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Spinal Muscular Atrophy

Treatment No. : RD0733
Dosage & Instructions: 15 drops in 15 ml of plain water twice a day, mornings and evenings.
Composition:
Hypericum D1
Melilotus D1
Vilburn op D3
Arinca D3
Belladonna D3
Secale corn D4
Arsen iodatum D4
Phosphorous D8
Ruhs tox D4
Treatment Type:
This remedy is a symptomatic treatment. A symptomatic treatment cannot eliminate the disease from its root but is able to considerably improve the patient's condition by easing his or her symptoms.
Contra-indications: None established
Special Instructions: Whereas this remedy can be safely used by teenagers, its use has not been evaluated in children under 12 years of age. Please do not administer to children under this age.
Storage: Store in a cool and dry place
Precautions: Keep away from the reach of children
Standard Packaging : 30 ml Drops

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One 30 ml bottle for $79.99
Two 30 ml bottles for $129.99

 

Condition Overview:

Spinal muscular atrophy (SMA) that is caused by a deletion of the SMN gene on chromosome 5 is an inherited progressive neuromuscular disorder characterized by degeneration of groups of nerve cells (motor nuclei) within the lowest region of the brain (lower brainstem) and certain motor neurons in the spinal cord (anterior horn cells). Motor neurons are nerve cells that transmit nerve impulses from the spinal cord or brain (central nervous system) to muscle or glandular tissue. Typical symptoms are a slowly progressive muscle weakness and muscle wasting (atrophy). Affected individuals have poor muscle tone, muscle weakness on both sides of the body without, or with minimal, involvement of the face muscles, twitching tongue and a lack of deep tendon reflexes. SMA is divided into subtypes based on age of onset of symptoms and maximum function achieved.

Spinal muscular atrophy is inherited as an autosomal recessive trait. Molecular genetic testing has revealed that all types of autosomal recessive SMA are caused by mutations in the SMN (survival motor neuron) gene on chromosome 5. Deletion of the NAIP (neuronal apoptosis inhibitory protein) gene that is close to the SMN gene is also associated with SMA. More patients with Werdnig Hoffman disease (SMA1) than other types of SMA have NAIP deletions. The relationship between specific mutations in the SMN gene and nearby genes and the severity of SMA is still being investigated so classification of SMA subdivisions is based on age of onset of symptoms and maximum function achieved, as opposed to the genetic profile. Other types of SMA exist with different prognoses.

 

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