Relevant bibliographies by topics / Motor neuron disease, MND

Academic literature on the topic 'Motor neuron disease, MND'

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Published: 4 June 2021
Last updated: 21 February 2023

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Journal articles on the topic "Motor neuron disease, MND"

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Oh, Seong-il, Jin-Sung Park, Jung-Joon Sung, and Seung Hyun Kim. "Clinical Scales Used in Motor Neuron Disease." Journal of the Korean Neurological Association 39, no. 2 Suppl (May 1, 2021): 77–86. http://dx.doi.org/10.17340/jkna.2021.2.22.

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Motor neuron diseases (MND) are heterogeneous spectra of disorders that that primarily affect the motor neurons (MN) resulting in motor nerve and muscle degeneration. The pathophysiological mechanisms of MN cell death are known to be combined with disturbance of proteostasis, ribonucleostasis and exaggerated neuro-inflammation. Amyotrophic lateral sclerosis is the prototypic disease of MND followed by spinal and bulbar muscular atrophy, spinal muscular atrophy, benign focal amyotrophy and other various diseases. Although diverse spectra of these diseases share common symptoms, significant differences are known in their clinical manifestations and their clinical progression. With increasing number of new clinical trials, the importance of selecting appropriate clinical scales for the monitoring of clinical progression in different types of MNDs should be emphasized. The purpose of this review is to illustrate different types of clinical scales and demonstrate how to utilize these in the clinical research field with consensus. With these efforts, we hope to be ready to understand different kinds of clinical scales in MND in participating global standard clinical trials.
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Chancellor, A. M., A. Hendry, F. I. Caird, C. P. Warlow, and A. I. Weir. "Motor Neuron Disease: A Disease of Old Age." Scottish Medical Journal 38, no. 6 (December 1993): 178–82. http://dx.doi.org/10.1177/003693309303800606.

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There is little information dealing specifically with motor neuron disease (MND) in the elderly. Given current epidemiological trends, geriatricians will be increasingly called upon to diagnose and manage this condition. We report four patients who presented within a six month period to a geriatric medical unit, and place this experience in the perspective of 229 patients from a population-based study of adult-onset MND in Scotland in 1989 and 1990. In 1990 Scotland had a crude annual incidence of MND of 2.25/100,000; the figure for those over 65 is four times greater. MND is more common in men, but the sex ratio was nearly equal over the age of 65. The risk of presenting with bulbar palsy was greater in women, and even higher in elderly women. This, together with increasing age, is the most important negative prognostic factor in MND. Problems with the diagnosis and management of MND in the elderly are highlighted.
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Zhao, Jing, Claire H. Stevens, Andrew W. Boyd, Lezanne Ooi, and Perry F. Bartlett. "Role of EphA4 in Mediating Motor Neuron Death in MND." International Journal of Molecular Sciences 22, no. 17 (August 30, 2021): 9430. http://dx.doi.org/10.3390/ijms22179430.

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Motor neuron disease (MND) comprises a group of fatal neurodegenerative diseases with no effective cure. As progressive motor neuron cell death is one of pathological characteristics of MND, molecules which protect these cells are attractive therapeutic targets. Accumulating evidence indicates that EphA4 activation is involved in MND pathogenesis, and inhibition of EphA4 improves functional outcomes. However, the underlying mechanism of EphA4’s function in MND is unclear. In this review, we first present results to demonstrate that EphA4 signalling acts directly on motor neurons to cause cell death. We then review the three most likely mechanisms underlying this effect.
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Chopra, Aarti, Ravi Kumar, and Girendra Kumar Gautam. "A review: Management of motor neuron diseases." IP Indian Journal of Neurosciences 7, no. 4 (January 15, 2022): 292–94. http://dx.doi.org/10.18231/j.ijn.2021.053.

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Motor neuron diseases are a group of chronic sporadic and hereditary neurological disorders characterized by progressive degeneration of motor neurons. These might affect the upper motor neurons, lower motor neurons, or both. The prognosis of the motor neuron disease depends upon the age at onset and the area of the central nervous system affected. Amyotrophic lateral sclerosis (ALS) has been documented to be fatal within three years of onset. This activity focuses on amyotrophic lateral sclerosis as the prototype of MND, which affects both the upper and the lower motor neurons and discusses the role of inter-professional team in the differential diagnosis, evaluation, treatment, and prognostication. It also discusses various other phenotypes of MND with an emphasis on their distinguishing features in requisite detail.
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Bobade, Shweta Shivaling, Mahesh Somnath Mali, and Komal Dattatray Pol. "A Review on Effect of Physical Activity as an Exogenous Factor and Cognitive Change in Motor Neuron Disease." International Journal of Research and Review 9, no. 7 (July 19, 2022): 119–31. http://dx.doi.org/10.52403/ijrr.20220714.

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Motor neuron disease (MND) is a terrible neurodegenerative illness with a poor prognosis and significant impairment. Despite recent advances in symptomatic care, there are few medicines that can affect survival. However, a better understanding of the underlying etiology would substantially aid the task of finding effective treatments. In the etiology of MND, many potential external risk factors have been hypothesized as part of a gene-environment interaction. Following reports of a greater than predicted incidence of MND in professional athletes, there has been an increasing interest in the role of intensive physical exercise in the development of the disease. Current hypotheses about the cellular and genetic causes of MND also support this conclusion. Epidemiological evidence, on the other hand, is contradictory and inconclusive. FTD/motor neuron disease is the name given to a motor neuronopathy that complicates frontotemporal dementia (FTD) (MND). FTD is marked by severe personality changes, abnormal social behavior, and executive difficulties caused by frontal and temporal neocortical atrophy. Bulbar palsy and limb amyotrophy are symptoms of motor neuron disease. Micro vacuolation of the cerebral cortex is the most common histological alteration, along with atrophy of the bulbar neurons and anterior horn cells of the spinal cord. Large pyramidal cortical neurons, surviving cranial nerve nuclei, and anterior horn cells all have ubiquitinated inclusion bodies. Evidence is accumulating that some patients with classical MND/amyotrophic lateral sclerosis (ALS) who are not regarded to be demented show frontal executive function abnormalities. Moreover, frontal lobe abnormalities have been demonstrated by neuroimaging. Keywords: MND, FTD, ALS, motor neuron, behavior, physical activity, cognitive change.
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MacDonald, Allycia, Merrilee Needham, and Anthony Alvaro. "078 Sensory nerve abnormalities in motor neuron disease." Journal of Neurology, Neurosurgery & Psychiatry 90, e7 (July 2019): A25.1—A25. http://dx.doi.org/10.1136/jnnp-2019-anzan.66.

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IntroductionElectrodiagnostic evaluation is crucial in establishing the diagnosis of motor neuron disease (MND) and excluding other pathologies. It is recommended that sensory nerve conduction studies (NCS) include the ulnar and sural nerves, and generally accepted that sensory nerves are normal in MND. There are however previous reports in the literature documenting variable sensory abnormalities in patients with MND. We sought to determine the frequency of unexplained sensory abnormalities seen on NCS in patients with MND.MethodsMedical records of patients attending our tertiary MND clinic over a 2 year period were reviewed. We identified 92 patients with a clinical diagnosis of MND for whom electrodiagnostic studies were available to review. Sensory abnormalities in patients without a clear underlying aetiology (eg. compressive neuropathies, diabetes) were considered unexplained.ResultsUnexplained sensory abnormalities were detected in at least one nerve in 18/92 (20%) patients. In 17 of those 18 patients, the ulnar sensory response was abnormal. 12 of 18 patients demonstrated abnormalities in 2 or more sensory nerves. Sensory abnormalities were present in 4 of 37 (10.8%) patients with bulbar onset MND and 14 of 55 (25.4%) patients with limb onset MND. Sensory symptoms were infrequently reported and did not correlate with abnormalities found on NCS.ConclusionsUnexplained sensory nerve action potential abnormalities are not uncommon in MND, with ulnar sensory responses the most frequently affected. These findings raise the possibility of sensory nerve pathology in patients with MND and suggest that the presence of unexplained sensory abnormalities should not exclude a diagnosis of MND.
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Higashihara, Mana, Parvathi Menon, Nimeshan Geevasinga, Mehdi AJVan den Bos, Matthew C. Kiernan, and Steve Vucic. "092 Motor neuron disease with malignancy: clinical and pathophysiological insights." Journal of Neurology, Neurosurgery & Psychiatry 90, e7 (July 2019): A29.3—A30. http://dx.doi.org/10.1136/jnnp-2019-anzan.80.

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IntroductionWhile some regard an association between motor neuron disease (MND) and malignancy as co-incidental, others have argued that it could represent a distinct clinical entity. The present study undertook in depth phenotyping along with assessment of cortical function to further explore disease pathophysiology in MND with malignancy (MND-M) patients.MethodsClinical features along with assessment of peripheral and cortical function was undertaken in 13 MND-M and results were compared to sporadic and familial MND cohorts.ResultsFrom a cohort 13 patients (10 males; aged 65.2±2.0 years), 30.8% were diagnosed with a haematological malignancy. The lower motor neuron phenotype predominated in the in the MND-M patients (χ2=10.8, P<0.01), with the upper motor neuron (UMN) score being significantly reduced in MND-M patients compared to sporadic and familial MND cohorts (χ2=6.84, P<0.01). The neurological deficits did not respond to treatment of the underlying malignancy in the majority of MND-M (92%) patients, and as such there were no significant differences in survival between the cohorts. Despite a paucity of UMN signs, cortical hyperexcitability was evident in MND-M patients, as indicated by reduction in short interval intracortical inhibition (P<0.01) and increase in motor evoked potential amplitude (P<0.01), that were similar to findings in sporadic and familial MND cohorts.ConclusionsThe present study suggests that MND-M falls within the spectrum of MND. A co-incidental association between MND and malignancy is underscored by cortical dysfunction and clinical findings which seems within the spectrum of abnormality evident in classical MND phenotypes.
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Sassani, Matilde, James Alix, Kathleen Baster, Mara Cercignani, Pamela Shaw, and Thomas Jenkins. "176 Motor fatigability in motor neuron disease." Journal of Neurology, Neurosurgery & Psychiatry 93, no. 9 (August 12, 2022): e2.136. http://dx.doi.org/10.1136/jnnp-2022-abn2.220.

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This study aimed to quantify, characterise and localise motor fatigue in people with motor neuron disease (MND) using a combination of clinical assessments, neurophysiology and muscle phosphorus-31 magnetic resonance spectroscopy (31P-MRS).We quantified fatigability using the fatigue index (FI) in twenty patients and 10 healthy controls. F-wave amplitudes, motor unit number index (MUNIX) and 31P-MRS were acquired pre- and post-maximal voluntary contraction to investigate fatigability at different sites of the motor system (spinal cord, peripheral nerve and muscle, respectively). Between-group differences and associations were assessed using regression models.There were no between-group differences in FI (p=0.115). MUNIX (p=0.008) and f-wave amplitude (p=0.024) declined significantly post-contraction in controls, but not in patients (MUNIX p=0.284, f-wave p=0.264). FI was associated with resting intracellular magnesium (R=0.869, p=0.001, FDR-corrected) in controls, but not patients. Resting magnesium and post-contraction MUNIX decrease were associated with greater fatigue in controls. A decrease in post-contraction f-wave amplitude was associated with greater fatigue in patients, after accounting for denervation (MUNIX) and magnesium.There is a differential response to fatigue in MND compared to healthy controls. Fatigability appears related to spinal excitability (f-waves) in patients, whereas peripheral (MUNIX) and muscular (magnesium) components predominate in healthy controls.
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Bak, S., E. N. Stenager, E. Stenager, J. Boldsen, and T. A. Smith. "Suicide in Patients with Motor Neuron Disease." Behavioural Neurology 7, no. 3-4 (1994): 181–84. http://dx.doi.org/10.1155/1994/148023.

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The aim of the present study was to assess, through an epidemiological study, whether suicide risk is increased in patients with motor neuron disease (MND). The study involved 116 patients with MND. In the study period 92 patients died, 47 males and 45 females. No patients committed suicide. The number of expected suicides was 0.27 for males and 0.12 for females, a total of 0.38. The difference between observed and expected suicides was not statistically significant for males and females.
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Lad, Tanuj S. "An ‘Acute’ Presentation of Motor Neuron Disease." Acute Medicine Journal 10, no. 3 (July 1, 2011): 140–41. http://dx.doi.org/10.52964/amja.0494.

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Abstract Motor neurone disease (MND) is a chronic condition which presents mainly in the seventh and eighth decades. It classically presents with a mixture of upper and lower motor neurone features, with a predilection for the limb muscles as the presenting feature. The case report outlined below describes acute respiratory failure requiring non invasive ventilation (NIV), at the time of diagnosis of MND. It highlights the need for the acute physician to be vigilant in the differing forms of presentation of this condition and its subsequent diagnosis and management.
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Dissertations / Theses on the topic "Motor neuron disease, MND"

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Watermeyer, Tamlyn Julie. "Emotional processing and social cognition in Amyotrophic Lateral Sclerosis (ALS)/Motor Neuron Disease (MND)." Thesis, King's College London (University of London), 2014. https://kclpure.kcl.ac.uk/portal/en/theses/emotional-processing-and-social-cognition-in-amyotrophic-lateral-sclerosis-als--motor-neuron-disease-mnd(e3552e39-2127-40a8-8035-357b66edd75d).html.

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Amyotrophic Lateral Sclerosis (ALS) is a debilitating and life–limiting neurodegenerative disorder that causes progressive muscle atrophy and spasticity. A small proportion of ALS patients experience co–morbid Frontotemporal Dementia (FTD). Milder cognitive–behavioural changes have been noted in ALS patients without dementia. In these patients, deficits in executive functioning, language, memory and behaviour have been documented. Recently, changes to emotional processing and social cognition (EMOSOC) in ALS have also been reported, albeit with inconsistent findings. The primary aims of the current thesis were i) to delineate the nature and extent of changes in EMOSOC in ALS and ii) to determine the relationship between such changes and interindividual differences in mood, behaviour, personality, empathy and ALS–related executive dysfunction. The results of the study indicate a profile of predominant executive dysfunction, with relative sparing of EMOSOC in non–demented ALS patients. However, the ALS patients did show impaired performance on a task requiring the attribution of thoughts and feelings to characters from cartoons and vignettes. ALS patients’ performance on EMOSOC tasks was predicted by their performance on tests of executive function, above and beyond mood, behaviour, personality and empathy variables. As a secondary aim, the impact of patients’ cognitive and behavioural changes on ALS caregivers’ outcomes (mood, perceived strain, burden and marital satisfaction) were examined. The data indicated patients’ behavioural dysfunction and functional impairment as key predictors of caregivers’ outcomes. Exploratory analyses revealed differences between patients’ and caregivers’ perceptions of patients’ personality, empathy and behaviour; these differences were associated with caregiver outcomes. In summary, the current thesis characterises the profile of EMOSOC changes in non–demented ALS and highlights the role of ALS–related executive dysfunction in these changes. It also assesses the relative impact of patients’ disease, cognitive and behavioural changes on ALS caregivers.
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Gopinath, Sumana. "Finding new genes causing motor neuron diseases." Thesis, The University of Sydney, 2006. http://hdl.handle.net/2123/1624.

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Abstract Neurodegenerative disorders are a diverse group of disorders that affect specific subsets of neurons. Motor neuron diseases, neurodegenerative disorders of motor neurons, are seen commonly as sporadic cases and less frequently as familial disease forms. The familial forms show genetic and phenotypic heterogeneity. Clinically motor neuron diseases may be seen as rapidly progressive disorders like amyotrophic lateral sclerosis, ALS or slowly progressive disorders like hereditary motor neuropathies, HMN. The only proven causes for motor neuron diseases are gene mutations that lead to motor neuron degeneration in familial disease forms. Only some of these genes have been identified and have contributed greatly to our understanding of the neurobiology of familial and sporadic disease forms. Identification of additional disease causing genes would help enhance our knowledge of the pathophysiological mechanisms underlying all forms of motor neuron disorders, which would lead to early diagnoses, effective prophylaxis and efficient therapies for these disorders. This study aimed to find gene mutations that cause rapid and slowly progressive familial motor neuron disorders in Australian families and to determine their relevance to sporadic forms of motor neuron disease. The familial forms of ALS show reduced disease penetrance, that is, not all gene mutation carriers manifest the disease. This study examines ALS penetrance in a group of Australian families. The most frequently observed mutations in ALS families are cytosolic superoxide dismutase/SOD1 gene mutations. In a collection of ALS families in our centre, families without the common SOD1 gene mutations were genotyped for other ALS genes and loci and studied using genetic linkage and haplotype analyses. Studies in a large Australian ALS family further confirmed genetic heterogeneity in non-SOD familial ALS, all known autosomal dominant ALS genes and chromosomal loci were excluded as cause of disease in this family. Such families can be studied further to identify additional disease genes and loci mapped in other ALS families. These families represent powerful resources for identification of additional ALS genes. Identifying the pathogenic genes in families with reduced disease penetrance may be more relevant to sporadic forms of disease. dHMN is a chronic neurodegenerative disorder predominantly affecting motor neurons. In a large Australian dHMN family, all the known dHMN genes and chromosomal loci were excluded as cause of disease. A genome wide microsatellite screen was performed in this family and genetic linkage was established to a novel 12.98 Mb locus on chromosome 7q34.2-q36. Candidate genes in this large interval will be screened based on their function and expression profile. Identification of a new dHMN locus provides the basis for future identification of a novel gene involved in motor neuron degeneration. Genes in dHMN have been shown to be pathogenic in ALS and Charcot Marie Tooth syndromes. The new locus for dHMN mapped in this project would lead to identification of a novel dHMN gene, which may elucidate the pathogenesis underlying a wide range of neurodegenerative disorders.
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Gopinath, Sumana. "Finding new genes causing motor neuron diseases." University of Sydney, 2006. http://hdl.handle.net/2123/1624.

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Doctor of Philosophy
Abstract Neurodegenerative disorders are a diverse group of disorders that affect specific subsets of neurons. Motor neuron diseases, neurodegenerative disorders of motor neurons, are seen commonly as sporadic cases and less frequently as familial disease forms. The familial forms show genetic and phenotypic heterogeneity. Clinically motor neuron diseases may be seen as rapidly progressive disorders like amyotrophic lateral sclerosis, ALS or slowly progressive disorders like hereditary motor neuropathies, HMN. The only proven causes for motor neuron diseases are gene mutations that lead to motor neuron degeneration in familial disease forms. Only some of these genes have been identified and have contributed greatly to our understanding of the neurobiology of familial and sporadic disease forms. Identification of additional disease causing genes would help enhance our knowledge of the pathophysiological mechanisms underlying all forms of motor neuron disorders, which would lead to early diagnoses, effective prophylaxis and efficient therapies for these disorders. This study aimed to find gene mutations that cause rapid and slowly progressive familial motor neuron disorders in Australian families and to determine their relevance to sporadic forms of motor neuron disease. The familial forms of ALS show reduced disease penetrance, that is, not all gene mutation carriers manifest the disease. This study examines ALS penetrance in a group of Australian families. The most frequently observed mutations in ALS families are cytosolic superoxide dismutase/SOD1 gene mutations. In a collection of ALS families in our centre, families without the common SOD1 gene mutations were genotyped for other ALS genes and loci and studied using genetic linkage and haplotype analyses. Studies in a large Australian ALS family further confirmed genetic heterogeneity in non-SOD familial ALS, all known autosomal dominant ALS genes and chromosomal loci were excluded as cause of disease in this family. Such families can be studied further to identify additional disease genes and loci mapped in other ALS families. These families represent powerful resources for identification of additional ALS genes. Identifying the pathogenic genes in families with reduced disease penetrance may be more relevant to sporadic forms of disease. dHMN is a chronic neurodegenerative disorder predominantly affecting motor neurons. In a large Australian dHMN family, all the known dHMN genes and chromosomal loci were excluded as cause of disease. A genome wide microsatellite screen was performed in this family and genetic linkage was established to a novel 12.98 Mb locus on chromosome 7q34.2-q36. Candidate genes in this large interval will be screened based on their function and expression profile. Identification of a new dHMN locus provides the basis for future identification of a novel gene involved in motor neuron degeneration. Genes in dHMN have been shown to be pathogenic in ALS and Charcot Marie Tooth syndromes. The new locus for dHMN mapped in this project would lead to identification of a novel dHMN gene, which may elucidate the pathogenesis underlying a wide range of neurodegenerative disorders.
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Lloyd, Catherine Margaret. "Aspects of cortical function in motor neurone disease." Thesis, Imperial College London, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.243835.

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Rewaj, Phillipa Jane. "Nature of language impairment in motor neurone disease." Thesis, University of Edinburgh, 2014. http://hdl.handle.net/1842/9744.

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Background: Language impairment associated with Motor Neurone Disease (MND) has been documented since the late 19th century, yet little is understood about the pervasiveness or nature of these deficits. The common clinical view among healthcare professionals is that communication difficulties can be attributed solely to the motor speech disorder dysarthria. Recent literature raises the possibility of more central processing deficits. Impairments in naming ability and comprehension of complex grammatical constructs have been frequently reported in some patients with MND. However, there is now growing evidence of spelling impairment, which could suggest the contribution of a more phonologically based deficit. In addition, the close relationship between MND and frontotemporal dementia (FTD) raises questions about the connection between the language impairments seen in MND patients and those documented in patients with the primary progressive aphasia (PPA) syndromes associated with FTD. Aims: This thesis examines the nature of speech and language deficits in people with MND and the extent to which expressive communication impairment can occur above and beyond dysarthria. In particular, the study explores: i) to what extent these language impairments can be attributed to deficits in working memory, executive functioning and/or disease severity; ii) what spelling errors can reveal about the integrity of lexical, phonological and orthographic processing; iii) whether similar patterns of impairment can be seen in PPA syndromes; iv) the relationship between language impairment and bulbar onset; and v) the impact these findings have on clinical management of MND patients. Methods: MND patients from across Scotland with changes in speech and/or language were tested using a neuropsychological battery of experimental and standardised tests of naming, spelling, syntactic comprehension, prosody and phonological and orthographical awareness. Patients were also screened for levels of dysarthria, executive functioning and working memory deficits, and results compared to those of matched controls. Findings: As a group, MND participants performed significantly worse than matched controls on measures of naming, spelling, orthographical awareness, grammatical comprehension, affective prosody and verbal fluency, but not working memory. However, based on patterns of individual impairment, of which spelling impairment formed a distinctive marker, the patient group divided into dichotomous subgroups, with 44% of participants categorised as ‘linguistically impaired’, while the remainder displayed little to no impairment. Those participants identified as linguistically impaired did not differ significantly from other MND participants on measures of disease severity, disease duration or dysarthria severity, although significantly more bulbar onset than limb onset participants were linguistically impaired. Spelling error patterns were suggestive of deficits at both a lexical and sublexical level, and were comparable to those reported in PPA literature. These findings suggest that dysarthria may be masking linguistic deficits in almost half of dysarthric MND patients, and highlight the importance of multidimensional assessment of language for effective clinical management.
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Brown-Wright, Sian Heledd. "Investigating metabotropic glutamate receptor 5 (mGlu5) as a novel therapeutic target in motor neuron disease (MND)." Thesis, University of Sheffield, 2018. http://etheses.whiterose.ac.uk/22583/.

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Wicks, Paul Jon Andrew. "The profile of cognitive, behehavioural and emotional change within MND [motor neurone disease]." Thesis, King's College London (University of London), 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.430936.

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Jones, Ross Alexander. "Comparative anatomy of the human neuromuscular junction." Thesis, University of Edinburgh, 2018. http://hdl.handle.net/1842/29629.

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The neuromuscular junction (NMJ), the synapse formed between lower motor neuron and skeletal muscle fibre, is known to be a target in a number of neurodegenerative conditions, including motor neuron disease (MND). Located in an accessible part of the peripheral nervous system, the NMJ can be used as a ‘model synapse’ in the context of ‘connectomics’ – the study of synaptic connectivity throughout the nervous system as a whole. Although the NMJ has been studied in a number of species, relatively little is known about its structure in humans, complicating the translation of animal models of disease to the human condition. Described here is the first detailed cellular and molecular characterization of the human NMJ. A standardized methodology for comparative morphometric analysis of NMJs was developed and validated (‘NMJ-morph’). NMJ-morph was used to generate baseline data for 2160 NMJs from a single litter of wild type mice, representing 9 distinct muscles across 3 body regions. Principal components analysis (PCA) revealed synaptic size and fragmentation to be the key determinants of synaptic variability. Correlation data revealed the pre-synaptic cell (motor neuron) to be a stronger predictor of synaptic morphology than the post-synaptic cell (muscle fibre). Other factors influencing synaptic variability were in a clear hierarchy: muscle identity accounted for more variation in synaptic form than animal identity, with side having no effect. Human tissue was obtained from 20 patients (aged 34 to 92 years) undergoing lower limb amputation, primarily for the complications of peripheral vascular disease (PVD). Muscle samples were harvested from non-pathological regions of the surgical discard tissue. 2860 human NMJs were analyzed from 4 distinct muscles (extensor digitorum longus, soleus, peroneus longus and peroneus brevis), and compared with equivalent NMJs from wild type mice. Human NMJs displayed unique morphological characteristics, including small size, thin axons, rudimentary nerve terminals and distinctive ‘nummular’ endplates, all of which distinguished them from equivalent mouse NMJs. The previous notion of partial occupancy in human NMJs was disproved. As in mice, the pre-synaptic cell was shown to correlate more strongly with NMJ morphology; in contrast to mice, the human NMJ was found to be relatively stable throughout its 90+ year lifespan. In support of the tissue harvesting procedure, patient co-morbidities (diabetes mellitus and vascular disease) did not significantly impact NMJ morphology. Super-resolution imaging of the NMJ revealed significant differences in the functional architecture of human and mouse active zones. Despite the smaller synaptic size in humans, the total quantity of active zone material was conserved between the species, suggesting a homeostatic mechanism to preserve effective neurotransmission. Parallel proteomic profiling demonstrated further species-specific differences in the broader molecular composition of the NMJ. The cellular and molecular anatomy of the human NMJ is fundamentally different to that of other mammalian species. These differences must be taken into account when translating animal models of disease to the human condition.
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Smith, Hayley-Jane. "The personal experience of carers of individuals with Motor Neurone Disease (MND) and their experiences of services." Thesis, University of Birmingham, 2009. http://etheses.bham.ac.uk//id/eprint/1221/.

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This thesis consists of research and clinical components and is submitted as partial fulfilment of a doctorate degree in Clinical Psychology. Volume 1, the research component, comprises of a literature review, an empirical paper and a public domain paper. The systematic literature review looks at evidence linking attachment and caregiving in adult couples. The empirical paper explores the experiences of individuals with a partners diagnosed with Motor Neurone Disease (MND). Lastly, a public domain provides a summary of the empirical paper. Volume II, the clinical component, contains clinical practice reports conducted within placements from adult, child, learning disability older adult specialities. The first report contains a behavioural and systemic formulation of a 3 year-old who was referred as her mother was having difficulties managing her behaviour. The second report describes an evaluation of the Experiences of practitioners interpreting and delivering Triple P (Positive Parenting Programme) groups in South Asian Community languages. The third report presents a single case experimental design concerning a behavioural approach to challenging behaviour displayed by a 7-year old boy with learning disabilities and autism. The fourth report is a case study of a Cognitive Behavioural approach used with a man diagnosed with Persistent Paranoid Delusional Disorder. Finally, the fifth report is an abstract of an oral case presentation of a small-scale service related project around a multiple family therapy group for adolescents with anorexia nervosa.
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Clabburn, Oliver. "Investigating the use of digital legacies with people affected by Motor Neurone Disease (MND) : an Interpretative Phenomenological Analysis." Thesis, Edge Hill University, 2018. http://repository.edgehill.ac.uk/10255/.

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Background: A video-based 'digital legacy' is a selection of videos which document a person's life, memories, achievements, or special family events. The videos are copied to a digital source to be specifically given to a child or young person to use in the future. A video-based digital legacy may either be purposefully recorded by the person living with MND (plwMND), or, compiled later by bereaved family members. To date, there is little published research about how children and young people are affected when a family member has MND and subsequently dies. As such, there is a dearth of literature on how to best support these young people. Objective: This research is investigating the views, perceptions and experiences of digital legacies with people affected by MND. Methods: The study is underpinned by Interpretative Phenomenological Analysis (IPA) meaning a small homogeneous sample was required using purposive methods of recruitment. Interviews were conducted and audio recorded with four plwMND regarding their experiences of creating a purposeful digital legacy for a child or young person in their family. Interviews were also conducted with three bereaved young people regarding their experiences of using a video legacy of a parent who had died from MND. Also, a sample of twenty healthcare professionals, specialists and experts were interviewed from across the United Kingdom regarding their perceptions on the use of digital legacies with plwMND, and, young people who are bereaved. Ethics: Ethical approvals were obtained from a Faculty of Research Ethics Committee at Edge Hill University (FREC), the Health Research Authority (HRA), and the National Research Service for Scotland. Discussion: 'The Model of Reciprocal Bonds Formation' and coining of the term 'autobiographical chapter' has been developed from this study. Creating a digital legacy provides a number of mutual challenges and benefits for both plwMND, and bereaved young people. Recommendations are provided regarding i) optimal 'windows of opportunity' in which the digital legacy is recorded/used; ii) actionable solutions for current policy/practice; iii) future directions for research.
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Books on the topic "Motor neuron disease, MND"

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Talbot, Kevin. Motor neuron disease. Oxford: Oxford University Press, 2008.

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Leigh, P. N., and Michael Swash, eds. Motor Neuron Disease. London: Springer London, 1995. http://dx.doi.org/10.1007/978-1-4471-1871-8.

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Talbot, Kevin. Motor neuron disease. Oxford: Oxford University Press, 2008.

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C, Williams A., ed. Motor neuron disease. London: New York, 1994.

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L, Mancini Raffaele, ed. Motor neuron disease research progress. New York: Nova Biomedical Books, 2008.

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Orrell, Richard William. Genetics of motor neuron disease. Manchester: University of Manchester, 1996.

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Talbot, Kevin. Motor neuron disease: A practical manual. Oxford: Oxford University Press, 2010.

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Talbot, Kevin. Motor neuron disease: A practical manual. Oxford: Oxford University Press, 2010.

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Motor neuron disease: A practical manual. Oxford: Oxford University Press, 2010.

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Motor neuron diseases: Causes, classification, and treatments. Hauppauge, N.Y: Nova Science Publishers, 2011.

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Book chapters on the topic "Motor neuron disease, MND"

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Rabin, Bruce A., and David R. Borchelt. "Motor Neuron Disease." In Cell Death and Diseases of the Nervous System, 429–43. Totowa, NJ: Humana Press, 1999. http://dx.doi.org/10.1007/978-1-4612-1602-5_20.

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Roy, Bhaskar, and Basil T. Darras. "Motor Neuron Disease." In Pediatric Electromyography, 199–220. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-61361-1_16.

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Sivak, Mark A. "Motor Neuron Disease." In Mount Sinai Expert Guides, 393–402. Chichester, UK: John Wiley & Sons, Ltd, 2016. http://dx.doi.org/10.1002/9781118621042.ch35.

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Brooks, Benjamin Rix, Roxanne Depaul, Yan De Tan, Mohammed Sanjak, Robert L. Sufit, and Joanne Robbins. "Motor Neuron Disease." In Foundations of Neurology, 249–81. Boston, MA: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4613-1495-0_18.

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Anderson, Janice R. "Motor Neuron Disease." In Atlas of Skeletal Muscle Pathology, 37–43. Dordrecht: Springer Netherlands, 1985. http://dx.doi.org/10.1007/978-94-009-4866-2_4.

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Joshua, Abraham M., and Zulkifli Misri. "Motor Neuron Disease." In Physiotherapy for Adult Neurological Conditions, 539–62. Singapore: Springer Nature Singapore, 2022. http://dx.doi.org/10.1007/978-981-19-0209-3_8.

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Oette, Mark, Marvin J. Stone, Hendrik P. N. Scholl, Peter Charbel Issa, Monika Fleckenstein, Steffen Schmitz-Valckenberg, Frank G. Holz, et al. "Motor Neuron Disease." In Encyclopedia of Molecular Mechanisms of Disease, 1351. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_8992.

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Talbot, Kevin, Martin R. Turner, Rachael Marsden, and Rachel Botell. "Genetics of MND." In Motor Neuron Disease, 69–84. Oxford University Press, 2009. http://dx.doi.org/10.1093/med/9780199547364.003.06.

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Talbot, Kevin, Martin R. Turner, Rachael Marsden, and Rachel Botell. "Organization of MND services." In Motor Neuron Disease, 48–57. Oxford University Press, 2009. http://dx.doi.org/10.1093/med/9780199547364.003.04.

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"Motor neurone disease (MND)." In Rapid Neurology and Neurosurgery, 108–10. Chichester, UK: John Wiley & Sons, Ltd, 2018. http://dx.doi.org/10.1002/9781119548898.ch26.

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Conference papers on the topic "Motor neuron disease, MND"

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Paula, Igor Roque de, Maria Alice Dias da Costa, Danielle Antoniazzi Kirscht Auermann D'Allembert Costa Sousa, Julia Magalhães Waybe Gonçalves, Marcela Ferreira de Andrade Rangel, Kamila Silva de Mattos, and Mariana Asmar Alencar. "Motor neuronic disease starting in the elderly and young adults." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.497.

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Abstract:
Introduction: Motor neuron diseases (MND) are degenerative disorders that affect motor neurons, leading to disability and dependence throughout their course. The onset of symptoms is variable and can occur in adults(A) and elderly(E), however little is known about the characteristics of the disease in different age groups. Objective: To investigate the characteristics and the difference between clinical and functional factors considering the onset of MND in the elderly and young adults. Method: There were 26 young adults and 26 elderly (≥60 years) evaluated, matched by gender and length of disease, treated at HC/UFMG. The following were investigated: demographic and clinical, using specific instruments (ALSFRS-R/BR and ALSAQ-40); fatigue (FSS); manual muscle strength; mobility and balance (SPPB). Analysis was performed descriptive and comparison (student t test, Mann-Whitney or X2), using SPSS, significance level of 0.05. Results: Differences were observed significant as to the place of onset of symptoms (p=0.034), presence of pain (p=0.034) and use of ambu (p=0.023). No significant differences were verified for the others: occurrence of falls (p=0.254), presence of comorbidities (p=0.158) and use of Riluzole (p=0.548), sit and stand (p=0.931), turn over in bed (p=0.402) and walk (p=0.740), total ALSFRS-R (p=0.656), MND severity level (p=0.307)strength muscular (p=0.940), SPPB (p=0.296), quality of life (p=0.686). Conclusion: The clinical and functional characteristics were similar between individuals who started the disease in the elderly and adult phase. However, it was observed a higher prevalence among the elderly with bulbar onset, which is thebeginning of the worst prognosis of disease progression.
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Aslam, Zaryab, Aisha Zahid Junejo, Aarish Memon, Ali Raza, Juveria Aslam, and Liaquat Ali Thebo. "Optical Assistance for Motor Neuron Disease (MND) Patients Using Real-time Eye Tracking." In 2019 8th International Conference on Information and Communication Technologies (ICICT). IEEE, 2019. http://dx.doi.org/10.1109/icict47744.2019.9001922.

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Ballard, Emily, Mike Mackie, Samiha Ismail, Reegan Puthussery, Hina Pattani, Joerg Steier, Philip Marino, et al. "Ventilation in Motor Neurone Disease (MND): what happens in practice." In ERS International Congress 2017 abstracts. European Respiratory Society, 2017. http://dx.doi.org/10.1183/1393003.congress-2017.pa2177.

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Hemsley, Bronwyn, Stuart Palmer, Wendy Goonan, and Stephen Dann. "Motor Neurone Disease (MND) and Amyotrophic Lateral Sclerosis (ALS): Social Media Communication on Selected #MND and #ALS Tagged Tweets." In Hawaii International Conference on System Sciences. Hawaii International Conference on System Sciences, 2017. http://dx.doi.org/10.24251/hicss.2017.455.

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Bird, Olivia, Matt Quint, and Kayode Adeniji. "Gastrostomy Safety in patients with Motor Neurone Disease (MND) in UK District General Hospital." In ERS International Congress 2017 abstracts. European Respiratory Society, 2017. http://dx.doi.org/10.1183/1393003.congress-2017.pa2149.

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Wilson, Eleanor. "8 Shifted deaths: the use of home mechanical ventilation for motor neurone disease (MND)." In Marie Curie Research Conference 2023, Monday 6 February – Friday 10 February 2023. British Medical Journal Publishing Group, 2023. http://dx.doi.org/10.1136/spcare-2023-mcrc.7.

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Seymour, John, Iain Wheatley, Elizabeth Spillan-Ind, and Timothy Ho. "Effect of gastrostomy insertion and age on the survival of patients with motor neuron disease (MND) using home non-invasive ventilation." In ERS International Congress 2019 abstracts. European Respiratory Society, 2019. http://dx.doi.org/10.1183/13993003.congress-2019.pa3958.

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Umpleby, Helen, David Oliver, Sandip Banerjee, and Lisa Vincent-Smith. "A novel collaborative approach in improving management outcomes in patients with motor neurone disease (MND)." In Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.pa2190.

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Bonnar, Kim, Nicola Denbow, Sarah Holmes, Clare Rayment, and Jenny White. "P-176 Improving care coordination for people living with motor neurone disease (MND) in the bradford area." In Transforming Palliative Care, Hospice UK 2018 National Conference, 27–28 November 2018, Telford. British Medical Journal Publishing Group, 2018. http://dx.doi.org/10.1136/bmjspcare-2018-hospiceabs.201.

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Thompson, F., P. Harbord, S. Ewles, F. Cull, D. Gibson, A. Sivaloganathan, A. Dushianthan, and J. Wilkinson. "P200 A review of domiciliary non-invasive ventilation for patients with motor neurone disease (MND) in a regional centre." In British Thoracic Society Winter Meeting 2018, QEII Centre, Broad Sanctuary, Westminster, London SW1P 3EE, 5 to 7 December 2018, Programme and Abstracts. BMJ Publishing Group Ltd and British Thoracic Society, 2018. http://dx.doi.org/10.1136/thorax-2018-212555.357.

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