Approach to

a patient with stroke

BY
DR OMER ELADIL
MBBS, MD, MHPE, MSC NEURO LONDON, FRCP LONDON

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 Objectives

By the end of this session you are expected to:

1. Define stroke-related terms

2. Classify stroke according to aetiology,

Pathophysiology and Anatomy

3. Outline clinical approach to stroke patients

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 Warm up Q1
Which of the following is expected in
cortical lesions more than in capsular
one?
A. Contralateral hemiplegia unequally
affected.
B. Contralateral hemiplegia equally affected.
C. Crossed hemiplegia and cranial nerve
defect.
D. Absent bladder and cerebellar dysfunction.

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Q2. Where is the lesion? 4
Q3
i. Describe the lesion
ii. What is your
diagnosis?

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Q4
i. Describe the
lesion
ii. What is your
diagnosis

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Q5
In a patient presented with difficulty in finding
words where he created his own language but
his fluency of speech remain intact.
Which lobe is more likely to be affected
A. Parietal
B. Temporal
C. Occipital
D. Frontal
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Q6
A patient failed to speak fluently with frequent
halting with clear difficulty in finding the right
words and whenever a question to be asked to
him she kept repeating it
Which lobe is more likely to be affected?
A. Parietal
B. Temporal
C. Occipital
D. Frontal

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Q7
A 29-year-old man presents complaining of visual
disturbance. Examination reveals a left superior
homonymous quadrantanopia. Where is the lesion
most likely to be?
Which lobe is more likely to be affected
A. Left temporal lobe
B. Right temporal lobe
C. Left parietal lobe
D. right parietal lobe

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Q8
A patient presented with right eye nystagmus
with right ptosis and miosis with ipsilateral loss
of corneal reflex and spinothalamic sensory
loss of the left limb.
Which artery is most likely to be affected
A. MCA
B. ACA
C. PCA
D. PICA
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Basic Rehearsal
for localization

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Circle of Willis-1

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Circle of Willis-2

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 Clinical manifestations of the HMFs:
Frontal Lobe

 Aphasia; expressive Broca's area

 Anosmia.
 Apathy, disinhibition and personality Changes
 Primitive reflexes (grasp, pout, palmomental)
 Perseveration
 Spastic paraparesis
 Mass effect
 Urinary and faecal incontinence
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 Clinical manifestations of the HMFs:
Parietal Lobe
1. Sensory inattention
2. Neglect
3. Apraxias
4. Astereognosis
5. Inferior homonymous quadrantanopias
6. Gerstmann's syndrome
i. Alexia
ii. Acalculia
iii. Agraphia
iv. Finger agnosia
v. Right-left disorientation
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 Clinical manifestations of the HMFs:
Temporal lobe
1. Wernicke's (receptive) aphasia neologisms
2. Superior homonymous quadrantanopia
3. Auditory agnosia
4. Prosopagnosia "face blindness"
5. Memory impairment

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 Clinical manifestations of the HMFs:
Occipital Lobe
1. Homonymous hemianopia
2. Anton’s syndrome: Denial
3. Balint’s syndrome: Failure of voluntary gaze,
with visual agnosia
4. Visual illusions: MICROPSIA/MACROPSIA
5. Colour agnosia
6. Prosopagnosia "face blindness"

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Cognitive function assessment-
Dominant hemisphere

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Cognitive function assessment-
Non-dominant hemisphere

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 Common basic questions

A. Localization: Where is the lesion?

B. Clinical Diagnosis: What is the lesion?

C. Aetiology: What is the nature of the lesion?

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 How to localize
common presentations
Neurology ∆
tells the clinical presenting deficit
NOT the anatomical interpretation

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 A. Localization
 At your level you are expected to determine
where is the lesion from the following sites:
1. Cortex
2. Internal Capsule
3. Brain stem
 Determine these three:
1. MRCS of the Upper, and the lower limbs
2. The affected cranial nerves, feature and site
3. Cortical dysfunction

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 Common Brain Lesions
Clinical 2. Internal
1. Cortex 3. Brain Stem
presentation Capsule

MRCS of the Equally Equally

Unequally affected
ULs & LLs affected affected

Cranial nerve
Ipsilateral Ipsilateral Contralateral
defect

To determine which
Higher mental lobe: Assess the
Intact Intact
Functions function mentioned
above
20-Nov-20 24
 Common Brain stem signs
Sign Where

Blindness Occipital lobe

Ipsilateral third nerve palsy with Midbrain

contralateral hemiplegia
Weber's syndrome

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 B. Clinical Diagnosis
1. What is the lesion?
Right/left Hemiplegia/paresis & the MRCS
2. What is the nature of the lesion?
Ischaemic/haemorragic (Lobar/ventricular/SAH)
3. Are there any other neurological deficit?
HMFs/Speech/Cranial nerves
4. What is the most affected vessel/s
(aided by neuroradiology MRI/MRV/MRI)
5. What is the prognostic scales?

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HOMUNCULUS

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 Common localizing signs
Sign Which artery
1. Contralateral hemiparesis and sensory Anterior cerebral artery
loss, lower limb > upper limb (ACA)
2. Sphincteric disturbances
1. Contralateral hemiparesis and sensory Middle cerebral artery
loss, upper limb > lower limb (MCA)
2. Contralateral homonymous hemianopia
3. Aphasia (Wernicke’s)
4. Gaze abnormalities.
1. Pure hemisensory loss Posterior cerebral
2. Contralateral homonymous hemianopia artery (PCA)
3. Visual agnosia
4. Disorders of reading (dyslexia)

1. Ipsilateral Cerebellar signs PICA lesion

2. Ipsilateral Horner's Lateral medullary
3. Contralateral limb sensory loss syndrome
(Wallenberg's)
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 c. Aetiology

 Modifiable and non modifiable

 For Infarction and for haemorrhage

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 Approach to
a patient with stroke

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 Introduction
 Stroke is defined as rapid onset of neurological
deficit lasting >24 as a result of a vascular lesion
 It is the third largest killer and the first major
cause of disability
 Traditionally classified into two major types:
1. Ischemic (85%)
2. Hemorrhagic (15%)
Other new classification separate TIA and
Thrombo-Hemorrhagic Stroke
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Ischaemic Stroke

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 Definition of Ischaemic Stroke
1. TIA: A transient episode of neurological
dysfunction caused by focal brain, spinal
cord or retinal ischaemia without acute
infarction
2. RIND: Reversible Ischaemic Neurological
Deficit
3. Minor stroke: Patients recover within a wk
4. Stroke in evolution: progressivewithin 24
hours of onset
5. Completed stroke: maximal within 6 hours
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 Risk Factors
Modifiable Non modifiable
 Hypertension  Age
 Sex
 Diabetes
 Ethnicity
 Heart disease  Genetic factors
A. Fib, Valvular, MI, endocarditis
 Smoking
 Dyslipidemia
 Pregnancy
 Bleeding Disorders
 Drug; Abuse, Anticoagulant
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 Ischaemic Classification

Aetiologically because of:

I. Thrombosis.
II. Embolism.
III. Systemic hypo-perfusion

The two commonest causes of young onset

stroke (less than 40 years) are:
Cardio embolism and carotid artery dissection

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 1- Thrombosis
Due to:
Large Vessel Disease
 Common & Internal
Carotids
 Circle of Willis & proximal
branches
Small Vessel Disease

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 2- Embolism
From:
 Heart

 Arterial system

 Venous system

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 3- Systemic Hypoperfusion
Due to:
Circulatory collapse.
Multiorgan involvement.

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National Institutes of Health Stroke Scale (NIHSS)
 To quantify the severity of strokes out of 42
 This score calculated from 11 components:
1. Level of consciousness (0-2)
2. Best gaze (0-2)
3. Visual fields (0-3)
4. Facial palsy (0-3)
5. Arm motor (0-4)
6. Leg motor (0-4)
7. Limb ataxia (0-2)
8. Sensory (0-2)
9. Best language (0-3)
10. Dysarthria (0-2)
11. Extinction and inattention (0-2)
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These 11 components are then summed and
the score correlates with stroke severity.

0 = No stroke symptoms
1-4 = Minor stroke
5-15 = Moderate stroke
16-20 = Moderate to severe stroke
21-42 = Severe stroke

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 Prevention of further stroke
 The recognition of risk factors
 Correction and modification
 Give Antiplatelets
(aspirin/Dipyridamole/Clopidogrel)
 Long term anticoagulation in atrial fibrillation
 Stop thrombogenic drugs, e.g. OCP

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Ticagrelor and its major metabolite reversibly
interact with the platelet P2Y12 ADP-receptor to
prevent signal transduction and platelet
activation

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Haemorrhagic Stroke

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 Classification - aetiology

 Hemorrhagic (15%) due to:

I. Intracerebral (ICH) /Intraventricular (IVH)
II. Subarachnoid (SAH)
III. Sub /extra dural (SDH/EDH)

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1. Intracerebral Hemorrhage

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 Subarachnoid Hemorrhage

 It is bleeding into the subarachnoid space

 It accounts for 5% of strokes.
 Due to:
 Saccular aneurysm rupture
 AVMs
 Diagnosis
 Head CT
 Lumbar Puncture (Xanthochromia)

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Calcification and not hge

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 Common Presentation
 Hemi.
 Mono.
 Craniopathy e.g (Amaurosis Fugax, 7th, 12th)

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 History salient features

 Risk factors: hypertension, smoking, diabetes

 Speech defects, swallowing, visual difficulties

 Headache, seizures and loss of consciousness

 Sensory loss and weakness of face and limbs

 Sphincteric disturbances

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 Examination salient features
 Cranipathy 2nd, 7th 12 th etc palsy
 Upper motor neuron signs
 Hemiplegic upper limb affects:
Shoulder abductor, elbow extensors, wrist
extensor, finger extensors
 Hemiplegic lower limb affects :
Hip flexors, knee flexors, dorsiflexors and
evertors of the foot
 Cortical sensory signs

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 Other systemic examinations
 The pulse for atrial fibrillation
 Blood pressure
 Carotid bruits
 Heart murmurs
 Thyroid gland and status
 Urine for sugar

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 Ischaemic stroke work up
 All patients should
have urgent CT scan
 Basic investigations
 Vitals stabilization

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 Initial Evaluation:
Emergency Investigations

All patients with suspected stroke should

have:

1. Non contrast brain CT or brain MRI

2. Serum glucose

3. Oxygen saturation

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Acute management: The first few hrs

Penumbra

Core

Clot in
Artery

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CT Scans of Stroke

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 Treatment approach

SUMMARY

 GENERAL

 ISCHAEMIC APPROACH

 HEAMORRHAGIC APPROACH

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 General plans
 Multidisciplinary
 Early hospital admission to a DSU/HDU
 Modification of risk factors
 Stabilization
 General care
 For ischaemic stroke:
Antiplatelets/Anticoagulant
 For haemorrhagic
Conservative
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Physiotherapy, speech therapy and occupational
therapy and rehabilitation

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Shoulder slings

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Hand splints

Foot slings

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Thanks

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