Free R.EEG.T. Exam Flashcards

Standardized electrode placement using 10% and 20% fractions of nasion-inion and preauricular distances. The fractions make placement reproducible across head sizes so recordings are comparable between patients and labs.

Letters denote brain region (Fp frontopolar, F frontal, C central, P parietal, T temporal, O occipital). Odd numbers are left hemisphere, even numbers are right, and 'z' marks the midline (Fz, Cz, Pz).

Located 10% of the nasion-to-inion distance above the nasion along the midline, then 10% of the transverse distance to the left. Correct measurement is essential because mislocated frontopolar electrodes distort frontal and eye-movement interpretation.

Provides a low-impedance electrical pathway between the electrode and scalp, reducing resistance, improving signal quality, and minimizing artifact. Poor contact raises impedance and introduces 60 Hz and pop artifact.

Keep impedances between 100 and 5,000 ohms (under 5 kilohms) and reasonably balanced. High or unequal impedance degrades common mode rejection and produces 60 Hz interference; re-prep the site rather than relying on filters.

Place electrodes around the wound, avoid direct contact to prevent infection and discomfort, and document the modification so the interpreter knows which positions were repositioned and why the montage deviates from standard.

The largest white-matter commissure connecting the cerebral hemispheres and enabling interhemispheric communication. Relevant to EEG because it underlies bilateral synchrony and the spread of generalized discharges.

The thalamus acts as a pacemaker generating and synchronizing cortical rhythms, including sleep spindles and the thalamocortical 3 Hz spike-and-wave of absence epilepsy. EEG largely reflects cortical postsynaptic potentials modulated by the thalamus.

Scalp EEG reflects summated excitatory and inhibitory postsynaptic potentials of cortical pyramidal neurons, not action potentials. Large synchronous populations are required for a deflection to be visible at the scalp.

Acetylcholine is the primary neurotransmitter generating REM sleep; brainstem cholinergic (REM-on) neurons interact reciprocally with aminergic (REM-off) neurons. Understanding state control aids correlation of EEG sleep patterns.

8-13 Hz posterior dominant rhythm seen in a relaxed adult with eyes closed; it attenuates with eye opening or attention. Slowing of the posterior dominant rhythm suggests encephalopathy or a structural process.

Beta: above 13 Hz (alert, drowsy, sedative-induced). Theta: 4 to under 8 Hz (drowsiness, children). Delta: under 4 Hz (deep sleep; pathologic if focal/persistent in awake adults).

A 7-11 Hz arch-shaped rhythm over the central (sensorimotor) regions that attenuates with contralateral movement or its intention. Recognizing mu prevents mislabeling a normal variant as abnormal.

Sharp, positive occipital transients occurring during visual scanning of a complex image in the awake patient with eyes open. A normal variant; not epileptiform, but can be confused with occipital sharp waves.

Sharp, positive occipital waves occurring in light sleep, often in runs. A normal sleep variant that must be distinguished from occipital epileptiform discharges.

Vertex sharp waves are sharp negative transients maximal at Cz in N1-N2 sleep. K-complexes are large biphasic transients (often with spindles) in N2. Both are normal sleep features, not epileptiform.

Wicket spikes (temporal arciform runs) and benign epileptiform transients of sleep (BETS/SSS) are normal variants frequently mistaken for epileptiform activity. Misidentification can lead to an incorrect epilepsy implication.

Referential montage measures each electrode against a common reference and best shows the amplitude/field of widespread activity. Bipolar montage links adjacent electrodes in chains and best localizes a focus by phase reversal.

In a bipolar chain, deflections pointing toward each other (or away) at adjacent channels localize the maximum of a discharge to the shared electrode. It is the key bipolar localization principle, not a sign of abnormality itself.

If the reference electrode is active (e.g., ECG, near a discharge), the artifact appears in all channels using that reference. Recognizing reference contamination prevents misreading shared activity as widespread cerebral activity.

A standard adult EEG uses the full 10-20 array, includes wakefulness and (when possible) drowsiness/sleep, runs at least about 20-30 minutes of artifact-free recording, and uses multiple montages for adequate sampling.

The differential amplifier's ability to cancel signals common to both inputs (e.g., 60 Hz). High CMRR with balanced low impedances suppresses environmental noise; degraded CMRR is a leading cause of mains artifact.

The ratio of input voltage to pen/display deflection (e.g., 7 microvolts/mm). Lower numeric sensitivity values yield larger deflections. Sensitivity must be adjusted so low-voltage records are not missed and high-voltage records are not clipped.

The LFF attenuates slow activity below its setting (typical 1 Hz or time constant 0.3 s). Raising it too high removes legitimate delta/slow waves and can mask slowing; lowering it admits sweat and movement artifact.

The HFF attenuates fast activity above its setting (typically 70 Hz). Set too low, it rounds spikes and muscle/fast activity, potentially blunting epileptiform sharpness; this can cause under-recognition of true spikes.

The 60 Hz notch filter suppresses mains interference but can attenuate or distort genuine activity near 60 Hz and masks an underlying impedance problem. Fix electrode contact first; use the notch as a last resort.

By the Nyquist principle the sampling rate must exceed twice the highest frequency of interest; clinical EEG typically samples at 256 Hz or higher. Under-sampling causes aliasing, falsely representing fast activity as slower waveforms.

A known square-wave or sine voltage applied to all channels verifies equal amplifier gain, filter settings, and pen/display response before recording. Unequal calibration invalidates amplitude and asymmetry interpretation.

Digitally acquired EEG referenced to a common reference can be reformatted into any montage, filter, and sensitivity after acquisition. This lets the interpreter re-examine events without re-recording the patient.

3-5 minutes of overbreathing induces hypocapnia and cerebral vasoconstriction, normally producing diffuse slowing (buildup) and notably activating absence (3 Hz spike-wave) epilepsy. Contraindicated in recent stroke, significant cardiopulmonary disease, sickle cell, or moyamoya.

Flashing light at varying frequencies tests for a photoparoxysmal response (generalized spike-wave) and helps assess photosensitive epilepsy. A photic driving response time-locked to the flash is a normal occipital finding.

A sleep-deprived recording increases the yield of epileptiform discharges, especially in generalized epilepsies, by promoting drowsiness and sleep, the states when many abnormalities appear. It is a planned activation, not an artifact source to suppress.

N1: vertex waves, slow eye movements. N2: spindles and K-complexes. N3: high-amplitude delta. REM: low-voltage mixed frequency, sawtooth waves, lowest chin tone. Correct staging supports identification of state-dependent abnormalities.

Eye movements create frontal deflections from the corneoretinal dipole: eye blink shows symmetric frontal downward deflections; lateral gaze produces out-of-phase frontotemporal deflections. Recognize so it is not read as frontal slowing/sharp waves.

Brief, high-frequency, spiky activity from scalp/facial muscle tension, often temporal and worse with jaw clenching. Reassure and reposition the patient or use slight HFF; do not mistake bursts for fast epileptiform discharges.

Regular sharp transients time-locked to the QRS complex, more common in short-necked patients and with reference issues. Use a simultaneous ECG channel to confirm timing; manage by re-referencing rather than mislabeling as periodic discharges.

An abrupt, single-channel high-amplitude transient with a sudden vertical jump from a momentarily disconnected or unstable electrode. It is confined to one electrode's derivations, distinguishing it from a cerebral discharge with a logical field.

Rhythmic 60 Hz contamination from environmental electrical sources, usually worsened by high/unbalanced impedance or a loose electrode. Correct impedance and remove offending devices before applying a notch filter.

Physiologic artifact arises from the patient (eye, muscle, ECG, sweat, pulse, glossokinetic). Technical artifact arises from equipment/environment (electrode pop, 60 Hz, cable movement). Source identification dictates the correct correction.

Sweat causes very-slow (under 0.5 Hz) undulating baseline sway; tongue movement (glossokinetic) produces slow potentials maximal frontally. Both are slow, non-cerebral, and corrected by cooling/drying or by reducing the LFF appropriately.

By convention a spike has a duration of 20-70 ms and a sharp wave 70-200 ms. Both are epileptiform when they stand out from background with a physiologic field; duration only differs, not clinical implication.

Generalized, symmetric, frontally maximal 3 Hz spike-and-wave discharges, classically activated by hyperventilation, are the signature of childhood/juvenile absence epilepsy and correlate with brief impaired awareness.

Repetitive lateralized sharp/spike complexes at near-regular intervals over one region. In a febrile patient with temporal PLDs, strongly suspect herpes simplex encephalitis; PLDs generally indicate an acute focal destructive process.

Bilateral, often frontally predominant waves with a characteristic three-phase morphology and an anterior-posterior lag, classically associated with metabolic/hepatic encephalopathy rather than a primary epileptic focus.

Alternating high-amplitude bursts and near-flat suppression, indicating severe diffuse cerebral dysfunction (deep anesthesia, hypothermia, severe anoxic injury). It signals critical depression of cortical activity and warrants prompt physician notification.

EEG performed in the brain-death evaluation requires a specialized technical protocol: extended interelectrode distances, increased sensitivity (e.g., 2 microvolts/mm), defined filters, and documentation of reactivity, following ACNS guidelines.

Neonatal EEG is discontinuous (tracé alternant/discontinu), has slower frequencies, and is interpreted by conceptional age. Applying adult criteria to a neonatal record leads to misinterpretation; age-appropriate norms are essential.

Benzodiazepines and barbiturates increase fast (beta) activity; many sedatives and anticonvulsants alter background and can suppress or slow it. Documenting current medications lets the interpreter avoid attributing drug effects to disease.

Document age, clinical question, medications, last seizure, sleep deprivation status, and relevant neurologic history. The reason for the study guides montage and activation choices and is essential context for clinical correlation.

If a technologist discovers an error in a patient's EEG report, the obligation is to report it through appropriate professional channels to the interpreting physician, maintaining accuracy and patient safety rather than concealing the mistake.