EEG in PD (continued)
| {Quynh Tran, 2016 #2603} | ↑ beta | spectral | gait | 4 PD, no control | Multiple lead, channel | power spectra density (PSD) and centroid frequency (CF) | GIF episodes were associated with significant increases in the high beta band (21-38Hz) across the central, frontal, occipital and parietal EEG sites The mean, maximum and minimum values of PSD and CF of the 4 frequency bands in each electrode"s location were taken as inputs of the classifier to | Quantification? Can't as there is no HC, |
| {Tard, 2016 #2604} | ERD/ERS | parkinsonian patients with freezing of gait (FoG, n = 12) or without freezing of gait (n = 13), and in aged-matched HC (n = 13) | event-related desynchronization/synchronization (ERD/ERS); Attention during step preparation was modulated by means of an auditory oddball discrimination task. EEG oscillations in different frequency bands were measured for the attentional stimulus and the motor stimulus. |
Over the 500 ms following the sound, low-frequency power increased in all three groups. This was followed by a power decrease in mid-range frequencies after both target and standard sounds in the healthy controls and in the non-FoG group. In contrast, EEG oscillations in the beta band were impaired in the FoG group, who notably failed to display event-related desynchronization after perceiving the sound. Conclusions: An attentional stimulus was able to trigger event-related desynchronization before motor preparation in the non-FoG group but not in the FoG group. Significance: In the FoG group, stimulus discrimination was maintained but the coupling between attention and motor preparation was impaired. Parkinsonian patients with freezing of gait did not display beta desynchronization Beta oscillations have a role in active immobilization (defined as a "sta tus quo" condition) (Engel and Fries, 2010) and are involved in the pathogenesis of bradykinesia. Premotor beta ERD is observed before movement onset (i.e. during motor prepa ration or execution) and is correlated with greater cellular excitability in the thalamocortical system beta ERS may correspond to the deactivation or active inhibition of the sensorimotor cortex | Can't: multiple lead, channel | |||
| {Singh, 2020 #2608} | ↑ beta | spectral | 13 PD FOG, 13 PD w/o FOG, 13 HC | scalp EEG during a lower-limb pedaling motor task, which required intentional initiation and stopping of a motor movement. | PDFOG+ patients exhibited attenuated theta-band (4–8 Hz) power and increased beta-band (13–30 Hz) power at midfrontal electrode Cz during pedaling. | |||
| Clouds of Care | This slide has some good source papers | |||||||
Limitations
| The EEG is thought to be primarily generated by cortical pyramidal neurons in the cerebral cortex that are oriented perpendicularly to the brain's surface. | The neural activity detectable by the EEG is the summation of the excitatory and inhibitory postsynaptic potentials of relatively large groups of neurons firing synchronously |
| biological and environmental electrical artifacts frequently | Most notable is the presence of low-amplitude, high-frequency activity arising from scalp muscles, often frontally dominant but seen throughout the tracing. REMs, resulting from saccades and spontaneous changes of gaze, may be seen as small, rapid deflections in frontal regions. Extremely large-voltage, diphasic potentials in frontal regions result from blinks. This occurs because the eye is a dipole, relatively positive at the corneal surface and negative at the retinal surface, and the eye moves characteristically upward during a blink according to Bell phenomenon, resulting in a moving charge and potential change. Since the positivity of the cornea rotates upward toward frontal electrode sites, a transient positivity, then negativity is recorded there. Another common artifact during the waking EEG is caused by swallowing and the related movement of the tongue, which similar to the eye is a dipole and causes a slow potential with superimposed muscle artifact |
| Not overall motor symptoms but only a specific domain, so not overall sPD population but PD with FOG | Mainly FOG in PD |
| variability in experimental settings |
|
| Small overall sample sizes across studies, the complexity of interpreting EEG data, thus difficult to harmonized, quantitative comparison |
Small n in {Quynh Tran, 2016 #2603}, {Tard, 2016 #2604} Multiple lead, channel, results only at certain electrode, multiple/different Regions of Interest |
Sleep EEG
| PD | |||
|---|---|---|---|
| Spectral power (REM mainly in stage 3 (N3)) | Scalp-Slow wave (SW) (< 1 Hz) | ↓ {Memon, 2023 #2386} | |
| delta power (1.0–4 Hz) |
Delta oscillation reflects the burst-pause firing pattern of the hyperpolarized thalamic cortex and corticothalamic neurons in synchronization (Steriade et al., 1993). Delta activity can be measured by delta power by Fourier analysis. Higher sleep quality, a biomarker of homeostatic sleep drive, as evidence shows that delta power is enhanced after prolonged wakefulness, but declines as sleep deepens. delta power is often accompanied by sleep duration and intensity (Davis et al., 2011 | ={Memon, 2023 #2386} | |
| Theta power 4-8 Hz | ={Memon, 2023 #2386} | ||
| Alpha power 9-12 Hz | ={Memon, 2023 #2386} | ||
| B power 12-30 Hz | ={Memon, 2023 #2386} | ||
| Slow-to-fast frequencies ratio: [(delta + theta)/(alpha + β)] | ↑ {Memon, 2023 #2386} | ||
| Delta power (1–4 Hz) | a deceased delta change accompanies higher sleep quality during REM period | ↑ {Memon, 2023 #2386} | |
| Theta power (4–8 Hz) | ={Memon, 2023 #2386} | ||
| B power (12–30 Hz) | ={Memon, 2023 #2386} |
Effect size
| Mean PD | Mean HC | % difference | SD PD | SD HC | %CV PD | %CV HC | CV (SD/Mean) | Effect size (d, vs CTL) | α | β | tail | T test (independent group) | N needed per group to detect the group difference (vs CTL) | Sample size per group in a clinical trial to detect 50% correction | Sample size per group in a clinical trial to detect 75% correction | |
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| These SD and CV values are all group parameters, not for difference! | ES | N per group | ||||||||||||||
| 150 | 100 | 150% | 75 | 50 | 50% | 50% | 0.5 | 0.78 | 0.1 | 0.7 | One | 12 | ||||
| 1.5 | 0.1 | 0.7 | One | 4 | ||||||||||||
| 1.5 | 0.1 | 0.8 | One | 5 | 0.75 | 17 | ||||||||||
| 1.5 | 0.05 | 0.8 | One | 7 | 0.75 | 23 | ||||||||||
| 1.18 | 0.1 | 0.7 | One | 6 | ||||||||||||
| 0.97 | 0.1 | 0.7 | One | 8 | ||||||||||||
| 0.97 | 0.1 | 0.8 | One | 11 | ||||||||||||
| 0.97 | 0.05 | 0.8 | One | 14 | 31 | |||||||||||
| 1.1 | 0.1 | 0.8 | One | |||||||||||||
| 0.97 | ||||||||||||||||
Uncertain Spans
| location | transcription | uncertainty |
|---|---|---|
Effect size / α / β | the α / β columns show values like 0.1 / 0.7, 0.1 / 0.8, 0.05 / 0.8. Some rows render the values with no decimal point separation (e.g. paddleocr token 01 07 One); visual confirmation reads them as 0.1, 0.7, 0.8, 0.05. | low confidence on a couple of 0.05 vs 0.1 cells in mid-page; the dominant pattern is documented in format_notes. |
Effect size / N needed per group | mid-table value 31 is shown in the right-most numerical column on the row that pairs with effect size 0.97; on the page the cell visibly aligns with that row. | matrix alignment: the 31 is listed under the Sample size per group ... 50% correction / N per group column. |
Sleep EEG / Davis et al., 2011 | the trailing closing parenthesis of (Davis et al., 2011 is not visible in the crop. | left out per direct-transcription policy; not auto-completed. |