Hello Kenderfox,
I am answering the question because of my own personal experience as
having either multiple sclerosis, lyme disease that has disseminated
to my neurological system, a combination of both (MS being a result of
Lyme, where the theories are now headed), or some other multi-focal
neuropathy. The amount of medical knowledge that I have amassed as a
result of this horrendous experience is ridiculous...and it angers
doctors, lest I actually know more than they do on several occasions!
While the mode in which I respond to most medical questions on Google
Answers is by mostly citing medical sources like journals, you have
made it clear that you want it broken down "Barney Style" (I'm going
to steal that phrasology from you, if that's okay), so I will ask that
you allow me to serve as your credible source, as any medical journal
or text to which I may refer you will only be filled with more arcane
medical jargon to confuse (and scare) you even more.
I will start this by breaking down the stupid medical terminology:
Multifocal:
This means that your father is NOT experiencing an isolated lesion
(inflammation) of the central or peripheral nervous system. His case
is presenting as many different areas of inflammation, occurring at
different times. For instance, on an MRI report for this, one might
read: "Multiple foci..." Foci being the place of inflammation.
Acquired: This means that, for whatever reason, what your father is
experiencing is not a result of some inherent genetic defect. He has
acquired this demyelinating process from a reason that is OUTSIDE of
his own body....now, that does NOT in any way mean that he has
contracted (caught) this from someone, like the term has come to be
stereotyped due to AIDS (as an Acquired Immune Deficiency Syndrome).
Rather, the term "acquired" in the medical realm has most commonly
come to refer to something that happens in the body as a result of
some environmental factor (stress, exposure to chemicals, pollution,
even a chronic unknown allergy that has caused the body to turn on
itself because it simply could not fight the invader any longer).
Demyelinating: Every nerve cell in our body is coated with a
protective sheath, called "myelin,? which is a fatty substance made up
of essential fatty acids, lipids, lecithin, etc?ALL GOOD THINGS FOR
YOUR DAD TO START TAKING, TODAY! When areas of the central or
peripheral nervous system inflame, the body rushes white blood cells
to that site in an effort to heal. Well, thanks, but no thanks,
because when they do that, and the body begins to heal that area, it
leaves scar tissue, which permanently impedes the signal from getting
through. Important: This doesn?t always happen. Just like a cut or
a scab on the outside of the body, a scar doesn?t always form! I have
had about 50 attacks to date (yeah, literally), and I have yet to have
any residual effects from any of it.
Okay, I cannot believe that I am about to refer you to a Walgreen?s
Web site, but they have a VERY comprehensive image of the myelin
sheath, and how it becomes frayed and damaged when that area inflames.
Go to: http://www.walgreens.com/library/health_topic/topic.jsp?docId=DS00188&alpha=M
In the middle of the page, there is a picture, click on that, and you
shall see the mechanism responsible. Remember, Myelin is just?.the
sheath. DE-myelinating means that the sheath is fraying or becoming
damaged. The simplest way to think of this is to think of each of our
nerve cells as an electrical cord. Ever have a dog or cat chew on the
cord? I sure have. When they do that, the plastic sheath becomes
damaged, and the signal is impeded from reaching its destination (in
your dad?s case, both his motor and sensory nerve tracts are being
affected, so this may mean that his brain will tell his arm to ?LIFT,?
but his arm won?t get the memo, or in the case of sensory, he may feel
an ice cube on his leg, and even though he knows it?s a damn ice cube,
that?s cold, his frayed wiring may communicate that message to his
brain as a hot sensation?.it?s weird, I know).
Sensory:
The sensory nerve tract is responsible for all things related to our
sense?.in the case of individuals who are demyelinating, this usually
entails experiencing a sensation of pins and needles, numbness, mixed
up hot/cold perception, pinprick sensations at random times (they
don?t hurt, it?s just like having one of the pins from the pins and
needles feeling when your leg falls asleep after sitting on it wrong).
Sensory disturbances can also include visual issues like double
vision, optic neuritis (color perception gets a little dodgy, though
usually only in one eye), hearing things like tinnitus (ringing), a
sensation of ear numbness, etc. The sensory system is a complete
mystery to most doctors, and many times, people with these issues will
experience sensations that doctors have never even fathomed?.like the
sensation of cold water and wet feathers tickling the top of the foot.
And?
Motor:
The motor nerve tract controls movement, both voluntary (arm, LIFT!)
and involuntary (heartbeat, swallowing, digestion, etc). When these
nerve sheaths become frayed (or demyelinate), weakness occurs. It?s
as simple as that.
I hope that the means by which I have broken down the terminology has
shed some good insight on your father?s condition. I will now move on
to speak specifically on the mechanism of MADSAM as a disorder,
unfortunately citing sources that may be chock-full of medical
terminology?if you have any questions at all, request clarification,
please!!!
According to www.neuro.org.tw/magpdf/13-1P24.PDF:
Multifocal acquired demyelinating sensory and motor (MADSAM)
neuropathy is characterized
by an asymmetric multifocal pattern of motor and sensory loss, and
conduction block and other features of
demyelination in nerve conduction studies. MADSAM neuropathy needs to
be differentiated from chron-
ic inflammatory demyelinating polyneuropathy (CIDP) and multifocal
motor neuropathy (MMN). In clas-
sic CIDP, there are symmetric proximal and distal weakness, sensory
deficit in both upper and lower
extremities and reduced deep tendon reflex. In MMN, limb weakness
without sensory loss is asymmetric
in the distribution of individual peripheral nerves and the weakness
typically begins in the distal upper
extremities. We report one patient with chronic progression of
asymmetric numbness and weakness in four
extremities. MADSAM neuropathy was diagnosed after extensive clinical
and laboratory evaluations. It is
very important to distinguish between CIDP, MADSAM neuropathy, and MMN
by clinical, laboratory, and histological features because of
different effective therapeutic strategies.
What they are saying here that I haven?t yet explained is that MADSAM
is an asymmetric disorder, meaning that it symptomology does not take
place in the same place of the body on both sides. Your dad is not
going to feel his symptoms symmetrically. That?s easy to understand
why: The left hemisphere of the brain controls the right side, and
vice versa. When areas of inflammation occur, they don?t follow the
rules of Algebra, ?What you do to one side, you must do to the other.?
Nope. It?s choice of inflammation areas are completely
unmathematical. Just?.whatever looks good to inflame.
They are also stating that it is IMPERATIVE that MADSAM be
distinguished from other, seemingly very similar, disorders, like
multifocal motor neuropathies (MMN). Can you guess one of the two
differences? MMN only affects the motor system, while MADSAM affects
both the sensory and motor tracts.
The other difference is one that is QUITE advantageous to your father:
MADSAM IS EXTREMELY responsive to therapy?MMN is NOT.
Here is an excerpt of an article differentiating the two, that also
speaks of therapy responsivity:
?Currently there are a num-ber of entities that can be put under the
heading of chronic acquired demyelinating neuropathy (CADP) based on
differing clinical presentations. In this scheme, CIDP is used only to
refer to patients with demyelinating neuropathies and generalized
symmetric weakness. In contrast, multifocal motor neuropathy (MMN) and
multi--focal acquired demyelinating sensory and motor neuropathy
(MADSAM) fall into the -category of asymmetrical, multifocal forms of
CADP. These are distinguished from each other only by the presence of
sensory involvement. In our opinion, there are pragmatic reasons for
splitting these clinical presentations into distinct entities.
Although each of these clinical subtypes shares some basic
similarities, there are important differences. MMN is usually
considered resistant to corticosteroid therapy and the first line
agent in this disorder is intravenous immunoglobulin (IVIg). -MADSAM
neuropathy can be responsive to prednisone or IVIg, and has a profile
more analogous to classic CIDP with regards to its laboratory features
and treatment response.?
(source: http://www.biomedcentral.com/1092-8480/3/119/abstract)
What your father has is also referred to as the Lewis-Sumner Syndrome,
named after the docs who discovered it as a variant of a CIDP.
?MADSAM neuropathy more closely resembles chronic inflammatory
demyelinating polyneuropathy and probably represents an asymmetrical
variant.?
(source: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10331353&dopt=Abstract)
Therefore, I think that it would be beneficial for you to read as much
as you can about CIDP, since there is A LOT more published on it.
Here are some links:
http://www.cidpusa.org/index.html
Here is a link to all of the articles the government has listed on Lewis Sumner:
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?CMD=search&DB=pubmed
Treatment:
Good news, right? Okay, here are some links to options:
http://www.cidpusa.org/treatment.html (oooh! That might be an even
better diagram of the nerve sheath!)
http://www.noridianmedicare.com/provider/pubs/med_a/policy/final/ak_wa/a2005_07.html
http://www.blackwell-synergy.com/doi/abs/10.1111/j.1600-0404.2005.00448.x
In sum, IVIG + Prednisone is prime for MADSAM?..
You might want to also look into cortocosteroids from short term
relief, as they are anti-inflammatory in nature.
Anything that induces an inflammatory response in the body should be
avoided at all costs (I await the onslaught of criticism from people
in the pharmaceutical or medical industries?bring it on, baby!), like
coffee. Also things that run the risk of inducing an inflammatory
response (beef, dairy, etc) should also be avoided. He should look
into getting a comprehensive allergen analysis, so he can increase his
chances of not inflaming.
As for natural anti-inflammatories:
Omega-3 essential fatty acids. Found in fish oils, EPA and DHA are
essential building blocks for the body's anti-inflammatory
prostaglandins (e.g., prostaglandin E1) and for turning off Cox-2 and
the body's proinflammatory cytokines (IL-1, IL-6, and TNFa). In
addition, omega-3 fatty acids block the activity of an enzyme that
breaks down joint cartilage. Daily dosage: 3 or more grams.
? Gamma-linolenic acid. Although GLA is an omega-6 fatty acid, it has
antiinflammatory properties. Relatively little GLA is converted to
arachidonic acid and prostaglandin E2. Instead, GLA increases
production of the antiinflammatory prostaglandin E1. Robert B. Zurier,
M.D., of the University of Massachusetts Medical Center, Worcester,
gave GLA supplements or placebos to 41 patients with rheumatoid
arthritis. Two-thirds of those receiving GLA had a 25 percent
reduction in their arthritic symptoms. Daily dosage: 2-3 grams.
? Vitamin E. Although Cox-2 and prostaglandin E2 levels rise with age,
animal studies have shown that vitamin E supplements reverse the
increase in Cox-2 and prostaglandin E2. Vitamin E also turns off
nuclear factor-kB (NF-kB) and activator protein-1 (AP-1), compounds
that turn on inflammatory genes. One recent study found that
arthritics taking supplements of natural vitamin E (600 mg twice
daily) for 12 weeks had their pain reduced by about half. Daily
dosage: 400-800 IU.
? Vitamin C. Long recognized for its anti-inflammatory properties, the
effects of vitamin C are enhanced by other nutrients. In a study of
people exposed to simulated sunlight, researchers found that vitamin C
and E worked synergistically to reduce skin inflammation. In a cell
study, Italian researchers noted that quercetin and vitamin C worked
together to protect cells from inflammation-induced damage. Daily
dosage: 1,000-2,000 mg.
? Polyphenols and Flavonoids. Researchers at Case Western Reserve
University, Cleveland, recently reported that the antioxidant
polyphenols in green tea had antiinflammatory properties by inhibiting
Cox-2 and TNFa. Genistein inhibits prostaglandin E2 and Cox-2, and
quercetin inhibits the activity of inflammation-promoting "adhesion"
molecules. It's likely that Pycnogenol, grape seed extract, and other
flavonoids work through similar mechanisms. Daily dosage: 25-500 mg.
? St. John's wort. Better known for its antidepressant effect, this
herb also has anti-inflammatory properties. In a laboratory
experiment, researchers from the University of Frieburg, Germany found
that hypericin, one of the constituents of St. John's wort, inhibited
NF-kB, which activates proinflammatory genes. Daily dosage: Because
product forms vary, follow label directions.
? Silymarin. A cell-culture study found that silymarin, the
antioxidant extract of milk thistle, inhibited Cox-2 formation. This
role of silymarin may partly explain why earlier cell-culture studies
found it to inhibit the growth of prostate, breast, and skin cancers.
Daily dosage: 100-200 mg.
? Ginger. With a long history as a folk medicine, ginger inhibits
Cox-2 and another proinflammatory compound, 5-lipoxygenase. This
simple herb and condiment contains almost 500 different compounds,
many of which are antiinflammatory, according to Thomas M. Newmark and
Paul Shulick, authors of Beyond Aspirin: Nature's Answer to Arthritis,
Cancer & Alzheimer's Disease (Holm Press, Prescott, Arizona, 2000).
Daily dosage: 100 mg.
? Rosemary. This common kitchen herb is rich in ursolic acid and many
of its derivatives. In laboratory experiments, Swedish researchers
found that the ursolic acid extract of rosemary was a potent inhibitor
of Cox-2 activity. Daily dosage: 100 mg.
? Curcumin. A natural pigment that accounts for the yellow color of
the spice turmeric, curcumin is also a powerful antioxidant. A recent
cell study by researchers at Cornell University, New York, found that
curcumin blocked the activity of Cox-2. The researchers suggested that
this property might explain some of the herb's anticancer effects.
Daily dosage: 2.8 mg.
? Cat's Claw. Known as una de gato and Uncaria tomentosa, this
Peruvian herb has a long history as a remedy for inflammatory
arthritis. Recent cell-culture and animal experiments at the Albany
Medical College, New York, found that cat's claw inhibited
inflammation by blocking the activity of NF-kB. Daily dosage: Because
products vary, follow label directions.
(source: http://www.thenutritionreporter.com/remedies_for_inflammation.html)
I hope, dear Kenderfox, that my answer has been of great use to you.
If for any reason, you are confused by any of the concepts, PLEASE ask
me for clarification. I am willing to continue to help you in
whatever way I can.
Oh, and please, don't be alone. Join messageboards, read, read,
read...the best way to combat a disease is to arm yourself with
knowledge. Doctor, heal thyself! :)
Peace Be With You and Your Father.
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