Muscle Atrophy and Hypertrophy

2015 ◽  
Author(s):  
Aziz Shaibani
Keyword(s):  
Motor Neuron ◽  
Muscle Atrophy ◽  
Muscle Hypertrophy ◽  
Conduction Block ◽  
Ulnar Neuropathy ◽  
Demyelinating Neuropathy ◽  
Motor Neuron Diseases ◽  
Axonal Flow ◽  
Tissue Replacement ◽  
Atrophy And Hypertrophy

Muscle atrophy is usually caused by interruption of axonal flow (axonal neuropathies, motor neuron diseases, etc.). If weakness is out of proportion to atrophy, conduction block due to demyelinating neuropathy should be suspected. Chronic myopathies and immobility may also cause atrophy, but no EMG evidence of denervation or myopathy is respectively found. The pattern of atrophy is often helpful to localize the lesion. Atrophy of the interossi and preservation of the bulk of the thenar muscles suggest ulnar neuropathy, but atrophy of both would suggest a C8 or plexus pathology. Muscle enlargement may be due to tissue replacement (fatt, amyloid), which can be confirmed by EMG and MRI, or may be due to real muscle hypertrophy from excessive discharges (neuromyotonia).

Muscle Atrophy and Hypertrophy

2018 ◽  
Author(s):  
Aziz Shaibani
Keyword(s):  
Magnetic Resonance Imaging ◽  
Magnetic Resonance ◽  
Muscle Atrophy ◽  
Muscle Hypertrophy ◽  
Resonance Imaging ◽  
Demyelinating Neuropathy ◽  
Motor Neuron Diseases ◽  
Fatty Replacement ◽  
Magnetic Resonance Imaging Mri ◽  
Atrophy And Hypertrophy

Muscle atrophy is usually caused by interruption of axonal flow [axonal neuropathies, motor neuron diseases (MNDs), etc.]. If weakness is out of proportion to atrophy, demyelinating neuropathy should be suspected. Chronic myopathies and immobility also may cause atrophy, but no electromyography (EMG) evidence of denervation or myopathy is found. The pattern of atrophy is often helpful to localize the lesions. Atrophy of the interossi and preservation of the bulk of the thenar muscles suggest ulnar neuropathy, but atrophy of both would suggest a C8 or plexus pathology. Muscle enlargement may be due to fatty replacement, which can be confirmed by EMG and magnetic resonance imaging (MRI), or due to real muscle hypertrophy from excessive discharges (neuromyotonia).

Lower Motor Neuron Disease with Accumulation of Neurofilaments in a Cat

1976 ◽  
Vol 13 (6) ◽  
pp. 428-435 ◽  
Author(s):  
M. Vandevelde ◽  
C. E. Greene ◽  
E. J. Hoff
Keyword(s):  
Spinal Cord ◽  
Motor Neuron ◽  
Motor Neuron Disease ◽  
Histological Examination ◽  
Muscle Atrophy ◽  
Motor Neurons ◽  
Nerve Cells ◽  
Lower Motor Neuron ◽  
Motor Neuron Diseases ◽  
Lower Motor Neuron Disease

A young cat had signs of tetraparesis that progressed to tetraplegia within a few weeks. Clinically, there was lower motor neuron disease with areflexia and muscle atrophy in all limbs. Degeneration of the motor neurons in the spinal cord was seen on histological examination. Ultrastructurally, the degeneration of nerve cells was characterized by abnormal proliferation of neurofilaments. These findings were compared to other motor neuron diseases and neurofibrillary accumulations in man and animals.

Persistent and transient ?conduction block? in motor neuron diseases

1993 ◽  
Vol 16 (9) ◽  
pp. 896-903 ◽  
Author(s):  
Dale J. Lange ◽  
Werner Trojaborg ◽  
T. Drake McDonald ◽  
David M. Blake
Keyword(s):  
Motor Neuron ◽  
Conduction Block ◽  
Motor Neuron Diseases ◽  
Transient Conduction

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

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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