H-reflex modulations during voluntary and automatic movements following upper motor neuron damage

1998 ◽  
Vol 109 (6) ◽  
pp. 475-483 ◽  
Author(s):  
Charles T. Leonard ◽  
Pamela M. Diedrich ◽  
Tamaki Matsumoto ◽  
Toshio Moritani ◽  
James A. McMillan
Keyword(s):  
Motor Neuron ◽  
H Reflex ◽  
Neuron Damage

Spasticity as an ictal pattern due to excitotoxic upper motor neuron damage

2012 ◽  
Vol 25 (3) ◽  
pp. 397-400 ◽  
Author(s):  
C. Liguori ◽  
M.G. Marciani ◽  
M. Albanese ◽  
R. Massa ◽  
F. Izzi ◽  
...  
Keyword(s):  
Motor Neuron ◽  
Neuron Damage

scholarly journals Intrathecal infusion of BMAA induces selective motor neuron damage and astrogliosis in the ventral horn of the spinal cord

2014 ◽  
Vol 261 ◽  
pp. 1-9 ◽  
Author(s):  
Hong Z. Yin ◽  
Stephen Yu ◽  
Cheng-I Hsu ◽  
Joe Liu ◽  
Allan Acab ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Motor Neuron ◽  
Ventral Horn ◽  
Neuron Damage ◽  
Intrathecal Infusion

scholarly journals Contribution of Aberrant Astrocytes to Motor Neuron Damage and Death in the SOD1G93A Rat Experimental Model of ALS

2020 ◽  
Author(s):  
Gabriel Otero Damianovich ◽  
Olga Cristina Parada ◽  
Pablo Díaz-Amarilla ◽  
Eugenia Eloísa Isasi ◽  
Carmen Isabel Bolatto Pereira ◽  
...  
Keyword(s):  
Motor Neuron ◽  
Experimental Model ◽  
Neuron Damage

scholarly journals Glial Cells in Amyotrophic Lateral Sclerosis

2011 ◽  
Vol 2011 ◽  
pp. 1-7 ◽  
Author(s):  
Jurate Lasiene ◽  
Koji Yamanaka
Keyword(s):  
Amyotrophic Lateral Sclerosis ◽  
Motor Neuron ◽  
Glial Cells ◽  
Motor Neurons ◽  
Premature Death ◽  
Active Role ◽  
Sporadic Als ◽  
Neuron Damage ◽  
Als Patients ◽  
Lateral Sclerosis

Amyotrophic lateral sclerosis (ALS) is an adult motor neuron disease characterized by premature death of upper and lower motor neurons. Two percent of ALS cases are caused by the dominant mutations in the gene for superoxide dismutase 1 (SOD1) through a gain of toxic property of mutant protein. Genetic and chimeric mice studies using SOD1 models indicate that non-neuronal cells play important roles in neurodegeneration through non-cell autonomous mechanism. We review the contribution of each glial cell type in ALS pathology from studies of the rodent models and ALS patients. Astrogliosis and microgliosis are not only considerable hallmarks of the disease, but the intensity of microglial activation is correlated with severity of motor neuron damage in human ALS. The impaired astrocytic functions such as clearance of extracellular glutamate and release of neurotrophic factors are implicated in disease. Further, the damage within astrocytes and microglia is involved in accelerated disease progression. Finally, other glial cells such as NG2 cells, oligodendrocytes and Schwann cells are under the investigation to determine their contribution in ALS. Accumulating knowledge of active role of glial cells in the disease should be carefully applied to understanding of the sporadic ALS and development of therapy targeted for glial cells.

scholarly journals Review of therapeutic options for spinal muscular atrophy

2021 ◽  
Vol 52 (2) ◽  
pp. 151-159
Author(s):  
Arun Singh ◽  
Monica Jain ◽  
Rupa Kapadia ◽  
Kumar Mahawar-Dhirendra ◽  
Shivankan Kakkar ◽  
...  
Keyword(s):  
Spinal Muscular Atrophy ◽  
Motor Neuron ◽  
Autosomal Recessive ◽  
Muscular Atrophy ◽  
Age Groups ◽  
Respiratory Muscles ◽  
Survival Motor Neuron ◽  
Medical Problems ◽  
The Us ◽  
Neuron Damage

Spinal Muscular Atrophy (SMA) is uncommon genetic (autosomal recessive) disease that deteriorates neuromuscular function of the affected person's body by causing lower motor neuron damage, progress in muscle atrophy and in advanced cases leads to paralysis of muscles. Mainly skeletal and respiratory muscles are involved. SMA is present due to lack of SMA proteins, which are encoded by survival motor neuron-1 (SMN-1) genes. In mutation of SMN-1 genes, deficiency of SMN proteins occurs. SMA affects all age groups, but mainly and most severely children younger than 6 months of age. At present, risdiplam is a treatment option and the drug has been approved by the US Food Drug and Administration on 7 August 2020. The availability of the drug has led to increased financial, ethical and medical problems. SMA affected populations are regularly challenged to these issues.

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