In the neurological evaluation of weakness, we distinguish between
upper motor neuron weakness and lower motor neuron weakness.

The anterior horn cells are somatotopically organized in the spinal cord.

Clinically characterized by selective involvement of muscles.
Currently there is no cure for MND, however there are medicines available to slow down the progress of the disease and manage your symptoms.
Talk to your GP before starting any complementary therapy to make sure that it isn’t harmful and is compatible with any other medicines you’re taking.

Stem cell treatment introduces new cells into the damaged tissue to treat disese or injury.Stem cell treatment have the potential of changing the face of human disease and alleviate suffering.Medical researches beleive thatadult and embryonic stem cells will soon be able to treat diabetes,cancer,cardiac failure,coeliac disese,parkinsons disease.Anterior horn cell is a disease which affects the nerve cells of the spinal cord.This disease has no treatment but recent development in stem cell therspy has opened up a avenue to replace the lost neural cells by stem cells.You cant talk about reactions because it comes when no other treatment remains and is the only option.

Anterior horn cell diseases.
Clinically characterized by selective involvement of muscles. EMG
findings are those of low CMAP amplitudes (fewer axons firing muscle fibers), normal SNAP amplitudes
(ventral horn cell axons are not sensory), relatively normal nerve conduction velocities (normal axons
camouflage dead ones), large “neurogenic” MUPs (normal axons take over muscle fibers of dead ones),
muscle histology shows type grouping and group atrophy (normal axons take over muscle fibers of dead
axons [type grouping] and then eventually die [group atrophy] and blood CK is normal (CK levels
become elevated if a muscle fiber breaks down, or if the muscle membrane becomes porous. Both
conditions allow CK to leak from the muscle fiber into the blood. In neurogenic atrophy (of anterior
horn cell or peripheral [axonal] nerve origin) the muscle membranes remain intact and thus CK levels
remain normal). Fasciculations (grossly) and fibrillations (only upon needle exam) are present.
Peripheral nerve diseases.
Clinically characterized by the associated findings of sensory and autonomic
abnormalities. EMG findings depend on whether it is primarily an axonal (axon cylinder) or
demyelinating neuropathy. Axonal EMG findings are those of low CMAP amplitudes (fewer axis
cylinders in a nerve means fewer muscle fiber firing), lower SNAP amplitudes if axons in a sensory
nerve, relatively normal nerve conduction velocities (normal axons camouflage dead ones), large
“neurogenic” MUPs (normal axons take over muscle fibers of dead ones), muscle histology shows type
grouping and group atrophy (normal axons take over muscle fibers of dead axons [type grouping] and
then eventually die [group atrophy] and blood CK is normal. Fasciculations and fibrillations are present.
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Spinal cord
Weakness
Demyelination
The EMG findings are those of relatively normal CMAP amplitudes (axis cylinders
are fine, so normal number of muscle fibers are activated), normal SNAP amplitudes (axis cylinders
are OK), reduced nerve conduction velocities (myelin loss=slowing), normal MUPs (axis cylinders
are OK), muscle histology is normal (axis cylinders are OK) and CK is normal (no muscle fibers are
dead!). No fasciculations or fibrillations.
You might wonder why normal myelinated fibers don’t camouflage the diseased fibers. In reality,
demyelinating neuropathies affect multiple focal areas of every nerve and you have normal segments
in between. Thus, you do not find “normal” and “abnormal fibers”, all the fibers are affected to
some degree. In axonal neuropathies some fibers are affected, others not. The normal fibers
conduct normally and thus you do not see significant slowing of nerve conduction velocities, but you
see drop in the SNAP and CMAP amplitudes.
Neuromuscular transmission defects.
Clinically characterized by abnormal fatigability; EMG
shows normal nerve conduction velocities, normal CMAP and SNAP amplitudes, decremental
CMAP responses to repetitive nerve stimulation; muscle histology is relatively normal; blood CK is
normal. No fasciculations or fibrillations.
Primary muscle diseases. Clinically specific patterns of muscle weakness may be noted; EMG shows
normal nerve conduction velocities with low CMAP amplitudes (fewer muscle fibers per motor
unit), normal SNAP amplitudes, smaller “myopathic” MUPs, muscle histology shows myopathic
changes; blood CK is elevated. Fibrillations are seen.
“SPEED PLAY”
Increased reflexes in a symptomatic limb suggest a central lesion, while reduced reflexes
suggest a peripheral lesion.
Bilateral sensory and motor deficits throughtout the body below a roughly horizontal level in
the trunk, with normal function above that level, indicates a spinal cord lesion