The document discusses stroke, including its pathophysiology, types, risk factors, and management categories. Key points include: - Stroke is caused by interrupted blood flow to the brain and can be ischemic (caused by clots or blockages) or hemorrhagic (caused by bleeding). - Major risk factors include age, gender, race, family history, diabetes, heart disease, smoking, hypertension, and obesity. - Strokes are classified based on location and cause, such as thrombotic, embolic, or hemorrhagic strokes. - Complications include sensory and motor deficits, speech/swallowing issues, and cognitive/emotional changes.

1. Stroke
Pathophysiology, Types, management categories, and
vascular syndromes
Amman ullah nazir
10th semester DPT (RCRS)

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.

3. Risk Factors
Nonmodifiable
 Age
 Gender (women more likely to die)
 Race (African Americans)
 Heredity

4. Risk Factors
Modifiable
 Asymptomatic carotid stenosis
 Diabetes mellitus
 Heart disease, atrial fibrillation
 Heavy alcohol consumption
 Hypercoagulability
 Hyperlipidemia
 Hypertension
 Obesity
 Oral contraceptive use
 Physical inactivity
 Sickle cell disease
 Smoking


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

10. Major Types of Stroke
Fig. 56-3

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.

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

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

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.

26. Anatomy of CBF (circle of Willis)
 Internal carotid artery
 Vertebral artery (entering through C6)
 Basilar artery
 Anterior cerebral artery
 Middle cerebral artery
 Posterior cerebral artery
 Posterior communicating artery
 Anterior communicating artery
 Superior cerebellar artery
 Inferior cerebellar artery
 Anterior inferior cerebellar artery
 Posterior inferior cerebellar artery

28. 5 Vascular Syndromes
 Anterior cerebral artery syndrome
 Middle cerebral artery syndrome
 Posterior cerebral artery syndrome
 Lacunar syndromes
 Internal carotid artery syndrome

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.

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.

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).

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