STROKE

Definition:
- Aka cerebral apoplexy, cerebrovascular disease/accident (CVA/CVD), brain attack
- A clinical syndrome characterized by the sudden development of a persisting focal neurological deficit as a result
of a vascular pathology
- Due to rapid loss of brain function as a result of disturbances in the blood supply to the brain
- A medical emergency & can cause permanent neurological complications & deaths
- Neurological deficits must persists for at least 24 hours to be considered a stroke

Epidemiology:
- 3rd leading cause of death & the most common cause of disability
- Incidence of stroke ↑ with age, doubling in every decade after 65/55 years of age
- M > W (1.25:1)
- Common in African-Americans, Mexican-Americans, Indian-Americans & Alaskan natives
- Rare in whites
- Most common type of stroke: Ischemic stroke
- Common type of stroke in young adults: Hemorrhagic stroke
- Most common type of stroke that results to death: Hemorrhagic stroke
- Death is W > M (60% higher in women)
Predictors of mortality
 Loss of consciousness  Lesion size
 Age  Persistent severe hemiplegia
 HPN  Multiple neurological deficits
 Heart disease  History of previous stroke
 DM

Etiology:
- Atherosclerosis – major contributory factor in stroke
 Characterized by plaque formation with an accumulation of lipids, fibrin, complex carbohydrates, &
calcium deposits on arterial walls that leads to progressive narrowing of blood vessels
 Sites of predilection:
a. Origin at the common carotid artery
b. Transition into the middle cerebral artery
c. Main bifurcation of the middle cerebral artery
d. Junction of the vertebral arteries with the basilar artery
- Risk factors for stroke:
Modifiable risk factors Non-modifiable risk factors
HPN – most important risk factor Age
Heart disease Race
- CAD ↑ risk by 2 times
- CAD accounts for the majority of subsequent deaths following stroke
- Atrial fibrillation & valvular heart disease ↑ risk of cerebral
infarction because both may cause cerebral emboli
- Atrial fibrillation ↑ risk by 5 times
- Rheumatic heart disease with atrial fibrillation ↑ risk by 17 times
Smoking – ↑ risk by 1.5 times Sex
DM – ↑ risk by 2 times Family history
Elevated fibrinogen – have ↑ levels in individuals who smoke & have high-
cholesterol diet
Hyperlipidemia – includes ↑ blood cholesterol, ↑ low density lipoprotein
(LDL), ↓ high density lipoprotein (HDL)
Erythrocytosis
Transient ischemic attack (TIA)
Obesity
Lack of exercise
Diet
Excessive alcohol consumption
History of previous stroke

- Classified according to mode of interruption of blood supply:

a. Ischemic
 The result of a thrombus, embolism, or conditions that produce low systemic perfusion pressures
  Lack of cerebral blood flow deprives the brain of needed oxygen & glucose, disrupts cellular
metabolism, & leads to injury & death of tissues
 The neurological deficits produced with systemic failure are global in nature with bilateral
neurological deficits
1. Thrombotic
 Results from platelet adhesion & aggregation on plaques
 Lead to ischemia, or occlusion of an artery with resulting cerebral infarction or tissue death
 Tends to affect large extracranial & intracranial blood vessels
 Gradual in onset
 About 32% are thrombotic in nature
2. Embolic
 Composed of bits or matter (blood clot, plaque) formed elsewhere & released into the
bloodstream, traveling to the cerebral arteries where they lodge in a vessel producing an
occlusion & eventually infarction
 Most common source of cerebral emboli: cardiovascular system (heart)
 Tends to affect small distal cortical branches of the cerebral artery
 Abrupt onset
 About 32% are embolic in nature
3. Lacuna
 Are small, circumscribed lesions, at most 1.5 cm in diameter, & frequently much smaller
 Affects small-diameter branches of the cerebral arteries (lenticulostriate artery, others)
 Strongly associated with HPN & diabetic microvascular disease
 Tend to occlude the deep penetrating branches of the large vessels which perfuse the
subcortical structures (internal capsule, basal ganglia, thalamus & brainstem)
 Often show early & progressive recovery with good ultimate outcome
 Gradual in onset
 About 18% are lacunar in nature
 Are consistent with specific anatomic sites: (pure motor versus pure sensory)
i. Pure motor lacunar stroke
 Associated with involvement of the posterior limb of the internal capsule, pons, &
pyramids
ii. Pure sensory lacunar stroke
 Associated with involvement of the ventrolateral thalamus or thalamocortical
projections
iii. Dysarthria/clumsy hand syndrome
 Involving the base of the pons, genu of anterior limb or the internal capsule
iv. Ataxic hemiparesis/hemiataxia
 Involving the pons, genu of internal capsule, corona radiate, or cerebellum
v. Sensory/motor (sensorimotor) stroke
 Involving the junction of the internal capsule & thalamus
vi. Dystonia/involuntary movements (hemichorea-hemiballismus)
 Choreoathetosis with lacunar infarction of the putamen or globus pallidus;
hemiballismus with involvement of the subthalamic nucleus
vii. Pseudobulbar palsy
 Multiple small lesions affecting the anterior limb of both internal capsule,
including the corticobulbar tract
 Presents with pseudobulbar affect, dysarthria, dysphonia, & facial weakness
viii. Central post-stroke (thalamic) pain syndrome
ix. Multi-infarct dementia
b. Hemorrhagic
 Abnormal bleeding into the extravascular areas of the brain are the result of rupture of a cerebral
vessel or trauma
 Results in ↑ ICP with injury to brain tissues & restriction of distal blood flow
 Closely linked to chronic HPN
 Arteriovenous malformation (AVM) – another congenital defect characterized by a tortuous tangle
of arteries & veins with agenesis of an interposing capillary system
 Sudden, severe cerebral bleeding can result in death within hours, because ICP rise rapidly &
adjacent cortical tissues are compressed or displaced (brainstem herniation)
 Abrupt in onset
1. Intracerebral
 Caused by rupture of a cerebral vessel with subsequent bleeding into the brain
 Occurs at the small site of small, deep penetrating arteries
  Primary cerebral hemorrhage – spontaneous hemorrhage typically occurs in small blood
vessels weakened by an atherosclerosis producing an aneurysm
 About 11% are Intracerebral in nature
2. Subarachnoid
 Occurs from bleeding into the subarachnoid space typically from a saccular or berry
aneurysm affecting primarily large blood vessels at the base of the brain
 Manifested by a severe headache followed by vomiting & signs of meningeal irritation
 Has a ↑ risk of hydrocephalus & coma
 About 7% are subarachnoid in nature

Clinical Manifestation:
1. Sensory impairments (anesthesia, hypoesthesia, dysesthesia, hyperesthesia, numbness)
 Lesion: Cortex (localized areas) or thalamus & adjacent structures (diffused)
2. Pain
 Central post-stroke (thalamic) pain – aka Dejerine-Roussy; involves the ventral posterolateral
thalamus & spinothalamic system; characterized by constant, severe burning pain with
intermittent sharp pains
3. Visual impairments
a. Visual loss (homonymous hemianopsia, monocular blindness)
 Lesion: optic radiation in the internal capsule (MCA) or the primary visual cortex (PCA)
 May also result to visual neglect/inattention, problems with depth perception & spatial
relationship
b. Paralysis of conjugate gaze
 Lesion: frontal lobe eye field (BA 8), CN 3, gaze centers in the pontine reticular
formation
 Result in forced gaze deviation – unopposed action of the intact eye muscles causes the
eye to deviate to the good side
 If lesion is at the hemispheres: looks away from the hemiplegic side
 If lesion is at the brainstem: looks toward the hemiplegic side
4. Motor impairments (weakness & paralysis)
 Lateral corticospinal tract versus anterior corticospinal tract
 Distal > proximal
 Selective loss of type II fast-twitch fibers
 ↓ number of functioning motor units & discharge firing rates due to degeneration of alpha
motor neurons
 ↑ effort & fatigability due to abnormal recruitment of motor units
 (+) denervation potentials
 ↑ coactivation of agonists & antagonists
5. Alterations in tone
 Flaccidity (hypotonicity) – present immediately after stroke (cerebral shock) & generally lasts for
a few days or weeks (if it persists, may indicate lesion to the cerebellum or primary motor
cortex)
 Spasticity (hypertonicity) – occur predominantly in anti-gravity muscles
6. Abnormal synergy patterns (obligatory synergies)
 Patient is unable to perform an isolated movement of a limb segment without producing
movement in the remainder of the limbs
Flexion synergy components Extension synergy components
UE Scapular retraction Scapular retraction
Shoulder abduction, ER Shoulder adduction, IR
Elbow flexion Elbow extension
FA supination FA pronation
Wrist & finger flexion Wrist & finger flexion
LE Hip flexion, abduction, ER Hip extension, adduction, IR
Knee flexion Knee extension
Ankle DF, inversion Ankle PF, inversion
Toe DF Toe PF
 Muscles usually not involved in synergy:
a. Finger extensors
b. Latissimus dorsi
c. Ankle evertors
d. Teres major
e. Serratus anterior
7. Abnormal reflexes
 Indicative of UMNL
  When spasticity & synergies emerge, hyperreflexia is seen consisting of the following:
 Stretch reflexes are hyperactive
 Clonus
 Clasp-knife response
 (+) Babinski reflex
 (+) Tonic reflexes (ATNR, STNR)
 (+) Associated reactions
8. Altered coordination
 Cerebellum versus Basal ganglia lesions
 Cerebellum lesions – produce cerebellar ataxia, weakness, problems with timing & sequencing
of muscles (diadodyskinesia)
 Basal ganglia lesions – produce bradykinesia & involuntary movements (Choreoathetosis,
hemiballismus)
9. Altered motor programming (apraxia)
 Lesion: premotor frontal cortex of either hemisphere, left inferior parietal lobe, & corpus
callosum
 Difficulty planning & executing purposeful movements that cannot be accounted for by any
other reason
 2 main types of apraxia:
a. Ideational apraxia – inability of the patient to produce movement either on command or
automatically
b. Ideomotor apraxia – unable to produce a movement on command but is able to move
automatically
 Other types of apraxia:
a. Kinetic apraxia – can perform gross task but not fine motor task
b. Dressing apraxia
c. Constructional apraxia
d. Verbal/oral apraxia – characterized by labored & dysprosodic productions resulting in errors
of omission, substitution, & repetition
e. Oculomotor apraxia – eye movements
10. Postural control & balance impairments
 Problems may exist in reactive postural control & anticipatory postural control
 Typically demonstrate asymmetrical weight bearing in sitting or standing, shifted toward the
stronger side
 Direction of fall is typically in the hemiplegic/weak side
 Ipsilateral/contraversive pushing/pusher’s syndrome – unusual motor behavior characterized by
active pushing with the stronger extremity toward the hemiparetic side, leading to a lateral
postural imbalance
11. Speech, language, & swallowing impairments
a. Aphasia
 Lesion: Cortex the dominant hemisphere (typically the left hemisphere)
 General term used to describe acquired communication disorder caused by brain
damage & is characterized by an impairment of language comprehension, formulation,
& use
Fluency Comprehension Repetition Aphasia Area affected
G Anomia Angular gyrus
G
G P
P
G
P
Conduction
Transcortical sensory
Wernicke’s
Arcuate fasciculus
Temporal lobe
Temporal lobe
G Transcortical motor Prefrontal lobe
G
P P
P
G
P
Broca’s
Isolation
Global
Frontal lobe
Watershed areas
Multilobe
 Summary of the Boston classification system of aphasia:
Type Language characteristics
Nonfluent
1. Broca Telegraphic, agrammatic expression often associated with apraxia
2. Transcortical motor Limited language output
3. Global Severe expressive & receptive reduction in language
4. Mixed transcortical Severe reduction in expression & reception
Fluent
1. Anomia Word-finding difficulty without other serious linguistic deficits
2. Conduction Phonemic paraphasic errors
 3. Wernicke Phonemic & semantic paraphasias
4. Transcortical sensory Fluent neologistic language
b. Dysarthria
 Lesions: Primary motor cortex in the frontal lobe, in the parietal lobe, or the cerebellum
 Refers to a category of motor speech disorders caused by lesions in parts of the CNS/PNS
that mediate speech production
c. Dysphagia
 Lesions: medullary brainstem (CN IX & X), large vessel pontine lesions, as well as in acute
hemispheric lesions (MCA & PCA)
 Dysfunction of the lips, mouth, tongue, palate, pharynx, larynx or proximal esophagus
 Problems:
 Delayed triggering of the swallowing reflex
 ↓ pharyngeal peristalsis
 ↓ lingual control
12. Perception impairments
 Lesion: Frequently in the right parietal cortex
 Include impairments in:
a. Body scheme/body image
 Refers to a postural model of the body including the relationship of the body parts to each
other & the relationship of the body to environment
 Impairments: unilateral neglect, anosognosia, somatoagnosia, right-left discrimination,
finger agnosia & anosognosia
b. Spatial relations
 Refers to a constellation of impairments that have in common a difficulty in perceiving the
relationship between & the self & two or more objects in the environment
 Impairments: figure-ground discrimination, form discrimination, spatial relations, position
in space, & topographical disorientation
c. Agnosia
 Impairments: visual object agnosia, auditory agnosia, tactile agnosia (astereognosis)
13. Cognition impairments
 Lesions involving the cortex
 Include impairments:
a. Alertness
 Lesion: prefrontal cortex & reticular formation
 Largely unaware of what is going on in the external environment
b. Attention
 Lesion: prefrontal cortex & reticular formation
 Inability to select & attend to a specific stimulus while simultaneously suppressing
extraneous stimuli
 Include impairments in sustained attention, selective attention, divided attention or
alternating attention
c. Orientation
 Lesion: prefrontal cortex, limbic system & limbic cortex
 Unable to provide information about self, time of day, physical or geographical location
d. Memory
 Lesion:
i. Short-term memory: limbic system, limbic association cortex, or temporal lobes
ii. Long-term memory: hippocampus of the limbic system
iii. Confabulation: prefrontal cortex
 Inability to store experiences & perceptions for later recall
 Short term memory versus long-term memory loss
 Confabulation – memory gaps may be filled with inappropriate words or fabricated stories
e. Confusion
 Lesion: bilateral prefrontal cortex
 Inability to understand the specific context of a conversation
f. Perseveration
 Lesion: premotor &/or prefrontal cortex
 Continued repetition of words, thoughts, or acts not related to current context
g. Executive function
 Lesion: prefrontal cortex
 Person is unable to engage in purposeful behavior, include volition planning purposeful
action, & effective performance
  Demonstrate impairments executive functions including: impulsiveness, inflexible
thinking, lack of abstract thinking, impaired organization & sequencing, ↓ insight,
impaired planning ability & impaired judgment
h. Dementia
 Lesion: multiple small infarcts of the brain (multi-infarct dementia)
 Characterized by progressive impairments in memory & cognition
 Demonstrate impairments executive functions including: impulsiveness, inflexible
thinking, lack of abstract thinking, impaired organization & sequencing, ↓ insight,
impaired planning ability & impaired judgment
i. Delirium
 A result of deprivation of oxygen to the brain, metabolic imbalance, adverse drug
reactions, sensory & perceptual losses, unfamiliar environment & inactivity
 Aka acute confusional state
 Characterized by a clouding of consciousness/dulling of cognitive processes & impaired
alertness
 Patient is inattentive, incoherent & disorganized with fluctuating levels if consciousness
14. Emotional status changes
 Lesion: frontal lobe, hypothalamus, & limbic system
a. Pseudobulbar affect (PBA)
 Aka emotional lability/emotional dysregulation syndrome
 Characterized by emotional outbursts of uncontrolled or exaggerated laughing or crying
with only slight provocation
b. Apathy
 Characterized by a shallow affect & blunted emotional responses
c. Euphoria
 Exaggerated feelings of well-being, ↑ levels of irritability or frustration, & social
inappropriateness
 Depression
 Lesion: left frontal lobe (acute stage) & right parietal lobe (subacute stage)
 Characterized by persistent feelings of sadness accompanied by feelings of hopelessness,
worthlessness &/or helplessness
 Left hemisphere > right hemisphere
15. Hemispheric behavioral differences
 Function of the hemispheres:
Left hemisphere Right hemisphere
Writing & language Emotional experience
Scientific skills Spatial awareness, dimensions
Math Music
Logic Creativity, imaginations
Lists Gestalt (whole picture)
LINEAR THINKING MODE HOLISTIC THINKING MODE
a. Left hemisphere damage
 Demonstrate difficulties in communication & in processing information in a sequential,
linear manner
 Described as cautious, anxious & disorganized
b. Right hemisphere damage
 Demonstrate difficulty in spatial-perceptual tasks & in grasping the whole idea of a task
or activity
 Described as quick & impulsive
 Overestimate their abilities while acting unaware of their deficits
Right brain injury Left brain injury
Visual-perceptual impariments Speech & language impairments
Difficulty sustaining a movement Difficulty planning & sequencing movements
(apraxia)
Quick, impulsive behavioral site Slow, cautious behavioral style
Difficulty grasping the overall organization or pattern, Disorganized problem solving
problem solving & synthesizing information
Often unaware of impariments, poor judgment Often very aware of impairments, anxious about poor
performance
Rigidity of though, difficulty with abstract reasoning Difficulty with processing delays
Difficulty with perception of emotions, expression of Difficulty with expression of positive emotion
negative emotions
Difficulty processing visual cues Difficulty processing verbal cues, verbal command
 Memory impairments, typically related to spatial- Memory impairments, typically related to language
perceptual information
16. Bladder & bowel alterations
 Urinary incontinence result from bladder hyperreflexia or hyporeflexia, disturbances of
sphincter control, &/or sensory loss
 Timed voiding/toileting schedule
 Bowel dysfunction: incontinence & diarrhea/constipation & impaction
 May require stool softeners & dietary/fluid modification
Pathophysiology:
Occlusion of a cerebral artery Rupture of a cerebral artery
↓ ↓ ↓
Loss of blood supply distal to the affected artery Blood is displaced in the brain parenchyma or
within the cerebral spaces
↓ ↓
Ischemia occurs  Cerebral  ↑ in ICP
↓ edema begins ↓
Focal infarction and an area of within minutes Brainstem herniation
viable but damaged cells
(ischemic penumbra) then
follows within minutes
↓
Ischemic cascade follows
↓
Further infarction

Categories:
I. According to management category:
1. Transient Ischemic Attack (TIA)
 Reflect local areas of retinal or cerebral ischemia of sufficient duration to cause neurological
signs & symptoms but is brief & does not persist long enough to develop a functionally
significant cerebral infarction
 May lasts for a few seconds or minutes without any sequelae, resolving within 24 hours
 In up to 30% of patients, a stroke will develop within 5 years
 Caused by occlusive episodes, emboli or reduced cerebral perfusion or cerebrovascular spasm
2. Reversible Ischemic Neurological Deficit (RIND)
 Impairments that resolve spontaneously as brain swelling subsides, generally within 3 weeks
3. Major stroke/Complete stroke
 Presence of stable, usually severe, impairments
4. Minor stroke
5. Stroke in evolution/Progressive stroke/Deteriorating stroke
 Used to refer to the patient whose neurological status is deteriorating after admission to the
hospital
 May be due to cerebral or systemic causes (cerebral edema, progressing thrombosis)
6. Young stroke
 Describe a stroke affecting persons younger than the age of 45
 May have potential for better recovery
II. According to vascular territory:
Cerebral blood flow (CBF)
 Circle of Willis
- Normal cerebral blood flow: 50-60 ml/100 g of brain tissue per minute
- Cerebral blood flow is usually maintained constantly by a number of cerebral autoregulatory
mechanisms
- Main blood supply to the brain is provided by:
a. Internal carotid arteries
 Gives off the ophthalmic & anterior choroidal arteries before bifurcating into the
MCA & ACA
b. Vertebral arteries
 Arises as a branch off the subclavian artery & unites together to form the basilar
artery (at the upper border of the medulla) & bifurcates to form the PCA (at the
upper border of the pons)
- Circle of Willis is composed of:
a. Anterior cerebral artery (ACA)
 b. Anterior communicating artery (Acomm)
c. Posterior cerebral artery (PCA)
d. Posterior communicating artery (Pcomm)
1. Internal carotid artery (ICA)
 Typically produces massive infarction in the region of the brain supplied by the MCA
 ACA may be preserved through the collateral circulation (Acomm)
 Significant edema is common with possible herniation, coma & death (mass effect)
 Amaurosis fugax syndrome – transient occlusion of the retinal branches of an ophthalmic artery
(branch of ICA) produces sudden, loss of vision in the eye (ipsilateral)
2. Anterior cerebral artery (ACA)
 The first & smaller of 2 terminal branches of the ICA
 Supplies the medial aspect of the cerebral hemisphere (frontal & parietal lobe) & subcortical
structures including the basal ganglia (anterior internal capsule, inferior/head caudate nucleus),
anterior fornix & anterior 4/5 of the corpus callosum
 Manifestation:
 Contralateral hemiparesis & sensory loss
 Greater involvement of the LE
 Dominant hemisphere: produces transcortical motor aphasia
3. Middle cerebral artery (MCA)
 2nd of the 2 main branches of the ICA
 Most common site of occlusion in stroke
 Supplies the entire lateral aspect of the cerebral hemisphere (frontal, temporal & parietal lobe)
& subcortical structures, including the internal capsule (posterior portion), corona radiate,
globus pallidus (outer part), most of the caudate nucleus, & the putamen
 Manifestation:
 Contralateral spastic hemiparesis & sensory loss of the face, UE, & LE
 Greater involvement of face & UE
 Dominant hemisphere: produces aphasia (Broca’s or Wernicke’s aphasia)
 Nondominant hemisphere: produces perceptual deficits (unilateral neglect,
anosognosia, apraxia, & spatial disorganization)
 Homonymous hemianopsia
4. Posterior cerebral artery (PCA)
 Aries as the terminal branches of the basilar artery
 Supplies the corresponding occipital lobe & medial & inferior temporal lobe, the upper
brainstem, midbrain & posterior diencephalon, including most of the thalamus
 Manifestation:
 Occlusion of the thalamic branches may produce hemianesthesia or central post-stroke
(thalamic) pain
 Homonymous hemianopsia
 Visual agnosia
 Prosopagnosia
 Temporal lobe ischemia results in amnesia
 Cerebral peduncle involvement results in contralateral hemiplegia
5. Vertebrobasilar artery
 Arises from the 2 vertebral arteries that join at the junction of the medulla & pons
 Supply the brainstem & cerebellum
 Can produce a variety of symptoms with both ipsilateral & contralateral signs
 Lesions involving the pons & medulla often cross the midline & cause bilateral features
 Often accompanied by cerebellar signs
 Cranial nerve lesions are very frequent & occur ipsilaterally
 Produces contralateral corticospinal signs
 Absence of aphasia & cognitive deficits
 Vertebrobasilar artery or brainstem syndromes:
Syndrome Artery Areas affected Manifestation
Weber Superior cerebellar Medial basal midbrain, CN Ipsilateral CN 3 palsy &
artery 3 contralateral hemiplegia
Benedikt Anterior inferior Tegmentum of midbrain, Ipsilateral CN 3 palsy &
cerebellar artery CN 3 contralateral loss of pain &
temperature
Locked-in Basilar artery B basal pons, B CST, B CBT Spared blinking & vertical gaze,
B hemiplegia, B cranial nerve
palsy, coma
Millard-Gubler posterior inferior Lateral pons, CN 6, 7 Ipsilateral peripheral facial palsy,
 cerebellar artery loss of conjugate gaze
Wallenberg or Vertebral artery or Lateral medulla, CN 5, 9, Horner’s syndrome, ipsilateral
lateral posterior inferior 10 ataxia, ipsilateral facial &
medullary cerebellar artery contralateral limbs sensory loss
syndrome
Dejerine Medial medulla, CN 12 Ipsilateral CN 12 palsy,
contralateral hemiparesis,
contralateral DCML loss
Marie-Foix Lateral pons Ipsilateral ataxia, contralateral
hemiparesis, contralateral hemi-
hypoesthesia
Foville Inferior medial pons, CN 7 Ipsilateral peripheral facial palsy,
contralateral hemiplegia, loss of
conjugate gaze
Raymond Ventral pons Ipsilateral lateral gaze weakness,
contralateral hemiplegia
Anton B PCA B PCA B visual loss & denial of
blindness
III. According to etiology:
1. Thrombotic
2. Embolic
3. Lacunar
4. Hemorrhagic

Complication:
1. Musculoskeletal
 Loss of ROM & contractures (in the affected side)
 Edema & pain
 Postural deformity
 Disuse atrophy & muscle weakness
 Osteoporosis
2. Neurological
 Seizures – common in ICA affectation
 Hydrocephalus – excessive accumulation of CSF within the cranial cavity
3. Cardiovascular/Pulmonary
 Thrombophlebitis/DVT – hallmark: rapid onset of unilateral leg swelling with dependent edema
 Cardiac impairments – deconditioning
 Pulmonary impairments – RLD, aspiration
4. Integumentary
 Skin breakdown, pressure sores & decubitus ulcer (bony prominence)
a. Shearing
b. Maceration

Differential Diagnosis:
- Seizure
- Brain tumor
- Encephalitis
- Abscess
- Trauma
- Syncope

Medical Management:
1. Diagnosis:
 Determined by CT scan, MRI or cerebral angiography
a. Pathologic diagnosis:
 Cerebral infarction (ischemia), intracerebral hemorrhage or subarachnoid hemorrhage
b. Anatomic diagnosis:
 Determining the location of the structural lesion, & affected cerebral artery
c. Etiologic diagnosis:
 Determine risk factors
 Occlusions versus ruptures (hemorrhages)
 Ruptures are usually the result of an embolism
2. Test & Measures:
a. Urinalysis – detects infection, DM, renal failure or dehydration
 b. Blood analysis – provides a complete blood count (CBC), platelet count, prothrombin time, partial
thromboplastin time, & erythrocyte sedimentation rate (ESR)
c. Fasting blood glucose level
d. Blood chemistry profile – indicates serum electrolytes & serum cardiac enzyme levels
e. Blood cholesterol & lipid profile
f. Thyroid function tests – accelerated atherosclerosis can result from hypothyroidism
g. Full cardiac evaluation – includes radiograph of the chest; electrograph (ECG) to detect arrhythmias
h. Echocardiography – may reveal valvular disease (a source of emboli) or other heart conditions such as CHF,
recent MI
i. Lumbar puncture – may be used to diagnose subarachnoid hemorrhage in the presence of focal neurological
deficit & nuchal rigidity
3. Imaging:
a. Computerized Tomography (CT) – most commonly used imaging technique, less expensive, reveals
structural lesions (hemorrhage, tumor, abscess)
b. Magnetic Resonance Imaging (MRI) – greater resolution of the brain & its structural detail is obtained with
MRI than CT scan (more sensitive in detecting small lacunar lesions especially in the brainstem &
cerebellum)
c. Positron Emission Tomography (PET) – allows imaging of regional blood flow & localized cerebral
metabolism; high cost & limited availability of PET scans limit the use in the routine evaluation of stroke
d. Transcranial & Carotid Doppler – non-invasive imaging of the neck & chest vessels
e. Cerebral Angiography – invasive & involves the injection of radiopaque dye into blood vessels with
subsequent radiography; provides visualization of the vascular system
4. Pharmacological interventions:
a. Anticoagulant therapy (heparin, Coumadin) – used to improve perfusion & reduce the risk of recurring clots
b. Antiplatelet therapy (aspirin) – long-term, low dose is used to ↓ the risk of recurrent stroke
c. Antihypertensive drugs
5. Neurosurgical interventions:
a. Endarterectomy – surgical removal of the lining & plaque of an artery; used to prevent stroke but not treat
acute strokes
b. Repair of a superficial rupture aneurysm or AVM (in hemorrhagic stroke)
c. Resection of a superficial unruptured AVM

Assessment/Examination:
 Purpose:
1. Determine the diagnosis & classification
2. Monitor recovery from stroke
3. Identify patients who are most likely to benefit from rehabilitation services & the most appropriate choice of a
setting
4. Develop a specific plan of care
5. Monitor progress toward projected goals through reevaluation
6. Determine if referral to another practitioner is indicated
7. Plan for discharge
 Assessment:
 Interviews
 Informal
 Unstructured
 Inventories
 Questionnaires
 Structured assessment
 Therapist gives a task to do then rates the performance
 Naturalistic observation
 Gather info in a natural setting that the activity occurs
 Elements:
a. Patient/Client history
b. Systems review
c. Test & measures
 Cognitive ability
 Orientation (to person, place, time & circumstance)
 Attention (selective, sustained, alternating, divided)
 Memory (immediate, short- & long-term)
 Follow instructions (one-, two-, & three-level commands)
 Arithmetic & abstract reasoning (grasp of information, abstract thinking & problem solving,
calculating ability, constructional ability)
 Mini-Mental Status Examination (MMSE) – valid & reliable quick screen of cognitive function
  Communication & language
 Close collaboration with the speech language pathologist (SLP)
 Aphasia (fluent versus non-fleunt) & neuromotor disorders (dysarthria, apraxia)
 To assess: test for reception first (being with a concrete task such as copying or matching &
proceed to more difficult task such as the reading of sentences for comprehension)  followed
by testing expression (repetition, naming, providing definitions)
 Minnesota Test for Differential Diagnosis of Aphasia
 The Boston Diagnostic Aphasia Examination
 The Western Aphasia Battery
 The Token Test
 Cranial nerve integrity
 Facial sensation (CN V)
 Facial movements (CN V, VII)
 Labyrinthine/auditory function (CN VIII)
 Swallowing difficulty (CN IX, X, XII)
 Visual field defects (CN II, optic radiation, visual cortex)
 Pupillary reflex (CN II, CN III)
 Extraocular movements (CN III, IV, VI)
 Sensory integrity
 Superficial
 Deep
 Combined/cortical
 Motor function
 Abnormal tone: flaccidity, spasticity
 Modified Ashworth scale (MAS)
Grading Description
0 No ↑ in muscle tone
1 Slight ↑ in muscle tone, manifested by a catch & release or by minimal resistance at the
end of the ROM when the affected part(s) is moved in flexion or extension
1+ Slight ↑ in muscle tone, manifested by a catch, followed by minimal resistance
throughout the remainder (less than half) of the ROM
2 More marked ↑ in muscle tone through the most of the ROM, but affected part(s)
easily moved
3 Considerable ↑ in muscle tone, passive movement difficulty
4 Affected part(s) rigid in flexion or extension
 Tardieu scale
Grading Description
0 No resistance throughout the course
1 Slight resistance throughout the course with no clear catch at a precise angle
2 Clear catch at a precise angle, followed by release
3 Fatigable clonus, < 10 seconds when maintaining pressure, appearing at a precise angle
4 Non-fatigable clonus, > 10 seconds when maintaining pressure at precise angle
 Pathological reflexes
 Obligatory synergies/abnormal involuntary movement (chorea, hemiballismus)
 To assess: check voluntary movement patterns
 Motor planning: apraxia
  To assess: patient is asked to touch nose, drink from a glass, put a pencil in a glass, strike
a match & blow it out & use scissors  patient is asked to perform without the objects
& with each hand
 Constructional apraxia: ask patient to copy a geometric design or draw the face of a
clock
 Dressing apraxia: ask patient to put on a coat
 Posture
 Sitting & standing
 Assess symmetry
 Postural Assessment Scale for Stroke Patients (PASS)
 Balance
 Static & dynamic balance (reactive postural control & anticipatory posture control)
 Static balance: assess steadiness
 Dynamic balance: assess balance from one posture to another (supine-to-sit, sit-to-stand),
against perturbations or in response to voluntary extremity movements
 Berg Balance scale (BBS)
 Fugl-Meyer test (FM-B)
 Gait & locomotion
 Observational gait analysis (OGA) – examine the movements occurring at the ankle, foot, knee,
hip, pelvis & trunk
 Physiologic, Household, Community Walker
 The 1-Meter Walk Test
 The 6-Minute Walk Test
 Functional status & activity level
 Assess ADLs & iADLs
 Barthel Index
 FIM
 Stroke Rehabilitation Assessment of Movement (STREAM)
 Work, community & leisure activities
 Occupational performance emphasizing self-care & iADL
 Stages of Motor Recovery
 Brunnstrom
Stage Description
Stage 1 Flaccidity (no movement of the limbs)
Stage 2 Beginning spasticity (minimal voluntary movement)
Stage 3 Peak spasticity (voluntary control of the movement synergies)
Stage 4 Spasticity begins to decline
Stage 5 Waning spasticity (more difficulty movement combinations are learned
Stage 6 Spasticity disappears
Stage 7 Recovery
 Bobath
Phase
Phase of flaccidity
Phase of spasticity
Phase of recovery
 OT
 Focus on UE function:
 Somatosensory assessment
 Mechanical & physiological components
 Voluntary movement
 Strength & endurance
 Functional performance
 Approach assessment:
1. Client-centered assessment
 Embraces a philosophy of respect for, & partnership with people receiving services
Law, Baptiste, Mills Canadian Occupational Performance Model
 Clients are qualified to make decisions about their occupational  Allow recipient of treatment to identify
functioning areas of difficulty & rate the importance
 More active role in defining goals & desired outcome of each area
 Interdependence in client-therapist relationship to enable the  Clients who sustained a stroke because
solution of performance dysfunction of multiple & extensive problems that
 OTs work with clients to enable them to meet their own goals this population experiences in
 Focus in the contexts in which client live, their roles & interests, & performance of areas of occupation
 their culture
 Client is “problem-definer” so becomes a “problem solver”
 Client evaluates own performance & set personal goals
2. Top-down approach assessment
 Starting point of evaluation: inquiry into role competency & meaningfulness
 Focused on the roles that are important to the client who sustained a stroke
 Discrepancies in past, present or future are identified to determine treatment plan
 First focuses on dysfunction of client factors
3. Standardized tools
 Clinical Picture Guidelines for Post-Stroke Rehabilitation
o Focused on task performance should be used
o Tools directly relate performance dysfunction observed during ADLs with the effect of
underlying skills necessary for independent performance of assessment
 Arnadottir Occupational Therapy Neurobehavioral Evaluation (A-ONE)
o Documents the way that dysfunction of client factors affects self-care & mobility tasks
 Assessment of Motor & Process Skills (AMPS)
o Use predominantly iADLs to evaluate underlying performance skills

Rehabilitation:
- Recovery & prognosis:
 Diachesis – transient inhibition of function, that accompanies acute stroke
 1st month – fastest measurable & functional recovery
 Type of stroke with best prognosis: Hemorrhagic stroke
 Type of stroke with worst prognosis: Hemorrhagic stroke
 In general, LE recovery is faster as compared to the UE
 Most recovery takes place within 3 months
 Minor additional measureable improvements within 6 months
 Golden period to treat stroke: 3 months (before was 6 months)
 Visual recovery is not as impressive as compared to motor/sensory recovery
 If visual impairment persists beyond a few weeks recovery less likely
Hand function
Poor Good
Complete arm paralysis at onset Some motor recovery by 4 weeks
No measurable grasp strength by 4 weeks
No initial motion by 3 weeks
If motion in one segment is not followed within a
week by the appearance of motion in a 2nd segment
- Goal:
 ↓ the impairments through therapy
 Achieve a maximum level of functional independence
 Minimize disability
 Successfully reintegrate back into home, family, & community
 Reestablish a meaningful & gratifying life
 PT
 Rehab approaches:
Approach Remarks
Crothers Active movement, encouraged participation, prevent contractures
Pohl Conscious muscle relaxation
Schwartz No bracing, motivation & environment simplification
Kabat, Voss & Knott Diagonals
Brunnstrom Synergies & reflexes
Phelps Extensive bracing, 15 modalities from massage to skill
Deaver Extensive bracing, emphasis on bed & wheelchair activities
Fay Phylogenetic plan
Doman-Delecato Patterning
Rood Sensorimotor
Bobath Reflexive inhibitory patterns (RIPs), Key points of control
Ayers Sensory integration
Carr & Shepherd Motor relearning program
Constraint induced Restrain non-affected side to encourage hemiplegic limb movement
movement therapy (CIMT)
Eclectic Combination of approaches
  OT
 Frame of reference (FOR):
FOR Description
NDTs Normalize tone, inhibit abnormal primitive reflex patterns & facilitate normal
movement
Utilization of specific handling techniques
Brunnstrom movement therapy Reflexes & primitive movement patterns are used to facilitate the recovery of
voluntary movement
Newly produced correct motion must be practiced to be learned
PNF Stimulation of proprioceptors inducing response of the neuromuscular
mechanism
Rood Sensory stimulation & by following the developmental sequence
Carr & Shepherd MRP Relearn effective strategies for performing functional movement
Biomechanical approach Focus on ROM, strength & endurance required to perform an occupation
Rehabilitative approach Emphasize on learning compensatory techniques, modification of social &
physical features of environment that inhibit function
Ecology of human performance Individuals influence context & vice versa