3. STROKE
• It is a cerebrovascular disorder also known as
cerebrovascular accident
• Occurs when there is obstruction in vessels
which impedes blood flow to a part of the
brain or haemorrhage into brain
• Results in death of brain cells
7. TYPES
1. ISCHEMIC STROKE
An ischemic stroke results from inadequate
blood flow to the brain from partial or complete
occlusion of an atery
It divides into thrombotic and embolic
8. a) THROMBOTIC STROKE
It occurs from injury to a vessels wall and
formation of blood clot
B) EMBOLIC STROKE
It occurs when an embolus lodge in and
occludes a cerebral artery
9. 2. HEMORRHAGIC STROKE
It is caused by bleeding into the brain tissue, the
ventricles or subarachnoid space
-primary intracerebral haemorrhage
-secondary intracerebral haemorrhage
10. PATHO-PHYSIOLOGY
Due to various etiological factors persisting for a
long time
There is disruption of the cerebral blood flow due
to obstruction of a blood vessels
Due to the obstruction of blood vessels, initially
there is abnormal infiltration of lipid in the intimal
layer of the artery
11. This fatty streaks further develops into the plague
This formation of the palgue may rupture which
may travel and occlude the vessels thus limiting the
blood flow causing cerebal ischemia
The ischemic cascade begins when cerebral blood
flow falls to less than 25ml/ 100 g/min
12. Due to the cerebral hypoxia, neurons cannot
longer maintain aerobic respiration
The mitochondria then switch to anaerobic
respiration, which generates large amount of
lactic acid
Initiation of anaerobic respiration
13. Neurons incapable of producing sufficient
quantities of adenosine triphosphate (ATP) to
fuel the depolarization processes of brain tissue
Maintenance of electrolyte balances begin to
fall and cell function ceases
Manifest features like syncope, hemiperesis,
weakness of the limb
15. Flaccid paralysis
COMMUNICATION LOSS
Dysarthria
Dysphasia
Apraxia
PERCEPTUAL DISTURBANCES
Headache
Pain and rigidity
Visual disturbances
Tinnitus, dizziness and hemiparesis
16. DIAGNOSTIC EVALUATION
Careful history and a complete physical and
neurologic examination
CT Scan
MRI
Cerebral angiography
Carotid duplex
Lumbar puncture for evidence of red blood
cells in cerebrospinal fluid
18. MANAGEMENT
DRUG THERAPY
Recombinant tissue plasminogen activator for
administered IV is used for re-establish blood
flow through a blocked artery to prevent cell
death
Acetylsalicylic acid is used within 48hrs
Platelet inhibitors and anti-coagulant e.g.
aspirin, warfarin
19. Calcium channel blockers e.g. nimodipine in
patient with subarachnoid hemorrhage
Temperature elevation e.g.acetoaminophen
Phenytoin for seizures
20. SURGICAL TREATMENT
Evacuation of aneurysm induced hematomas
or cerebral hematomas larger than 3cm
Aneurysm involves clipping wrapping or
coiling the aneurysm to prevent right bleeding
Merei Retriver removes blood clots in patient
who are experiencing ischemic stroke
21.
22. MULTIPLE SCLEROSIS
• It is defined as an auto-immune disease that
affects the CNS and is characterized by the
loss/or damage of myelin sheath
23. TYPES
1. RELAPSING/ REMITTING MULTIPLE
SCLEROSIS (RRMS)
Characterized by periods of flaretips and
remission
2. PRIMARY PROGRESSIVE MULTIPLE SCLEROSIS
This type of multiple sclerosis is usually slow
continuous, periodically progressive and
results in worsening of disease in a period of
time
24. 3. SECONDARY PROGRESSIVE MULTIPLE SCLEROSIS
(SPMS):
This types is initially diagnosed and disappear but
relapse in over a time period (approximately within
10 years) and then becomes steady and disease
worsening develops
4. PROGRESSIVE RELAPSING MULTIPLE SCLEROSIS
(PRMS)
This multiple sclerosis has a steady worsening
pattern with acute relapses
27. PATHO-PHYSIOLOGY
Due to various contributing factors (chronic
inflammation, viral infestation, injury)
Results in the loss of myelin, disappearance of
oligodendrocytes and proliferative astrocytes
Initially myelin sheath of neurons in brain and
spinal cord are interfered but nerve fibres are
not effected
28. Changes in the myelin results in plaque
formation which will be scattered throughout
the CNS
Loss of myelin results in noticeable impairment
of function
With the destruction of axons in late stage
impulse are totally blocked
Results in permanent loss of nerve function
29. CLINICAL FEATURES
A. MOTOR MANIFESTATION
-weakness or paralysis of limbs, trunk & head
-diplopia
-scanning speech
-spasticity of muscles
B.SENSORY MANIFESTATION
-numbness and tingling
-blurred vision
33. MANAGEMENT
- Corticosteroids to treat acute exacerbation by
reducing edema and inflammation at the site
of demyelination
- Immunosuppressive therapy
- Antispasmodic
- Nutritional therapy