Encephalopathic Patterns

Encephalopathic Patterns

When a patient is unresponsive without lateralizing exam findings and the etiology of the coma is in question, an EEG can be helpful to further assess the degree of the coma and perhaps give insight into the etiology or localization of the underlying pathology. With repeated EEGs, just like with repeated physical examinations, the evolution of the EEG pattern can help determine prognosis.

In general, there is a continuum of EEG findings that correspond to the severity of a diffuse clinical encephalopathy. Extremes of normalcy or abnormality at both ends of this continuum are fairly easy to recognize, and what lies in between can be categorized as mild, moderate, or severe based on some basic reproducible EEG findings.

Mild: As the level of arousal becomes clouded there is corresponding mild slowing of the EEG. It may begin with slowing of the posterior dominant rhythm, but as the depth of encephalopathy increases, there are increasing amounts of theta and then delta activity intermixed with the background. These changes are independent of the etiology of the encephalopathy.

Moderate: With worsened cerebral function, there is increased theta and delta range slowing. Background organizational features such as anterior-posterior gradients and the posterior dominant rhythm become difficult recognize, but the EEG background retains some variability in response to stimulation and there is usually evidence of discernible state changes.

Severe: Eventually there is loss of normal state changes that control wakefulness and sleep, and the EEG becomes monotonous in appearance and unresponsive to external or internal stimulation. At the far extreme of a severe diffuse encephalopathy, there is a loss of all cortical activity and the EEG shows electrocerebral silence.

Within these general patterns of encephalopathy, there can be more specific findings that suggest particular etiologies.

A. EEG Background

Symmetry	Background EEG Frequency	PDR	Continuity	Reactivity	State Changes	CAPE	Voltage	AP Gradient	Breach Effect
Symmetric	Beta	Present (specify frequency)	Continuous: <1% suppression (<10 µV) or attenuation (≥10 µV but <50% of background voltage)	Reactive	Present with normal stage N2 sleep transients	Present	High ≥150 µV	Present	Present
Mild asymmetry (<50% voltage OR 0.5–1 Hz difference)	Alpha	Absent	Nearly continuous: 1–9% suppression or attenuation	Unreactive	Present but with abnormal stage N2 sleep transients	Absent	Normal ≥20 to <150 µV	Absent	Absent
Marked asymmetry (≥50% voltage OR >1 Hz difference)	Theta	Unclear	Discontinuous: 10–49% suppression or attenuation	SIRPIDs only	Present but without stage N2 sleep transients	Unknown/unclear	Low 10 to <20 µV	Reverse	Unclear
	Delta		Burst-suppression or Burst-attenuation: 50–99% suppression or attenuation	Unclear	Absent		Suppressed <10 µV
			Suppression: >99% suppression or attenuation	Unknown

Additional features if there is burst suppression:

Localization of Bursts	G / L / BI / UI / Mf
Highly Epileptiform Bursts	Present or Absent
Identical Bursts	Present or Absent

Symmetry

Normal

• Symmetric

Mild Abnormal

• <50% voltage asymmetry
• 0.5–1 Hz frequency difference

Severe

• ≥50% voltage asymmetry
• >1 Hz frequency difference

Background Frequency

• Beta
• Alpha
• Theta
• Delta

Continuity

Normal

• Continuous: <1% suppression

Mild

• Nearly continuous: 1–9% suppression

Moderate

• Discontinuous: 10–49%

Severe

• Burst suppression: 50–99%
• Suppression: >99%

Reactivity

• Reactive
• Unreactive
• SIRPIDs only
• Unknown

State Changes

• Normal N2 sleep transients
• Abnormal N2 transients
• Absent

CAPE

• Present
• Absent
• Unclear

Voltage

• High ≥150 µV
• Normal ≥20–<150 µV
• Low 10–<20 µV
• Suppressed <10 µV

AP Gradient

• Present
• Absent
• Reverse

Breach Effect

• Present
• Absent
• Unclear

Slow Posterior Dominant Rhythm

Diffuse theta slowing

Diffuse delta slowing

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Generalized Periodic Discharges with Triphasic Morphology, previously known as Triphasic Waves are a periodic pattern of waveforms that have three phases and are generally most prominent in the anterior leads. These waveforms often have a subtle time lag between anterior and posterior regions. Their presence tends to be associated with metabolic encephalopathy, often of hepatic or renal origin, but they are nonspecific and may be seen in a variety of toxic-metabolic encephalopathies.

Generalized Rhythmic Delta Activity (GRDA) frontally predominant – previously known as Frontal Intermittent Rhythmic Delta Activity (FIRDA): This is an intermittent pattern of rhythmic monomorphic delta waves seen with mild to moderate diffuse encephalopathies. It tends to occur with subcortical white matter disease more than cortical disease, but the etiology is usually nonspecific. It becomes more pronounced as the patient becomes drowsier.

Dominant Frequency is in the alpha range with loss of reactivity previously known as Alpha Coma This monomorphic pattern of diffuse alpha frequencies that are more prominent in the anterior than the posterior regions of the brain typically occurs in the setting of hypoxic-ischemic injury. It looks like a normally organized background turned upside-down (or more accurately, frontside-back). The prognosis for independent living following development of this EEG pattern is poor. It can also be seen with anesthetic sedation so the context matters.

Dominant Frequency is in the beta range but it is usually intermixed delta with loss of reactivity previously known as Beta Coma. This pattern of diffuse beta frequently is associated with a drug overdose. These faster frequencies seen can be seen with sedatives such as barbiturates and benzodiazepines. The overall prognosis is better compared to other coma patterns if the patient is supported through the overdose period assuming there is no other cerebral injury.

Dominant frequency is a beta delta pattern previously known as a Spindle Delta Coma In contrast to the beta predominant pattern, there are bursts of beta activity riding over large slow polymorphic delta waves that are maximal centrally and can be seen in encephalopathy from a variety of etiologies. It is a nonspecific pattern.

Burst Suppression Pattern is an extreme pattern that can be seen in severe coma states or can be induced iatrogenically by anesthesia or for the treatment of status epilepticus. This is an alternating pattern of bursts of higher voltage activity separated by periods of relatively suppressed cerebral activity. This pattern is typically described by its ratio of burst period to suppression period. When the bursts are lost and the suppression periods become continuous, then the pattern is called background suppression with no apparent cerebral activity over 2 microvolts.

Electrocerebral Silence or Inactivity These studies, also called brain death studies, are now rarely used. They were frequently requested in transplant centers as a confirmatory test to document brain death in association with the clinical examination. The principal limitation EEG for the purpose of establishing a diagnosis of brain death is that it only records cortical activity and cannot reveal useful information about brainstem activity. Other tests such nuclear medicine test for cerebral perfusion or evoked potentials have largely supplanted the usefulness of the EEG. In addition, there are no EEG criteria for the very young, and the presence of small populations of cortex that cannot generate sufficient voltages above 2 microvolts cannot be revealed by an EEG.

When other ancillary tests are unavailable, an EEG for the purpose of establishing electrocerebral inactivity (ECI) is still sometimes performed. Reversible factors that suppress cerebral activity need to be excluded, and the study must be performed according to a strict criteria:

Exclusion Criteria:

• Overdose of CNS depressants
  • barbiturates, benzodiazepines, methaquinolone and meprobamate
• Hypothermia (T < 32.2C)
• Cardiovascular shock (BP < 80mmHg)
• Severe metabolic or endocrine disorders

Technical requirements of a brain death study.

• At least 8 scalp electrodes and reference electrodes
• Interelectrode impedance between 100-10,000 ohms
• Document testing integrity of entire system
• Interelectrode distances of > 10 cm
• Sensitivity < 2mV/mm
• Time constant 0.3-0.4 second
• EKG channel
• Test EEG reactivity to external stimulation
• Recording time at least 30 minutes
• Qualified technologist (rEEG,T)

Electrocerebral Inactivity (ECI) with respiratory and ECG artifacts. Note the scale legend shows a 40 microvolt amplitude. There is no waveform that could be considered generated by the cortex.

Periodic Discharges These discharges occur with a regular periodicity throughout the EEG and can be generalized, regional/lateralized, or bilateral and independent. Generalized periodic discharges (GPDs) are more frequently associated with severe encephalopathy and can been seen after a severe hypoxic/ischemic event. Lateralized Periodic Discharges (LPDs) are seen in a variety of clinical settings including herpes encephalitis, acute stroke, tumor, or as the aftermath of nonconvulsive status epilepticus. Bilateral independent lateralized discharges are rare and suggest that multifocal injury to the brain such as occurs in the setting of shower emboli resulting in multifocal strokes or aggressive metastatic brain cancer. While Periodic Discharges are not an epileptogenic pattern per se, they are associated with pathological processes where seizures often occur.

Generalized Periodic Discharges (GPDs) in the setting of a hypoxic ischemic injury after cardiac arrest

Right Temporal Lateralized Periodic Discharges (LPDs) in the setting of herpes encephalitis

LPD+

LRDA