This document is a comprehensive presentation on strokes, covering their introduction, classification, epidemiology, etiology, risk factors, pathophysiology, clinical features, investigations, and prognosis, aimed primarily at final year bachelor of physiotherapy students. Key learning objectives include understanding stroke definitions, causes, syndromes, clinical features, and the necessary investigations. It also discusses the various types, symptoms, and recovery related to strokes, along with references and questions for further assessment.

1. DEPARTMENT OF
NEUROSCIENCES.
DATTA MEGHE COLLEGE OF
PHYSIOTHERAPY. NAGPUR.

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

8. INTRODUCTION AND CLASSIFICATION
STROKE

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)

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

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)

30. VERTIBRO-BASILARARTERY
SYNDROMES
 Medial medullary syndrome
(VA)
 Lateral medullary (Wallenberg's)
syndrome (PICA)
 Complete basilar artery
syndrome (locked-in syndrome)
 Med inferior pontine syndrome
 Lateral inferior pontine syndrome
(AICA)
 Medial midpontine syndrome
 Lateral midpontine syndrome
 Medial superior pontine syndrome
 Lateral superior pontine syndrome

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

34. CLINICALFEATURES AND
INVESTIGATIONS OF STROKE.

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

49. HEMISPHERIC BEHAVIORAL
DIFFERENCES

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

56. TESTSAND MEASURES
 Urine analysis
 CBC count
 Blood sugar level
 Blood cholesterol & lipid profile
 Cardiac evaluation
 Lumbar puncture

57. IMAGING
 CT Scan.
 Magnetic Resonance Imaging (MRI).
 Cerebral Angiography.

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.

60. SUMMARY
 Introduction
 Etiology, epidemiology
 Risk factors, warning signs
 Pathophysiology, syndromes
 Clinical features
 Investigations and prognosis

61. REFERENCES
 O’ Sullivan SB, Schmitz TJ. Stroke. Physical rehabilitation.
7th ed., New Delhi: Jaypee Brothers, 2007, chapter 15, P(592-
661)
 Darcy A. Umphred. Neurological Rehabilitation, 6th ed.,
Mosby Elsevier, Missouri.Chapter 23, P(711-752).

62. QUESTIONS
 Define stroke and explain causes.
 Describe various syndromes occurring in stroke.
 Illustrate various clinical features and prognosis of stroke