cerebrovascular accidents

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Anatomy Of The Brain Mollie Rowley Second year medical student

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Page 1: Cerebrovascular Accidents

Anatomy Of The BrainMollie RowleySecond year medical student

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Learning objectives

0 Anatomical language0 The main bones of the skull0 External and internal (sagittal) view of the brain0 The forebrain, midbrain and hindbrain0 The Circle of Willis

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Anatomical language for the brain

Before we go any further however, let’s go through the basics…Anatomy of the brain comes with its own weird and wonderful language. Understanding the anatomy of the brain becomes a lot easier as soon as you understand the language that comes with it.

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Anatomical language for the brain

rostra means beak/nose, soRostral means closer to the nose Cauda means tail (ie cauda equina), soCaudal means closer to the spine

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Anatomical Language for the brain0 The brain is folded into

Gyri and sulci0 Gyri (singular gyrus) are

the raised bumps of the folds

0 Sulci (singular sulcus) are the grooves between the folds

0 The longitudinal fissure (aka the median fissure) splits the two halves of the cerebrum

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Anatomical language for the brain

0 Grey Matter is matter composed of unmyelinated neuron bodies, neurons and glial cells

0 White matter is matter composed of myelinated axons and glial cells and is the lipid content of the myelin sheaths that makes this area appear white

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Anatomical language for the brain

There are 3 layers covering the brain:0 The dura mater is the outermost layer.

As its name might suggest its very durable and coats the whole of the brain and spinal cord in one continuous sheath

0 The arachnoid mater is the middle layer. All cerebral veins, arteries and cranial nerves lie beneath this layer in an area known as the subarachnoid space

0 The pia mater is a vascular membrane that intimately covers all gyri and sulci of the brain

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The SkullA quick revision of the main bones of the skull

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A brief overview of the brainExternal Structures

Cerebrum

Cerebellum

brainstemPons

Medulla

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A Brief Overview of the BrainInternal Structures

Sagittal section of the brain

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Functional areas of the brainThe brain is grouped into 3 areas based loosely on embryological formation:0 The Forebrain – cerebrum and

the diencephalon0 The Midbrain –tegmentum and

tectum0 The Hindbrain – cerebellum,

medulla oblongata and pons

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The forebrainThe cerebrum

0 Also known as the telencephalon0 Thought to be the seat of humanity

as its so well developed in humans0 Composed of two hemispheres (left

and right) divided by the median fissure

0 Commissures (tracts of axons crossing the midline) connect these two hemispheres, the largest of which is the corpus callosum

0 Covered in a 2-4mm thick layer of grey matter - the cerebral cortex

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Lobes of the Cerebrum0 The lobes of

the cerebrum are described in terms of the skull bones they lie behind

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The cerebrum

Functions of the cerebral cortex include:0 Sensory perception0 Memory0 Planning/execution of voluntary movement0 Language0 Consciousness0 Self Awareness0 Cognitive functions

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The cerebrum

Brodmann’s map divides the cerebral cortex into 52 different functional areas that are either motor, sensory or associational.

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The forebrainThe diencephalon

Composed of the hypothalamus, thalamus, epithalamus and subthalamusThe hypothalamus:0 thermoregulation and triggering

sleep0 part of the limbic system

(generates goal directed behaviours - eating, drinking etc.)

0 Controls many endocrine functions via connections to the pituitary gland

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The forebrainThe diencephalon

The Epithalamus:0 Regulates circadian rhythm0 Contains the pineal gland

The Thalamus has multiple functions:0 Emotion (limbic system)0 Memory (frontal cortex)0 Sensory and motor0 Pain and visual attention0 Sleep/wakefulness and arousal

The Subthalamus is involved in movement

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The Midbrain

The mesencephalon2 parts: 0 Tegmentum - receives

cranial nerves III – V and contains substantia nigra

0 Tectum – receives cranial nerves II and VIII; mediates visual/auditory reflexes

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The hindbrainThe Cerebellum

Makes up ¼ brain mass and ½ the brain’s total neuronsCortex is composed of grey matter folded into folia separated by transverse fissuresWhite matter is called arbor vitae “tree of life”Concerned with high level functions:0 timing and execution of a

voluntary movement0 Learning new motor skills0 Cognition

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The hindbrainPons and Medulla Oblongata

The centres for life support functions of the brain0 Pons consists mainly of nerve fibres connecting the

cerebellar hemispheres, forebrain, midbrain and spinal cord

0 Medulla consists of 2 pyramids separated by a median fissure

0 Descending fibres cross from left to right in the medulla, known as the decussation of the pyramids

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The Circle of Willis0 Circle of Willis is meant to

be the brain’s insurance mechanism against arterial blockages which could cause CVAs

0 If one artery is blocked other arteries in the circle can compensate to continue supplying the affected area with blood

0 In reality the circle of Willis is often too small to be effective and isn’t really able to cope with large scale CVAs

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The Circle of Willis0 The Internal Carotid

arteries and the vertebral arteries form the main blood supply

0 They meet in the middle via the two posterior communicating arteries and the basilar artery

The basilar and vertebral arteries supply the brainstem

Internal Carotid arteries

Vertebral arteries

Posterior communicating artery

Basilar artery

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Internal Carotid arteries

Vertebral arteries

Posterior communicating artery

Basilar artery

The Circle of WillisThe Internal carotids branch form the anterior cerebral arteries. these supply:0 the medial surface of the

frontal and parietal lobes0 1 inch of brain either side

of the median fissure0 Occlusion can damage

motor nuclei cranial nerves V, VII and XII affecting movement of jaw, lips and tongue respectively

The Anterior communicating artery links the 2 anterior cerbral arteries

Anterior cerebral arteriesAnterior communicating artery

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Internal Carotid arteries

Vertebral arteries

Posterior communicating artery

Basilar artery

The Circle of Willis0 Middle cerebral

arteries supply lateral parts of cerebral hemispheres except occipital and inferior temporal lobe

0 Anterior choroidal arteries supply thalamus and hypothalamus and various important forebrain groups

Anterior cerebral arteryAnterior communicating artery

Middle cerebral artery

Anterior choroidal artery

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Internal Carotid arteries

Vertebral arteries

Posterior communicating artery

Basilar artery

The Circle of WillisPosterior cerebral arteries supply:0 Occipital lobe0 Inferior temporal lobe0 MidbrainSuperior and inferior cerebellar arteries supply:0 Pons0 Medulla 0 CerebellumPontine arteries supply medial parts of pons and medulla

Anterior cerebral arteryAnterior communicating artery

Middle cerebral artery

Posterior cerebral artery

Superior cerebellar artery

Inferior cerebellar artery

Pontine arteries

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Summary

The brain has a 3 layer covering which allows it to be suspended in CSFThe brain is divided anatomically into many different areas.It is composed of three functional parts:0 The Forebrain – higher functions and endocrine regulation0 The Midbrain – cranial nerves and substantia nigra0 The Hindbrain – coordination, movement and life support

functionsThe circle of Willis ensures a high arterial blood supply with the possibility of compensatory blood supply in a CVA

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Thank you for your time

0 Any questions?

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Pathophysiology of a Cerebrovascular Accident

By Tim Sale and Nicola Tribley

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Aims:• Define a stroke• Distinguish

between types• Explain what goes

wrong

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A stroke is an acute neurological deficit, lasting

longer than 24 hours.

A Transient Ischaemic Attack (TIA) is an acute neurological

deficit lasting less than 24 hours.

Definitions:

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3rd most common cause of death in developed world

More common in men

25% of patients die

More likely to occur in the morning

More common in Black Africans

The Facts…

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Types of C.V.A...

Ischaemic stroke/ Infarction – 80-90%Small vesselLarge vessel stenosisCardio-embolic

Haemorrhagic – 10-20%

TIA – Transient Ischaemic Attack

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Large Vessel Disease

Also called Large vessel stenosis

Rupture of a local plaque

Most common type

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Cardio-embolic Stroke

Common embolic source

Atrial fibrillation

Valvular changes

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Small Vessel Disease/ Lacunar Infarct025% of strokes

0 Infarcts in the deep (perforating) arteries, from branches of the middle cerebral artery

0Very localised, lesions (<5mm) are in the deep brain – lots of important structures!

0 (37% putamen, 16% pons, 14% thalamus and 10% caudate)

0Microatheroma (main cause) and Lipohyalinosis (thickening of arteriolar wall and reduction in lumen diameter)

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Haemorrhagic• Intraparenchymal- 8-13% of

strokes

• Resulting haematoma can damage surrounding brain tissue due to increase in pressure

• Hypertension damage to vessel walls (most common)

• Anuerysm/ arteriovenous malformation rupture

• Altered hemostasis (coagulation disorders)

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Cellular Changes↓blood flow =↓O₂

Na˖/K˖ pump fails(Na˖ accumulates in cell)

H₂O enters cell causing it to swell

Swelling causes ↑intracranial pressure

Further ↓bloodflow

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Also…0High Na˖ causes cells to continually depolarise

=EXCITOTOXICITY

0↑Ca2˖ enters cell leading to necrosis and Inflammation (via cytokine release)

Cells with CBF <10ml/100g tissue/min will die within minutes of a stroke - the ‘core’

Cells with CBF <25ml/100g tissue/min can remain viable for several hours - the ‘penumbra’

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Anterior Cerebral Artery

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Middle Cerebral Artery

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Posterior Cerebral Artery

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Features Anatomy Prognosis

Total Anterior Circulation Infarct (15%)TACI

1. High cerebral dysfunction

2. Hemanopia3. Ipsilateral

motor/sensory deficit

Middle Cerebral Artery occluded

High mortality

Poor outcome

Partial Anterior Circulation Infarct (35%)PACI

2/3 of TACI features

Middle cerebral artery/

Anterior Cerebral artery branch occluded

Fair

High chance of recovery

Lacunar Circulation Infarct (25%)LaCI

Motor/ sensory/ataxichemipareisis

Occlusion of small, deep perforating artery

Often good recovery

PosteriorCirculation Infarct (25%)PoCI

1.Cranial nerve palsy2.Contralateral motor/sensory deficit/cerebral deficit/hemanopia

Brain stem/ cerebellum/ occipital lobe

Good recovery

High reoccurrence

Categorizing strokes

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Possible causes and differential diagnosis of cerebro-vascular

accidents

Zeenat Umerji

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What is stroke?

A sudden attack of weakness due to an interruption to the flow of blood to the brain. Usually affects one side of the body.

Either: Ischeamic (50% cerebral hemisphere, 25%

brainstem, 25% lacunar) heamorrhagic from prolonged reduction of BP

Varies in severity from a passing weakness/tingling in a limb (TIA) to profound paralysis, coma or death

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Causes Chief causes:

Thrombosis Atherothromboembolism Heart emboli CNS bleed (BP increased, trauma, aneurism

rupture)

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Causes Rare causes:

Vasculitis Venus sinus thrombosis

Young patients: Thrombophilia Vasculitis subarachnoid haemorrhage Venus-sinus thrombosis Carotid artery dissection

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Presentations

Cerebral hemisphere infarcts: initially flaccid then spastic contra-lateral hemiplegia, contra-lateral sensory loss, hemianopia, dysphasia

Brainstem infarction: quadriplegia (paralysis affecting all four limbs), disturbances of gaze & vision, locked-in syndrome

Lacunar infarcts: poor motor/sensory signs, ataxia, intact cognition/consciousness

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Differential diagnosis

CNS tumour Subdural haemorrhage Seizure (Todd's palsy) Hypoglycaemia Hyperglycemia Drug overdose (if comatose) Meningitis Migraine

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Differential diagnosis

CNS tumour Subdural haemorrhage Seizure (Todd's palsy) Hypoglycaemia Hyperglycemia Drug overdose (if comatose) Meningitis Migraine

Altered consciousnessHemiparesisSigns of trauma

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Differential diagnosis

CNS tumour Subdural haemorrhage Seizure (Todd's palsy) Hypoglycaemia Hyperglycemia Drug overdose (if comatose) Meningitis Migraine

Altered consciousnessHemiparesis (Todd's paralysis)History of seizuresSeizure medication

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Differential diagnosis

CNS tumour Subdural haemorrhage Seizure (Todd's palsy) Hypoglycaemia Hyperglycemia Drug overdose (if comatose) Meningitis Migraine

When glucose is ≤50 or ≥300Altered consciousnessHemiparesis (Todd's paralysis)

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Differential diagnosis

CNS tumour Subdural haemorrhage Seizure (Todd's palsy) Hypoglycaemia Hyperglycemia Drug overdose (if comatose) Meningitis Migraine

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Questions?

Thank you for listening :)

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Investigations for Cerebrovascular Accident (CVA) / Stroke

By Rosie Vincent9th Nov 2012

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How would you know someone is having a stroke?

• FAST (Face, Arms, Speech, Time)

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What are the Signs and Symptoms?• All strokes tend to be sudden onset, occasionally with

further progression over a few hours. Focal signs relate to distribution of the affected artery, but collateral supplies cloud the issue. You can not reliably differentiate between ischemic and haemorrhagic strokes but some pointers are: • Ischemic (A): Carotid bruit, AF, past TIA, IHD• Haemorrhagic (B): Menigism, severe headache, and coma

within hours.

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Other Symptoms• Difficulty swallowing• Excessive drooling• Choking• Difficulty walking• Change in vision (double vision/loss of vision) • Eyes fail to move in unison• Difficulty with balance• Clumsiness• Loss of coordination• Symptoms typically occur on one side of the body• Less common symptoms of a stroke may include:

• Altered smell sense, Headache, Dizziness, Excessive sleepiness, Excessive salivation, Drooping eyelid, Trismus (can’t open mouth), Vertigo, Urinary incontinence, Memory loss, Confusion, Delusions, Coma, Impotence, Generalised weakness, Fatigue

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Investigation/Examination• Needs to be prompt!• Confirm the clinical diagnosis (exclude other causes

e.g. Tumour)• Distinguish between haemorrhage and ischemic

infarction• Look for underlying causes for the stoke, therefore we

can reduce risk factors and prevent further strokes• Identify where the stroke has occurred, what has been

damaged and how it is affecting the patient- So we can start to plan treatment/management and rehabilitation.

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Awareness and consciousness – Glasgow coma scale/AVPU

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Cranial Nerve Exam• Cranial nerves 1 and 2 originate from the cerebrum,

whereas 3-12 originate from the brain stem. Therefore strokes in these areas may affect the function of these nerves.

• You know what each one does so think about what symptoms you might get e.g.• 1 (Olfactory)= altered smell• 2(Optic)= loss of vision (total/ partial), Pupil Un-

reactive to light• 9(Glossopharyngeal)=?

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Neurological Exams• Motor and Sensory examination• If the area of the brain affected contains one of the three

prominent Central nervous system pathways—the spinothalamic tract, corticospinal tract, and dorsal column (medial lemniscus), symptoms may include:• hemiplegia and muscle weakness of the face• numbness• reduction in sensory or vibratory sensation

• In most cases the symptoms are usually on just 1 side of the body, with the defect in the brain on the opposite side (depends on which part of the brain is affected)

• BE CAREFUL - The symptoms do not always mean there is a stroke- as these pathways also travel in the spinal cord and lesions there can produce the same symptoms.

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Cerebral Cortex• If the cerebral cortex is involved the CNS pathways can again be

affected, but also can produce the following symptoms:• Aphasia (inability to speak or understand language from involvement

of Broca's or Wernicke's area)• Apraxia (altered voluntary movements)• Visual field defect• Memory deficits (involvement of temporal lobe)• Hemineglect (involvement of parietal lobe)• Disorganized thinking, confusion, hypersexual gestures (with

involvement of frontal lobe)• Anosognosia (persistent denial of the existence of a, usually stroke-

related, deficit)• If the ''cerebellum'' is involved, the patient may have the following

symptoms:• trouble walking• altered movement coordination• vertigo and or disequilibrium

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Stroke Classification (Bamford/Oxford classification)• Total Anterior Circulation Infarct (TACI)

• Combination of new higher cerebral dysfunction (eg,dysphasia); homonymous visual field defect; and ipsilateral motor and/or sensory deficit of at least two areas of face, arm and leg.

• Partial Anterior Circulation Infarct (PACI) • Two of the three components of the TACI syndrome with higher cerebral

dysfunction alone, or with a motor/sensory deficit more restricted than those classified as LACI

• Posterior Circulation Infarct (POCI) • Ipsilateral cranial nerve palsy with contralateral motor and/or sensory

deficit;bilateral motor and/or sensory deficit; disorder of conjugate eye movement; cerebellar dysfunction without ipsilateral long tract deficits; or isolated homonymous visual field defect.

• Lacunar Infarct (LACI)• Pure motor > 2/3 face, arm, leg Pure sensory > 2/3 face, arm, leg Pure

sensorimotor > 2/3 face, arm, leg Ataxic hemiparesis, No higher dysphasia or visuospatial or hemianopia or vertebrobasilar problems

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Investigations - Bloods

• Baselines FBC, U+E Clotting and ESR

• Random Glucose -Do they have hypoglycaemia or hyperglycaemia. Diabetes??

• Lipid Profile –Do they have hyperlipidaemia

• Hyperhomocysteinaemia?• Hyperviscosity - Polycythaemia?• Infection- Vasculitis?• Prothrombotic States –

Thrombophilla? (Blood clotting disorders)

• Syphilis?

• Thrombocytopenia?• Genetic Tests: Check for Fabry’s

disease and CADASIL

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CT- Computerised Tomography• CT has the advantage of being available 24 hours a day • Non-Contrast CT is the gold standard for haemorrhage,

haemorrhage on MR images can be quite confusing. • On CT 60% of infarcts are seen within 3-6 hours and

virtually all are seen in 24 hours. • The overall sensitivity of CT to diagnose stroke is 64% and

the specificity is 85%.• It may be difficult to identify early cerebral infarction• Posterior fossa and brainstem regions may not be visible

• May not detect small infarcts especially lacunar infarcts

• Can not differentiate between old infarcts and old intracerebral haemorrhages

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MRI- Magnetic Resonance Imaging • Not as easily available as takes longer to organise • Has a specific sequence (stroke sequence) called

Diffusion-weighted imagine (DWI)- this becomes positive within minutes-hours of stroke onset as a white ‘light bulb’ which remains for 2-3 weeks

• DWI can detect the haemorrhage as early as CT• Much better at visualising the posterior fossa• More sensitive to small infarcts (95%)• You can differentiate between old infarcts and haemorrhages (with MRI + gradient echo)

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CT vs. MRIIn summary MRI is a lot easier to diagnose due to DWI changes being so apparent, making the diagnosis relatively easy for the non-specialist...

BUT CT can differentiate between infarction and haemorrhage instantly, and is faster to carry out, therefore it is usually the 1st line approach and is carried out ASAP after patients admission

CT MRI

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Investigation for Signs of Hypertension

• Retinopathy- Ophthalmoscopy/Fundoscopy• Nephropathy- U+E’s (Urea:Creatinine) Renal

ultrasound, Urinalysis • Big heart- CXR• Blood Pressure commonly high in early stroke but

usually do not treat! It may harm the patient and even a 20% decrease may compromise brain perfusion as auto regulation is impaired

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Investigation for Signs of Cardiac sources of Emboli

• 24 tape ECG – Do they have AF?• CXR - Enlarged left atrium?• Echocardiogram (Transoesophageal is more sensitive

than transthoracic) Looking for:• Mural thrombus due to AF or a hypokinetic segment of

cardiac muscle post-MI• Valvular lesions which could be due to ineffective

endocarditis or rheumatic heart disease• Patient foramen ovale (especially in younger patient)

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Signs of Carotid Artery Stenosis• Carotid Doppler Ultrasound• CT/MRI Angiography

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Assessing handicap, disability and independence in daily life

• Two people with the same impairment (e.g. Paralysed arm) may have different disabilities (One can dress and the other cannot)

• Treatments are usually aimed at reducing disability and improving quality of life, not curing disease.

• Usually use Barthel’s Index of activities of daily living to establish the patient’s degree of independence from any help. You score the patient on the following aspects of daily living, and total the scores, gaining a value from 0-20 (20 = completely able).

• For example: Bowels0 = incontinent (or needs to be given

enema) 1 = occasional accident (once/week) 2 = continent • This is also carried out for:

• Bladder• Grooming• Toilet use• Feeding• Transfer• Mobility• Dressing• Stairs

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Summary

After carrying out these investigations and examinations on a patient you should know:• If they had a stroke•What type of stroke it was•Where the stroke occurred•What caused the stroke•What the stroke’s effects have been on the patient Knowing this will now enable you to inform the patient what has happened to them, and together you will be able to decide on treatment/management that is best tailored to the patients needs.

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The End

Q&A

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Cases

CVA

Ella Ward-Baker

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Case 1

• 55 year old woman presents Tuesday morning feeling faint.

• Notable left-sided hemiparesis and dysarthria.• Consequently unable to break her fall as she

fell

What other relevant information might we need?

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Onset and duration

• Came on within 5 minutes (walking from home to the bus stop)

• Resolved after 10 minutes• Followed by another episode that came on

within 5 minutes of arriving at hospital

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Other necessary information

Prior to episode Mrs X had been getting ready for work…

• No chance of head traumaNo history of bleeding disorders…Past medical history of Hypertrophic

cardiomyopathy• Less likely to be haemorrhagic stroke

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Other necessary information

What does the medication reveal?• Bisoprolol 7mg/day – used to treat hypertension• Hypertension is a risk factor for both ischaemic

and haemorrhagic stroke, exacerbated by patient’s hypertrophic cardiomyopathy

Family history?Mother and father both died of MI

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Investigations

• CT scan• Labs: U&Es, FBC, Glucose• ECG• Carotid Doppler• Physical examination

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• CT Scan:

No sign of haemorrhageNo sign of infarction – may not appear for 6-24

hours or up to one week (if at all)

Investigations

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Left hypertrophic cardiomyopathy…

Don’t be misled into thinking this woman’s symptoms are because of a cardiac emergency, however this may be another factor leading to her stroke…

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ECG

• Left hypertrophic cardiomyopathy…• Patient also known to have paroxysmal AF…

Emboli more likely to form due to impeded passage of blood through the heart

From there, emboli may travel easily to brain, causing stroke

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Other results

• Bloods: Normal• Carotid Doppler – no sign of stenosis• Physical examination – no bruits, BP 148/78,

slightly tachycardic, aforementioned neurological symptoms

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Management

• AlteplaseTissue Plasminogen activatorThrombolytic treatment

• WarfarinBecause of intermittent AFInhibits factors… II VII IX X

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Criteria for Atleplase:• Present within 3 hours of symptoms (as

infarcted tissue more prone to bleeding)• CT rules out haemorrhage (would be bright

white bleed on CT)• Thrombolysis must take place in specific stroke

unit (reason why there is always a bed kept spare on the ward)

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Non-Pharmacological interventions(MDT)

• Physiotherapy – Important to encourage patient to use affected limbs/relearn use…

- Even once partial use is regained, muscle wasting from inactivity may be a problem

• Speech and Language Therapy (SALT) – helping to prevent psychological problems associated with inability to communicate

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• Occupational Therapist – help the patient by providing strategies and coping methods to deal with disability

- Enables patient to begin/continue with daily tasks/ work/ self-care etc

• Dietician – fair enough to tell a patient to ‘cut down on salt’, but that doesn’t generally help in itself…

• Psychological Support

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Some points about this case

• Highlighted the importance of patient understanding• On questioning, Mrs X claimed to have no medical

conditions• On further questioning, hypertension treatment was

mentioned… • Mrs X then confirmed she had high blood pressure but

that she ‘felt fine’• She had made no connection between hypertension and

the possible risks - ‘why would that effect my brain?’• Patient understanding…

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• Patient now worried about returning home to house where she lives alone

• Again, understanding firstly of the risks of having another stroke, but also what and how the medication she is on should help her

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Case 2

• 62 year old man having breakfast with his wife when he develops a severe headache and weakness in left arm.

What other relevant information might we need?

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Relevant information• Pain InfoSevere pain localised to head

• OnsetOver 2 hours

• Duration Ongoing

• Seizure post-admission

• Trauma?No evidence of trauma

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Other relevant information

• Past medical history:-History of Hypertension and hyperlipidaemia-Hip operation in past 4 weeks-Has smoked all his life-No previous stroke

• Medication historyWafarin 5mg daily

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Investigations

• Vital signs• CT• FBC, Electrolytes• Echocardiograph – to show cardiac mural

thrombus • ECG – possible AF• Plain Chest Radiograph• Prothrombin Time & Partial Thromboplastin Time

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• Normal bloods

• Clear Echo, ECG, CXR

• Slightly prolonged PT&PTT – Related to Warfarin

• BP 160/100 – Not severely hypertensive, so do not treat

hypertension as emergency – lack of evidence as to whether this is helpful

Results

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CT

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Intracerebral Haemorrhage

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Management• Anticonvulsants (Seizures most common with ICH than

other strokes)• Maintain perfusion of the brain- Keep hydrated (Consider saline)- Consider intubation if airway patency becomes a problem• IV vitamin K & Prothrombin complex- Reverse anticoagulation treatment• Send Type & Screen bloods to blood bank• MDT

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Thank you