7.3 Neurological Disorders & EEG Correlation

Why Clinical Correlation Is on the Exam

The content outline explicitly lists neuropathology (tumors, encephalopathy, vascular), neurological disorders, head trauma/TBI, psychiatric disorders, and correlation of history with EEG patterns. The technologist is the person who reads the order, takes the history, watches the patient, and records the tracing simultaneously - so the exam tests whether you can connect the clinical picture to the expected EEG and recognize when a finding is a critical value that demands provider notification.

The guiding principle: a focal, fixed, polymorphic abnormality points to a structural lesion; a diffuse abnormality points to a global process (toxic, metabolic, anoxic, infectious, degenerative).

Structural and Vascular Lesions

The breach rhythm is a classic exam point: over a craniotomy or skull defect, the missing bone no longer attenuates the signal, so activity is higher in amplitude and sharper locally. It is a normal physical effect of the skull defect and must not be called epileptiform.

Diffuse and Metabolic Encephalopathies

A frequent sample-question theme is which processes cause diffuse slowing. The answer is the global ones - meningitis, encephalitis, anoxia, and toxic-metabolic states - whereas a focal mass (meningioma, abscess, thrombosis) tends to cause focal slowing.

• Toxic-metabolic encephalopathy (hepatic, uremic/renal, hypoglycemic, anoxic): generalized theta/delta slowing; triphasic-morphology generalized periodic discharges (GPDs) are classic in hepatic and renal failure and are typically reactive to stimulation (which helps distinguish them from epileptiform discharges).
• Anoxic brain injury (post-cardiac arrest): generalized slowing, burst-suppression, GPDs, or in the worst case electrocerebral inactivity - patterns with major prognostic weight, so accurate, reactive-tested recording is critical.

Infectious and Degenerative Disorders

The periodicity interval is a high-yield discriminator: ~0.5-2 s for LPDs and CJD, but much longer (4-15 s) for SSPE. Knowing the interval lets the technologist describe the pattern accurately for the reader.

Other Conditions and Their EEG Relationships

• Narcolepsy: characterized by sleep-onset REM periods (SOREMPs) - REM appearing abnormally early after sleep onset. (A classic sample-question answer is 'REM onset sleep.')
• Psychiatric disorders: the routine EEG is often normal in primary psychiatric disease; the EEG is frequently ordered to exclude an organic or epileptic cause. The technologist should not expect a specific 'psychiatric' pattern.
• Dementias (e.g., Alzheimer disease): generalized slowing and loss of the normal posterior rhythm in advanced disease; early disease may be near-normal.
• Migraine, syncope, nonepileptic events: the EEG helps distinguish these from seizures; capturing a typical event with no ictal correlate is itself diagnostically valuable - documenting that a 'spell' had no EEG change supports a nonepileptic diagnosis.
• Sleep disorders: narcolepsy's SOREMPs are detected on the multiple sleep latency test; the technologist who records sleep must label stages accurately because the clinical question often hinges on sleep architecture.

Basic Cardiac Rhythms and the EEG

The outline lists basic cardiac rhythms and rhythms associated with EEG changes because cardiac events masquerade as neurologic ones. A simultaneous ECG channel is standard so the reader can correlate. A cardiac arrhythmia or asystole can cause a convulsive syncope with diffuse EEG slowing/attenuation that recovers when perfusion returns - distinguishing this cerebral hypoperfusion pattern from a primary seizure is a classic correlation point.

The technologist should recognize that a regular sharp deflection time-locked to the QRS is cardiac artifact, not cerebral activity, and that a sudden diffuse attenuation coinciding with a dropped heartbeat points to a cardiac cause.

The Technologist's Correlation Responsibilities

Clinical correlation is an active recording task, not after-the-fact interpretation:

1. Extract the clinical question from the order and history so the recording targets it (montage, activations, duration, extra electrodes).
2. Test and document reactivity (response to eye opening, noxious or auditory stimulation) - especially important to separate reactive metabolic GPDs from epileptiform patterns and to assess comatose patients.
3. Apply seizure precautions and ensure patient safety when a seizure or high-risk pattern is anticipated.
4. Recognize critical values - electrographic seizure, status epilepticus, herpes-pattern temporal LPDs, new burst-suppression, deterioration - and notify the provider promptly.
5. Annotate, do not diagnose: describe what you see ('continuous left temporal polymorphic delta, non-reactive') and let the physician assign the clinical meaning.