MULTIPLE SCLEROSIS

Presented by:
Magaling, Julius Christian T.
Roque, Patrick
Vasallo, Rusella Paulina R.
Multiple Sclerosis
(MS) is a progressive disease that attacks the central
nervous system (CNS) and affects multiple systems of
the body through attacks on the nervous system. MS
affects individuals of all races and socioeconomic groups
and is seen all over the world. It is most common in
white women of northern European descent.
Pathophysiology

MS is currently believed to be an immune-mediated

disorder mediated by a complex interaction of the
individual's genetics and as yet unidentified
environmental insults. Damage is believed to be
caused by the patient's own immune system. The
immune system attacks the nervous system, possibly
as a result of exposure to a molecule with a similar
structure to one of its own.
Pathophysiology
Lesions
The name multiple sclerosis refers to the scars (scleroses
– better known as plaques or lesions) that form in the
nervous system. MS lesions most commonly
involve white matter areas close to the ventricles of
the cerebellum, brain stem, basal ganglia and spinal
cord; and the optic nerve.
MS destroys oligodendrocytes, the cells responsible for
creating and maintaining a fatty layer—known as
the myelin sheath—which helps the neurons
carry electrical signals.
Pathophysiology
Inflammation
the inflammatory process is caused by T cells, a kind of lymphocyte.
Lymphocytes are cells that play an important role in the body's
defenses. In MS, T cells gain entry into the brain via the previously
described blood–brain barrier. Evidence from animal models also point
to a role of B cells in addition to T cells in development of the disease.
The T cells recognize myelin as foreign and attack it as if it were an
invading virus. This triggers inflammatory processes, stimulating other
immune cells and soluble factors like cytokines and antibodies. Leaks
form in the blood–brain barrier, which in turn cause a number of other
damaging effects such as swelling, activation of macrophages, and
more activation of cytokines and other destructive proteins
Frequency
United States
According to the National Multiple Sclerosis Society,
250,000-300,000 individuals in the United States are
affected by MS. Approximately 1 person per 1000
population in the United States is believed to have the
disease.
International
Worldwide, approximately 1.1 million people are
affected by multiple sclerosis.
Mortality/Morbidity

Life expectancy is shortened only slightly with

multiple sclerosis (MS), and the survival rate is linked
to disability. Usually, death is due to secondary
complications (50-66%), such as pulmonary or renal
causes, suicide, primary complications, and causes
other than MS seen in the general population.
Race

Multiple sclerosis is seen in all parts of the world and

in all races, but whites of northern European descent
have the highest incidence.
Sex
The female-to-male ratio for multiple sclerosis is 2:1.
Age
Multiple sclerosis disease is usually diagnosed in
persons aged 15-45 years; however, it can occur in
persons of any age. The average age at diagnosis is 29
years in women and 31 years in men.
Causes
The cause of multiple sclerosis (MS) is not known.
Environmental factors and a genetic predisposition,
which affect an individual's chance of acquiring the
disease, appear to play a role.

Identical twin studies have shown up to a 60% risk of

one twin's developing MS if the other is affected. The
first-degree family members (children or siblings) of
people affected with MS have a 3-5% risk of
developing MS.
Causes
Geography is clearly an important factor in the
equation. Persons from the equatorial regions of the
world have a much lower incidence than those in the
southernmost and northernmost regions. If an
individual lives in an area with low incidence of MS
until age 15 years, that person's risk is low; however, if
an individual lives in an area with a high incidence
until age 15 years, the risk of developing MS is high.
Classification
 Relapsing-remitting --by unpredictable relapses followed by periods of
months to years of relative quiet (remission) with no new signs of disease
activity. Deficits suffered during attacks may either resolve or
leave sequelae, the latter being more common as a function of [Link]
describes the initial course of 85–90% of individuals with [Link]
deficits always resolve between attacks, this is sometimes referred to
as benign MS, although patients will still accrue some degree of disability
in the long term. 
Secondary progressive (sometimes called "galloping MS") describes
around 65 % of those with an initial relapsing-remitting MS, who then
begin to have progressive neurologic decline between acute attacks
without any definite periods of remission. Occasional relapses and minor
remissions may appear. The median time between disease onset and
conversion from relapsing-remitting to secondary progressive MS is
19 years.
Classification
 Primary progressive-- describes the approximately 10–15% of
individuals who never have remission after their initial MS
[Link] is characterized by progression of disability from
onset, with no, or only occasional and minor, remissions and
[Link] age of onset for the primary progressive
subtype is later than for the relapsing-remitting, but similar to
mean age of progression between the relapsing-remitting and
the secondary progressive. In both cases it is around 40 years
of age.
Progressive relapsing-- describes those individuals who, from
onset, have a steady neurologic decline but also suffer clear
superimposed attacks. This is the least common of all subtypes.
Symptoms
Visual disturbances
-- patch of blurred vision, red-to-orange or red-to-gray distortions (color
desaturation), or monocular visual loss (loss of vision in one eye).
Visual symptoms due to optic nerve inflammation (optic neuritis) in
multiple sclerosis usually are accompanied or preceded by eye pain. 
Limb weakness with or without difficulties with coordination and
balance may occur early. 

Muscle spasms, fatigue, numbness, and prickling pain are common

symptoms. 

loss of sensation, speech impediment (typically a problem articulating

words), tremors, or dizziness.
Symptoms
decreased concentration, 
attention deficits, 
some degree of memory loss
inability to perform sequential tasks, or 
impairment in judgment.
Other symptoms may include:
depression
manic depression
paranoia
an uncontrollable urge to laugh and weep.
individuals may experience sexual dysfunction or reduced bowel and bladder
control. Heat appears to intensify multiple sclerosis symptoms for about 60%
of those with the disease. Pregnancy seems to reduce the number of attacks,
especially during the third trimester.
Diagnosis
MRI (magnetic resonance imaging) scans with intravenous
gadolinium helps to identify, describe, and in some instances
date lesions in the brain (plaques). 

An electro-physiological test, evoked potentials, examines the

impulses traveling through the nerves to determine if the
impulses are moving normally or too slowly. 

examining the cerebro-spinal fluid that surrounds the brain

and spinal cord may identify abnormal chemicals (antibodies)
or cells that suggest the presence of multiple sclerosis.
Differential Diagnosis
Lyme Disease
Lyme disease is known to cause intermittent neurologic events. Some of the
most frequent problems include Bell's palsy, nonspecific symptoms of
numbness, fatigue and amnesia. CSF findings may resemble those found in
the MS, and MRI may show a white matter disease. History of tick bites,
rashes and arthralgia should be sought after. Screening for Lyme titer and/or a
Lyme PCR in the CSF or blood should help in diagnosis.

Systemic Lupus Erythematosus

Systemic lupus erythematosus may cause multiple neurologic pathology such
as optic abnormalities, encephalopathy, transverse myelitis, strokes. One
needs to look for systemic abnormalities, such as elevated antinuclear
antibody, leukopenia, hematuria, elevated erythrocyte sedimentation rate. On
some occasions lupus erythematosus and MS may be found in the same
patient.
Differential Diagnosis

Tropical Spastic Paraparesis
  

Tropical spastic paraparesis is a retroviral disease caused by HTLV-1 virus. It is

uncommon in the continental United States, but may be seen infrequently in
patients who resided for some time around the Caribbean Sea Basin. The major
clinical manifestations are progressive spastic paraparesis or generalized white
matter disease.

Behçet
 Syndrome
Behçet syndrome can cause MRI findings that are very similar to MS. However, the
main distinguishing features of this condition are oral and genital ulcersand uveitis,
as well as possible involvement of lungs, joints, intestines, and heart. This group of
patients may present with either quadriparesis, pseudobulbar palsy, cranial
neuropathy, cerebellar ataxia or cerebral venous thrombosis.

 
Differential Diagnosis
Sarcoidosis and Sjogren's Syndrome

Sarcoidosis and Sjogren's syndrome may show lesions on MRI that resemble those found in
Multiple Sclerosis. These are autoimmune conditions that affect multiple organ systems and
should not be confused with MS. A chest X-ray may show granulomatous disease of the
lungs, and meningeal enhancement is seen in patients with CNS involvement. Oligoclonal
bands and IgG are raised in CSF of patients with sarcoidosis. Central nervous system
involvement and the course of the disease may show striking similarity to MS. Angiotensin-
converting enzyme determination may be used for further differential diagnosis. It may be
elevated in either serum or CSF but is not reliably abnormal.
Vitamin B-12 Deficiency and Tertiary Syphilis

Vitamin B-12 deficiency and tertiary syphilis may result in dorsal column abnormalities and
dementia. These two conditions need to be ruled out when patients present with the above
mentioned symptoms as their chief complaints.
Leukodystrophies of Adulthood

Leukodystrophies of adulthood (metachromatic leukodystrophy, Krabbe's disease, adrenal
leukodystrophy, ) show large areas of involvement on the MRI scan where no normal white
matter can be found.

  
Treatment
Medications
Drugs that are commonly used for multiple sclerosis include:
Corticosteroids. The most common treatment for multiple sclerosis, corticosteroids reduce the
inflammation that spikes during a relapse. Examples include oral prednisone and intravenous
methylprednisolone.
Interferons. These types of drugs — such as Betaseron, Avonex and Rebif — appear to slow the
rate at which multiple sclerosis symptoms worsen over time. But interferons can cause serious
liver damage.
Glatiramer (Copaxone). Doctors believe that glatiramer works by blocking your immune
system's attack on myelin. You must inject this drug subcutaneously once daily. Side effects
may include flushing and shortness of breath after injection.
Natalizumab (Tysabri). This drug is designed to work by interfering with the movement of
potentially damaging immune cells from your bloodstream to your brain and spinal cord.
Tysabri is generally reserved for people who see no results from or can't tolerate other types of
treatments. This is because Tysabri increases the risk of progressive multifocal
leukoencephalopathy — a brain infection that is usually fatal.
Mitoxantrone (Novantrone). This immunosuppressant drug can be harmful to the heart, so it's
usually used only in people who have advanced multiple sclerosis.
Treatment
Therapies
A physical or occupational therapist can teach you
stretching and strengthening exercises, and show you
how to use devices that can make it easier to perform
daily tasks.
Procedures
Plasma exchange (plasmapheresis) looks a little like
dialysis as it mechanically separates your blood cells
from your plasma, the liquid part of your blood.
Plasma exchange is sometimes used to help combat
severe symptoms of multiple sclerosis relapses,
especially in people who are not responding to
intravenous steroids.
Thank You