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of conduction in human nerve fibers.
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The cause of autoimmune disease is
uncontrolled
inflammation, this inflammatory reaction in limited to a particular
group of cells only.
In alzheiners the neurons in the brain are affected. In Thyroditis the
thyroid gland is inflamed. In vasculitis the blood
vessels are inflamed. In Fibromyalgia the fibrous covering
around the muscles is affected. In CIDP & Multiple Sclerosis
the Myelin around the nerves is a target and
destruction of Myelin
If you are wondering what is inflammation. The
answer is all of us have a built in protective force or army
called the immune system. In rare cases a invader comes
(bacteria, bug, virus, chemical) . This invader will induce
a immune attack, in some invaders proteins resemble the
human tissue. Any attack that takes place on the invader
will mistakenly attack similar human tissue. That is a autoimmune
inflammatory disease.
Each cell in our body is programmed to live for
a certain time. They will perform cellular suicide when the
time comes. Our antiageing treatments are based on re
programming the cycle of aptosis.
In CIDP our own Immune System
turns on to attack the Myelin around the nerves. If the
attack is on peripheral Myelin around the nerves in arms and
legs it is called CIDP or Guilliane Barre Syndrome. If the
attack is targeting central Myelin located in the brain or
spinal cord then the diseases is called Multiple Sclerosis.
Suppose the attack is against both central and peripheral
Myelin then the disease it will be called ALS or Lugaric
disease. In CIDP nerves can be attacked in any part of the
body, eye, ears, throat, stomach, heart but the treatment
remains the same.
The treatments that CIDPUSA recommends are simple and
inexpensive, directed against the attacking organism in the
particular disease. All the treatments are available in our
autoimmune E.Book, " the flame within". The treatments
are from University studies all over the world. No medical center in the
Western world is aware of all these treatments. A few
specialty clinics in the USA do offer these treatments in
the field of rheumatology. Nanotech Lahore facility became
the first Medical center to adopt all these treatments. cIf you need the name of the clinics
which practice these methods please contact us , we do
charge $10 TO GIVE YOU THE NAMES OF THOSE DOCTORS.
W e have written complete treatment guidelines of all
autoimmune disorders in our E-Book .
Chronic Inflammatory
Demyelinating Polyradiculoneuropa
What
is Autoimmunity:
Autoimmune
disease occurs when the immune system initiates a specific
response against a self protein . The response of
the immune system is misdirected and results usually after
exposure to infecting organisms or chemical toxins.
Autoimmune diseases
result from a dysfunction of the immune system in which the
body attacks its own organs, tissues, and cells. Physicians
and scientists have identified more than 80 clinically
distinct autoimmune diseases. Several are well known,
including rheumatoid arthritis, multiple sclerosis, type 1
diabetes, and systemic lupus erythematosus; others are less
familiar, including autoimmune hepatitis, Sjögren’s
syndrome, autoimmune ear disease, and pemphigus.
Collectively, these diseases afflict millions of Americans,
an estimated 5 to 8 percent of the population – 14 to 22
million persons. The social and financial burdens imposed by
these chronic, debilitating diseases include poor quality of
life, high health care costs, and substantial loss of
productivity. We have calculated that autoimmune diseases is
the number one diseases process in the world, the main cause
of ageing and the number one killer of animals and humans on
planet earth.
CIDPUSA has done
20 years of research and produced a
autoimmune diseases prevention e-book our Bestseller.
Written by Dr
Imran Khan
Introduction
to CIDP:
CIDP is an autoimmune disease, which
affects the motor and sensory nerves by destroying the
myelin sheaths surrounding the nerves. The myelin sheath
is a fatty covering acting as an (insulator which helps
conduction) to the fibers of nerves. Myelin wraps around
the axon and helps electrical current flow down the axon
(just like wrapping tape around a leaky water hose would
help water flow down the hose).
Above is a illustration of how Myelin is
wrapped around the axon. This protects the axon and
helps in electrical conduction in the nerve. Below is an
example of how electrical impulses travel in a nerve.
However, the myelin insulation does not
cover the entire axon. Rather there are breaks in the
wrapping. These breaks are called
nodes of Ranvier. The distance between these
nodes is between 0.2 and 2 mm. Action potentials
traveling down the axon "jump" from node to node. This
is called saltatory conduction
which means "to leap". Saltatory conduction is a faster
way to travel down an axon than traveling in an axon
without myelin
See a example of salutatory conduction shockwave needed.
(opens in a new window).
See a video of conduction in a nerve. (opens in a
new window
Saltatory conduction. Nerve
impulses move quickly by jumping from node to node.
When portions of the myelin sheath are destroyed, the
message must travel via the axon which is less efficient
and slower as compared to the jumping currents of
salutatory conduction.
 Myelin sheath under a microscope. Other
then CIDP & GBS, Polio & Leprosy damages myelin in
peripheral nervous system .
Multiple sclerosis damages myelin in the central nervous
system. Schwann cell makes myelin in the PNS (Nerves).
Oligodendrocyte makes myelin in the CNS (Brain).
Without this covering, nerves lose the
ability to transmit electrical impulses from the brain
to the muscles. There is evidence that the inflammation
of this neural tissue is caused by the autoimmune
process to the sheath of the nerves. CIDP is thought to
be the chronic variety of Guillain-Barre Syndrome (GBS).
There are two types of CIDP: chronic progressive, and
relapsing. In chronic progressive patients, the disease
gradually worsens over time. Relapsing patients show
recurrent attacks with some improvement between attacks.
This disease is characterized by progressive
weakness and loss of neurological function in the legs and
arms. Most patients with this disorder present with a case
of progressive weakness for months. The course of the
disease is characterized by periods of relapses and
remissions. CIDP is slightly more prevalent in young adults,
it can occur at any age, and statistics show that men are
twice as likely as women to contract this disease. Some
typical symptoms include: symmetric tingling in the proximal
and distal extremities, weakness or paralysis of the
muscles. The onset is gradual over the course of at least 8
weeks. Statistics show that 70% of patients diagnosed with
CIDP presented with only sensory symptoms later developed
motor symptoms over the course of 2-3
years.
Figure 2: This figure shows a
representation of a demyelinated nerve
A. Demyelination at the paranodal region
(solid arrow). Arrow head points to the node of Ranvier.
B. Demyelination of a nerve segment (solid
arrow) between the two nodes of Ranvier (arrow heads). This
finding is frequently observed in the nerve biopsy of CIDP.
How is it
related to the immune system?
The main reason CIDP is considered an immune
disorder is that it because inflammation is seen in the
nerve tissue, anti inflammatory treatment helps this
condition. It is very difficult to diagnose and can be
diagnosed through a number of methods which are discussed
below. Although the etiology remains unknown, both humoral
and cell-mediated immune mechanisms contribute to the
pathogenesis. Immune or inflammatory mechanisms are thought
to be the root cause of many disorders that, like CIDP,
reflect damage to the peripheral nerves and affect sensory
function. This turns out to be the most definite role of the
immune system in the development of CIDP; the mutation of
the macrophage to cause macrophage-mediated inflammation,
ultimately resulting in the demyelination of the nerves.
Another characteristic of CIDP, which leads to its
classification as an autoimmune disorder, is the evidence of
preexisting infections immediately prior to the development
of the disease in a significant number of patients. Studies
show that in 70% of GBS patients (Guillain-Barre Syndrome),
the acute form of CIDP, have pre-existing infections prior
to the development of symptoms. Although the pathology of
the infections preceding CIDP are studied less frequently,
statistics show that at the very least relapses are strongly
correlated with infection .
The specific pathway for induction of the
autoimmunity associated with CIDP is unknown. The current
research cannot eliminate the possibility of an antibody
mediated self-reactivity or a T-cell mediated self
reactivity. The possibility that infection is a possible
stimulus to the development of CIDP can support either
pathway. Infections are capable of inducing co-stimulatory
activity on antigen presenting cells that present low levels
of the specific peptide being attacked, in this case myelin.
Another pathway is that of molecular mimicry. In this
situation, antibodies or T-cells generated in response to an
infectious agent cross-react with self antigens. A molecular
mimic is a foreign antigen closely related in structure to a
self peptide allowing an antibody mediated response mounted
toward the mimicked peptide to also effect the self-protein
.
What
components of the immune system are involved?
T-Cells:
The most widely explained
mechanism for the demyelination of nerve cells in CIDP is a
macrophage-mediated inflammatory response. Endoneurial
inflammatory changes with T cell infiltrates and macrophage
associated demyelination are present on nerve biopsies in
patients in the acute phase of CIDP (Mahad, et al,
2002). These endoneurial lymphocytes are associated with the
increase expression of mRNA for Tumor Necrosis Factor alpha
(TNF alpha), Interferon gamma (INF gamma) and Interluekin-2
(IL-2) (Mahad, et al, 2002).. TNF alpha is involved
in local inflammation and endothelial activation. INF gamma
causes macrophage activation, increased expression of MHC
molecules and Ig class switching. INF gamma also suppresses
the less damaging TH2 response in favor of the inflammation
mediation of TH1. IL-2 is a crucial chemokines for the
adaptive immune response and aids in the proliferation of
T-cells. All of these proteins are either produced by
T-cells, Natural Killer Cells or Macrophages, or add to the
existence of T-cells and cause the initial inflammatory
response associated with infection (Janeway, 2001).
Activated T lymphocytes are increased in the peripheral
blood of CIDP patients. This diagnostic evidence coupled
with the relative success of T-cell suppressive treatment
makes the case for a possible malfunction in the TH1
inflammatory response.
Antibodies and Complement:
These components of the
immune system play a role in the pathogenesis of CIDP in the
presence of a blood-nerve barrier breakdown. (after the
demyelination has begun)
The current research debates
whether CIDP is associated with a specific antibody response
against neural antigens (van Doorn, 2000). Antibodies
against selected neuroblastoma cells have been found in 40%
of patients with CIDP and GBS in comparison with only 4% in
other neuropathies (van Doorn, 2000). This, however, is far
from conclusive as to the direct pathology of the disease,
as other groups show no antibody interaction with myelin
proteins or glycolipid cell-surface receptors (van Doorn,
2000).
Some forms of CIDP can be
diagnosed using autoantibody serums to tubulin. Tubulin is a
molecule which mediates many cell processes specifically
cell division and movement of materials within cells. The
suggested mechanism for the autoantibody to tubulin involves
both IgG and IgM antibodies capable of binding to the
tubulin epitope. This pathology was present in 10% of
patients with CIDP (Washington University, 2003).
Another specific immunologic
interference occurring in 26% of patients with CIDP is an
interaction between IgG antibodies and Schwann cell
processes. Schwann cells are the cells that wrap themselves
around nerves making a protective barrier for the nerve
fibers. Schwann cells are the individual cells making up the
myelin protective sheaths. This suggests that a patient
presenting with symptoms of CIDP could possibly have an
autoantibody response against cell schwann cells. This
response tags the self-protein for natural killer cell
destruction.
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