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Multiple Sclerosis

Multiple Sclerosis
Is a chronic demyelinating disease
that affects th.e myelin sheath of the
neurons in the central nervous
system.
The myelin sheath is essential for
normal conduction of nerve impulses.
Impairments causes slowing of nerve
conduction.

Pathophysiology
Predisposing
factors:
Age (20-40
y.o)
Gender
(common in
females)

Precipitating
factors:
Unknown
Viral
infections(epste
in-barr virus)
Autoimmune
disease

Pathophysiology

Clinical patterns
DISEASE CATEGORY

DEFINITION

RELAPSING-REMITTING

EPISODES OF ACUTE WORSENING WITH A


RECOVERY AND A STABLE COURSE BETWEEN
RELAPSES

SECONDARY PROGRESSIVE

GRADUAL NEUROLOGIC DETERIORATION


WITH OR WITHOUT SUPERIMPOSED ACUTE
RELAPSES IN A CLIENT WHO PREVIOUSLY HAD
RELAPSING-REMITTING MULTIPLE SCLEROSIS

PRIMARY PROGRESSIVE

GRADUAL, NEARLY CONTINUOUS


NEUROLOGIC DETERIORATION FROM THE
ONSET OF MANIFSTATIONS

PROGRESSIVE RELAPSING

GRADUAL NEUROLOGIC DETERIORATION


FROM THE ONSET OF MANIFESTATIONS BUT
WITH SUBSEQUENT SUPERIMPOSED
RELAPSES

Clinical manifestations
Muscle symptoms:
Loss of balance
Muscle spasms
Numbnessor abnormal sensation in any area
Problems moving arms or legs
Problems walking
Problems withcoordinationand making small movements
Tremorin one or more arms or legs
Weaknessin one or more arms or legs
Bowel and bladder symptoms:
Constipationand stool leakage
Difficulty beginning to urinate
Frequent need to urinate
Strong urge to urinate
Urine leakage (incontinence)
Tingling, crawling, or burning feeling in the arms and legs
Painfulmuscle spasms
Eye symptoms:
Double vision
Eye discomfort

Clinical manifestations
Sexual symptoms:
Problems with erections
Problems with vaginal lubrication
Speech and swallowing symptoms:
Slurred or difficult-to-understand speech
Trouble chewing and swallowing
Fatigueis a common and bothersome symptoms as
MS progresses. It is often worse in the late afternoon.
Fever, hot baths, sun exposure, and stress can
trigger or worsen attacks.

Medical management
Medications used to slow the progression of multiple sclerosis are taken on a longterm basis, they include:
1. Interferons (Avonex, Betaseron, or Rebif), glatiramer acetate (Copaxone),
mitoxantrone (Novantrone), and natalizumab (Tysabri)
2. Fingolimod (Gilenya )
3. Methotrexate, azathioprine (Imuran), intravenous immunoglobulin (IVIg) and
cyclophosphamide (Cytoxan) may also be used if the above drugs are not
working well
4. Steroids may be used to decrease the severity of attacks.
5. Medications to control symptoms may include:
6. Medicines to reduce muscle spasms such as Lioresal (Baclofen), tizanidine
(Zanaflex), or a benzodiazepine
7. Cholinergic medications to reduce urinary problems
8. Antidepressants for mood or behavior symptoms
9. Amantadine for fatigue

Medical management
Six disease-modifying drugs are approved by the FDA for treatment of
multiple sclerosis:
1. Interferon beta-1b (Betaseron). Given in subcutaneous (under the
skin) injections every other day.
2. Interferon beta-1a (Avonex). Given as weekly intramuscular
injections.
3. Interferon beta-1a (Rebif). Given in subcutaneous injections three
times a week.
4. Glatiramer acetate (Copaxone). Given daily in subcutaneous
injections.
5. Natalizumab (Tysabri). Given by intravenous infusion once every four
weeks.
6. Mitoxantrone (Novantrone). Given intravenously once every three
months for 2 -3 years at most.

Surgical management
Deep Brain Stimulation
Severe and disabling tremor that occurs with the slightest
movement of the limbs may be helped by an implanted
device that stimulates an area of thebrain.
The person is awake for part of the procedure, but the
scalp is numbed. A small hole is drilled in the skull, and
tiny wire electrodes are placed in the brain. A small
battery-powered device (generator) similar to a
pacemaker is implanted in the chest and connected to
the electrodes in the brain by a wire. The procedure takes
3 to 4 hours, although it may take up to 8 hours in some
cases.
Deep brain stimulation for tremor caused by multiple
sclerosisis still experimental, expensive, and not widely
available.

Guillian Barre
Syndrome

an inflammatory disease (autoimmune) with unknown


origin
involves the degeneration of the myelin sheath of the
peripheral nerves
affects 1 to 4 in every 100,000 of the population
results to acute, rapid segmental demyelination of
peripheral nerves and some cranial nerves
producing ascending weakness with dyskinesia (inability
to execute voluntary movements), hyporeflexia
(subnormal or absent reflexes), and paresthesias
(numbness)

Myelin is a complex substance that covers nerves,


providing insulation and speeding the conduction of
impulses from the cell body to the dendrites. It is
produced by Schwann cells that are spared, allowing for
remyelination in the recovery phase of the disease

Assessment & Diagnosis


Symmetric weakness, upward progression of motor
weakness, loss of deep tendon reflexes, limb paresthesis
A history of a viral illness is suggestive of the diagnosis.
Spinal tap (lumbar puncture)
Elevated protein levels are detected in CSF evaluation
Nerve Function test
Electromyographyreads electrical activity in your
muscles to determine if your weakness is caused by
muscle damage or nerve damage
Nerve conduction studiesassess how your nerves and
muscles respond to small electrical stimuli.

Pa t h o p h y s i o l o g y

`
Predisposing Factor

Precipitating Factor

Age: Can occur at any


age
Mostly Diagnosed
(30 - 50)

Post Infection to
Campylobacter Jejuni

Sex: Common on both


sexes

Poor Hygiene
Stress
Diet
Lifestyle

Pa t h o p h y s i o l o g y

Campylobacter Jejuni enters the


body by multifenestrated
(Having fenestrae or windowlike
openings) cells.

Innate Immune Response results


in the uptake of pathogens by
immature antigen presenting
cell
Innate Immune Response results
in the uptake of pathogens by
immature antigen presenting
cell

Pa t h o p h y s i o l o g y

Migration to lymph nodes and


Activates
CD4 T cells that recognize
antigens
From the infectious pathogen
B Cells and Th2 Cells are
activated
(produces cell mediated and
humoral
Response)
Antibodies are produced
Activates complement system
Phagocytosis of Bacteria

Pathogen and
Host
have identical
amino acids
sequences

Molecular Mimicry

Pa t h o p h y s i o l o g y

Immune responses directs


against capsular components
produce antibodies that cross
react with myelin
Lymphocytes and Macrophages
Circulate in the blood and
eventually
locates the myelin
Defects in
Stripping of
propagation
Myelin
of electrical
Lymphotic
And Axonal
nerve
infiltration
of spinal
Damage
impulses
Roots and Per. Nerves

Pa tho p h ysiolog y

Acute progressive
ascending
weakness of upper,
lower limbs and
hyporeflexia
Sensory
Changes
Paresthesi
as

GUILLIAN BARRE
SYDROME

Cranial Nerve
Involvement
Facial Droop

Dull Aching
Pains of
lower back,
flank,
proximal
legs

Pa th op h ysiolo g y

If Treated:

If not Treated:

Plasma Exchange
(IVIG)
Physical Therapy
and Exercise
Medication

Extensive axonal
destruction
Ascending weakness
progresses

Good prognosis

DEATH

Weakening of the
Diaphragm
and Respi. Muscles
Respiratory Distress
Syndrome
Bad prognosis:
Respi. Arrest and Shock

Medical Management

This syndrome presents a medical emergency in


view of rapid progression and neuromuscular
respiratory failure, requiring ICU admission.
Mechanical ventilation may be necessary to
support pulmonary function and adequate
oxygenation, and may be required for an
extended period.

Medical Management

Plasmapheresis consists of the plasma and separating it


from the actual blood cells. The blood cells are then put back
into the body, which manufactures more plasma to make up
for what was removed. It is used to remove antibodies from
the bloodstream, thereby preventing them from attacking
their targets. It does not directly affect the immune
system's ability to make more antibodies, and therefore may
only offer temporary benefit.

IVIG is ablood productadministeredintravenously. It


contains pooled, polyvalent,IgG(immunoglobulin(antibody)
G) extracted from theplasmaof over one thousand blood
donors.
Both therapies used to directly affect and decrease the
circulating peripheral nerve myelin antibody

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