocephalus, and syncope. Note the bursts of rhythmic delta activity with bi-anterior predominance. There is also slowing of posterior background rhythms.
Fig. 3. Continuous generalized slowing. This is from a 73-yr-old man with a several year history of memory loss and recently increased confusion. Note the slightly irregular, continuous, 5- to 6-Hz activity evident biposteriorly as well as more diffusely in this tracing.

neoplastic processes, dementing illnesses, and even in multifocal conditions, such as multifocal, bihemispheric vascular insults. Indeed, because EEG offers relatively poor spatial resolution, as vascular events accrue in the CNS, the tracing may lose its focal/multifocal quality and may appear diffusely slow. Likewise, focal abnormalities may have less distinctive EEG signatures amid the diffuse slowing caused by an encephalopathy; focal details are lost. It is also important to remember that generalized slowing is a normal feature of the drowsy or sleep tracing. One must take stock of the patient's state when interpreting whether the observed slowing is pathological or merely reflective of state.

Triphasic waves (Fig. 4) represent a special type of generalized continuous slowing. The key features that distinguish triphasic waves from other forms of slowing include their typical triphasic morphology and a phase lag. The waves themselves are usually medium- to high-voltage slow waves occurring at a frequency of 1.5 to 2.5 Hz. They typically occur in a bilaterally symmetric, bisynchronous fashion. Although they may wax and wane somewhat in amplitude and frequency during the recording, they tend to exhibit a somewhat monotonous appearance. Triphasic waves usually show a phase lag of 25 to 140 ms across the anterior-posterior axis. This phase lag is more commonly observed in an anterior-to-posterior direction than vice versa.

Triphasic waves suggest a toxic-metabolic encephalopathy, most commonly a hepatic encephalopathy. However, this pattern is not specific for hepatic encephalopathy. Triphasic waves can also be observed in other metabolic disorders, such as uremia, hyperthyroidism, hypercalcemia, hypoglycemia, hyponatremia, and lithium intoxication. Alzheimer's disease and other dementias; prion diseases; structural pathologies, such as stroke and subdural hematoma; and cerebral carcinomatosis can also demonstrate this pattern. Triphasic waves may be quite difficult to differentiate from triphasic-appearing epileptiform morphologies, blunted sharp and slow wave complexes. This is even more problematic because both may equally occur in similar clinical settings, such as in uremic encephalopathy.


Coma refers to a clinical state in which a person exhibits a decreased level of consciousness with eyes closed and no purposeful responses to applied stimuli. Just as in milder encephalopathy conditions, the depth of the coma is paralleled by helpful EEG findings. In lighter forms of coma, the EEG may show some responsivity to stimuli with higher voltage and more prominent slowing. As the coma deepens, a blocking type response ensues, in which stimuli produce a voltage drop and attenuation of background activity. Finally, in deeper coma, the EEG becomes unreactive to patient stimulation.

Causes of coma are many and may include toxic-metabolic or hypoxic-ischemic encephalopathies as well as supratentorial or infratentorial structural pathologies. The EEG in coma may show several possible patterns, some of which can help identify etiology and some of which may have prognostic implications.

When coma is caused by nonconvulsive status epilepticus (Fig. 5), the EEG can be extremely helpful because it not only quickly establishes etiology, but may also permit assessment of subsequent anticonvulsant treatment efficacy. In no other instance is the specificity of the EEG in coma higher than in nonconvulsive status epilepticus. Keep in mind, however, that although the EEG may identify the cause of coma as an epileptic encephalopathy, there may be an as yet unidentified disturbance acting as a precipitant, for instance, hypoxic-ischemic encephalopathy, uremia, stroke, and so on. The EEG provides an immediate assessment of treatment efficacy in abolishing the epileptiform activity.

Discharge With Phase Reversal Eeg

Fig. 4. Triphasic waves. This is derived from the EEG of a 46-yr-old man with hepatic encephalopathy. Note the bi-anteriorly predominant waveforms with triphasic morphology. There are no clear phase reversals or embedded sharp elements, and a subtle phase lag is evident along the anterior-posterior axis of the tracing.

Fig. 4. Triphasic waves. This is derived from the EEG of a 46-yr-old man with hepatic encephalopathy. Note the bi-anteriorly predominant waveforms with triphasic morphology. There are no clear phase reversals or embedded sharp elements, and a subtle phase lag is evident along the anterior-posterior axis of the tracing.

Discharge With Phase Reversal Eeg

Fig. 5. Nonconvulsive status epilepticus. This tracing is from a 13-yr-old boy with absence epilepsy and a new prolonged confusional state. Note the incessant, bisynchronous, very high amplitude 3-Hz spike-and-wave pattern. The patient was quite confused, but could repeat if reminded to do so. This indicates absence status epilepticus.

Fig. 5. Nonconvulsive status epilepticus. This tracing is from a 13-yr-old boy with absence epilepsy and a new prolonged confusional state. Note the incessant, bisynchronous, very high amplitude 3-Hz spike-and-wave pattern. The patient was quite confused, but could repeat if reminded to do so. This indicates absence status epilepticus.

Focal slowing in the EEG of a comatose patient may suggest a structural cause, such as a supratentorial structural lesion. Such lesions often produce coma in the setting of various cerebral herniation syndromes via mechanical compression of pontomesencephalic tegmental zones important in "alerting" the cortex and permitting wakefulness.

Generalized burst suppression (Fig. 6) is another common EEG pattern observed in coma. The bursts occur in a quasi-periodic fashion and may contain admixed sharp and/or spike and slow waves. Myoclonic jerks can accompany the bursting. Asynchronous bursting may reflect disordered interhemispheric cortical connectivity. Asymmetric burst voltage often signifies asymmetric cortical injury and/or raises the suspicion of a breach effect or an overlying fluid collection. The quasi-periodic bursts and suppressive intervals vary in duration with the depth of the coma. As the coma deepens, the bursts of activity become shorter and more infrequent and the suppressive intervals widen. This pattern reflects an exceptionally profound level of depressed consciousness. It is often observed during induction of general anesthesia. It is also the desired EEG pattern during administration of barbiturate therapy for refractory status epilepticus or to help control increased intracranial pressure after traumatic brain injury. Burst suppression suggests a poor prognosis, depending on the etiology. In the setting of a toxin- or medication-induced coma, the prognosis may be far better than in hypoxic-ischemic injury or trauma, in which burst suppression patterns may suggest a poor outcome.

Monotonous monorhythmic patterns can also be observed in the EEG of a comatose patient. Persistent, diffuse 8- to 12-Hz activity in a comatose patient is known as alpha coma (Fig. 7). This pattern, at first glance, may resemble normal background activity. However, the 8- to 12-Hz activity appears diffusely, not over posterior head regions, as in the normal waking background rhythm. Additionally, the pattern is completely unreactive to exogenous stimuli. Typical precipitants of alpha coma include brainstem lesions and hypoxic-ischemic mechanisms. It may also be observed as an ante mortem pattern as the patient progresses from burst suppression to electrocerebral inactivity (ECI). Alpha coma is, thus, thought to imply a very poor prognosis, particularly in the setting of anoxic injury. However, rare case reports have shown neurological recovery from this EEG pattern. Beta coma, theta coma, and delta coma are less common unre-active monomorphic EEG patterns whose prognostic significance is less clear.

Comatose patients can exhibit an EEG that seems to show features of normal sleep. Spindles, vertex waves, and K-complexes can be observed with cyclic variability. The EEG is distinguishable from normal sleep, however, because the patient is unarousable and the EEG does not react to applied stimuli. This pattern is sometimes referred to as spindle coma. These features associated with the EEG of sleep may disappear as the coma deepens.

Cheyne-Stokes respirations in a comatose patient may have a specific EEG correlate. An alternating pattern consisting of low-voltage irregular periods followed by higher-voltage slowing mirrors the respiratory rhythm changes. The cyclic alternating pattern may represent the effects of a cortical release phenomenon on the pacemaker function of the brainstem arousal system.

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  • Eric
    What causes generalized continuous slowing?
    1 year ago
  • Bildad
    What does bihemisphiric slowing mean?
    4 months ago
  • Kiara Wallace
    What is mild slowing on EEG?
    1 month ago

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