MULTIPLE
SCLEROSIS
DONE BY :
MANAR ALFALLEH
EMAN ALADLY
GROUP A1
Multiple sclerosis (MS) is a chronic
autoimmune disease affecting the central
nervous system (the brain and spinal cord),
in its most typical form, is characterized by
lesions separated both in space and time
in the CNS.
PATHOPHYSIOLOGY :
MS is autoimmune disease where T lymphocyte attack myelin of the white matter
.of brian, spinal cord and optic nerve
The regions of white matter Interspersed with foci of Inflammation and
. demyelination known as plaques, which are often located near venules
The demyelination process lead to reduction of in the conduction velocity with
distortion and ultimatly loss of information conveyed by impulse traffic along CNS
. "tract pathways "clinical deficit
CNS function return with resolution of the inflammation and oedema, and also
.remylination
This pathologlcal sequence corresponds to the clinical pattern of MS relapses,
. with symptoms being present for a period then resolving partially or completely
AETIOLOGY :
.Causes of MS are unknown
There are working hypothesis for the cusation
: of MS
Enviromental eg : viral infection, vitamin D
defiecency .
Genetic eg :HLA-DRB1 gene .
EPIDEMOLOGY :
MS is more common in females than males
(approximately 3:1). It may develop at any age,
though its first onset is rare in children and the
elderly. The usual age of presentation is between 20
and 40 years. In the UK ; its prevalence is
approximately 1 in 1000 .
انقر فوق األيقونة إلضافة صورة
CLINICAL
FEATURES :
Presentation
Common modes of
presentation of MS
:include
,visual disturbance •
,limb weakness •
• sensory
disturbances .
VISUAL DISTURBANCE :
Optic (retrobulbar) neuritis is a characteristic Visual disturbance that may herald the
onset of MS. The underlying pathology is inflammatory de- myelination of one or
:(less commonly) both optic nerves. Symptoms of unilateral optic neuritis include
;pain around one eye, particularly on eye movement •
blurred vision, which may proceed to complete monocular blindness within days •
;or weeks
,loss of colour vision •
pink, swollen optic disc on fundoscopy – if the of inflammatory demyelination is •
,area immediately behind the optic nerve head
,visual field defect – typically a central scotoma in the affected eye •
.relative afferent pupillary defect •
Other visual disturbances at the onset of
MS include diplopia, often associated
with vertigo and nausea, hence
indicative of a brainstem plaque.
Examination in these circumstances may
reveal an internuclear ophthalmoplegia.
Sensory and motor presentations imply a lesion in the spinal
cord or cerebral hemi- spheres. For example: spasticity, muscle
. weekness, parasethesia and pain
is a lesion in the posterior )Lhermitte phe- nomenon(
columns of the cervical spinal cord may produce the near-
pathognomonic symptom of rapid tingling sensations
.shooting down the arms or legs on neck flexion
occurs In some patients, where )Uhthoff phenomenon(
motor, sensory or indeed visual symptoms are temporarily
.much worse after a hot bath
: Other presentations
Trigeminal neuralgia,
cognetive desfunction,
bladder disturbances
and impotance.
Course of the disease : The usual temporal
pattern of symptom
evolution In a patient
presenting in one of the
above ways is that
Relapsing _ remitting disease (70 – 80 %) clinical features worsen
Secondary progressive disease (10 _20%) over days or weeks,
reach a plateau and
Primary progressive disease then gradually resolve,
Progressive Relapsing disease (rare) partially or completely,
over weeks or months.
In the initial episodes there may near-complete or
complete symptomatic resolution "Relapsing _ remitting
disease " . However, subsequent episodes of
demyelination may leave some residual disability, the
patient eventually entering a secondary phase of steady
progres- sion without resolution "Secondary progressive
disease".
Some patients , particularly those presenting in middle
life with a spastic paraparesis, will have no clear-cut
relapses and remissions (primary progressive disease).
The natural history of MS in individual patients is
very variable. Some patients may have one or more
initial episodes and then no symptoms for many
.years
Occasionally the illness is hyperacute, with death
occurring within months, but the average life
expectancy in patients with progressive disease
.exceeds 25 years from onset
DIAGNOSIS OF MS
diagnosis of MS has been
clinical, based on the occurrence of at least two lesions in the
CNS with appropriate clinical charachteristics, separated in time
and space.
Investigations :
1-MRI - First line diagnositic test
-periventricular white matter. - brainstem
- cerebellum. - spinal cord
*some MS patients may have false-negative MR scans.
* abnormalities seen in MRI are not specific to MS (cerebral small
vessel disease may appear similar
2- visual evoked potentials
tests the function of the visual pathway from the retina
to the occipital cortex.
measures the conduction of the visual pathways from
the optic nerve, optic chiasm, and optic radiations to the
occipital cortex
Show delayed conduction ;optic neuritis
Using flashing
checkerboard pattern
As stimulus for the
retina
3- Lumber pPuncture - CSF examination
*pleocytosis : increace in cell counts - particularly
WBCs (lymphocytes - Tcells - & macrophages)
* oligoclonal banding : immunoglibulin (IgG), the
presence of these proteins indicates inflammation of the
central nervous system.
differential diagnoses of MS include:
● for relapsing and remitting disease
● sarcoidosis,
● systemic lupus erythematosus,
● TIA;
● for progressive disease
● motor neurone disease,
● spinal and cerebellar degenerations.
MANAGEMENT
NO CURE IS YET AVAILABLE FOR MS but
▪ management of an acute relapse,
high-dose methylprednisolone, intravenously or
orally
(500 mg to 1 g daily for 3–5 days.
▪ modification of the course of the disease,
trials of immunosuppressant
drugs, e.g. azathioprine, methotrexate, but side
effects over weight benefit
immunotherapeutic agents eg ; interferon-beta and
glatiramer acetate- 30% reduction in relapse
frequency
Mnoclonal antibody, natalizumab is twice as
effective as interferon-beta.
chemotherapeutic agent, is an alternative to
natalizumab, but also has potentialy serious
adverse effects, including cardio toxicity and a risk
(0.2%) of acute leukaemia.
control of symptoms
Spasticity.. Baclfen, dantrolene, botilinum toxin
Cerebellar tremor.. Clonazepam or gabapentein
Blaadder disturbance.. Anticholonergic, treat
unriary infection prmptly
Pain and paraxosymal symptoms like seziures..
Carbamazepine
Depression.. TCA, SSRI
THANK YOU
