EEG Non-Epileptiform Abnormalities 2 — Questions and Answers
Question 1: Focal polymorphic delta activity (PDA) over the right temporal region in an awake adult most strongly suggests:
- Normal drowsiness
- A structural lesion in the right temporal area (Correct answer)
- Generalized metabolic encephalopathy
- Medication effect from benzodiazepines
Correct answer: A structural lesion in the right temporal area
Focal polymorphic delta activity is a highly localizing finding indicating structural pathology (tumor, stroke, abscess) disrupting normal cortical-subcortical connections in the region where it appears.
Focal polymorphic delta activity (PDA) is continuous, irregular (polymorphic) slow activity confined to one brain region, and is the most reliable EEG indicator of a focal structural lesion. It results from disruption of subcortical white matter connections to the overlying cortex, preventing normal faster rhythmic activity. Common causes include tumor, stroke, hemorrhage, abscess, or traumatic injury. PDA persists across states (wake and sleep), distinguishing it from the intermittent rhythmic delta of encephalopathy. The location correlates well with the lesion site. Loss of faster frequencies and lack of reactivity in the affected area increase the specificity. Neuroimaging should follow any new focal PDA finding.
Question 2: Generalized background slowing with intermittent frontal rhythmic delta activity (FIRDA) in an adult typically indicates:
- Focal frontal lobe epilepsy
- Diffuse encephalopathy or deep midline dysfunction (Correct answer)
- Normal aging changes
- Posterior fossa tumor
Correct answer: Diffuse encephalopathy or deep midline dysfunction
FIRDA (now called generalized rhythmic delta activity with frontal predominance or GRDA) is a non-specific finding indicating diffuse cerebral dysfunction from metabolic, toxic, or structural causes affecting deep midline structures.
Frontal intermittent rhythmic delta activity (FIRDA), reclassified by ACNS as generalized rhythmic delta activity (GRDA), consists of 1.5-3 Hz rhythmic, sinusoidal delta waves maximal bifrontally. Despite its frontal predominance, it does not indicate frontal lobe pathology. It reflects diffuse cerebral dysfunction from metabolic encephalopathy (hepatic, uremic, hypoxic), medication toxicity, increased intracranial pressure, or deep midline structural lesions affecting the diencephalon. It is distinguished from focal PDA by its bilateral, rhythmic nature and from epileptiform activity by its sinusoidal (not sharp) morphology. GRDA may also be seen in generalized epilepsy syndromes, where it should be distinguished from epileptiform patterns.
Question 3: An asymmetry in the posterior dominant rhythm amplitude, with the right side consistently 50% lower than the left, suggests:
- Normal variant — mild asymmetry is always benign
- Possible structural or functional abnormality of the right hemisphere (Correct answer)
- Left hemisphere hyperexcitability indicating seizure focus
- Electrode application error only
Correct answer: Possible structural or functional abnormality of the right hemisphere
Amplitude asymmetry greater than 50% of the posterior dominant rhythm suggests dysfunction on the lower-amplitude side, potentially from a structural lesion, prior surgery, or cortical atrophy.
The posterior dominant rhythm (PDR) normally shows mild amplitude asymmetry (up to 50% difference is considered within normal limits by some authors). Consistent asymmetry exceeding 50%, with the right side lower, suggests right hemisphere pathology — either a structural lesion (tumor, stroke, cortical atrophy), subdural collection, or prior surgery disrupting cortical generators. This is sometimes called 'amplitude depression.' However, before concluding pathology, the technologist must rule out technical causes: electrode impedance differences, scalp edema, skull defect (breach rhythm produces HIGHER amplitude), or hair-related contact issues. Frequency asymmetry of the PDR (slower on one side) is generally more significant than amplitude asymmetry.
Question 4: Generalized voltage attenuation (low-voltage EEG) with amplitudes below 20 µV throughout may be caused by:
- Caffeine ingestion in the last hour
- Scalp edema, subdural fluid, or certain medications such as barbiturates (Correct answer)
- Hyperventilation artifact
- Photic driving response
Correct answer: Scalp edema, subdural fluid, or certain medications such as barbiturates
Generalized low voltage can result from physical barriers between brain and electrodes (scalp edema, subdural effusions, thick skull) or from cortical suppression by medications like barbiturates, hypothermia, or severe diffuse brain injury.
Low-voltage EEG (generalized amplitudes below 20 µV) has both benign and pathological causes. Technical causes include high electrode impedances and scalp conditions. Benign: approximately 7-10% of normal adults have low-voltage recordings as a constitutional variant, often with preserved reactivity. Pathological causes include: (1) physical barriers — scalp edema, subdural fluid collections, thick skull; (2) cortical suppression — barbiturates, anesthetic agents, hypothermia; (3) severe diffuse brain injury — anoxic encephalopathy, advanced neurodegenerative disease. The key clinical distinction is reactivity: benign low-voltage records show normal alpha blocking with eye opening, while pathological cases may show unreactive patterns. In the most severe form, electrocerebral inactivity (ECI) may support a brain death determination.
Question 5: Excessive beta activity (above 25 µV) generalized across the recording is most commonly associated with:
- Temporal lobe epilepsy
- Sedative or anxiolytic medication use such as benzodiazepines (Correct answer)
- Posterior fossa tumor
- Normal hyperventilation response
Correct answer: Sedative or anxiolytic medication use such as benzodiazepines
Generalized excessive beta activity is most commonly a pharmacological effect of benzodiazepines, barbiturates, or other sedative-hypnotic medications, which enhance GABAergic inhibition and increase fast cortical activity.
Excessive generalized beta activity (>25 µV or >30 µV by some criteria) is most commonly pharmacological, caused by benzodiazepines, barbiturates, chloral hydrate, and other GABA-enhancing sedatives. These medications increase cortical fast activity by enhancing inhibitory interneuron synchronization. The beta is typically diffuse, symmetric, and maximal in frontal-central regions. Other causes of increased beta include: anxiety/alertness (normal low-amplitude beta), hyperthyroidism, and breach rhythm (focal beta increase over skull defects). Focal or asymmetric beta excess may suggest a structural lesion — either a skull defect (breach rhythm with increased amplitude) or a lesion on the side with reduced beta.
Question 6: What does the term 'electrocerebral inactivity' (ECI) refer to in EEG?
- Normal low-voltage pattern during deep sleep
- Absence of cerebral electrical activity above 2 µV at maximum sensitivity, used as an adjunct in brain death determination (Correct answer)
- Background slowing to theta range
- Intermittent suppression during burst-suppression pattern
Correct answer: Absence of cerebral electrical activity above 2 µV at maximum sensitivity, used as an adjunct in brain death determination
Electrocerebral inactivity is the absence of EEG activity above 2 µV when recorded with maximum sensitivity, interelectrode distances of at least 10 cm, and a recording duration of at least 30 minutes, used as an adjunct test in brain death evaluation.
Electrocerebral inactivity (ECI) is defined as no identifiable cerebral electrical activity above 2 µV at maximum amplifier sensitivity (2 µV/mm). The ACNS criteria for ECI recording include: minimum 8 scalp electrodes with interelectrode distances ≥10 cm, impedances between 100-10,000 ohms, 30-minute minimum recording, sensitivity of 2 µV/mm, 1-30 Hz filter settings, and testing for reactivity. ECG and other physiological monitors must be included to distinguish artifacts. ECI is used as an adjunctive test for brain death determination in many jurisdictions. Reversible causes (hypothermia <32°C, sedative drugs, severe metabolic derangement) must be excluded before ECI can support a brain death diagnosis.
EEG Non-Epileptiform Abnormalities 2
Focal polymorphic delta activity (PDA) over the right temporal region in an awake adult most strongly suggests: