Multiple Sclerosis & other

demyelinating diseases
Caucasus International University
2018
 Multiple Sclerosis

Multiple sclerosis (MS) is a progressive disease

that destroys patches of myelin in the brain and
spinal cord, disrupting neuronal signals in the
CNS and leading to sensory disorders and
weakened musculature.
 Multiple Sclerosis
This disease, which varies greatly in intensity
among individuals who have it, is characterized
by periods of relapse (disability) and remission
(recovery).
 Multiple Sclerosis - etiology
The cause of MS is incompletely understood.

It is known MS to be an autoimmune disease in

which the immune system attacks the myelin
around axons in the CNS, thereby interfering
with the conduction of signals along the
axons.
 Multiple Sclerosis - etiology
The immune system cells called lymphocytes
break down the myelin, and then
macrophages consume the remains through
phagocytosis.
The damage is also accompanied by
inflammation, which can destroy the axons
themselves.
Multiple Sclerosis - MRI
Multiple Sclerosis - MRI
Diagnosis - oligoclonal bands
 Oligoclonal bands are abnormal discrete
bands seen on CSF gel electrophoresis.
They result MOTOR from the synthesis of
large amounts of relatively homogeneous
immunoglobulin by individual plasma cell
clones in the cerebrospinal fluid (CSF).
Diagnosis - oligoclonal bands
Diagnosis - oligoclonal bands
 Multiple sclerosis – acute
treatment
 Corticosteroids, such as oral prednisone and intravenous
methylprednisolone, are prescribed to reduce nerve
inflammation. Side effects may include insomnia,
increased blood pressure, mood swings and fluid
retention;

 Plasma exchange (plasmapheresis). The liquid portion of

part of blood (plasma) is removed and separated from
blood cells. The blood cells are then mixed with a protein
solution (albumin) and put back into body.

 Plasma exchange may be used if your symptoms are

new, severe and haven't responded to steroids.
Multiple sclerosis – immunomodulatory
treatment (remission)
 Beta interferons. These medications are among the most commonly
prescribed medications to treat MS. They are injected under the skin
or into muscle and can reduce the frequency and severity of
relapses.

 Glatiramer acetate (Copaxone). This medication may help block your

immune system's attack on myelin and must be injected beneath the
skin. Side effects may include skin irritation at the injection site.

 Dimethyl fumarate (Tecfidera). This twice-daily oral medication can

reduce relapses. Side effects may include flushing, diarrhea, nausea
and lowered white blood cell count.

 Fingolimod (Gilenya). This once-daily oral medication reduces

relapse rate.
 Neuronal Regeneration
 If a nerve is severed in the PNS,
macrophages invade and destroy the axon
distal to the injury.


 Axon filaments can grow peripherally from

the injured site at an approximate rate of
1.5 mm a day within regeneration tubes
formed by the surviving Schwann cells that
surrounded the original axons
Neuronal Regeneration
 Acute disseminated
encephalomyelitis (ADEM)
 Acute disseminated encephalomyelitis
(ADEM), as the name would suggest, is
featured by a monophasic acute
inflammation and demyelination of white
matter typically following a recent (1-2
weeks prior) viral infection or vaccination
 Acute disseminated
encephalomyelitis (ADEM)
 Unlike multiple sclerosis, symptoms are more
systemic rather than focal and include fever,
headache, decreased level of consciousness
varying from lethargy to coma, seizure, and
multifocal neurologic symptoms such as
hemiparesis, cranial nerve palsies, and
movement disorders; behavioural changes like
depression, delusions, and psychosis may
dominate the symptoms.
Acute disseminated
encephalomyelitis
 Neuromyelis optica (NMO)
 Closely related severe demyelinating
diseases caused by an autoantibody to the
aquaporin-4 water channel. The classic
presentation of NMO is with the triad of
optic neuritis, longitudinally extensive
myelitis, and positive anti-AQP4 antibody.
 Neuromyelis optica (NMO)
 NMO is characterized by bilateral optic
neuritis and myelitis resulting in blindness
and paraplegia.

 Although the two usually present

concurrently, it is not uncommon for one to
precede the other by up to several weeks;

 Additionally, it is now recognized that some

patients present with unilateral optic nerve
involvement.
Neuromyelis optica (NMO)
Neuromyelis optica (NMO)