Stroke presentation 1

8/7/2019 Stroke presentation 1

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StrokeA syndrome of rapid onset (usually focal) neurological deficit lasting>24 hours or leading to death- Kumar and Clark


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Both result in (temporary or semi/permanent) focal

neurological dysfunction. The main difference is duration of

the neurological deficit.

24hrs = Stroke (can also progress)

10.5% of people who have a TIA will have a stroke within 90

days. Half of these will occur within 48 hour of the initial TIA.

(Johnson et al, 2000, JAMA).


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TIA/Stroke Signs &SymptomsHemianopic/bilateral

(rare) visual lossAmaurosis fugax

Diplopia

Gaze paresis

Nystagmus

Aphasia (receptive orexpressive)

Hemifacial paresis (rare)

Facial sensory loss

Hemi/tetra (rare)

paresis

Paresthesia

Sensory loss

Transient global

amnesia (rare)

Loss of consciousness

(rare)

Confusion

Headache

Agnosonosia

Hemineglect

Vomiting

Choking

Ataxia

Vertigo

Areflexia initially

Exaggerated

reflexes later


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TIA/Stroke Signs &Symptoms

Cranial nerves

Cerebellum

Cerebral cortex

Spinal tracts

(or motor/sensory cortex)

Brain stem


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Stroke- ROSIER ScoreAfter excluding hypoglycaemia

Score of >0 makes stroke likely (although scores of 0 to -2 do not rule it out).


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TIA- ABCD2 ScoreIf no neurological signs remaining at presentation

Score of >4 requires patient to be urgently reviewed and assessed for

secondary prevention within 24 hours.


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Differential diagnosis

It is important to distinguish stroke from the following:

Conversion disorder

Fainting

Seizure/Todds palsy

Hypoglycaemia

Hyperglycaemia

Other toxic/metabolic abnormalities

Silent MI

MS

Vestibulitis

Bells palsy

CNS tumourMigrane

Brain herniation

Cerebral abscess

Chronic subdural haematoma

Encephalitis

Importance of risk factors and witnesses!


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Arterial supply to neck and head


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Gadolinium enhanced MR angiogram


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Principle sites of stenoses


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Areas of supply of three cerebral arteries


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Arteries of the brainstem


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Some of the structures at risk during brainstem infarction


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Structure Affected Normal Function Clinical signs

Corticospinal tracts Motor function (esp. fine) Hemiparesis or tetraparesis

Medial lemniscus and

spinothalamic tracts

Conveys sensory information Sensory loss

Oculomotor system Co-ordination of visual system Diplopia

Vth nerve nuclei Facial sensation Facial numbness

VIIth nerve nucleus Motor innervation to muscles

of facial expression

Facial weakness

Vestibular connections Balance, rotation and gravity Nystagmus and vertigo

IXth and Xth nerve nuclei Taste, swallowing, speech Dysphagia and dysarthria

Brainstem and cerebellar

connections

Various inc. Speech and

balance

Dysarthria, ataxia, hiccups

and vomiting

Sympathetic fibres Homeostasis Horners syndrome

Reticular formation Regulatory esp.consciousness and

habituation

Coma, altered consciousness

Upper brainstem infarction Various Locked-in syndrome

Lower brainstem infarction Various Pseudobulbar palsy


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Severe middle cerebral artery infarct


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Bilateral subdural haematoma in CT (left ) and T1 MRI (right)


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Pathophysiology of Stroke


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Aims

1. Brain vascular physiology

2. Pathophysiology haemorrhagic, ischaemic and others

3. TIA pathophysiology


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Brain Physiology

Brain is 2% of body weight 20% total oxygen

Blood flow:

- Total flow: 750ml/min (15% C.O.)

- Average flow: 50-55ml/min/100g

- Ischaemia:


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Brain Physiology

Cerebral perfusion pressure = MAP (mean arterial

pressure) ICP (intracranial pressure)

Cranium


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Cerebral perfusion pressure = MAP (mean arterial

pressure) ICP (intracranial pressure)

Intrinsic regulatory mechanisms

Stroke will be caused by:

a) Breakdown

b) Intervention

Brain Physiology


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Stroke pathophysiology

Stroke

Ischaemia Haemorrhage

Blood vessel

disease

Cardiac

disease

Haematological

disorders

Some underlying causes:

Intracerebral

causes

Extracerebral/

Trauma


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Pathophysiology ofischaemic stroke

Trigger is low oxygen

Initiation of viscous circles

Cell

membrane

Synaptic

cleft

Intra-

cellular

Dirnagl, U. et al. Trends in Neurosciences 1999; 22: 391-7.


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Pathophysiology ofischaemic stroke

Mechanisms of injury and cell death can be both fast or

prolonged:

1. Excitotoxicity (fast - minutes)

2. Inflammation and oedema (prolonged hours to days)3. Apoptosis (prolonged hours to days)

Dirnagl, U. et al. Trends in Neurosciences 1999; 22: 391-7.


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Stroke pathophysiology

Stroke

Ischaemia Haemorrhage

Some underlying causes:

Intracerebral

causes

Extracerebral/

Trauma

Haematological

disorders

Cardiac

disease

Blood vessel

disease


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Pathophysiology ofhaemorrhagic stroke

Risk factors untreated hypertension, atherosclerosis

Can occur as a result of an intracerebral haemorrhage

arteries in the brain are thin-walled

Leads to mass effect lesion

Ultimately the pathology arises as a result of ischaemia

+/- change in intracranial pressure


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Other causes of stroke

Can be as a result of trauma in particular extradural or

subdural haemorrhage

Less common causes include:

- Arteriovenous malformations

- Intraventricular haemorrhage in babies


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Pathophysiology ofTIA

Sadat U et al. J Neurol Neurosurg Psychiatry 2010;81:286-289

Acute

symptomatic

Recentlysymptomatic

Documents

Stroke presentation 1