Stroke Medical Student Handout Version 1.

0 October 2014
Northampton General Hospital
See www.strokeeducation.co.uk for latest version

Introduction
Welcome to Northampton General Hospital and the stroke service. We are an incredibly busy service
seeing over 1000 strokes each year comparable with Leicester and Nottingham so there is lots to see and
learn. We are very keen that you take an active rather than passive role during your time with us and
follow some of the patients through.

Wards and Clinics

The Hyperacute stroke unit is on Eleanor ward and there are daily ward rounds and board round. Please
attend punctually at 9 am. Holcot ward is more rehabilitation and we have a weekly midday MDT. We
would be impressed if you speak to therapists and spend some time with them. Understanding the role of
rehabilitation is key.

Clinics are held below Holcot ward in the Elderly care outpatient department. Please attend at 9 am or 2
pm depending on which clinic you are down to attend. If we have room you may well be asked to see and
present new patients.

Basics
A useful definition of stroke is a neurological deficit of presumed vascular origin lasting for greater than 24
hours. However we are moving to a more image based diagnosis with radiological evidence of brain
infarction or haemorrhage as the definition. All patients would usually have a CT but this may miss small
ischaemic strokes which can only be seen on MRI but some patients cannot tolerate MRI imaging for
differing reasons. In these patients we must adopt a pragmatic approach and diagnose and manage a
stroke on clinical grounds.

Types of Stroke

Ischaemic 80-85% Haemorrhagic 10% Subarachnoid haemorrhage 5%

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Basics facts
• Anterior circulation: that part of the brain perfused by the internal carotid artery
• Posterior Circulation: that part of the brain perfused by the vertebral artery and its branches
• Cerebral cortex level the right sided deals with sensation and vision from the left side of your
world and movement on the left side

The Brain Circulation

• The brain is 1-2% of body weight
• The brain gets 10% of cardiac output
• The brain is very sensitive to any vascular injury
• It has very little glucose storage
• It has no oxygen storage
• Hypoperfused neurones die within minutes

Hypoperfusion due to
• Obstruction of the vessel by a local thrombotic clot or embolism
• Low Blood pressure e.g. due to shock causing ‘watreshed infarcts’
• Haemorrhage so the vessel downstream is underperfused

Stroke Circulation
Look at the diagram below. It’s a bit like a tube map. How does a thrombus get from
• The Left ventricle to the right lateral medulla (clue – perfused by PICA)
• The Left Ventricle to the anterior cerebral artery

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Why do Strokes happen
There are many different causes. One must look for causes based on the incidence of that condition in
that population. Dissection is common in those under 40, AF is common in those over 80. Carotid stenosis
is commoner in smokers.

Ischaemic 80-85% Haemorrhagic 10% Subarachnoid haemorrhage

Atherosclerosis e.g. carotid Chronic Hypertension Saccular aneurysms
stenosis – large vessel strokes Cerebral Amyloid Angiopathy Arteriovenous Malformations
Arteriosclerosis – small vessel Anticoagulants Unknown
strokes Arteriovenous Malformations
Arterial Dissection Cavernomas
AF and embolism Tumours
Cardiac thrombus and embolism
Vasculitis
Antiphosphilipid syndrome
Thrombophiia
CADASIL
Hyperhomocysteinaemia
Fabry’s disease

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Risk Factors
These are mainly risk factors for the above causes. Some are modifiable and others not. Goal is to modify
and reduce risk to prevent a first or a subsequent stroke. The key is always to prevent stroke rather than
have to treat it.

Ischaemic 80-85% Haemorrhagic 10% Subarachnoid haemorrhage

Age Age Hypertension
Smoking Chronic Hypertension Smoking
Hypertension Cerebral Amyloid Angiopathy Family History
Diabetes Anticoagulants Age less important
Cholesterol Arteriovenous Malformations
Alcohol Cavernomas
Tumours

Pathophysiology

Infarction - at least 4 mechanisms

• Large vessel : atherosclerosis and ruptured plaque occludes artery or sends a shower of clot distally

• CardioEmbolism: AF, LV mural thrombus, PFO

• Small vessel disease : oocclsuion of thin thready arterioles causing lacunar strokes seen in the basal
ganglia, thalamus, internal capsule and pons

• Low flow: e.g. sepsis and hypotension or perioperative. Causes a 'watershed infarct' at the border
between ACA and MCA and MCA and PCA

Haemorrhage

• Deep bleeds due to Fragile small penetrating vessels - in the basal ganglia, thalamus,
internal capsule and pons . Main risk is HTN

• Lobar bleeds: Cerebral Amyloid angiopathy in the young. AV malformations, cavernomas

• Subarachnoid haemorrhage: Saccular/berry aneurysms and AVMs

Clinical Presentation and clues

• Strokes present with maximal disability at onset
• Improve usually over following days and weeks
• Unilateral neurology – face,leg,arm, vision
• Come on with no prodrome

The FAST test is useful for laypersons and paramedics in spotting early signs. In most cases stroke is not
subtle and a very straightforward diagnosis

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Key Clinical Findings
Anterior Circulation
• Hemiparesis face/arm/trunk/leg– side C/L stroke
• Hemisensory loss – side C/L stroke
• Homonymous Hemianopia – to side C/L stroke
• Dysphasia if Left Frontal/Parietal/Temporal lobe
affected
• Neglect/Extinction if right parietal cortex affected
Posterior Circulation
• Hemianopia on the C/L side
• Vertigo, Diplopia
• Weakness usually on C/L side
• Hiccoughs, Dysarthria, ataxia
• Facial weakness may be on same side of stroke
and limb weakness on other side
• Cranial nerve palsies
• Horner’s syndrome – miosis, mild ptosis,
enophthalmus

These can be subclassified by the Bamford or Oxford Community Stroke Classification

Subtype Clinical Common

Aetiology
All three of
(1) New, higher cerebral dysfunction (e.g. dysphasia)
Total Anterior
(2) Homonymous visual field defect Thrombo-
Circulation (TAC)
(3) Ipsilateral motor and / or sensory deficit of at least two areas out Embolism
Syndrome
of face, arm and leg.
If drowsy with unilateral weakness, last two factors are assumed
Partial Anterior 2 of 3 criteria of TACI
Thrombo-
Circulation (PAC)
Embolism
syndrome
(1)Pure motor: Complete or incomplete weakness of 1 side, involving
the whole of 2 of 3 of the body areas of face, arm and leg).
(2)Pure sensory: Sensory symptoms and/or signs, same distribution as
Lacunar (LAC) Thrombosis
above with no higher signs e.g. dysphasia, apraxia etc.
syndrome Lipohyalinosis
(3) Pure Sensori-motor : Combination of the above. Includes
dysarthria (“clumsy hand syndrome”) and dysphasia
(4) Ataxic hemiparesis: Hemiparesis with ipsilateral cerebellar ataxia
Any stroke affecting brainstem, cerebellar or occipital lobes
Ipsilateral cranial nerve palsy with contralateral motor and / or
Posterior sensory deficit
Thrombo-
Circulation (POC) Bilateral motor and / or sensory deficit.
Embolism
Syndrome Disorder of conjugate eye movement
Cerebellar dysfunction without ipsilateral long tract signs
Isolated homonymous hemianopia

Stroke Investigations
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 Investigations About
FBC/ESR Anaemia, Raised ESR in Giant cell arteritis or vasculitis
U&E/LFT/Lipids Baseline renal function, exclude diabetes, hypercholesterolaemia
Glucose
ECG Look for AF and NSTEMI/STEMI. If no AF and you suspect the patient mayhave
intermittent Paxysmal AF then arrange a 7 day tape
CXR All patients but smokers especially – assume smokers have a lung tumour until proven
otherwise
Carotid duplex Ischaemic strokes with good recovery in whom you would refer for Endarterectomy if
you find symptomatic stenosis (narrowing > 70% on the side of the stroke or TIA
Echocardiogram If there is a murmur or abnormal ECG or cardiac symptoms and in all younger patients
Non Contrast CT All patients as early as possible but 100% within 12 hours
MRI When the CT is normal and there is diagnostic uncertainty or there are atypical signs.
Unable to do if shrapnel, metal foreign bodies, pacemakers, claustrophobia
Exotic There are many other tests but please discuss with consultant first e.g. vascultis
screens, TOE, thrombophilia screens etc.

Stroke Management
Ischaemic 80-85%
Thrombolysis:
• Aged <=80 and within 4.5 hrs
• Aged > 80 and within 3 hr
Antiplatelet: Aspirin 300 mg for
up to to 2 weeks and then
Clopidogrel 75 mg long term
Statin and cholesterol reduction
Warfarin or Novel anticoagulant if
in AF e.g dabigtran within 2
weeks
Endarterectomy if > 70% stenosis
in symptomatic artery
Hemicraniectomy if malignant
MCA syndrome
Rehabilitation
Haemorrhagic 10% Subarachnoid haemorrhage 5%
Surgical Admit Neurosurgical centre
• Very little evidence of • Coiling of aneurysm
benefit except Cerebellar • Clipping of Aneurysm
haemorrhage > 3 cm Nimodipine
• Shunting for those with IV fluids
acute hydrocephalus Rehabilitation after
Look for and treat any
underlying causes
Long term BP control
Conservative
Rehabilitation

Specific Issues
Action About
Thrombolysis • All patients needs a CT brain first to ensure no haemorrhage on the CT scan
• Doctor must be sure Clinically a stroke as CT can be normal early
• Must ensure BP < 185/110 mmHg
• Aim for Door to Needle of < 30 minutesDo not give if h/o bleeding from anywhere
that cannot be controlled, severe hypertension, underlying cancer that can bleed,
aneurysms, previous Haem Stroke, Ischaemic stroke < 3/12 ago, trauma or head
injury
• Risks are Intracerebral haemorrhage bleeding from gut or retroperitoneal or
anywhere, anaphylaxis, angioedema (tongue swells
Atrial Fibrillation • Major risk factor for ischaemic stroke
• Anticoagulation reduces Stroke risk by 2/3rds
• All TIA/Stroke patients automatically have an elevated CHADS2 or CHADSVASC score
and need full anticoagulation with warfarin or one of the enw oral anticoagulants

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Stroke Complications: Prevent and manage these

• Cerebral oedema: seen in the first 72 hours and brain swells and ICP goes up as brain within bony box
- the skull. Can require hemicraniectomy in selected patients.

• Bleeding: ischaemic strokes can bleed and this is called haemorrhagic transformation. Haemorrhagic
strokes and particularly SAH can rebleed.

• Low Na: SIADH is seen with some strokes. The Na is low. There is inappropriate retention of water.
Serum osmolality low. Treat by restricting water. In SAH the low Na may be due to kidneys peeing out
lots of Na and the treatment is N-Saline.

• Vasospam: Seen with SAH. The large cerebral arteries spasm and this can cause an ischaemic stroke.
Seen in large SAH. Use Nimodipine to prevent.

• Venous thromboembolism (DVT/PE): use calf compression devices or low dose LMWH. Early
mobilisation. In those with large haemorrhagic strokes and IVC filter may be needed.

• Aspiration and Hospital acquired Pneumonia: Prevent through checking patient can salely swallow
and if not using an NG tube and speech and language therapists to hekp assess and monitor.

• Pressure ulcers: prevent with frequent turning, nutrition, hydration and good nursing care

• Seizures : usually seen after 6months

• Further stroke: seen in up to 15% depending on cause per year. Reduce risk with secondary
prevention especially anticoagulation if AF and ischaemic stroke

• Myocardial infarction: these patients often have coexisting IHD

• Sepsis: from chest or urine

• Death: from PE, MI, Infection

• Shoulder damage and pain: shoulder held together by muscles. If arm weak head of humerus can
move and can lead to pain and deformity.

• Depression: low mood is common. Consier starting an antidepressant,

• Falls: these are part of rehabiliation and some patients can try to walk.

• Pain syndromes: seen classically with contralateral thalamic strokes. Difficult to treat.

• Spasticity: the affected side is tight and flexed and this can reduce function and give abnroaml
positions. Prevent with good positioning, antispasmodics may be useful e.g. bacloften or Botulinum
toxin can be used.

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• Urinary Incontinence: exclude UTI and treat. Regular toileting. Treat any detrusor overactivity.
Bladder training. Only exceptionally should a catheter be left in.

Rehabilitation

Early expert and comprehensive stroke rehabilitation is key to reducing death and disability and improving
functional outcomes. The Stroke Unit Trialists Collaboration showed using a meta analysis of 23 trials that
when comparing a specialised multi-disciplinary stroke service with care either on an elderly care unit or
general medical ward that those on the stroke unit where more likely to be alive, at home and
independent at 1 year. The nurses are key working with the medical and therapy staff to coordinate
everything.

Physiotherapy (Blue) Occupational Therapy (Green) Speech and Language

Look at strength, muscle, tone,
balance and gait and involved in
the physical aspects of stroke
and working to improve these.
Specialists as well in chest
physiotherpay helping to
improve respiratory function and
prevent chest infections
Work to convert physical
abilities into useful functionality
e.g. able to wash, dress, feed
oneself, cook a meal, perform
complex tasks
Assessing swallowing safety and
preventing aspiration
Assessing language and helping
dysphasia and dysarthic patients to
regain communication skills

We are very fortunate in NGH that we have a community stroke team who can provide rehabilitation at
home very quickly and early and so allow patients home. This helps to improve outcomes. The goal for all
patients is functional independence.

Other important MDT partners

• Neurologist: providing BOTOX to manage spasticity

• Dietetics: ensuring patients having sufficient calorific input

• Social workers: helping to provide carers

• Palliative care team: for those who need end of life support

• Diabetic team: those with diabetes

• Anticoagulation team: counselling patients and monitoring anticoagulant usage

• Psychology: supporting patients with psychological issues 0- depression, anxiety etc.

• Gastroenterologists: insertion of PEG tubes for feeding