Application of clinical neurophysiology to clinical trials involving motor neuron diseases

2004 ◽  
pp. 689-697
Author(s):  
Mark B. Bromberg
Keyword(s):  
Clinical Trials ◽  
Motor Neuron ◽  
Clinical Neurophysiology ◽  
Motor Neuron Diseases

Clinical Trials in Motor Neuron Diseases

1999 ◽  
Vol 14 (3) ◽  
pp. 173-179 ◽  
Author(s):  
Robert G. Miller
Keyword(s):  
Clinical Trials ◽  
Motor Neuron ◽  
Motor Neuron Diseases

Correlate the NCS and Needle EMG of Motor Neuron Diseases Using FIS System

2020 ◽  
Author(s):  
Amit Mayavanshi ◽  
Himanshu A Patel ◽  
Palak A Parikh
Keyword(s):  
Motor Neuron ◽  
Motor Neuron Diseases

Commissural fiber degeneration in motor neuron diseases

2020 ◽  
Vol 21 (5-6) ◽  
pp. 321-323
Author(s):  
Peter Bede ◽  
Rangariroyashe H. Chipika
Keyword(s):  
Motor Neuron ◽  
Motor Neuron Diseases

scholarly journals Kinesin Mutations Cause Motor Neuron Disease Phenotypes by Disrupting Fast Axonal Transport in Drosophila

Genetics ◽  
1996 ◽  
Vol 144 (3) ◽  
pp. 1075-1085 ◽  
Author(s):  
Daryl D Hurd ◽  
William M Saxton
Keyword(s):  
Motor Neuron ◽  
Axonal Transport ◽  
Action Potentials ◽  
Light And Electron Microscopy ◽  
Synaptic Membrane ◽  
Slow Axonal Transport ◽  
Fast Axonal Transport ◽  
Motor Neuron Diseases ◽  
Transmitter Secretion ◽  
Axon Terminals

Abstract Previous work has shown that mutation of the gene that encodes the microtubule motor subunit kinesin heavy chain (Khc) in Drosophila inhibits neuronal sodium channel activity, action potentials and neurotransmitter secretion. These physiological defects cause progressive distal paralysis in larvae. To identify the cellular defects that cause these phenotypes, larval nerves were studied by light and electron microscopy. The axons of Khc mutants develop dramatic focal swellings along their lengths. The swellings are packed with fast axonal transport cargoes including vesicles, synaptic membrane proteins, mitochondria and prelysosomal organelles, but not with slow axonal transport cargoes such as cytoskeletal elements. Khc mutations also impair the development of larval motor axon terminals, causing dystrophic morphology and marked reductions in synaptic bouton numbers. These observations suggest that as the concentration of maternally provided wild-type KHC decreases, axonal organelles transported by kinesin periodically stall. This causes organelle jams that disrupt retrograde as well as anterograde fast axonal transport, leading to defective action potentials, dystrophic terminals, reduced transmitter secretion and progressive distal paralysis. These phenotypes parallel the pathologies of some vertebrate motor neuron diseases, including some forms of amyotrophic lateral sclerosis (ALS), and suggest that impaired fast axonal transport is a key element in those diseases.

Fatigue in motor neuron diseases

2012 ◽  
Vol 22 ◽  
pp. S198-S202 ◽  
Author(s):  
Alon Abraham ◽  
Vivian E. Drory
Keyword(s):  
Motor Neuron ◽  
Motor Neuron Diseases

scholarly journals Evaluation of peripherin in biofluids of patients with motor neuron diseases

2021 ◽  
Author(s):  
Daniele Sabbatini ◽  
Flavia Raggi ◽  
Susanna Ruggero ◽  
Mara Seguso ◽  
Jessica Mandrioli ◽  
...  
Keyword(s):  
Motor Neuron ◽  
Motor Neuron Diseases
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