Stroke intro

1. STROKE
HANINE HASSAN
MPT- PEDIATRIC NEUROLOGY

2. Learning Objectives
Definition
Risk Factors
Types of Stroke
Brief assessment
Treatment Goals

3. Definition
Rapidly developing clinical signs of focal (or global) disturbance of
cerebral function, with symptoms lasting 24 hours or longer or
leading to death, with no apparent cause other than of vascular
origin. (WHO)

6. Types
Stroke is classified into two major types:
o Brain ischemia due to thrombosis, embolism, or systemic
hypoperfusion - 80%
o Brain hemorrhage due to intracerebral hemorrhage (ICH) or
subarachnoid hemorrhage (SAH) -20%

7. Ischemic Stroke
•Ischemia is the complete loss of blood flow to a tissue.
•Failure to deliver adequate oxygen and glucose to brain tissue, resulting in
neuronal dysfunction and possible cell death.
•Focal ischemia reflects loss of blood flow to particular vascular territory.
•Major anastomosis of the arteries lessen the effect of ischemic damage.

8. Pathophysiology of cerebral ischemia and
ischemic infarction
Vascular factors: loss of oxygen & glucose supply
Metabolic factors: collapse of energy producing process, ultimately with
disintegration of cell membranes.
Vascular factors:
center of ischemic stroke is a zone of infarction.
Depends on degree & duration
Margins of infarct there is only minimal or no parenchymal damage.

10. Metabolic factors:
Neurotransmitters namely glutamate & aspartate released form the
ischemic cells excite neurons and cause influx of sodium and calcium.
Causing irreversible cell death.
There is production of free radicals which leads to pre-oxidation and
disruption of outer cellular layer.

11. Hemorrhagic stroke
Primary intracerebral hemorrhage
Spontaneous brain hemorrhage.
Defined as non-traumatic hemorrhage within brain parenchyma
of brain.
Chronic hypertension & degenerative changes in cerebral arteries.
Mostly involves penetrating branches located in basal ganglia,
thalamus, brainstem, cerebral white matter or cerebellum.

12. Abrupt onset of symptoms that evolve gradually & steadily over
minutes, hours or days.
Prognosis for neurologic recovery may be better than that following
an ischemic infarct, since lesions are characterized by tissue
compression rather than tissue destruction.

14. Subarachnoid hemorrhage:
Often disastrous
If hemorrhage is massive  death.
Clinical sequela of sudden headache, vomiting, collapse, relative
preservation of consciousness with few lateralizing signs, neck stiffness is
diagnostic of SAH

18. Assessment
History: Associated LOC, fall, seizures, time of onset, headache, nausea, vomiting.
Weakness: Static vs progressive.
Limb: Upper limb Vs lower limb. Facial weakness.
Aphasia, dysarthria, Blurring of vision, swallowing difficulty, urinary incontinence
Functional capacity at the time of onset and the progression.
Details of the hospitalization.
Progression of symptoms. Improvement in the status in general and weakness. Any
regression in the condition.
Transition assessment.
GCS when applicable.
FIM

19. Treatment Goals Post-Stroke
Short term goals
• Patient and family education
• Decrease pain
• Prevent secondary
complications
• Improve joint mobility
Long term goals
• Functional independence in
ADLs
• Improve muscle strength
• Reduce abnormal muscle
tone
• Improve balance and
coordination

20. Impairments associated with stroke
Clinical presentation varies depending on anatomic distribution of affected
vessel, extent of lesion & presence of secondary complications.
Rehabilitation should focus on remediating or compensating for impairments
affecting functional activities.
Many volitional tasks require interlimb coordination, motivation, attention,
sensory guidance, conceptual understanding of task & intact problem solving
abilities.

22. References
O’ Sullivan SB, Schmitz TJ. Stroke. Physical rehabilitation. 7th ed.,
New Delhi: Jaypee Brothers, 2019.
Darcy A. Umphred. Neurological Rehabilitation, 5th ed., Mosby
Elsevier, Missouri, 2012.