General
- Records variations in electrical activity from different areas of the head
- Represents a compound electrical field that originates mainly from postsynaptic potentials.
- The electric field is measured in the form of a voltage difference between two points, and each channel of an EEG represents the difference between two specific sites.
- These can be averaged to a single common reference point or measured between EEG electrodes.
- The ‘10– 20’ system is commonly used but does not always provide adequate anterior temporal coverage and so is often supplemented with additional electrodes.
Recording
- Scalp,
- Cortical surface
- For example, subdural strips or grids (electrocorticography, ECoG) or
- Within brain (stereoencephalography, SEEG) via depth electrodes
Indication
- Diagnosis and management of seizure disorders (main)
- Non-convulsive use
- Monitoring for burst suppression (e.g. induced barbiturate coma)
- Differential diagnosis of diffuse encephalopathy, including:
- Differentiating psychogenic unresponsiveness from organic:
- A normal EEG indicates
- Psychiatric unresponsiveness OR
- Locked-in syndrome
- Non-convulsive status epilepticus (seizures):
- Absence or complex partial status
- Subclinical focal abnormalities: e.g. PLEDs (see below), focal slowing…
- Specific patterns diagnostic for certain pathologies: e.g.:
- Periodic lateralizing epileptiform discharges (PLEDs):
- May occur with any acute focal cerebral insult (e.g. herpes simplex encephalitis (HSE), abscess, tumour, embolic infarct):
- Seen in 85% of cases of HSE (onset 2–5 d after presentation),
- If bilateral is ≈ diagnostic of HSE
- Subacute sclerosing panencephalitis (SSPE) (pathognomonic pattern):
- Periodic high voltage with 4–15 secs separation with accompanying body jerks
- No change with painful stimulation (differential diagnosis includes PCP overdose)
- Creutzfeldt-Jakob disease:
- Myoclonic jerks.
- EEG → bilateral sharp wave 1.5–2 per second (early → slowing; later→ triphasic).
- May resemble PLEDs, but are reactive to painful stimulation (most PLEDs are not)
- Triphasic waves:
- Not really specific.
- May be seen in hepatic encephalopathy, post-anoxia, and hyponatremia
- Objective measure of severity of encephalopathy:
- Usually used for anoxic encephalopathy
- Periodic spikes with seizures indicates <5% chance of normal neurologic outcome, with high mortality.
- Poor prognosticators
- Alpha coma
- Burst suppression
- Electrocerebral silence
- Differentiating hydranencephaly from severe hydrocephalus
- As a clinical confirmatory test in the determination of brain death
Evaluation
- Assessment & treatment of known or suspected status epilepticus
- Applied after witnessed or suspected event when the patient has not returned to baseline.
- Helpful to assess depth of treatment and non-convulsive events.
- Persistent altered mental status of uncertain etiology
- Suspected drug overdose/intoxication
- Supratentorial brain injury with exam out of proportion to injury
- Any critically ill patient with unexplained altered mental status (with or without known CNS injury)
- Neuroprognostication
- Post cardiac arrest and hypoxic/ischemic injuries
- Following other acute brain injuries
- As a component of multimodality monitoring
- Particularly in aneurysmal subarachnoid hemorrhage (SAH) to detect secondary ischemia
- When deep sedation or paralysis is used in patients at high risk of seizure
- Post cardiac arrest if targeted temperature management (TTM)
- Intracranial pressure crisis requiring paralysis
- Preop evaluation
- Interictal EEG → Video telemetric EEG → Cortical grid electrodes/ Depth electrode
Clinical analysis
- What is hypsarrhythmia?
- A chaotic, high-amplitude, generalized electroencephalographic pattern characteristic of infantile spasms
- What is phase amplitude coupling
- Oscillations from different frequency bands are not isolated and independent; consequently, they can interact with each other in the form of modulation
- This interaction of oscillations across different frequency bands is referred to as “cross-frequency coupling”11121314. Multiple forms of cross-frequency coupling have been analysed including phase/amplitude12151617; phase/phase18192021; amplitude-to-amplitude2223; and phase-frequency1114. Phase-amplitude coupling (PAC) is the most-studied type of cross-frequency coupling and is thought to be responsible for integration across populations of neurons. Low frequency brain activity controls the information exchange between brain regions by modulating the amplitude of the high frequency oscillations. PAC thus quantifies the modulation of the amplitude of high frequency oscillation, typically 30–100 Hz, with the phase of slow rhythm, typically 5–12 Hz
Electrode location
Electrode | Common Name |
Fp1 and Fp2 | Frontopolar or frontal polar |
F7 and F8 | Anterior temporal |
F3 and F4 | Superior frontal |
Fz | Frontal midline |
T7 and T8 (T3 and T4) | Midtemporal |
C3 and C4 | Central |
Cz | Vertex or central midline |
P7 and P8 (T5 and T6) | Posterior temporal |
P3 and P4 | Parietal |
Pz | Parietal midline |
O1 and O2 | Occipital |
Sp1 and Sp2 | Sphenoidal |
A1 and A2 | Auricular |
To be sorted
- 49-year-old woman is referred with a 1-year history of medically refractory epilepsy. Electrographically, both interictally and ictally, this patient’s seizures were consistent with left mesial temporal onset. However, no definite abnormalities were observed on MRI. Assuming left hemisphere dominance for language, neuropsychological data were suggestive of left temporal lobe dysfunction. Some intact verbal memory scores raised a question that the left mesial temporal lobe structures were intact. Wada test: Language lateralized to the left hemisphere. She underwent invasive electrocorticographic (ECoG) monitoring with a left mesial temporal (LMT) strip, basal temporal strips (anterior, LAT and posterior, LPT), and an 8 × 8 electrode grid with the upper five rows located frontoparietally (contacts 1-40) and the lower three rows over the lateral temporal neocortex (contacts 41-64). All seizures were electrographically stereotyped. Electrographic onset preceded clinical onset and consisted of fast activity of 80-100 Hz isolated to the contact at LG41. Six to nine seconds later this abruptly transitioned to a 2.5-Hz spike and wave pattern involving the mesial and basal temporal contacts. Which one of the following statements is most accurate?
- The epileptogenic zone is the zone whose resection or disruption is both necessary and sufficient to eliminate seizures hence is only determinable postoperatively once seizure freedom has been gained. As such, epilepsy surgery targets the ictal onset zone and areas involved in early seizure organization, which generally tend to coincide or intersect with the epileptogenic zone. The ictal onset zone is defined as the area where the ictal discharge is first detected, regardless of its morphology, before the clinical manifestations of the seizure. Identifying that area (using ECoG and/or nuclear imaging), a major prerequisite for successful resective epilepsy surgery, requires familiarity with electrographic ictal patterns. Early ictal patterns seen on the ECoG include rhythmic sinusoidal waves, irregular spike discharge, spike and wave activity, low-voltage fast activity, and high-frequency oscillations. An appropriate broad definition of an electrocorticographic ictal discharge is any electrodecremental or rhythmic pattern that represents a considerable deviation from the baseline, whether or not it contains apiculate waveforms. In general, it is believed that ictal onsets consisting of fast frequency activity indicate the proximity of the recording electrodes to the ictal onset zone whereas slower ictal onsets tend to represent propagated activity. In this case, seizure onset was from the anterosuperior temporal gyrus (LG41) with spread to the hippocampus (mesial and basal contacts). There are several caveats to this: the epileptogenic zone may be more extensive than the ictal onset zone hence resection may not eliminate seizures (or adjacent areas become capable of initiating seizures), the majority of epilepsy surgery patients only remain seizure free on antiepileptic drugs, the epileptogenic zone and the ictal onset zone may be separate, e.g. the epileptogenic zone in a “clinically silent” area and the seizure becomes clinically manifest only after it propagates to the temporal lobe (ECoG will localize ictal onset to temporal lobe but resection will not eliminate the seizure generator).
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