Charcot-Marie-Tooth disease (CMT)

[Guest guest]

Dear Andrea,

 

Namaste.

 

Medical background:

 

Charcot-Marie-Tooth disease (CMT) is one of the most

common inherited neurological disorders, affecting

approximately 1 in 2,500 people in the United States.

The disease is named for the three physicians who

first identified it in 1886 - Jean-Martin Charcot and

Pierre Marie in Paris, France, and Howard Henry Tooth

in Cambridge, England.

 

CMT, also known as hereditary motor and sensory

neuropathy (HMSN) or peroneal muscular atrophy,

comprises a group of disorders that affect peripheral

nerves. The peripheral nerves lie outside the brain

and spinal cord and supply the muscles and sensory

organs in the limbs. Disorders that affect the

peripheral nerves are called peripheral neuropathies.

 

The neuropathy of CMT affects both motor and sensory

nerves.

 

Unlike other neurological disorders, CMT usually isn't

life-threatening, and it almost never affects the

brain. It causes damage to the peripheral nerves —

tracts of nerve cell fibers that connect the brain and

spinal cord to muscles and sensory organs.

 

Symptoms:

- A typical feature includes weakness of the foot and

lower leg muscles, which may result in foot drop and a

high-stepped gait with frequent tripping or falls.

- Foot deformities, such as high arches and hammertoes

(a condition in which the middle joint of a toe bends

upwards) are also characteristic due to weakness of

the small muscles in the feet.

- In addition, the lower legs may take on an " inverted

champagne bottle " appearance due to the loss of muscle

bulk.

- Later in the disease, weakness and muscle atrophy

may occur in the hands, resulting in difficulty with

fine motor skills. Although sensory nerves are also

involved, patients rarely notice significant numbness

or pain.

 

Onset of symptoms is most often in adolescence or

early adulthood, however presentation may be delayed

until mid-adulthood. The severity of symptoms is quite

variable in different patients and some people may

never realize they have the disorder. Progression of

symptoms is very gradual. CMT is not fatal and people

with most forms of CMT have a normal life expectancy.

 

Types of Charcot-Marie-Tooth disease:

 

There are many forms of CMT disease.

- The principal types include CMT1, CMT2, CMT3, CMT4,

and CMTX. CMT1 is the most frequent and results from

abnormalities in the myelin sheath. There are three

main types of CMT1. CMT1A is an autosomal dominant

disease resulting from a duplication of the gene on

chromosome 17 that carries the instructions for

producing the peripheral myelin protein-22 (PMP-22).

The PMP-22 protein is a critical component of the

myelin sheath. An overabundance of this gene causes

the structure and function of the myelin sheath to be

abnormal. Patients experience weakness and atrophy of

the muscles of the lower legs beginning in

adolescence; later they experience hand weakness and

sensory loss. Interestingly, a different neuropathy

distinct from CMT1A called hereditary neuropathy with

predisposition to pressure palsy (HNPP) is caused by a

deletion of one of the PMP-22 genes. In this case

abnormally low levels of the PMP-22 gene result in

episodic, recurrent demyelinating neuropathy. CMT1B is

an autosomal dominant disease caused by mutations in

the gene that carries the instructions for

manufacturing the myelin protein zero (P0) which is

another critical component of the myelin sheath. Most

of these mutations are point mutations, meaning a

mistake occurs in only one letter of the DNA genetic

code. To date, scientists have identified more than 30

different point mutations in the P0 gene. As a result

of abnormalities in P0, CMT1B produces symptoms

similar to those found in CMT1A. The gene defect that

causes CMT1C, which also has symptoms similar to those

found in CMT1A, has not yet been identified.

 

CMT2 is less common than CMT1 and results from

abnormalities in the axon of the peripheral nerve cell

rather than the myelin sheath. Recently a mutation was

identified in the gene that codes for the kinesin

family member 1B-beta protein in families with CMT2A.

Kinesins are proteins that act as motors to help power

the transport of materials along the train tracks

(microtubules) of the cell. Another recent finding is

a mutation in the neurofilament-light gene, identified

in a Russian family with CMT2E. Neurofilaments are

structural proteins that help maintain the normal

shape of a cell. Genes that cause other forms of CMT2

have not yet been identified.

 

CMT3 or Dejerine-Sottas disease is a severe

demyelinating neuropathy that begins in infancy.

Infants have severe muscle atrophy, weakness, and

sensory problems. This rare disorder can be caused by

a specific point mutation in the P0 gene or a point

mutation in the PMP-22 gene.

 

CMT4 comprises several different subtypes of autosomal

recessive demyelinating motor and sensory

neuropathies. Each neuropathy subtype is caused by a

different genetic mutation, may affect a particular

ethnic population, and produces distinct physiologic

or clinical characteristics. Patients with CMT4

generally develop symptoms of leg weakness in

childhood and by adolescence they may not be able to

walk. The gene abnormalities responsible for CMT4 have

yet to be identified.

 

CMTX is an X-linked dominant disease and is caused by

a point mutation in the connexin-32 gene on the X

chromosome. The connexin-32 protein is expressed in

Schwann cells-cells that wrap around nerve axons,

making up a single segment of the myelin sheath. This

protein may be involved in Schwann cell communication

with the axon. Males who inherit one mutated gene from

their mothers show moderate to severe symptoms of the

disease beginning in late childhood or adolescence

(the Y chromosome that males inherit from their

fathers does not have the connexin-32 gene). Females

who inherit one mutated gene from one parent and one

normal gene from the other parent may develop mild

symptoms in adolescence or later or may not develop

symptoms of the disease at all.

 

Causes:

A nerve cell communicates information to distant

targets by sending electrical signals down a long,

thin part of the cell called the axon. In order to

increase the speed at which these electrical signals

travel, the axon is insulated by myelin, which is

produced by another type of cell called the Schwann

cell. Myelin twists around the axon like a jelly-roll

cake and prevents dissipation of the electrical

signals. Without an intact axon and myelin sheath,

peripheral nerve cells are unable to activate target

muscles or relay sensory information from the limbs

back to the brain.

 

CMT is caused by mutations in genes that produce

proteins involved in the structure and function of

either the peripheral nerve axon or the myelin sheath.

Although different proteins are abnormal in different

forms of CMT disease, all of the mutations affect the

normal function of the peripheral nerves.

Consequently, these nerves slowly degenerate and lose

the ability to communicate with their distant targets.

The degeneration of motor nerves results in muscle

weakness and atrophy in the extremities (arms, legs,

hands, or feet), and the degeneration of sensory

nerves results in a reduced ability to feel heat,

cold, and pain.

 

The gene mutations in CMT disease are usually

inherited. Each of us normally possesses two copies of

every gene, one inherited from each parent. Some forms

of CMT are inherited in an autosomal dominant fashion,

which means that only one copy of the abnormal gene is

needed to cause the disease. Other forms of CMT are

inherited in an autosomal recessive fashion, which

means that both copies of the abnormal gene must be

present to cause the disease. Still other forms of CMT

are inherited in an X-linked fashion, which means that

the abnormal gene is located on the X chromosome. The

X and Y chromosomes determine an individual's sex.

Individuals with two X chromosomes are female and

individuals with one X and one Y chromosome are male.

In rare cases the gene mutation causing CMT disease is

a new mutation which occurs spontaneously in the

patient's genetic material and has not been passed

down through the family.

 

 

Teatment:

There is no cure for CMT, but physical therapy,

occupational therapy, braces and other orthopedic

devices, and even orthopedic surgery can help patients

cope with the disabling symptoms of the disease.

 

Physical and occupational therapy, the preferred

treatment for CMT, involves muscle strength training,

muscle and ligament stretching, stamina training, and

moderate aerobic exercise. Most therapists recommend a

specialized treatment program designed with the

approval of the patient's physician to fit individual

abilities and needs. Therapists also suggest entering

into a treatment program early; muscle strengthening

may delay or reduce muscle atrophy, so strength

training is most useful if it begins before nerve

degeneration and muscle weakness progress to the point

of disability.

 

Stretching may prevent or reduce joint deformities

that result from uneven muscle pull on bones.

Exercises to help build stamina or increase endurance

will help prevent the fatigue that results from

performing everyday activities that require strength

and mobility. Moderate aerobic activity can help to

maintain cardiovascular fitness and overall health.

Most therapists recommend low-impact or no-impact

exercises, such as biking or swimming, rather than

activities such as walking or jogging, which may put

stress on fragile muscles and joints.

 

Many CMT patients require ankle braces and other

orthopedic devices to maintain everyday mobility and

prevent injury. Ankle braces can help prevent ankle

sprains by providing support and stability during

activities such as walking or climbing stairs.

High-top shoes or boots can also give the patient

support for weak ankles. Thumb splints can help with

hand weakness and loss of fine motor skills. Assistive

devices should be used before disability sets in

because the devices may prevent muscle strain and

reduce muscle weakening. Some CMT patients may decide

to have orthopedic surgery to reverse foot and joint

deformities.

 

Ongoing research includes efforts to identify more of

the mutant genes and proteins that cause the various

disease subtypes, efforts to discover the mechanisms

of nerve degeneration and muscle atrophy with the hope

of developing interventions to stop or slow down these

debilitating processes, and efforts to find therapies

to reverse nerve degeneration and muscle atrophy.

 

One promising area of research involves gene therapy

experiments. Research with cell cultures and animal

models has shown that it is possible to deliver genes

to Schwann cells and muscle. Another area of research

involves the use of trophic factors or nerve growth

factors, such as the hormone androgen, to prevent

nerve degeneration.

 

Source: U.S. National Institute of Neurological

Disorders and Stroke and the Muscular Dystrophy

Association

 

Pranic Healing:

 

1. Invoke and scan before, during and after

treatment.

 

2. General sweeping several times.

 

3. Localized through sweeping on the front and back

solar plexus and the liver alternately with LWG and

LWO. Energize with LWG, LWB and LWV. Apply more

localized sweeping.

 

4. Localized sweeping on the brain, the forehead

chakra, crown chakra, ajna chakra and the back head

minor chakra. Energize the chakras with LWG and more

of ordinary LWV.

 

5. Localized thorough sweeping on the throat and

throat minor chakras. Energize with LWG and more of

ordinary LWV.

 

6. Localized thorough sweeping on the spine and both

sides of the spine. Start from the base of the back

of the head to the end of the tailbone with LWV.

Visualize the energy penetrating into the spinal

column and nerves.

 

7. Localized thorough sweeping on the thymus gland,

the front and back heart chakra. Energize the heart

chakra through the back heart with LWG and more of

ordinary LWV. Visualize the energy going through the

back heart making the heart chakra brighter and

bigger.

 

8. Localized thorough sweeping on the navel, sex and

perinium minor chakra. Energize them with LWR.

 

9. Localized thorough sweeping on the armpits, both

arms, hands, hips, both legs, and the feet with

emphasis on their minor chakras alternately with LWG

and LWO. Energize the chakras with LWR then with LWV.

 

10. Localized thorough sweeping on the front and back

spleen. Do not energize.

 

11. Scan the basic and meng mein chakra frontally and

sideways.

 

The normal size of the meng mein chakra is 1/2 to 2/3

of the average size of the other major chakras.

 

12. Localized thorough sweeping on the basic chakra.

Energize the basic chakra with LR or LWR. You may

simultaneously visualize the chakra to increase its

size to 1 to 2 inches bigger in diameter.

 

13. Localized thorough sweeping on the meng mein

chakra.

Energize with LR or LWR.

Do no visualize the meng mein becoming bigger; it will

pulsate and rotate faster even without visualizing it.

 

14. Rescan frontally and sideways the basic and meng

mein chakras. Get feedback from patient.

 

If the patient feels dizzy or experiences pain at the

back of the head, immediately apply localized sweeping

from the back of the head to the tail end of the

spine. Apply thorough sweeping on the basic and the

meng mein until the patient is relieved.

 

You may tone down steps 12 to 14 by using white to

energize the basic and the meng mein chakras. Steps

12 to 14 may be used with the precautions listed on

pp. 102-103 of the Advanced Pranic Healing by Master

Choa Kok Sui.

 

15. Apply distributive sweeping several times in

front and back.

 

16. Stabilize and release projected energy.

 

17. Repeat treatment 3 times per week.

 

 

Recommend for patient:

 

1. Daily proper practice of the Meditation on Twin

Hearts and blessings. This is maybe done individually

or together as a family.

 

2. Regular bath in warm salt water solution.

 

3. Balanced healthy nutritious diet. Regular

physical exercise and/or physiotherapy.

 

4. Engage in normal enjoyable activities.

 

5. Do regular service for the good of others and

tithing.

 

6. Character-building.

 

Love,

 

Marilette.

 

 

 

 

 

 

=====

Pranic Healing is not intended to replace orthodox medicine, but rather to

complement it. If symptoms persist or the ailment is severe, please consult

immediately a medical doctor and a Certified Pranic Healer . ~ Master Choa Kok

Sui

 

Miracles do not happen in contradiction to nature, but only to that which is

known to us in nature. ~ St. Augustine

 

Ask or read the uptodate pranic healing protocols by joining the group through

http://health./

 

For the latest International Information regarding GMCKS Pranic Healing, visit

http://www.pranichealing.org.

 

 

 

Finance: Get your refund fast by filing online.

http://taxes./filing.html