2. STROKE
(INTRODUCTION, CLASSIFICATION AND
CLINICAL FEATURES)
DR. NEHA INGALE CHAUDHARY
MPT (Neuro)
PROFESSOR & HEAD
DR. SACHIN CHAUDHARY
MPT (Cardio-respi. Physiotherapy)
PROFESSOR & HEAD
DATTA MEGHE COLLEGE OF PHYSIOTHERAPY.
Nagpur.
3. PREFACE
This PPT is intended primarily for Bachelor of
Physiotherapy (BPTh) Final year students those are under
preparation for their University Examination.
I have attempted to cover different areas of stroke.
Despite my best efforts there might have some errors.
I like to thank all those who have helped me.
Dr. Neha Ingale Chaudhary
Dr. Sachin Chaudhary
4. CONTENT
Sr. No. Topic Slide No
1 Objectives 5- 6
2 Introduction of stroke and Transient Ischemic Stroke. 9-11
3 Epidemiology , Etiology , Risk factors and warning signs 12-17
4 Pathophysiology 18-19
5 Classification and syndromes 20-33
6 Red flags 33
7 Clinical features 34-55
8 Investigations and Prognosis 56-59
9 Summary 60
10 References 61
11 Questions 62
5. GENERALOBJECTIVES OF THE
SYLLABUS
At the end of the session student should be able to
understand –
The definition, epidemiology, Pathophysiology, and
classification of stroke.
The clinical features and the investigations done for
stroke.
The investigations and prognosis outcome of stroke.
6. LEARNING OBJECTIVES
Sr. no Learning objectives domain level criteria
1 Explain Stroke, etiology,
Pathophysiology.
Cognitive Must know All
2 Explain different types
and syndromes of Stroke.
Cognitive &
Psychomotor
Must know All
3 Explain clinical features
of stroke
Cognitive &
Psychomotor
Must know All
4 Explain investigations
required and prognostic
features of stroke
Cognitive &
Psychomotor
Must know All
7. CHAPTER CONTENT
Sr. No. Topic Slide No
1 Introduction 5- 6
2 Transient ischemic attack 9-11
3 Epidemiology , Etiology , Risk factors and warning signs 12-17
4 Pathophysiology 18-19
5 Classification and syndromes 20-32
6 Red flags 33
7 Clinical features 34-55
8 Investigations and Prognosis 56-59
9. INTRODUCTION
Stroke is an acute onset of neurological dysfunction
due to an abnormality in cerebral circulation with
resultant signs & symptoms which corresponds to
involvement of focal areas of the brain
10. ACC. TO WHO
It is defined as the sudden onset of neurological
deficits due to an abnormality in cerebral
circulation with the signs and symptoms lasting for
more than 24 hours or longer
11. TRANSIENT ISCHEMIC ATTACK
It is defined as the sudden onset of neurological
deficits due to an abnormality in cerebral
circulation with the signs and symptoms lasting
for less than 24 hours
12. EPIDEMIOLOGY
Third leading cause of death
The incidence of stroke is about 1.25 times greater
for males than females
Most common cause of disability among adults
13. ETIOLOGY
Atherosclerosis.
Cerebral Thrombus.
Cerebral embolus.
Embolism from the heart (cardiac origin)
Intracranial hemorrhage.
Subarachnoid hemorrhage.
Intracranial small vessel disease.
Arterial aneurysms and Arterio-venous malformation.
Haematological disorders (haemoglobinopathies, leukemia)
Atherothromboembolism
14. MISCELLANEOUS RARE CAUSES OF
STROKE
Infective endocarditis & HIV infection
Tumour, Hypoglycemia, Chronic meningitis
Perioperative stroke (hypotension and boundary zone infarction,
trauma, dissection of neck arteries, paradoxical embolism, fat
embolism, infective endocarditis)
Migraine, Snake bite
Inflammatory bowel disease (Ulcerative and Crohn's colitis)
15. RISK FACTORS
Smoking
Obesity
Lack of physical exercise or
sedentary life style
Diet & excess alcohol
consumption
Oral contraceptives
Infection (meningeal
infection)
Psychological factors
Vasectomy
Ageing & gender
Positive family history
Circadian and seasonal factors
Heart disease
Diabetes mellitus
Hypertension
Peripheral arterial disease
Blood pathology
Hyperlipidemia , TIA
Non Modifiable Modifiable
16. STROKE EARLYWARNING SIGN
F- Face Drooping
A- Arm Weakness
S- Speech Difficulty
T- Time To Call Hospital
17. OTHER THAN FAST SIGN-
Sudden Weakness, Numbness Of Leg
Sudden Confusion Or Trouble In Understanding
Sudden Trouble In Seeing or Walking
Sudden Severe Headache With No Known Cause
Other important but less common stroke symptoms include:
Sudden nausea, fever, & vomiting distinguished from a viral
illness by speed of onset
Brief loss of consciousness (fainting, confusion, convulsions)
18. PATHOPHYSIOLOGY
Ischemia results in irreversible cellular damage with a
core area of focal infarction within minutes
Transitional area surrounding core is termed ischemic
penumbra & consists of viable but metabolically
lethargic cells
Ischemia produce cerebral edema, that begins within
minutes of insult & reaches a maximum by 3 to 4 days.
19. Swelling gradually subsides & generally disappears by 2 - 3 weeks.
Edema elevates ICP, leading to intracranial HT & neurological
deterioration associated with contra lateral & caudal shifts of brain
structures.
Cerebral edema is the most frequent cause of death in acute stroke
& is characteristic of large infarcts involving MCA & ICA.
20. CLASSIFICATION
Depending on the cause
Hemorrhagic stroke
Intracranial hemorrhage
Subarachnoid hemorrhage
Signs of raised ICP will be evident with a history
of a traumatic accident
21. Contd…
Ischemic stroke
Thrombotic: more common. Usually occurs in the sleeping
hours. Characterized by gradual onset of symptoms
Embolic: Occurs in the waking hours of the day. Sudden
onset of symptoms preceded by giddiness in most
conditions
22. Depending on the severity
Mild stroke: symptoms subside with no deficit in a week
period.
Moderate stroke: symptoms recover in a period of 3 - 6
months with minimal neurological deficit.
Severe stroke: no complete recovery of the symptoms, even
after 1 year. Always ends up with severe neurological deficit.
23. Depending on the duration
Acute stroke: to a period of one week or until spasticity develops
Sub acute stroke: after the development of spasticity & last for a
period of 3-12 months
Chronic stroke: more than 12 months
24. Depending on the artery
involved-
Depending on the artery
involved-
MCA Syndrome
ACA Syndrome
PCA syndrome
Vertebro basilar artery
syndrome
Vertebral, basilar artery
Internal carotid artery
Lacunar syndrome
25. MCA SYNDROME
Contralateral hemiplegia (UL &
face >LL)
Contralateral hemi sensory loss
(UL & face more affected than
LL)
Ideomotor apraxia
Ataxia of contra lateral limb
Contralateral Homonymous
hemianopia
Left hemisphere infarction
Contralateral neglect
Possible Contralateral visual
field deficit
Aphasia: Broca’s (expressive)
or Wernicke’s (receptive)
26.
27. ACASYNDROME
Contralateral Hemiplegia or
monoplegia of LL (LL >UL)
Contralateral sensory loss of
LL
Urinary incontinence
Problems with imitation &
bimanual task
Abulia (akinetic mutism)
Apraxia
Amnesia
Contralateral grasp reflex,
sucking reflex
28.
29. PCA SYNDROME
Coordination disorders such as
tremor or ataxia
Contralateral homonymous
field deficit
Cortical blindness
Cognitive impairment
including memory impairment
Contralateral sensory
impairment
Thalamic syndrome (severe
pain from touch or temp.
changes)
Weber’s syndrome
(Contralateral hemiplegia &
third nerve palsy)
31. Locked-in syndrome (LIS)
Acute hemiparesis rapidly progressing to tetraplegia & lower bulbar
paralysis (CN V through XII are involved)
Initially patient is dysarthric & dysphonic & progresses to mutism
There is preserved consciousness & sensation
Horizontal eye movements are impaired but vertical eye movements
& blinking remain intact.
Communication can be established via these eye movements.
32. LACUNAR SYNDROME
Caused by small vessel disease
of deep white mater
Pure motor Lacunar stroke
Pure sensory Lacunar stroke
Ataxic hemiparesis
Dysarthria
Clumsy hand syndrome
Sensory/motor stroke
Dystonia/involuntary
movements
33. RED FLAG
Changes in neurological status
Symptoms Possible causes Management
Decreased level of
arousal
enlargement of pupil
on the side of stoke
sudden change in
muscle tone and /or
deep tendon reflexes
Cerebral edema
Another attack of
stroke
Cease treatment and
seek immediate
medical attention
35. PRIMARYIMPAIRMENT
1. Altered sensation
Pain (central pain or thalamic pain syndrome) characterized by
constant, severe burning pain with intermittent sharp pains
Hyperalgesia
Loud sound, bright light etc. may trigger pain
36. 2. Vision
Homonymous hemianopia, a visual field defect, occurs
with lesions involving the optic radiation (MCA) or to
primary visual cortex (PCA)
Visual neglect & problems with depth perception, and
spatial relationships
37. 3. Weakness
Usually seen in the contralateral side of the lesion
MCA stroke are more common so weakness is largely seen in
the UL in clinical practice
Distal muscle are more affected than proximal muscles
Mild weakness of ipsilateral side
38. 4. Alteration of tone
Flaccidity (hypotonicity) is present immediately after stroke
also called as cerebral shock.
Spasticity (hypertonicity) emerges in about 90 percent of cases
39. 5.Abnormal synergy
Extremity Flexion synergy
components
Extensor synergy
components
Upper extremity Scapular
retraction/elevation or
hyperextension
Shoulder abduction,
external rotation
Elbow flexion*
Forearm supination
Wrist and finger flexion
Scapular protraction
Shoulder adduction*,
internal rotation
Elbow extension
Forearm pronation*
Wrist and finger flexion
Lower extremity Hip flexion*, abduction,
external rotation
Knee flexion
Ankle dorsiflexion,
inversion
Toe dorsiflexion
Hip extension, adduction*,
internal rotation
Knee extension*
Ankle plantarflexion*,
eversion
Toe plantarflexion
40. Muscles not involved in either synergy
Latissimus dorsi
Teres major
Serratus anterior
Finger extensors
Ankle evertors
41. 6. Abnormal reflexes
Initially, hyporeflexia with flaccidity & later hyperreflexia
Clonus, & positive Babinskie
▪ Asymmetric tonic neck reflex (ATNR) present most of times.
Associated reactions are also present by stimulation of yawning,
sneezing, or coughing.
42. 7. Altered co ordination
Proprioceptive loss can result in sensory ataxia.
Strokes affecting cerebellum typically produce cerebellar ataxia
(e.g. Basilar Artery Syndrome, Pontine Syndromes) & motor
weakness.
Basal ganglia involvement (PCA syndrome) may lead to
bradykinesia or involuntary movements.
43. 8. Altered motor programming
Lesions of premotor frontal cortex of either hemisphere, left
inferior parietal lobe, & corpus callosum can produce Apraxia.
Apraxia is more evident with left hemisphere damage than right
and is commonly seen with aphasia.
▪ Ideational apraxia
▪ Ideomotor apraxia
44. 9. Postural Control & Balance
Impairments in steadiness, symmetry, & dynamic stability.
Reactive postural control and Anticipatory postural control
affected.
Pusher syndrome: Active pushing with stronger extremities
toward affected side, leading to lateral postural imbalance.
45. 10. Speech, Language, and Swallowing
Lesions of dominant hemisphere.
Aphasia: impairment of language comprehension, formulation,
and use.
Dysarthria: Motor speech disorders -lesions of CNS or PNS.
Dysphagia: Lesions affecting medullary brainstem (CN IX and
X), large vessel pontine lesions, acute MCA and PCA lesion
46. 11. Perception and Cognition
Disorders of body scheme/body image, spatial relations, and
agnosias.
Result of lesions in right parietal cortex & seen more with left
hemiplegia than right.
47. 12. Emotional Status
Pseudobulbar affect (PBA), also known as emotional liability
or emotional dysregulation syndrome.
▪ emotional outbursts or exaggerated laughing or crying.
Lesions of brain affecting frontal lobe, hypothalamus, & limbic
system
Depression is extremely common
48. 13. Bladder and Bowel Function
Common during acute phase.
Urinary incontinence- bladder hyperreflexia or hyporeflexia,
loss of sphincter control, or sensory loss.
Bowel function affection: Incontinence & Diarrhea or
Constipation
50. INDIRECT IMPAIRMENTS
1. Musculoskeletal changes
Loss of ROM & Contractures.
Disuse atrophy & muscle weakness.
Osteoporosis, results from decreased physical activity, changes
in protein nutrition, hormonal deficiency, & calcium deficiency.
51. 2. Neurological signs
Seizures occur in a small % of patients - more common in
occlusive carotid disease than in MCA disease
Hydrocephalus - rare but can occur with subarachnoid or
intracerebral hemorrhage.
52. 3. Thrombophlebitis & deep venous thrombosis (DVT)
Commonest complications for all immobilized patients.
53. 4. Cardiac Function
Stroke as a result of underlying coronary artery disease (CAD) -
impaired CO, cardiac decompensation, & rhythm disorders.
If problems persist, can alter cerebral perfusion & produce
additional focal signs (e.g., mental confusion).
Cardiac limitations in exercise tolerance
54. 5. Pulmonary Function
Decreased lung volume, decreased pulmonary perfusion & vital
capacity & altered chest wall excursion
Aspiration- due to Dysphagia.
55. 6. Integumentary
Pressure sore/ decubitus ulcer.
Fragile skin- reduced blood supply to epidermis.
The skin breaks down over bony prominences from pressure,
friction, shearing, and/or maceration
58. RECOVERYAND PROGNOSIS
Fastest in first weeks after onset
Measurable neurological & functional recovery –
in first month after stroke.
Continue to make measurable functional gains for months or years
after insult.
Late recovery of function- seen in patients with chronic stroke
undergoing extensive functional training
59. VARIATION OF RECOVERY
Recovery depends on severity of stroke .
Depends on type of stroke – hemorrhagic or ischemic.
Varies from individual to individual.
Depends on intensity of therapy.
Depends on age of the patient.
62. QUESTIONS
Define stroke and explain causes.
Describe various syndromes occurring in stroke.
Illustrate various clinical features and prognosis of stroke