Altered cortical activation during a motor task in ALS

Stanton, Biba; Williams, Victoria C.; Leigh, P. Nigel; Williams, Steven; Blain, Camilla; Jarosz, Józef; Simmons, Andrew

doi:10.1007/s00415-006-0513-4

Cited by 76 publications

(51 citation statements)

References 43 publications

(69 reference statements)

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“…Initial observations were of a “boundary shift” in regional cerebral blood flow measured using positron emission tomography (PET) in ALS patients during a joystick task [Kew et al, 1993]. Further support stems from the observation of widened cortical BOLD activation in ALS patients during functional MRI (fMRI)‐based motor tasks [Mohammadi et al, 2011; Stanton et al, 2007b]; reduced binding of the PET GABA A ligand [ 11 C]‐fluamzenil [Lloyd et al, 2000; Turner et al, 2005a]; reduced GABA MR spectroscopy peak in the motor cortex [Foerster et al, 2012], and elevated Glx (glutamate and glutamine) peak in the medulla [Pioro et al, 1999]. …”

Section: Discussionmentioning

confidence: 99%

“…Additional analysis variables pertinent to neural signal interpretation include the selection of baseline period and frequency band of interest. Furthermore patient groups may differ in the degree to which they actively participate in a task, and this severely limits the conclusions that can be drawn from tasks of motor imagery (Kasahara et al, 2012; Lulé et al, 2007; Stanton et al, 2007a, 2007b). Riluzole administration could possibly dilute the reported ALS group effects, although analysis of the five remaining patients revealed a directionally similar trend.…”

Section: Discussionmentioning

confidence: 99%

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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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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

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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“…[82][83][84][85] Increased sensorimotor activation was also reported in the hemisphere ipsilateral to the movement. 84 A spatial shift of recruitment to more anterior regions of the premotor cortex during upper limb movement was also observed in patients with ALS.…”

Section: Fmrimentioning

confidence: 94%

The Present and the Future of Neuroimaging in Amyotrophic Lateral Sclerosis

Agosta¹,

Chiò²,

Cosottini³

et al. 2010

AJNR Am J Neuroradiol

116

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SUMMARY:In patients with ALS, conventional MR imaging is frequently noninformative, and its use has been restricted to excluding other conditions that can mimic ALS. Conversely, the extensive application of modern MR imagingϪbased techniques to the study of ALS has undoubtedly improved our understanding of disease pathophysiology and is likely to have a role in the identification of potential biomarkers of disease progression. This review summarizes how new MR imaging technology is changing dramatically our understanding of the factors associated with ALS evolution and highlights the reasons why it should be used more extensively in studies of disease progression, including clinical trials.ABBREVIATIONS: ALS ϭ amyotrophic lateral sclerosis; ALSFRS ϭ ALS Functional Rating Scale; Cho ϭ choline; Cr ϭ creatine; CST ϭ corticospinal tract; DTI ϭ diffusion tensor imaging; FA ϭ fractional anisotropy; FLAIR ϭ fluid-attenuated inversion recovery; fMRI ϭ functional MR imaging; FTD ϭ frontotemporal dementia; FUS/TLS ϭ fused in sarcoma/translocated in liposarcoma gene; GM ϭ gray matter; 1 H-MR spectroscopy ϭ proton MR spectroscopy; L ϭ left; LMN ϭ lower motor neuron; MD ϭ mean diffusivity; mIns ϭ myo-inositol; MT ϭ magnetization transfer; MTR ϭ MT ratio; NAA ϭ N-acetylaspartate; ns ϭ not significant; PD ϭ proton density; R ϭ right; SOD1 ϭ superoxide dismutase 1; SPM ϭ statistical parametric mapping; TDP-43 ϭ TAR DNA-binding protein gene; UMN ϭ upper motor neuron; VBM ϭ voxel-based morphometry; WM ϭ white matter A LS, also known as motor neuron disease, is a neurodegenerative disorder characterized by a progressive muscular paralysis reflecting degeneration of motor neurons in the primary motor cortex, brain stem, and spinal cord. The phenotypic expression of ALS is highly heterogeneous and determined by 4 elements: 1) body region of onset, 2) relative mix of UMN and LMN involvement, 3) rate of progression, and 4) cognitive impairment.1 In approximately 5%-10% of patients, the disease is inherited; 20% of these individuals have a mutation of the SOD1 gene; approximately 2%-5%, of the TARDBP (TDP-43) gene; and 2%-4%, of the FUS/TLS gene. 2Most patients with ALS, however, have no obvious family history and have sporadic ALS.2 To date, the only specific marker of sporadic ALS is the presence of inclusions staining positively for ubiquitin and TDP-43 in degenerating motor neurons. 3Despite technical advances in medicine in the last century, the diagnosis of sporadic ALS relies on the interpretation of clinical symptoms and signs (ie, signs suggestive of combined UMN and LMN degeneration, together with disease progression compatible with a neurodegenerative disorder). Paraclinical and laboratory tests are used only to exclude "ALS-mimic" syndromes. 4,5 In ALS, the absence of a disease marker for UMN and LMN involvement has 2 main negative consequences. First, the delay from onset of the disease to diagnosis of ALS can vary between 13 and 18 months 6,7

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“…Increased sensorimotor activation has also been reported in the brain ipsilateral to the movement [80]. In addition, reduced activation in the dorsolateral prefrontal cortex has been observed, providing further evidence for the existence of frontal lobe function deficits in patients with ALS [81].…”

Section: Functional Mrimentioning

confidence: 68%

“…A general pattern of cortical reorganization was found for motor function in patients with ALS when compared with that seen in normal subjects [24], with increased activation of the contralateral sensorimotor cortex, supplementary motor area, basal ganglia, and cerebellum demonstrated on fMR images during motor tasks [24,25,80,81]. Increased sensorimotor activation has also been reported in the brain ipsilateral to the movement [80].…”

Section: Functional Mrimentioning

confidence: 84%

Neuroimaging in Amyotrophic Lateral Sclerosis

et al. 2011

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Summary: Amyotrophic lateral sclerosis (ALS) is a motor neuron disease characterized by progressive degeneration of upper motor neurons (UMN) and lower motor neurons (LMN). While LMN dysfunction can be confirmed by electromyography (EMG) and muscle biopsy, UMN involvement is more difficult to detect, particularly in the early phase. Objective and sensitive measures of UMN dysfunction are needed for early diagnosis and monitoring of disease progression and therapeutic efficacy. Advanced magnetic resonance imaging (MRI) techniques, such as diffusion, perfusion, magnetization transfer imaging, functional MRI, and MR spectroscopy, provide insight into the pathophysiological processes of ALS and may have a role in the identification and monitoring of UMN pathology. This article provides an overview of these neuroimaging techniques and their potential roles in ALS.

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Altered cortical activation during a motor task in ALS

Abstract: We conclude that alterations in cortical function in ALS differ in sensorimotor and prefrontal regions. Importantly, we have shown that these changes do not reflect confounding by weakness or task difficulty, but are likely to be related to upper motor neuron pathology in ALS.

Cited by 76 publications

References 43 publications

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

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

The Present and the Future of Neuroimaging in Amyotrophic Lateral Sclerosis

Neuroimaging in Amyotrophic Lateral Sclerosis

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