The value of P300 in the diagnosis of cognitive impairment in stroke

Ladurner, G.; Schimke, Hannes; Wranek, Ursula; Klimesch, Wolfgang

doi:10.1016/0167-4943(90)90038-8

Cited by 10 publications

(7 citation statements)

References 25 publications

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“…In our patients, the latency of the P300 response significantly changes after stroke, being longer when compared with that of normal subjects, throughout the observation window of 6 months. The P300 latency has been reported to be similar in normal controls and in stroke patients without dementia; by contrast, a longer P300 latency was found in stroke patients with dementia [28]. The authors conclude that the increased latency was because of lower cognitive ability of stroke patients with dementia.…”

Section: Discussionmentioning

confidence: 89%

The role of P300 in the recovery of post‐stroke global aphasia

Nolfe

Cobianchi

Mossuto-Agatiello

et al. 2006

Euro J of Neurology

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Seventeen right-handed patients suffering from global aphasia caused by a recent stroke in the left-hemisphere were studied. Passive P300 auditory event related potential paradigm was applied every months for 6 months. Aachen subtests were used for evaluating comprehension. Only a minority of the patients displayed the P300 at the baseline. Those patients had the best outcome at the Aachen comprehension subtest. Latency and amplitude changed over time in an unpredictable way. The number of patients presenting with the P300 also fluctuated, since some patients could regain the potential, whereas some other patients could lose that from month to month. Passive P300 is a monitor of recovery following global aphasia. A single passive P300 recording is useful for prognostic purposes. Repairing mechanisms in the first 6 months have a non-linear trend.

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Section: Discussionmentioning

confidence: 89%

The role of P300 in the recovery of post‐stroke global aphasia

Nolfe

Cobianchi

Mossuto-Agatiello

et al. 2006

Euro J of Neurology

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“…The P3 component of the brain event-related potentials (ERPs) obtained with the classic oddball paradigm is used in clinical practice for the assessment of dementia Pfefferbaum et al, 1984;Goodin and Aminoff, 1986;Ladurner et al, 1990;Wranek et al, 1990Wranek et al, , 1992. Current knowledge still gives an incomplete picture of P3 generators but many researchers suggest a crucial role of the mesial temporal lobe structures (Halgren et al, 1980(Halgren et al, , 1986McCarthy and Wood, 1987;Smith et al, 1990;Grunwald et al, 1995) and the inferior parietal lobe (Knight et al, 1989).…”

Section: Introductionmentioning

confidence: 99%

Delayed visual P3 in unilateral thalamic stroke

et al. 2000

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The P3 potential is accepted as a neurophysiological correlate of memory and attention. Delayed latencies were reported in different forms of dementias. Although the generator sites are still under debate, the thalamus may play a crucial role.The aim of this study was to investigate the influence of an unilateral thalamic ischaemic infarction on P3 generation.The event-related P3 component of six patients (2 male, four female; mean age 47 years, range 22]63 years) with unilateral thalamic ischaemic infarction was studied and compared to age-matched controls (five male, nine female; mean age 45.8 years; range 22]69 years). All patients underwent full clinical examination, CCT, and MRI scan. P3 potentials were recorded with a visual three stimulus discrimination paradigm. The mean P3 latency of the patient group to the target stimulus was delayed (469.7 ms, SD = 36.8) compared with the controls (378.8 ms, SD = 51.5; P , 0.05). The mean P3 latency to the unexpected stimulus was delayed in patients with thalamic infarction compared with controls [477 ms (SD = 46.6) vs. 381.2 ms (SD = 48.5); P , 0.001). Delayed P3 components of the event-related potential (ERP) were recorded in six patients with unilateral thalamic infarction, suggesting an important role of the thalamus in the generation of the P3 potential.

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“…and decisional processes (e.g., the P300 and more specifically the P3b subcomponent) 24,25,[27][28][29][30][31][32] are suppressed or delayed in the lesioned hemisphere while stroke patients undertake speeded tasks, relative to ERPs in the healthy hemisphere. However, the majority of studies have selectively examined patients with right hemisphere lesions in the context of spatial neglect 23,25,26,28,31,[33][34][35][36][37][38][39] , which does not wholly account for the broader incidence of slowed contralesional responding.…”

Section: -26mentioning

confidence: 99%

Neurophysiological mechanisms underlying post-stroke deficits in contralesional perceptual processing

Pearce,

Loughnane,

Chong

et al. 2023

Preprint

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Slowed responding to sensory inputs presented in contralesional space is pervasive following unilateral cerebral stroke, but the causal neurophysiological pathway by which this occurs remains unclear. To this end, here we leverage a perceptual decision-making framework to disambiguate information processing stages between sensation and action in 30 unilateral stroke patients (18 right hemisphere, 12 left hemisphere) and 27 neurologically healthy adults. By recording neural activity using electroencephalography (EEG) during task performance, we show that the relationship between strokes in either hemisphere and slowed contralesional response times is sequentially mediated by weaker target selection signals in the contralateral hemisphere (the N2c ERP), and subsequently delayed evidence accumulation signals (the centroparietal positivity). Notably, asymmetries in CPP and response times across hemispheres are associated with everyday functioning. Together, these data suggest a plausible neurophysiological pathway by which post-stroke contralesional slowing arises and highlight the utility of neurophysiological assessments for tracking clinically relevant behaviour.

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The value of P300 in the diagnosis of cognitive impairment in stroke

Cited by 10 publications

References 25 publications

The role of P300 in the recovery of post‐stroke global aphasia

The role of P300 in the recovery of post‐stroke global aphasia

Delayed visual P3 in unilateral thalamic stroke

Neurophysiological mechanisms underlying post-stroke deficits in contralesional perceptual processing

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