Multiple Sclerosis: Demyelination-Damages The Myelin Sheath and Neurons This Damage Slows Down or

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MULTIPLE SCLEROSIS

MULTIPLE SCLEROSIS
Abbreviated MS, also known as disseminated sclerosis or encephalomyelitis
disseminate.
Is an immune-mediated, progressive demyelinating disease of the CNS.
It is an autoimmune disease in which the body’s very own immune system attacks the
CNS‘s cells and underlying tissues.
Demyelination- damages the myelin sheath and neurons this damage slows down or
blocks messages between your brain and your body, leading to the symptoms of MS.

MS is grouped into the following four types:


 Relapsing-remitting: Periods of neurological dysfunction followed by partial or full
recovery.
 Primary-progressive: Steady decline with periods of minimal recovery (fairly uncommon).
 Secondary-progressive: Initial pattern of relapse and recovery, which becomes steadily
progressive over time.
 Progressive-relapsing: Progressive from onset with clear exacerbations (rare).

Causes of multiple sclerosis

 Virus (ESPREIN-BARR)

SIGN & SYMPTOMS

 Fatigue
 Depression
 Weakness
 Numbness
 Difficulty in coordination
 Loss of balance
 Pain
 Spasticity ( muscle hypertonicity )
 Visual disturbances
I. Blurring of vision
II. Diplopia ( double vision )
III. Patchy blindness ( scotoma )
IV. Total blindness

DIAGNOSTIC PROCEDURE

 A neurological exam may show reduced nerve function in one area of the body, or
spread over many parts of the body. This may include:

 Abnormal nerve reflexes


 Decreased ability to move a part of the body
 Decreased or abnormal sensation
 Other loss of nervous system functions

 An eye examination may show:

 Abnormal pupil responses


 Changes in the visual fields or eye movements
 Decreased visual acuity
 Problems with the inside parts of the eye
 Rapid eye movements triggered when the eye moves

 Diagnosis requires evidence of 2 or more neurologic dysfunction


 EEG: demonstrates abnormalities in brain waves in one -third of patients.
 MRI scan of the brain and MRI scan of the spine are important to help diagnose and
follow MS
 CT scan: Demonstrates brain lesions, ventricular enlargement or thinning.
 Evoked potentials: Visual (VER), brainstem auditory (BAER), and somatosensory
(SSER) are abnormal early in a high percentage of patients with definite or suspected
MS.

SURGICAL MANAGEMENT

Surgery options include:

 Deep brain stimulation for tremor. 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 the brain. Neurological performs the surgery to implant the device.
 Implantation of a drug catheter or pump, for spasticity. People who have severe pain or
spasticity may benefit from having a catheter or pump placed in the lower spinal area to
deliver a constant flow of medicine, such as baclofen (Lioresal).

MEDICAL MANAGEMENT

 There is no known cure for multiple sclerosis at this time. However, there are therapies
that may slow the disease. The goal of treatment is to control symptoms and help you
maintain a normal quality of life.

 Medications used to slow the progression of multiple sclerosis are taken on a long-term
basis, they include:

 Interferons (Avonex, Betaseron, or Rebif), glatiramer acetate (Copaxone),


mitoxantrone (Novantrone), and natalizumab (Tysabri) are approved for treating
MS
 Methotrexate, azathioprine (Imuran), intravenous immunoglobulin (IVIg) and
cyclophosphamide (Cytoxan) may also be used if the above drugs are not working
well

 Steroids may be used to decrease the severity of attacks.

 Medications to control symptoms may include:

 Medicines to reduce muscle spasms such as Lioresal (Baclofen), tizanidine


(Zanaflex), or a benzodiazepine
 Cholinergic medications to reduce urinary problems
 Antidepressants for mood or behavior symptoms
 Amantadine for fatigue

 The following may help MS patients:

 Physical therapy, speech therapy, occupational therapy, and support groups


 Assistive devices, such as wheelchairs, bed lifts, shower chairs, walkers, and wall
bars
 A planned exercise program early in the course of the disorder
 A healthy lifestyle, with good nutrition and enough rest and relaxation
 Avoiding fatigue, stress, temperature extremes, and illness

 Household changes to ensure safety and ease in moving around the home are often
needed.

NURSING DIAGNOSIS
 Impaired Physical Mobility related to neuromuscular impairment, decreased strength
and fatigue
Nursing Interventions:
 Encourage and facilitate early ambulation and other ADLs when possible.
 Facilitate transfer training by using appropriate assistance of persons or devices when
transferring patients to bed, chair, or stretcher.
Encourage appropriate use of assistive devices in the home setting.
Provide positive reinforcement during activity.
Allow patient to perform tasks at his or her own rate.
Keep side rails up and bed in low position. This promotes a safe environment.
Turn and position every 2 hours or as needed.
Maintain limbs in functional alignment (e.g., with pillows, sandbags, wedges).
Perform passive or active assistive ROM exercises to all extremities.
Encourage coughing and deep-breathing exercises.
Encourage liquid intake of 2000 to 3000 ml/day unless contraindicated.
Initiate supplemental high-protein feedings as appropriate.
Administer medications as appropriate. Antispasmodic medications may reduce muscle
spasms or spasticity that interfere with mobility.
NURSING DIAGNOSIS
 Acute Pain
NURSING INTERVENTION
 Monitor v/s and pain scale to provide baseline data for comparison
 Promote bed rest /chair (recliner) during toxic stage
 Determine patient acceptable level of pain
 Provide comfort measure such as touching to promote non pharmacological pain
management

NURSING DIAGNOSIS
 Risk for Injury
NURSING INTERVENTION
 Provide bed rest
 Remove environmental barriers to ensure safety
 Guide patient when ambulating if appropriate

NURSING DIAGNOSIS
 Fatigue
NURSING INTERVENTION
 Promote bed rest /chair (recliner) during toxic stage
 Provide quiet environment ; limit visitor as needed
 Energy conservation and activity management 

REFERENCE:

Textbook of Medical –Surgical Nursing,11th edition;Brunner and Suddarth’s


Medical-Surgical nursing, 7th edition; Joyce m. Black
Straight A’s in Pathophysiology Lippincott Williams & Wilkins
Pathophysiology Lippincott Manual of Nursing Practice

MENDERO COLLEGE
Tiguma Pagadian City

S.Y 2010-2011

NCM-104

Multiple Sclerosis
Submitted by

Manas Norhana C.

Submitted to

MS. Czarmecris Lee V. Tumanda

Demyelination is the major underlying factor responsible for the symptoms


of multiple sclerosis (MS). Demyelination is the destructive removal
ofmyelin, an insulating and protective fatty protein which sheaths nerve cells
(neurons). More specifically, the myelin is wrapped around the long
extensions of neurons called axons. During MS relapses, patches of white
matter in the central nervous system that normally contain tracts of
myelinated neurons become inflamed and lose their myelin. These patches
of demyelination are known as lesions.

The cause and precise mechanism of demyelination is not clearly understood


but there is good evidence that the body's own immune system is at least
partially responsible. Acquired immune system cells called T-cells are known
to be present at the site of lesions. Other immune system cells
called macrophages (and possibly mast cells as well) also contribute to the
damage.

Myelin is produced by special "glial cells" in the central nervous system


called oligodendrocytes. Oligodendrocytes and axons have a many to many
relationship - that is one oligodendrocyte produces myelin for several axons
and one axon has several oligodendrocytes producing its myelin. In MS, it is
not just the myelin that is destroyed but also these oligodendrocytes and
occasionally even the axons themselves.
Axons use an electrochemical mechanism to transmit nerve impulses -
the action potential. This requires sodium and potassium ions to pass
through a semi-permeable membrane around the nerve. It is believed that
the myelin not only insulates and encases this electrochemical process but
also actively assists it. When axons become demyelinated, they transmit the
nerve impulses 10 times slower than normal myelinated ones.

During periods of MS remission, the oligodendrocytes repair the damaged


axons in a process called remyelination. However, very often the
oligodendrocytes are also destroyed which delays or prevents remyelination
from happening. Additionally, another kind of glial cell, calledastrocytes,
cause scar tissue to form in place of the myelin. Scar tissue does not
perform the same function as the myelin. As the disease reaches its more
advanced phases, the axons themselves are often destroyed as well.

Demyelination links: 

Legend:

Pathophysiology Medical treatment

Diagnostic procedure Nursing diagnosis &

Nursing intervention
Sign & symptoms

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