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Motor neuron disease can affect either upper motor neurons (UMNs) or lower motor neurons (LMNs). Motor neuron disease describes a collection of clinical disorders, characterized by progressive muscle weakness and the degeneration of the motor neuron on electrophysiological testing. The term "motor neuron disease" has varying meanings in ...
Mitochondrial myopathies are diseases caused by mutations related to mitochondria, and thus are generally inherited from the mother with variable expressivity due to heteroplasmy. Kearns–Sayre syndrome; Mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes (MELAS) Myoclonic epilepsy with ragged red fibers (MERRF)
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Collins, Joseph. Progressive Bulbar Palsy. ‘’The Treatment of Diseases of the Nervous System: A Manual for Practitioners’’. W. Wood and Company. (1900) Swash M, and Desai J. Motor Neuron Disease: Classification and nomenclature. ALS and Other Motor Neuron Disorders. 1:105-112. (2000) Kadekawa J et al.
To this day, terminology around these diseases remains confusing because in the United Kingdom motor neurone disease refers to both ALS specifically and to the spectrum of ALS, PMA, PLS, and PBP. In the United States the most common terms are ALS (both specifically for ALS and as a blanket term) or Lou Gehrig's disease. [citation needed]
Spinal and bulbar muscular atrophy (SBMA), popularly known as Kennedy's disease, is a rare, adult-onset, X-linked recessive lower motor neuron disease caused by trinucleotide CAG repeat expansions in exon 1 of the androgen receptor (AR) gene, which results in both loss of AR function and toxic gain of function.
There is currently no known pharmacological treatment to hereditary motor and sensory neuropathy. However, the majority of people with these diseases are able to walk and be self-sufficient. [3] Some methods of relief for the disease include physical therapy, stretching, braces, and sometimes orthopedic surgery.
Hirayama disease, also known as monomelic amyotrophy (MMA), [1] [2] is a rare motor neuron disease first described in 1959 in Japan. Its symptoms usually appear about two years after adolescent growth spurt and is significantly more common in males, with an average age of onset between 15 and 25 years.