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Very simple and understandable explanation of MS...

Dec 08, 2008 - 3 comments

Multiple Sclerosis

Multiple Sclerosis (MS) is an acquired inflammatory, demylenating disease of the Central Nervous System (CNS). MS is a leading cause of disability in young adults. It strikes people in the prime of their lives, usually between 20 and 40 years of age. It is estimated that more than 400,000 individuals, two-thirds of whom are female, in the United States are afflicted by the disease, at a national cost of nearly $10 billion per year.

In MS, cells of the immune system invade the CNS and destroy myelin (the fatty material that insulates the neurons in the brain and spinal cord), leading to demyelination of the axon and damage to the axon itself. In response, other CNS cells produce a hardened sclerotic lesion (plaque) around the multiple demyelinated sites. Not all lesions are associated with neurological dysfunction and, depending on their location, areas of demyelination may not cause clinical symptoms or signs. Such lesions are referred to as "silent lesions."

Etiology of MS

The cause of MS remains unknown. Both genetic and environmental factors have been implicated in the disease. Some combination of genetic susceptibility and one or more environmental triggers appears to be the most likely explanation.

Clinical Features of MS
Sensory Problems:
Sensory complaints occur in 20-50% of patients and are often the earliest symptoms of MS that bring the patient to the doctor. Symptoms such as disturbances in feeling in the extremities or in the trunk occur because sensory pathways in the spinal cord are impaired. These disturbances, commonly called paresthesias, include tingling, crawling sensations, tight-band feelings, and feelings of swelling. Another common complaint is an electric sensation that goes down the back and legs with head and neck motion; this is called Lhermitte’s sign.

Optic Neuritis:

Optic neuritis occurs as the presenting symptoms in 15-20% of patients with MS. It rarely involves both eyes simultaneously, but may appear on one side followed by a later appearance on the other. Optic neuritis usually starts with blurred vision, which is followed by vision loss, most often in one spot (scotoma), but sometimes in the entire field of vision. Complaints often include dimming of vision, photophobia, and pain that is aggravated by eye movement.


Corticospinal tract involvement, particularly spasticity, occurs with the initial attack of MS in 30-40% of patients and is present in about 60% of patients with progressive disease. Spasticity occurs when opposing groups of muscles that are responsible for maintaining an upright posture, such as the calf, thigh, buttock, groin, and occasionally the back, contract and relax at the same time. Most patients complain of heaviness, stiffness, or pain in an extremity. Usually the legs are more involved than the arms.


Gait and balance disturbances are common in patients with MS and are the initial complaint in about 15% of cases. They are more common in patients with progressive disease, with 50% reporting extremity ataxia (shaky movements or unsteady gait) or intention tremors.

Bladder Dysfunction:

Bladder dysfunction, which occurs in almost two-thirds of patients within their disease course, can be a very disabling feature of MS. Symptoms include urinary frequency, urgency, hesitancy, and incontinence. Retention or the inability to empty the bladder completely increases the risk for, and the frequency of, urinary tract infection.

Bowel Dysfunction:

Constipation is common in patients with MS and is often aggravated by the patients’ reluctance to drink water because of associated urinary problems. Constipation can be prevented by adequate fluid intake and a high fiber intake. Fecal incontinence is less frequent and usually occurs from diarrhea resulting from other illness (laxative overdose or diet).


Fatigue, the single most common complaint of people with MS, is often one of the most debilitating symptoms. It occurs in as many as 75% of patients with MS and interferes with work or family and social life. Fatigue from MS commonly occurs late in the afternoon when the body and environmental temperature rise and often subsides in the early morning when temperatures fall. It can also occur as a result of over-activity or over-work. Relief of fatigue may be achieved by cooling off and resting.

Heat Sensitivity:

Heat is a common aggravating factor in MS. With a one-degree elevation in temperature, new symptoms may appear or old ones may reappear. The elevation in temperature may be due to environmental heat, fever from an infection, or exercise. Although heat does not bring on an attack, it is a good idea for patients with MS to stay indoors during the hottest part of a summer day and to avoid heat from sunbathing, saunas, or hot showers.

Cognitive and Emotional Dysfunction:

Cognitive and emotional changes are common in MS, affecting approximately one-half of patients with MS. Of this group, approximately 40% have mild dysfunction, and 10% severe dysfunction. There is controversy as to whether MS-related cognitive problems are a reaction to the emotional distress of the disease or are caused by the lesions themselves. The most common cognitive deficits involve memory, reasoning, verbal fluency, and speed of information processing. Cognitive dysfunction can significantly affect the patients’ employment or everyday activities, and it is important that these symptoms are discussed and treated.

Natural Course of MS

The natural course of MS is highly variable and it is impossible to predict the nature, severity, or timing of progression in a given patient; however, there are a few guidelines to follow. For instance, a patient with numbness or tingling (sensory problems) tends to have a better prognosis than those with spasticity or paralysis (balance or coordination problems). Another factor that influences prognosis is age of onset. Disease progression tends to be more rapid in patients who experience their first symptoms after age 40. Other factors predictive of rapid progression include male gender, frequent attacks, and burden of disease as detected by magnetic resonance imaging (MRI). The course of MS over the first 5 years can provide a clue to the progression of the disease over the next 10 years. In a series of patients, 90% of those with minimal disability 5 years after disease onset were still ambulatory at 15 years.

Classifications of MS

Clinically definite MS is further categorized according to disease course. Relapsing-remitting MS is characterized by symptoms that develop over a period of a few hours to a few days, followed by recovery and a stable course between relapses. Approximately 80% of patients are initially diagnosed with relapsing-remitting MS. Almost 50% of patients with relapsing-remitting MS eventually develop secondary-progressive (SP) MS characterized by gradual neurological deterioration with or without superimposed acute relapses. If there is continual disease progression from onset with only minor fluctuation the classification becomes primary-progressive (PP). PP-MS occurs in approximately 10% of patients, mainly those who are older than 40 years at onset. Progressive-relapsing MS, a rare form of the disease, is characterized by gradual neurological deterioration from the onset of symptoms and subsequent superimposed relapses.

Diagnosis and Treatment of MS

A diagnosis of MS should be confirmed by a qualified neurologist, who would subsequently recommend appropriate treatments accordingly.

Realistic Expectations

Despite being told that none of these drugs is a cure for MS and that therapy is unlikely to reverse existing disabilities, patients with MS often hope that their disabilities will disappear and that no further exacerbation will occur. Failure to achieve these outcomes is likely to be very discouraging, therefore patients and their families require continual support and understanding. Education is crucial to maintaining patient compliance with treatment. In addition to the patient-support program provided by each drug supplier, the individual health care provider will be looked to for guidance on all aspects of treatment.

Source: E. Torage Shivapour, M.D.
University of Iowa Hospitals and Clinics, Department of Neurology

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198419 tn?1360245956
by sllowe, Dec 08, 2008
This is very good! Thanks for posting this Heath!

Avatar universal
by danielle47, Apr 25, 2009
Wow, what a great article, thanks for the posting, helps me with questions on monday with neurologist.  i have a single demylenating lesion (14mm cc x 5 ap x 4 tr) in the c4 spine.  in 2004 i woke up one morning with numbness on one side of face, went to dentist and confirmed the numbness, sent to neuro, mri of brain showed nothing.  6 mos to a year later i had a diffiult time with vertigo, saw another neuro and nothing found.  in sept 08, had blurred vision and pain over right eye and bad headaches, nothing definitive mri negative of brain.  neuro opthamologist indicated the optic nerve wasn't swollen, however didn't rule out pseudopapilladema, a month later symptoms subsided.  brings me to today.  i had major back surgery due to degenerative disc disease and herniatiion of l5-s1 on 2/23/09.  surgery went well, developed uti from cathetor, so we think, while in hospital and passed out next night in hospital for 20-25 seconds, very weak and developed anemia from surgery, so they think, doc said it was unusual, they typically don't see patients become anemic from this procedure, but I did.  Went home and passed out again and back to a local hospital.  had tilt table test, carotids, eeg, ct, nothing showed and back home three days later.  glad to be home, feeling better with my back, but just after i got out of second hospital, i woke up one morning with the most excruciating pain in my neck with radiation down left arm to elbow, discovered in shower that i could not feel under my arm down to the last two digits on my right hand, still do not have feeling and hot and cold sensations are absent.  still cannot feel when i a applying underarm deodorant.  i called surgeon in nyc and he ordered an mri of my cervical spine to make sure when i passed out in hospital that my neck had not been hurt.  got mri, thank god i did.  went to see dr. in nyc with films and he told me that it was not my neck hurting from a bulge or herniation, but in fact i needed to see a neuro immediately as i have a sizable demylenating lesion that was causing this problem.  had appt with neuro, went through 3 mri's of head, spine an thoracic with and without contrast, confirmed demylenating lesion, leading differential but couldn't rule out other etiologies, and had a evoke potential test that confirmed a slowing of nerve to brain in arms correlating with where the lesion sits.  i had a lumbar puncture, protein elevated and igg synthesis elevated confirming blood brain barrier damage, however no oglioclonal banding, which i have learned would make sense due to the location of the lesion.  nyc dr thinks this could be the beginning of ms, however doc on long island thinks this to be a single demylenatiing process, like a bells palsy per se, but still awaiting the final report on some more blood work done.  autoimmune panel, vitamin b12, immunofix panel, cardiolipin ab, and one other.  not sure what the report shows, but i am very scared and uncomfortable with what is happenning with my body, not to mention the fatigue and cognitive things that i have been showing.  memory is not good, words escape me and can't seem to get a good handle on things.  i have suffered depression in the last 5-6 years and tried to go off medicine, but can't.  i am just writing in hopes someone may be able to help me with some questions for my doc on monday april 27 09.  the wait and see approach is somewhat uncomfortable for me since i have been going through some unusual things in the past 5 years, without any significant finding until this one lesion that is actively demylenating.  doc on long island put me on decadron for the swelling and inflammation and neurontin due to the pain i experience daily.  i also experienced a very heavy feeling in the upper body as to where it made doing anything at home or even driving difficult due to the heaviness i was feeling.  i am weaning on the decadron (which has provided me some relief), will be finished with first 6 day course on tuesday, doc said if symptoms return i may need to go on them again.  i am not sure this would be best because i know steroids of that magnitude are dangerous long term.  would it be beneficial to talk to do about an interferon?  i know this is long winded, sorry, but i hope if you took the time to read it you may be able to help me some.  by the way, facial numbness was discovered in my 41st year, lesion showed itself in my 46th year, any thoughts on this.  thank you so much for your time, i am absolutely confused by all this and hope for some answers.  i know ms is very difficult to diagnose when there are no brain lesions, that is what makes this so hard.  thanks for taking the time to read, you can email  me at ***@****

992734 tn?1257183651
by wtaylor, Aug 04, 2009
I am in the military and was experiencing severe leg pain with headaches and memory loss, got a mri and the Doc found brain lesions 3 to be exact. I was referred to nuero and have been seeing him for 3 months since then I have black spots in central vision in right eye also have swallowing problems, constipation, urinary problems. My headaches are mostly on the right side in the temple and in the eye itself,  my eyes stay bood shot and nothing relieves the headaches. I am fatigued all the time cant go outside and play with my kids, my eyes are sensative to light I have numbness and tingling in fingers and feet, I have tremors  and muscle spasms. I have more symtoms but the point is I am getting tired of the runaround and nuero saying it is a possible brain injury, what kind of questions should I ask the Dr.? to explain these symptoms.

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