Laser evoked potentials in amyotrophic lateral sclerosis

Simone, I. L.; Tortelli, Rosanna; Samarelli, V.; D’Errico, Eustachio; Sardaro, Michele; Difruscolo, Olimpia; Calabrese, Rita; Francesco, Vito De Vito; Livrea, Paolo; Tommaso, Marina de

doi:10.1016/j.jns.2009.09.023

Cited by 20 publications

(16 citation statements)

References 52 publications

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“…3,6,[27][28][29][30][31][32] Our results show that pain is not related to patients' gender or age, disease duration, bulbar or spinal disease onset, nutritional or respiratory status. This is consistent with two recent studies, 14,29 but not with another one 2 which reported that pain was more prevalent in the later stages of ALS. Higher statistical power, due to a larger population in this latter study, might explain this contradictory result.…”

Section: Discussionsupporting

confidence: 93%

“…30 Our results confirm previous reports about pain involving more frequently neck and limbs, especially shoulder. 3,6,28,29,33 A negative correlation between pain intensity and muscle testing was found, 14 but until now, only one study has looked for a correlation between proximal muscular deficit and shoulder pain. 33 Our results confirm this correlation.…”

Section: Discussionmentioning

confidence: 99%

“…10 Also, somatosensory and laser cortical evoked potentials could be decreased or delayed in relation to motor cortex hypofunction. 10,13,14 Although, these data suggest that ALS involve not only the motor but also the somatosensory system, limited information is available regarding the epidemiology and the characteristics of neuropathic pain in patients with ALS. Moreover, as ALS is regarded as a disease solely involving motor neurons, the algorithm proposed by Treede et al 15 cannot be used for the diagnosis.…”

Section: Is There Pain With Neuropathic Characteristics In Patients Wmentioning

confidence: 99%

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Is there pain with neuropathic characteristics in patients with amyotrophic lateral sclerosis? A cross-sectional study

et al. 2015

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 99%

Section: Is There Pain With Neuropathic Characteristics In Patients Wmentioning

confidence: 99%

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Is there pain with neuropathic characteristics in patients with amyotrophic lateral sclerosis? A cross-sectional study

et al. 2015

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“…Moreover, comparing ALS patients in this advanced stage of disease to subjects in the previous stage 2B, it is noteworthy that WM of both hemispheres were impaired, with a more marked impairment of long associative tracts. This pattern of spreading of ALS-related pathology towards extra-motor neocortices, such as prefrontal and postcentral cortices, is consistent with the striking clinical evidence of cognitive and behavioral dysfunctions and nociceptive alterations mostly described in ALS patients with severe clinical pictures and longer disease course [ 12 , 67 , 68 ]. Moreover, histochemical data by Brettschneider et al [ 23 ] about dissemination of TDP-43 lesions across brain areas with ongoing disease have revealed a wider spreading of TDP-43 pathology towards prefrontal cortices in advanced ALS patients also affected by executive dysfunctions.…”

Section: Discussionsupporting

confidence: 84%

Microstructural Changes across Different Clinical Milestones of Disease in Amyotrophic Lateral Sclerosis

et al. 2015

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Neurodegenerative process in amyotrophic lateral sclerosis (ALS) has been proven to involve several cortical and subcortical brain regions within and beyond motor areas. However, how ALS pathology spreads progressively during disease evolution is still unknown. In this cross-sectional study we investigated 54 ALS patients, divided into 3 subsets according to the clinical stage, and 18 age and sex-matched healthy controls, by using tract-based spatial statistics (TBSS) diffusion tensor imaging (DTI) and voxel-based morphometry (VBM) analyses. We aimed to identify white (WM) and gray matter (GM) patterns of disease distinctive of each clinical stage, corresponding to specific clinical milestones. ALS cases in stage 2A (i.e., at diagnosis) were characterized by GM and WM impairment of left motor and premotor cortices and brainstem at ponto-mesenchephalic junction. ALS patients in clinical stage 2B (with impairment of two functional regions) exhibited decreased fractional anisotropy (FA) (p<0.001, uncorrected) and increased mean (MD) and radial diffusivity (RD) (p<0.001, uncorrected) in the left cerebellar hemisphere and brainstem precerebellar nuclei, as well as in motor areas, while GM atrophy (p<0.001, uncorrected) was detected only in the left inferior frontal gyrus and right cuneus. Finally, ALS patients in stage 3 (with impairment of three functional regions) exhibited decreased FA and increased MD and RD (p<0.05, corrected) within WM underneath bilateral pre and postcentral gyri, corpus callosum midbody, long associative tracts and midbrain, while no significant clusters of GM atrophy were observed. Our findings reinforce the hypothesis that the neurodegenerative process propagates along the axonal pathways and develops beyond motor areas from early stages, involving progressively several frontotemporal regions and their afferents and efferents, while the detection of GM atrophy in earlier stages and its disappearance in later stages may be the result of reactive gliosis.

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“…Even though increased processing of experimental nociceptive stimuli was recently evidenced in ALS patient [66], the study of pain in the context of ALS was out of the scope of the present research which essentially took advantage of the characteristic of an animal model of the disease at a pre-symptomatic stage. Thus, we here demonstrated that rats expressing hSOD1 G93A develop more severe pain hypersensitivity after peripheral nerve injury.…”

Section: Resultsmentioning

confidence: 99%

Enhanced neuroinflammation and pain hypersensitivity after peripheral nerve injury in rats expressing mutated superoxide dismutase 1

Berger

Deumens

Goursaud

et al. 2011

J Neuroinflammation

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BackgroundNeuroinflammation and nitroxidative stress are implicated in the pathophysiology of neuropathic pain. In view of both processes, microglial and astroglial activation in the spinal dorsal horn play a predominant role. The present study investigated the severity of neuropathic pain and the degree of glial activation in an inflammatory- and nitroxidative-prone animal model.MethodsTransgenic rats expressing mutated superoxide dismutase 1 (hSOD1G93A) are classically used as a model for amyotrophic lateral sclerosis (ALS). Because of the associated inflammatory- and nitroxidative-prone properties, this model was used to study thermal and mechanical hypersensitivity following partial sciatic nerve ligation (PSNL). Next to pain hypersensitivity assessment, microglial and astroglial activation states were moreover characterized, as well as inflammatory marker gene expression and the glutamate clearance system.ResultsPSNL induced thermal and mechanical hypersensitivity in both wild-type (WT) and transgenic rats. However, the degree of thermal hypersensitivity was found to be exacerbated in transgenic rats while mechanical hypersensitivity was only slightly and not significantly increased. Microglial Iba1 expression was found to be increased in the ipsilateral dorsal horn of the lumbar spinal cord after PSNL but such Iba1 up-regulation was enhanced in transgenic rats as compared WT rats, both at 3 days and at 21 days after injury. Moreover, mRNA levels of Nox2, a key enzyme in microglial activation, but also of pro-inflammatory markers (IL-1β and TLR4) were not modified in WT ligated rats at 21 days after PSNL as compared to WT sham group while transgenic ligated rats showed up-regulated gene expression of these 3 targets. On the other hand, the PSNL-induced increase in GFAP immunoreactivity spreading that was evidenced in WT rats was unexpectedly found to be attenuated in transgenic ligated rats. Finally, GLT-1 gene expression and uptake activity were shown to be similar between WT sham and WT ligated rats at 21 days after injury, while both parameters were significantly increased in the ipsilateral dorsal region of the lumbar spinal cord of hSOD1G93A rats.ConclusionsTaken together, our findings show that exacerbated microglial activation and subsequent inflammatory and nitroxidative processes are associated with the severity of neuropathic pain symptoms.

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Laser evoked potentials in amyotrophic lateral sclerosis

Cited by 20 publications

References 52 publications

Is there pain with neuropathic characteristics in patients with amyotrophic lateral sclerosis? A cross-sectional study

Is there pain with neuropathic characteristics in patients with amyotrophic lateral sclerosis? A cross-sectional study

Microstructural Changes across Different Clinical Milestones of Disease in Amyotrophic Lateral Sclerosis

Enhanced neuroinflammation and pain hypersensitivity after peripheral nerve injury in rats expressing mutated superoxide dismutase 1

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