2. Introduction
Stroke or Cerebrovascular Accident (CVA) or brain attack is
the sudden loss of neurological function caused by an
interruption of the blood flow to the brain.
5. Epidemiology
Stroke is the fourth leading cause of death and the leading
cause of long-term disability among adults in the United
States.
Incidence in Males >Females
The incidence of stroke increases dramatically with age,
doubling in the decade after 65 years of age.
6. Pathophysiology
Interruption of blood flow for only a few minutes sets in
motion a series of pathological events.
Complete cerebral circulatory arrest results in irreversible
cellular damage with a core area of focal infarction within
minutes.
The transitional area surrounding the core is termed the
ischemic penumbra and consists of viable but metabolically
lethargic cells.
Ischemia triggers a number of damaging and potentially
reversible events, termed ischemic cascade.
7. Etiology and Pathophysiology
Brain requires continuous supply of O2 and glucose for
neurons to function
If blood flow is interrupted
Neurologic metabolism is altered in 30 seconds
Metabolism stops in 2 minutes
Cell death occurs in 5 minutes
8. Cont..
Ischemic strokes produce cerebral edema, an accumulation of
fluids within the brain that begins within minutes of the insult and
reaches a maximum by 3 to 4 days.
It is the result of tissue necrosis and widespread rupture of cell
membranes with movement of water from the blood into brain
tissues.
The swelling gradually subsides and generally disappears by 2 to 3
weeks.
Significant edema can elevate intracranial pressures(normal 5 to
15mmhg), leading to intracranial hypertension and neurological
deterioration associated with contralateral and caudal shifts of brain
structures (brainstem herniation).
9. 2 Types of Stroke
Classification based on underlying pathophysiologic findings
Ischemic
Thrombotic
Embolic
Hemorrhagic
Intracerebral haemorrhage
Subarachnoid haemorrhage
11. Ischemic Stroke
Result of inadequate blood flow to brain due to partial or
complete occlusion of an artery
Constitute 85% of all strokes
Most patients with ischemic stroke do not have a decreased
level of consciousness in the first 24 hours
Symptoms often worsen during first 72 hours d/t cerebral
edema
12. Ischemic Stroke
1: Thrombotic stroke
Thrombosis occurs in relation to injury to a blood vessel wall →
blood clot
Result of thrombosis or narrowing of the blood vessel
Two-thirds are associated with HTN and diabetes
Often preceded by a TIA
Most common cause of stroke(mcq)
13. Ischemic Stroke
2: Embolic stroke
Embolus lodges in and occludes a cerebral artery
Results in infarction and edema of the area supplied by the vessel
Second most common cause of stroke
Majority of emboli originate in heart, with plaque breaking off from the
endocardium and entering circulation
Associated with sudden, rapid occurrence of severe clinical symptoms
Patient usually remains conscious although may have a headache
14. Hemorrhagic Stroke
Account for approximately 15% of all strokes
Result from bleeding into the brain tissue itself or into the
subarachnoid space or ventricles
15. Hemorrhagic Stroke
Intracerebral hemorrhage
Bleeding within the brain caused by a rupture of a vessel
Hypertension is the most important cause
Commonly occurs during activity
Often a sudden onset of symptoms that progress over
minutes to hours b/c of ongoing bleeding
Manifestations include neurologic deficits, headache,
Nausea & Vomiting, decreased levels of consciousness,
and HTN
16. Hemorrhagic Stroke
Subarachnoid hemorrhage
Bleeding into cerebrospinal space between the arachnoid and pia mater
Commonly caused by rupture of a cerebral aneurysm
17. Management Categories
Transient ischemic attack (TIA); Temporary interruption of blood supply to
the brain.
Major stroke; stable, usually severe, impairments
Deteriorating stroke; neurological status is deteriorating after
admission to the hospital. This change in status may be due to cerebral
or systemic causes (e.g., cerebral edema, progressing thrombosis).
Young stroke; persons younger than the age of 45
18. Transient ischemic attack (TIA)
Temporary interruption of blood supply to the brain.
Symptoms of focal neurological deficit may last for only a few
minutes or for several hours, but do not last longer than 24 hours.
No residual brain damage or permanent neurological dysfunction.
TIAs may result from a number of different etiological factors
including occlusive episodes, emboli, reduced cerebral perfusion
(arrhythmias, decreased cardiac output, hypotension,
overmedication with antihypertensive medications, ) or
cerebrovascular spasm.
19.
20.
21. NEUROLOGICAL COMPLICATIONS AND
ASSOCIATED CONDITIONS IN STROKE
Altered Consciousness
Sensory deficits
Motor Deficits
Disorders of Speech and Language(dysarthria)
Dysphagia
Cognitive Dysfunction
Altered Emotional Status
Hemispheric Behavioral Differences
Perceptual Dysfunction
Seizures
Bladder and Bowel Dysfunction
Cardiovascular and Pulmonary
Dysfunction
Deep Venous Thrombosis and
Pulmonary Embolus
Osteoporosis and Fracture Risk
22.
23. Altered Consciousness
Coma, decreased arousal levels) may occur with extensive brain
damage (e.g., large proximal MCA occlusion).
The Glasgow Coma Scale is the gold standard used to document level
of coma
Three areas of function are examined: eye opening, best motor
response, and verbal responses
The Glasgow Coma Scale (GCS) is a gold standard
instrument used to document level of consciousness
in acute brain injury. Three areas of function are
examined: eye opening, best motor response, and verbal response.
Total GCS scores range from a low of
3 to a high of 15.
A total score of 8 or less is indicative
of severe brain injury and coma, a score between 9 and
12 is indicative of moderate brain injury, and a score
from 13 to 15 is indicative of mild brain injury.8
The Rancho Los Amigos Scale, or Levels of Cognitive
Functioning (LOCF), is widely used in rehabilitation
24.
25. Cerebral Blood Flow (CBF)
Auto regulation
Normal flow of 50 to 60 ml/100 g of brain tissue per minute.
High energy requirements and very little metabolic reserves.
Brain requires a continuous, rich perfusion of blood to deliver
oxygen and glucose to the tissues.
Cerebral flow represents approximately 17 percent of
available cardiac output.
29. Anterior Cerebral Artery Syndrome
It supplies the medial aspect of the cerebral hemisphere (frontal
and parietal lobes) and subcortical structures, including the basal
ganglia (anterior internal capsule, inferior caudate nucleus),
anterior fornix, and anterior four fifths of the corpus callosum.
Because the anterior communicating artery allows perfusion of
the proximal anterior cerebral artery from either side, occlusion
proximal to this point results in minimal deficit.
The most common characteristic of ACA syndrome is contralateral
hemiparesis and sensory loss with greater involvement of the
lower extremity because the somatotopic organization of the
medial aspect of the cortex includes the functional area for the
lower extremity.
30.
31. Middle Cerebral Artery Syndrome
Supplies the entire lateral aspect of the cerebral hemisphere
(frontal, temporal, and parietal lobes) and subcortical
structures, including the internal capsule (posterior portion),
corona radiata, globus pallidus (outer part), most of the
caudate nucleus, and the putamen.
Occlusion of the proximal MCA produces extensive
neurological damage with significant cerebral edema.
Increased intracranial pressures typically lead to loss of
consciousness, brain herniation, and possibly death.
32. Cont.. The most common characteristics of MCA syndrome are
contralateral spastic hemiparesis and sensory loss of the face,
upper extremity (UE), and lower extremity (LE), with the face and
UE more involved than the LE.
aphasia… inability to speak
produce perceptual deficits (e.g., unilateral neglect,
anosognosiaAnosognosia is a deficit of self-awareness, a condition
in which a person who suffers some disability seems unaware of the
existence of his or her disability., apraxia, and spatial
disorganization).
Homonymous hemianopsia (a visual field defect) is also a common
finding.
The MCA is the most common site of
occlusion in stroke.
33.
34. Posterior Cerebral Artery Syndrome
The two posterior cerebral arteries are terminal branches of the
basilar artery and each supplies the corresponding occipital
lobe and medial and inferior temporal lobe . It also supplies the
upper brainstem, midbrain, and posterior diencephalon,
including most of the thalamus.
Occlusion proximal to the posterior communicating artery
typically results in minimal deficits owing to the collateral blood
supply from the posterior communicating artery (similar to ACA
syndrome).
35. Cont..
Occlusion of thalamic branches may produce
hemianesthesia (contralateral sensory loss) or central post-
stroke (thalamic) pain.
Occipital infarction produces homonymous hemianopsia,
visual agnosiaa condition in which a person can see but
cannot recognize or interpret visual information, due to a
disorder in the parietal lobes., prosopagnosia, or, if bilateral,
cortical blindness.
Temporal lobe ischemia results in amnesia (memory loss).
36.
37. Internal Carotid Artery Syndrome
Occlusion of the internal carotid artery (ICA) typically produces massive
infarction in the region of the brain supplied by the middle cerebral
artery.
The ICA supplies both the MCA and the ACA.
If collateral circulation to the ACA from the circle of Willis is absent,
extensive cerebral infarction in the areas of both the ACA and MCA can
occur.
Significant edema is common with possible uncal herniation, coma, and
death (mass effect).
38. Vertebrobasilar Artery Syndrome
The vertebral arteries arise from the subclavian arteries and
travel into the brain along the medulla where they merge at
the inferior border of the pons to form the basilar artery.
The vertebral arteries supply the cerebellum (via posterior
inferior cerebellar arteries) and the medulla (via the
medullary arteries).
The basilar artery supplies the pons (via pontine arteries), the
internal ear (via labyrinthine arteries), and the cerebellum (via
the anterior inferior and superior cerebellar arteries).
The basilar artery then terminates at the upper border of the
pons giving rise to the two posterior cerebral arteries
39. Cont…
Occlusions of the vertebrobasilar system can produce a wide
variety of symptoms with both ipsilateral and contralateral
signs, because some of the tracts in the brainstem will have
crossed and others will not.
Numerous cerebellar and cranial nerve abnormalities also
are present.
Locked-in syndrome (LIS) occurs with basilar artery
thrombosis and bilateral infarction of the ventral pons.
LIS is a catastrophic event with sudden onset.
40. Cont..
Patients develop acute hemiparesis rapidly progressing to
tetraplegia and lower bulbar paralysis (CN V through XII are
involved).
Initially the patient is dysarthric and dysphonic but rapidly
progresses to mutism (anarthria).
consciousness and sensation is preserved thus the patient
cannot move or speak but remains alert and oriented.
Horizontal eye movements are impaired but vertical eye
movements and blinking remain intact. Communication can
be established via these eye movements.
41. Lacunar Syndromes
Caused by small vessel disease deep in the cerebral white
mater (penetrating artery disease).
Associated with hypertensive hemorrhage and diabetic
microvascular disease.
Consistent with specific anatomic sites.
Pure motor lacunar stroke is associated with involvement of the
posterior limb of the internal capsule, pons, and pyramids.
Pure sensory lacunar stroke is associated with involvement of
the ventrolateral thalamus or thalamocortical projections.
42. Cont..
Dysarthria/ clumsy hand syndrome (involving the base of the pons,
genu of anterior limb or the internal capsule)
Ataxic hemiparesis
Deficits in consciousness, language, or visual fields are not seen in
lacunar strokes as the higher cortical areas are preserved.
43. MEDICAL DIAGNOSIS OF STROKE
History and examination
Tests and measures
Use of NIHSS National Institutes of Health Stroke Scale
Blood analysis
Imaging .. CT scan, MRI
Pharmacologic Management or surgical management…
Thrombolytics tPA.. Tissue plasminogen activator
Anticoagulants (e.g., warfarin [Coumadin], heparin, dabigatran
etexilate [Pradaxa])
Antiplatelet therapy (e.g., acetylsalicylic acid [aspirin]; clopidogrel
bisulfate [Plavix]; dabigatran etexilate [Pradaxa]; ticlopidine
hydrochloride [Ticlid])
Antihypertensive agents (e.g., ACE inhibitors, alpha-blockers
[Minipress], beta-blockers, calcium channel blockers, direct
vasodilators, diuretics, postganglionic neuron inhibitors
Angiotensin II receptor antagonists (telmisartan [Micardis], losartan
potassium [Cozaar])
Antispastics, anticonvulsants, antidepressants.
44. Physical therapy Interventions in stroke patient
Strategies to Improve Motor Learning
Interventions to Improve Sensory Function
Interventions to Improve Hemianopsia and Unilateral Neglect
Interventions to Improve Flexibility and Joint Integrity
Interventions to Improve Strength
Interventions to Manage Spasticity
Interventions to Improve Movement Control
Strategies to Improve Upper Extremity Function
Strategies to Improve Lower Extremity Function
Interventions to Improve Functional Status
Interventions to Improve Postural Control and Balance
Interventions to Improve Gait and Locomotion
Interventions to Improve Aerobic Capacity and Endurance
45. QUESTIONS ????
A TIA is characterised by
a) Neurological symptoms lasting for less than 24 hours
b) Neurological symptoms lasting for more than 24 hours but
less than 1 week
c) Neurological symptoms lasting for more than 1 week but
less than 6 weeks
d) Neurological symptoms lasting for more than 6 weeks
46. Cont..
A 55 year old woman presents with contralateral spastic
hemiparesis and sensory loss of the face, upper
extremity (UE), and lower extremity (LE), with the face
and UE more involved than the LE is characterized by
the following vascular syndrome.
a) MCA
b) PCA
c)PCA
d) None of the above
47. Stroke posture
ntigravity positions is common; for example, a spastic
upper extremity is typically held fixed against the body
with the shoulder adducted, elbow flexed, forearm
supinated with wrist/fingers flexed. In the supine position, the
lower extremities are typically held in extension, adduction
with plantarflexion, and inversion
(Table 5.3).18 Limbs that appear floppy and lifeless
(e.g., a lower
48. All stroke
he patient with brain
injury who has a condition called optic ataxia can recognize an object
using focal vision but cannot use visual information to accurately
guide the hand to the object (impaired ambient vision).
The opposite occurs in a patient with stroke experiencing visual
agnosia. The patient cannot recognize common objects, but can use
the ambient visual system to reach and grasp an object
or navigate an environment. Vision also contributes to righting
reactions of the h
Patients with stroke who exhibit topographical disorientation will have
difficulty navigating their environment and understanding the
relationship of one place
to another.
Soma