This Is MS Multiple Sclerosis Knowledge & Support Community

kaliej wrote:There are many other centers other centers available on the internet.Why don't people go for others?

Liberation wrote:Neurologists told me that currently they believe that in spms and ppms autoimmunity is not the primary culprit, eventhogh if it is there. Probably, this is the reason why they do not give any immunmodulatory drugs for ppms patients.

CVfactor wrote:So in RRMS the main target is the Myelen sheath (white matter) while there may be some secondary damage to the axons. The white matter damage is what shows up on MRI's as lesions.

In SPMS and PPMS the main damage is to axons (grey matter).

So, my question is that if either type of MS is not autoimune why are not the other structures of the neuron such as the cell body (soma) effected. Why is it that only specific areas of the neuron are targets?

[color=blue]WebMD[/color] wrote:Gray Matter: Those regions of the brain and spinal cord that are made up primarily of the cell bodies and dendrites of nerve cells rather than myelinated axons.

CVfactor wrote:

Liberation wrote:Neurologists told me that currently they believe that in spms and ppms autoimmunity is not the primary culprit, eventhogh if it is there. Probably, this is the reason why they do not give any immunmodulatory drugs for ppms patients.

I often hear this a lot on this site. But lets look at a Nueron:



So in RRMS the main target is the Myelen sheath (white matter) while there may be some secondary damage to the axons. The white matter damage is what shows up on MRI's as lesions.

In SPMS and PPMS the main damage is to axons (grey matter).

So, my question is that if either type of MS is not autoimune why are not the other structures of the neuron such as the cell body (soma) effected. Why is it that only specific areas of the neuron are targets?

Glial cells serve nerve cells by insulating them with layers of fats and proteins called myelin. Myelin coatings are necessary for nerve signals to be transmitted normally; when the sheaths are lost, disorders involving impairment in sensation, movement and cognition such as multiple sclerosis or amyotrophic lateral sclerosis develop. Glial cells named oligodendrocytes produce myelin around nerves of the central nervous system, while those named Schwann cells make myelin that insulates peripheral nerves.

I'm still not sure if there's any sort of connection between MS & HNPP, although my family's situation raises intriguing questions.

HNPP means that MY peripheral nerves are unable to handle physical stress to them due to a missing myelin gene. Some other "named" peripheral neuropathies, such as CIDP, sound more like inflammation caused by other reasons, such as viruses, etc.

Also, just for the sake of background information in this discussion, I should have mentioned that the myelin in the CNS (brain & spinal cord) is made up of oligodendrocytes, whereas the myelin covering of the peripheral nerves (all other nerves in the body) is from Schwann cells instead.

So, my LP shows that I have both O-bands in my spinal fluid (plus whatever else they look for) and the extensive round of EMGs they gave me (I call it The Day of the Long Needles ) show I have carpal tunnel in both wrists & both elbows (at least). That's what puts the PP (Pressure Palsies) into HNPP. (I also have a brain that's Chock Full O' MS-specific Lesions, but who's counting at this point?)

My cousin with MS has had 2 unsuccessful carpal tunnel surgeries (possible HNPP), although my dad had a recent MRI of his brain showing only that he had, well, a "normal" 87-year-old brain. My dad, cousin, and I have footdrop, but my neuros shrug that there's no way to figure out whether my footdrop & hand tremors are due to MS or HNPP or both.

Also, FYI - both the "named" PNs like CIDP & HNPP and also the generic, unnamed PN condition can show remarkably similar symptoms to MS. Just check out the generic PN pages at Mayo: http://www.mayoclinic.com/health/periph ... hy/DS00131

The term "peripheral neuropathy" in general just refers to a group of symptoms within the PNS, which includes the sensory nerves, muscles, and organs, affecting things like bowel & bladder issues as well. PN can be the result of genetics (me), diseases, vitamin deficiencies, etc., which is why I always feel obligated to remind undx'd sufferers (who don't test as well as I do ) of the possibilities.

Another note: HNPP is a malfunction of the same gene (missing part) as CMT, Charcot-Marie-Tooth (doubled gene), a much more common hereditary neuropathy. They're often mentioned together when you do research.

NHE wrote: For clarification...

[color=blue]WebMD[/color] wrote:Gray Matter: Those regions of the brain and spinal cord that are made up primarily of the cell bodies and dendrites of nerve cells rather than myelinated axons.

NHE

Multiple sclerosis (MS) is a chronic disease that is characterized by central nervous system (CNS) inflammation, demyelination, and neurodegeneration. Although the pathophysiology of MS is not completely understood, it is clear that much of the underlying disease process is clinically silent and continues even when patients are not experiencing symptoms. Most patients initially present with relapsing/remitting MS, in which acute disease episodes are separated by a return to normal or near-normal neurologic function. Eventually, most patients transition to secondary progressive MS, which is defined by the gradual accumulation of irreversible neurologic impairment. A consensus has recently begun to emerge that the long-term progressive disability in patients with MS is due to irreversible neurodegeneration, and that inflammation is less prominent in the later stage of the disorder. MS lesions exhibit extensive axonal transection and degeneration, and may involve both gray matter and white matter. Demyelination alone does not appear to cause axonal injury, and most axons survive transitory demyelination. However, axons that are chronically demyelinated are at substantial risk of degeneration. This may reflect the loss of important nerve growth factors that are produced by surrounding oligodendrocytes and that are essential for axonal survival. The gradualaccumulation of axonal injury probably contributes to the long-term atrophy of the CNS that is often observed in patients with chronic MS, and to the eventual progression of neurologic impairment. Early initiation of disease-modifying therapy may therefore help to slow long-term neurodegeneration and disease progression in patients with MS. (Adv Stud Med. 2009;9(2):37-41)