Bereitschaftspotential in amyotrophic lateral sclerosis (ALS): lower amplitudes in patients with hyperreflexia (spasticity)

Westphal, K. P.; Heinemann, H. A.; Grözinger, B.; Kotchoubey, B. J.; Diekmann, V.; Becker, Wolfgang; Kornhuber, H. H.

doi:10.1111/j.1600-0404.1998.tb07372.x

Cited by 24 publications

(12 citation statements)

References 8 publications

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“…This has been attributed to motor neuron loss, which could extend beyond the primary motor cortex and involve the SMA. Similarly, electrophysiological substrates of movement preparation are altered in patients with advanced ALS [25], and premotor potentials are more severely attenuated in ALS patients with intense spasticity [26]. In addition, our patients without pre-inspiratory potentials used NIV for longer daily durations (table 1).…”

Section: Heterogeneity Among Patientsmentioning

confidence: 75%

“…The EEG recording therefore lasted ⩾120 breaths at the end of the steady-state period. All epochs exhibiting EEG artefacts, spurious EEG activity exceeding 20% of the baseline background signal or intense electro-oculographic activity were discarded (median rejection rate 38% [21][22][23][24][25][26][27][28][29][30][31][32][33][34][35][36][37][38][39]). On the averaged tracings, a slow negative shift starting between 2 and 0.5 s before inspiration was identified as pre-motor activity based on visual inspection by two observers blinded to the recording condition.…”

Section: Signal Processing Electroencephalographic Datamentioning

confidence: 99%

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Cortical drive to breathe in amyotrophic lateral sclerosis: a dyspnoea-worsening defence?

et al. 2016

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Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease causing diaphragm weakness that can be partially compensated by inspiratory neck muscle recruitment. This disappears during sleep, which is compatible with a cortical contribution to the drive to breathe. We hypothesised that ALS patients with respiratory failure exhibit respiratory-related cortical activity, relieved by noninvasive ventilation (NIV) and related to dyspnoea.We studied 14 ALS patients with respiratory failure. Electroencephalographic recordings (EEGs) and electromyographic recordings of inspiratory neck muscles were performed during spontaneous breathing and NIV. Dyspnoea was evaluated using the Multidimensional Dyspnea Profile.Eight patients exhibited slow EEG negativities preceding inspiration (pre-inspiratory potentials) during spontaneous breathing. Pre-inspiratory potentials were attenuated during NIV (p=0.04). Patients without pre-inspiratory potentials presented more advanced forms of ALS and more severe respiratory impairment, but less severe dyspnoea. Patients with pre-inspiratory potentials had stronger inspiratory neck muscle activation and more severe dyspnoea during spontaneous breathing.ALS-related diaphragm weakness can engage cortical resources to augment the neural drive to breathe. This might reflect a compensatory mechanism, with the intensity of dyspnoea a negative consequence. Disease progression and the corresponding neural loss could abolish this phenomenon. A putative cognitive cost should be investigated.

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Section: Heterogeneity Among Patientsmentioning

confidence: 75%

Section: Signal Processing Electroencephalographic Datamentioning

confidence: 99%

Cortical drive to breathe in amyotrophic lateral sclerosis: a dyspnoea-worsening defence?

et al. 2016

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“…For example, marked alterations of early visual event-related potential components [43] show that visual cortical areas are indeed altered in the ALS disease process. Also, impaired initiation and inhibition of movements implies the supplementary motor area and right prefrontal cortex [8,44,45]. …”

Section: Discussionmentioning

confidence: 99%

Extent of cortical involvement in amyotrophic lateral sclerosis – an analysis based on cortical thickness

et al. 2013

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BackgroundBesides the defining involvement of upper and lower motor neurons, the involvement of extramotor structures has been increasingly acknowledged in amyotrophic lateral sclerosis (ALS).MethodsHere we investigated a group of 14 mildly to moderately affected ALS patients and 14 age-matched healthy control participants using cortical thickness analysis. Cortical thickness was determined from high resolution 3D T1 magnetic resonance images and involved semiautomatic segmentation in grey and white matter, cortical alignment and determination of thickness using the Laplace method. In addition to a whole-cortex analysis a region of interest approach was applied.ResultsALS patients showed regions of significant cortical thinning in the pre- and postcentral gyri bilaterally. Further regions of cortical thinning included superior and inferior parietal lobule, angular and supramarginal gyrus, insula, superior frontal, temporal and occipital regions, thus further substantiating extramotor involvement in ALS. A relationship between cortical thickness of the right superior frontal cortex and clinical severity (assessed by the ALS functional rating scale) was also demonstrated.ConclusionsCortical thickness is reduced in ALS not only in motor areas but in widespread non-motor cortical areas. Cortical thickness is related to clinical severity.

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“…Previous EEG investigations in ALS largely focused on evoked movement-related cortical potentials (MRCPs), time-locked to movement onset and averaged over many trials. The impact on these measures appears most prominent in patients with a high burden of UMN dysfunction [Bizovičar et al, 2013;Inuggi et al, 2011;Westphal et al, 1998], with MRCPs particularly reduced in patients with PLS [Bai et al, 2006]. Event-related potentials (ERPs) have also revealed abnormal neural correlates of attention control [Pinkhardt et al, 2008], particularly within a bulbar-onset sub-group [Mannarelli et al, 2013].…”

Section: Cortical Neurophysiological Dysfunction In Als and Plsmentioning

confidence: 99%

Altered cortical beta‐band oscillations reflect motor system degeneration in amyotrophic lateral sclerosis

Proudfoot

Rohenkohl

Quinn

et al. 2016

Human Brain Mapping

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Continuous rhythmic neuronal oscillations underpin local and regional cortical communication. The impact of the motor system neurodegenerative syndrome amyotrophic lateral sclerosis (ALS) on the neuronal oscillations subserving movement might therefore serve as a sensitive marker of disease activity. Movement preparation and execution are consistently associated with modulations to neuronal oscillation beta (15–30 Hz) power. Cortical beta‐band oscillations were measured using magnetoencephalography (MEG) during preparation for, execution, and completion of a visually cued, lateralized motor task that included movement inhibition trials. Eleven “classical” ALS patients, 9 with the primary lateral sclerosis (PLS) phenotype, and 12 asymptomatic carriers of ALS‐associated gene mutations were compared with age‐similar healthy control groups. Augmented beta desynchronization was observed in both contra‐ and ipsilateral motor cortices of ALS patients during motor preparation. Movement execution coincided with excess beta desynchronization in asymptomatic mutation carriers. Movement completion was followed by a slowed rebound of beta power in all symptomatic patients, further reflected in delayed hemispheric lateralization for beta rebound in the PLS group. This may correspond to the particular involvement of interhemispheric fibers of the corpus callosum previously demonstrated in diffusion tensor imaging studies. We conclude that the ALS spectrum is characterized by intensified cortical beta desynchronization followed by delayed rebound, concordant with a broader concept of cortical hyperexcitability, possibly through loss of inhibitory interneuronal influences. MEG may potentially detect cortical dysfunction prior to the development of overt symptoms, and thus be able to contribute to the assessment of future neuroprotective strategies. Hum Brain Mapp 38:237–254, 2017. © 2016 Wiley Periodicals, Inc.

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Bereitschaftspotential in amyotrophic lateral sclerosis (ALS): lower amplitudes in patients with hyperreflexia (spasticity)

Cited by 24 publications

References 8 publications

Cortical drive to breathe in amyotrophic lateral sclerosis: a dyspnoea-worsening defence?

Cortical drive to breathe in amyotrophic lateral sclerosis: a dyspnoea-worsening defence?

Extent of cortical involvement in amyotrophic lateral sclerosis – an analysis based on cortical thickness

Altered cortical beta‐band oscillations reflect motor system degeneration in amyotrophic lateral sclerosis

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