Cortical neurophysiology of ALS
<p>The experiments described in this thesis aimed to investigate the neurophysiological consequences, at the cortical level, of the neurodegenerative condition, amyotrophic lateral sclerosis (ALS). A principle tenet of this study was that ALS is, first and foremost, a disorder of the cortical...
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| Format: | Thesis |
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2016
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| _version_ | 1826317294165295104 |
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| author | Proudfoot, M |
| author2 | Turner, M |
| author_facet | Turner, M Proudfoot, M |
| author_sort | Proudfoot, M |
| collection | OXFORD |
| description | <p>The experiments described in this thesis aimed to investigate the neurophysiological consequences, at the cortical level, of the neurodegenerative condition, amyotrophic lateral sclerosis (ALS). A principle tenet of this study was that ALS is, first and foremost, a disorder of the cortical motor system, the precise pathological mechanisms of which remain incompletely understood. Furthermore, the degree to which neurodegeneration can be evidenced before the onset of symptoms is thus far uncertain, and the optimal means by which to measure therapeutic response has yet to be determined.</p> <p>Chapter 1 introduces relevant key concepts in ALS and briefly summarises three studies completed in the early phases of pursuit for the above degree. These studies respectively considered presmyptomatic cellular ALS pathology, quantitation of disease progression and eyetracking assessment of cognitive dysfunction. Chapter 2 describes magnetoencephalography, the investigative technology utilised in the subsequent experimental chapter. In chapter 3, the effects of ALS on movement related modulation of neuronal oscillations are determined. An excessive peri-movement desynchronisation and delayed post-movement rebound was described. Functional connectivity between cortical regions at rest is appraised in chapter 4. ALS appeared to result in quite striking increases in functional connectivity, in keeping with the fMRI literature and in support of diminished intracortical inhibitory influences. The functional communication from the motor cortices is directly considered during active motor performance in chapter 5. ALS related reductions in beta-band coherence were noted in both corticospinal and inter- hemispheric communication.</p> <p>In conclusion, the results demonstrated considerable support for proposed excitotoxic disease mechanisms and were in alignment with reported findings in other neurodegenerative diseases. Finally, a pilot study by which the neural mechanisms for cognitive impairment in ALS are explored via antisaccade performance is described. While underpowered, the experimental design showed promise for future application. </p> |
| first_indexed | 2024-03-06T22:40:55Z |
| format | Thesis |
| id | oxford-uuid:5b8673f7-8eb2-4bf2-b3b8-d901fa134007 |
| institution | University of Oxford |
| last_indexed | 2025-02-19T04:36:12Z |
| publishDate | 2016 |
| record_format | dspace |
| spelling | oxford-uuid:5b8673f7-8eb2-4bf2-b3b8-d901fa1340072025-02-05T07:58:48ZCortical neurophysiology of ALSThesishttp://purl.org/coar/resource_type/c_db06uuid:5b8673f7-8eb2-4bf2-b3b8-d901fa134007Clinical NeuroscienceAmyotrophic Lateral SclerosisORA Deposit2016Proudfoot, MTurner, MNobre, K<p>The experiments described in this thesis aimed to investigate the neurophysiological consequences, at the cortical level, of the neurodegenerative condition, amyotrophic lateral sclerosis (ALS). A principle tenet of this study was that ALS is, first and foremost, a disorder of the cortical motor system, the precise pathological mechanisms of which remain incompletely understood. Furthermore, the degree to which neurodegeneration can be evidenced before the onset of symptoms is thus far uncertain, and the optimal means by which to measure therapeutic response has yet to be determined.</p> <p>Chapter 1 introduces relevant key concepts in ALS and briefly summarises three studies completed in the early phases of pursuit for the above degree. These studies respectively considered presmyptomatic cellular ALS pathology, quantitation of disease progression and eyetracking assessment of cognitive dysfunction. Chapter 2 describes magnetoencephalography, the investigative technology utilised in the subsequent experimental chapter. In chapter 3, the effects of ALS on movement related modulation of neuronal oscillations are determined. An excessive peri-movement desynchronisation and delayed post-movement rebound was described. Functional connectivity between cortical regions at rest is appraised in chapter 4. ALS appeared to result in quite striking increases in functional connectivity, in keeping with the fMRI literature and in support of diminished intracortical inhibitory influences. The functional communication from the motor cortices is directly considered during active motor performance in chapter 5. ALS related reductions in beta-band coherence were noted in both corticospinal and inter- hemispheric communication.</p> <p>In conclusion, the results demonstrated considerable support for proposed excitotoxic disease mechanisms and were in alignment with reported findings in other neurodegenerative diseases. Finally, a pilot study by which the neural mechanisms for cognitive impairment in ALS are explored via antisaccade performance is described. While underpowered, the experimental design showed promise for future application. </p> |
| spellingShingle | Clinical Neuroscience Amyotrophic Lateral Sclerosis Proudfoot, M Cortical neurophysiology of ALS |
| title | Cortical neurophysiology of ALS |
| title_full | Cortical neurophysiology of ALS |
| title_fullStr | Cortical neurophysiology of ALS |
| title_full_unstemmed | Cortical neurophysiology of ALS |
| title_short | Cortical neurophysiology of ALS |
| title_sort | cortical neurophysiology of als |
| topic | Clinical Neuroscience Amyotrophic Lateral Sclerosis |
| work_keys_str_mv | AT proudfootm corticalneurophysiologyofals |