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Emergency Medical Services

Stroke Training Curriculum


2. Anatomy & Physiology
Aetiology and Pathogenesis
Symptoms & Diagnosis
Risk Factors
Introduction
Stroke is an acute heterogeneous syndrome caused by several disorders leading to an
occlusion or rupture of blood vessels supplying brain tissue. After deprivation of
oxygen supply, some neurons die within minutes, resulting in irreversible brain injury.
Around the area of necrosis, there is an area in which the blood supply is marginally
sufficient to keep these cells alive, but currently dysfunctional. This is called the
ischaemic penumbra.1

If reperfusion is not performed in a timely manner, or if additional injury is added, a


time-related death of the neurons located in the penumbra occurs. Therefore, ‘time is
brain’ summarises the fact that brain function is lost for every second treatment is
delayed.1

1. Kollmar R, Schwab S. Ischaemic stroke: acute management, intensive care, and future perspectives. British Journal of Anaesthesia 2009;99(1):95–101.
Stroke facts1

INSUFFICIENT SUPPLY OF BLOOD


STROKE IS A MEDICAL TO AN AREA OF THE BRAIN
EMERGENCY CAUSES A LACK OF OXYGEN AND
NUTRIENTS

STROKE OCCURS WHEN THE IF BLOOD FLOW IS NOT


BLOOD SUPPLY TO AN AREA OF RESTORED, BRAIN TISSUE WILL
THE BRAIN IS BLOCKED OR DIE CAUSING PERMANENT
REDUCED DISABILITY

1. Kollmar R, Schwab S. Ischaemic stroke: acute management, intensive care, and future perspectives. British Journal of Anaesthesia 2009;99(1):95–101.
Anatomy & Physiology
The brain receives information through our five senses: touch, smell, taste, sight and hearing. It can store
information in our memory and can assemble it in a way that has meaning for us. It controls our thoughts, speech,
memory, body movement and also major organ functions. The primary functions of the nervous system are to
monitor, integrate and respond to information inside and outside the body.2
ANATOMICAL AND FUNCTIONAL STRUCTURE OF THE CNS
In general, the human nervous system consists of the central nervous system (CNS) and the peripheral nervous
system (PNS). The CNS is composed of the brain and spinal cord.2 The PNS is composed of 12 pairs of cranial
nerves and 31 pairs of spinal nerves originating from the brain or the spinal cord. It is supported and protected by
the surrounding skin, skull, meninges and cerebrospinal fluid. 2,3

Figure 1. Meninges of the central nervous parts4


2. Mayfield Brain & Spine: Anatomy of the brain [Internet]. © Mayfield Clinic; 1998-2018;1-7 [cited 2019 April 12]. Available from: https://d3djccaurgtij4.cloudfront.net/pe-anatomybrain.pdf 3. Woolsey TA, Hanaway J, Gado MH. The
Brain Atlas: A Visual Guide to the Human Central Nervous System. 4th edition. Hoboken (NJ): John Wiley & Sons; 2017. . 4. File: Meninges-en-svg. In Wikimedia Commons; [cited 2019 April 12]. Available from:
https://commons.wikimedia.org/wiki/File:Meninges-en.svg
Anatomy & Physiology

The brain comprises of three main parts (Figure 2)2:


❖ Cerebrum
❖ Cerebellum
❖ Brainstem

Figure 2. Internal anatomy of the brain.2


The surface of the cerebrum is called the cortex and contains nerve cells which are grey giving the cortex its colour
and name (grey matter). Beneath the cortex are long connective fibres between neurons and axons (white
matter).2

2. Mayfield Brain & Spine: Anatomy of the brain [Internet]. © Mayfield Clinic; 1998-2018;1-7 [cited 2019 April 12]. Available from: https://d3djccaurgtij4.cloudfront.net/pe-anatomybrain.pdf
Anatomy & Physiology
The cerebrum consists of the right and left hemisphere and is the largest part of the brain. 2

It is sub-divided into the frontal lobe, parietal lobe, temporal lobe and occipital lobe (Figure 3).2

Figure 3. External anatomy of the brain.2

2. Mayfield Brain & Spine: Anatomy of the brain [Internet]. © Mayfield Clinic; 1998-2018;1-7 [cited 2019 April 12]. Available from: https://d3djccaurgtij4.cloudfront.net/pe-anatomybrain.pdf
Anatomy & Physiology2
FRONTAL LOBE 2 PARIETAL LOBE
• Personality, behaviour and emotions • Interpreting language and words
• Judgment, problem solving and planning • Sense of touch, pain and temperature
• Speech - speaking and writing (Broca’s • Interpreting signals from vision, hearing,
area) motor, sensory and memory
• Body movement, intelligence, • Spatial and visual perception
concentration and self awareness

TEMPORAL LOBE
• Understanding language (Wernicke’s area) cerebellum OCCIPITAL LOBE
• Memory • Interpreting vision: colour, light,
• Hearing movement
brainstem
• Sequencing and organisation
The cerebellum (Figures 2 & 3) is located under the temporal and occipital lobes of the cerebrum. Its function is to
coordinate muscle movements, maintain posture and balance. It also has an important role in motor learning.2

The midbrain, pons and medulla form the brainstem (Figure 2), which acts as a relay centre connecting the cerebrum and
the cerebellum to the spinal cord. Many important functions such as breathing, heart rate, sleeping, swallowing or
coughing are regulated here.2

The brain is protected by the skull on the outside.2


2. Mayfield Brain & Spine: Anatomy of the brain [Internet]. © Mayfield Clinic; 1998-2018; 1-7 [cited 2019 April 12]. Available from: https://d3djccaurgtij4.cloudfront.net/pe-anatomybrain.pdf
Anatomy & Physiology
FUNCTIONAL AREAS OF THE BRAIN.5

Figure 4. Functional areas of the brain.5


5. Functional areas of the brain. [Cited 2019 April 12]. Available from
https://www.google.com/search?q=functional+areas+of+the+brain&source=lnms&tbm=isch&sa=X&ved=0ahUKEwirqf14NLhAhUVtHEKHQrHCUgQ_AUIDigB&biw=1366&bih=606#imgrc=XjS2YbQfiiXXbM:
Anatomy & Physiology
PROTECTION OF THE CNS2
Then there are three layers of tissue which are called meninges (Figure 5). The meninges cover and protect
the brain and the spinal cord. The inner layer is the pia mater, the middle layer is the arachnoid mater, and
the outermost layer is the dura mater.

The dura mater is a thick and strong membrane which closely aligns to the inside of the skull. It creates small
compartments, the falx and the tentorium. The falx separates the right and the left hemisphere and the
tentorium separates the cerebrum from the cerebellum.

Figure 5. Meninges of the central nervous parts4


2. Mayfield Brain & Spine: Anatomy of the brain. © Mayfield Clinic; 1998-2018; 1-7 [cited 2019 April 12]. Available from: https://d3djccaurgtij4.cloudfront.net/pe-anatomybrain.pdf 4. File: Meninges-en-svg. In Wikimedia Commons; [cited
2019 April 12]. Available from: https://commons.wikimedia.org/wiki/File:Meninges-en.svg
Anatomy & Physiology
CEREBROSPINAL FLUID2
CEREBROSPINAL FLUID2

Cerebrospinal fluid (CSF) flows around and within the


brain and spinal cord to cushion it from injuries. It is
produced inside fluid-filled cavities called ventricles.
These contain within them a structure called choroid
plexus that makes the colourless CSF. Two lateral
ventricles, deep in the cerebral hemisphere, are
connected to a third ventricle through the foramen of
Figure 6. CSF is produced inside the ventricles deep within the brain. CSF fluid
Monro. The third ventricle is connected to a fourth circulates inside the brain and spinal cord and then outside the subarachnoid
space. Common sites of obstruction: 1) foramen of Monro, 2) aqueduct of
ventricle through the aqueduct of Sylvius. From there, Sylvius, and 3) obex.2

CSF flows into the subarachnoid space to cushion the


brain.

2. Mayfield Brain & Spine: Anatomy of the brain [Internet]. © Mayfield Clinic; 1998-2018;1-7 [cited 2019 April 12]. Available from: https://d3djccaurgtij4.cloudfront.net/pe-anatomybrain.pdf
Anatomy & Physiology
THE ANATOMY
THE ANATOMY OF THE CEREBRAL SYSTEM2 CIRCULATORY SYSTEM2
OF THE CEREBRAL
CIRCULATORY

To function, the brain is dependant upon an adequate supply of both oxygen and nutrients, which are provided by a network of blood
vessels. Blood is carried to the brain by two paired arteries, the carotid arteries and the vertebral arteries (Figure 7).
• Internal carotid arteries supply most of cerebrum. • The venous circulation of the brain is very different
than the rest of the body. Usually arteries and veins
• Vertebral arteries supply the cerebellum, brainstem, run together as they supply and drain specific areas
and the underside of the cerebrum. of the body.
• After passing through the skull, the right and • The major vein collectors are integrated into the
left vertebral arteries join together to form dura to form venous sinuses which collect the blood
the basilar artery. from the brain and pass it to the internal jugular
veins.
• The basilar artery and the internal carotid arteries
“communicate” with each other at the base of the • The superior and inferior sagittal sinuses drain the
brain called the circle of Willis (Figure7). cerebrum, the cavernous sinuses drains the anterior
skull base.
• The communication between the internal carotid
and the vertebral-basilar systems is important Figure 7. Top view of the circle of Willis. The
• All sinuses eventually drain to the sigmoid sinuses,
internal carotid and vertebral-basilar systems are
because if a major vessel is blocked, it is then still joined by the anterior communicating (Acom) and which exit the skull as the jugular veins.
possible for the collateral blood flow to come across posterior communicating (Pcom) arteries.2
the circle of Willis and prevent brain damage.

2. Mayfield Brain & Spine: Anatomy of the brain [Internet]. © Mayfield Clinic; 1998-2018;1-7 [cited 2019 April 12]. Available from: https://d3djccaurgtij4.cloudfront.net/pe-anatomybrain.pdf
Anatomy & Physiology
AUTOREGULATION

Cerebral autoregulation is the mechanism by which cerebral blood flow (CBF) remains relatively constant despite
changes in cerebral perfusion pressure (CPP).6

Changes in CPP or mean arterial blood pressure (MAP) that would increase or reduce CBF can be compensated for by
adjusting cerebrovascular resistance. CBF is regulated better than in most other organs; even with mean arterial
pressure variations of between 60 and 150 mm Hg in the normotensive human. CBF is relatively but not absolutely
constant with changes by only a few percentage points. This is different with acute neurological patients where CPP
is highly important.6

6. Markus HS. Cerebral perfusion and stroke. Journal of Neurology, Neurosurgery & Psychiatry 2004;75(3):353–361.
What is a stroke?
A STROKE IS A MEDICAL EMERGENCY! 7,8

A STROKE OCCURS WHEN THE BLOOD FLOW TO A PART


OF THE BRAIN IS INTERRUPTED8,9

LACK OF BLOOD SUPPLY MEANS THAT NOT ENOUGH OXYGEN OR


NUTRIENTS REACH THE BRAIN AND THE BRAIN CELLS BECOME
DAMAGED OR PERMANENTLY DESTROYED9

DEPENDING ON WHICH PART OF THE BRAIN IS AFFECTED,


DIFFERENT SYMPTOMS CAN OCCUR8,9

IF NOT TREATED IN TIME, A STROKE CAN HAVE EMOTIONAL,


PHYSICAL OR EVEN FATAL CONSEQUENCES8,9 Watch video from webpage , below the
slide section

7. Saver JL. Time is brain- Quantified. Stroke 2006; 37: 263-266. 8. Mayfield Brain & Spine: Stroke. © Mayfield Clinic; 1998-2018;1-6 [cited 2019 April 21]. Available from: https://d3djccaurgtij4.cloudfront.net/pe-stroke.pdf 9. What is
stroke. National Stroke association® [cited 2019 April 12]. Available from: https://www.stroke.org/understand-stroke/what-is-stroke/
What happens when a stroke occurs? 10

Blood flow stopped 0 min

Brain tissue paralysed


Instant onset of early
symptoms
Minutes
Brain tissue dies

Embolic stroke
12 hours
10. Ichai C, Quintard H, Orban JC. Metabolic disorders and critically ill patients. From pathophysiology to treatment. France (Paris): Springer-Verlag; 2012.
What happens when a stroke occurs? 10

Blood flow stopped 0 min

Brain tissue paralysed

Minutes
Brain tissue dies

The sooner blood flow is restored -


the more brain death is prevented

12 hours
10. Ichai C, Quintard H, Orban JC. Metabolic disorders and critically ill patients. From pathophysiology to treatment. France (Paris): Springer-Verlag; 2012.
Clot formation – a quick review11,12

11. Smith SA, Trevers RJ, Morrissey JH. How it all starts: initiation of the clotting cascade. Critical reviews in biochemistry and molecular biology 2015;50(4):326-336. 12. Coagulation. Wikipedia, the free encyclopedia. 2019 [cited
2019 April 21]. Available from: https://en.wikipedia.org/wiki/Coagulation
Aetiology and Pathogenesis of Cerebral Infarct
The World Health Organisation defines a stroke as neurological impairment “caused by the interruption of the blood
supply to the brain, usually because a blood vessel bursts or is blocked by a clot. This cuts off the supply of oxygen and
nutrients, causing damage to the brain tissue. The most common symptom of a stroke is sudden weakness or numbness
of the face, arm or leg, most often on one side of the body. Other symptoms include: confusion, difficulty speaking or
understanding speech; difficulty seeing with one or both eyes; difficulty walking, dizziness, loss of balance or
coordination; severe headache with no known cause; fainting or unconsciousness”.13

The effects of a stroke depend on which part of the brain is damaged and how severely it is affected. A very severe
stroke can cause sudden death.13

There are two different types of stroke:8

1. Ischaemic stroke

2. Haemorrhagic stroke

8. Mayfield Brain & Spine: Stroke. © Mayfield Clinic; 1998-2018;1-6 [cited 2019 April 21]. Available from: https://d3djccaurgtij4.cloudfront.net/pe-stroke.pdf 13. Stroke, Cerebrovascular accident. World Health Organisation [cited 2019, April
12]. Available from: https://www.who.int/topics/cerebrovascular_accident/en/
Aetiology and Pathogenesis of Cerebral Infarct
In addition, there is also transient ischaemic attacks (TIA), defined as “brief episodes of neurological dysfunction
resulting from focal cerebral ischaemia not associated with permanent cerebral infarction”.14

An ischaemic stroke is caused by a thrombotic or embolic occlusion of a cerebral artery. The rupture of a blood vessel
with bleeding into the brain parenchyma or subarachnoid space is known to lead to a haemorrhagic stroke.8 Both types
of strokes deplete the brain of oxygen and nutrients and cause affected brain cells to die.9

When blood flow to the brain is blocked for only a short time, this is known as a transient ischaemic attack (TIA). It is
important to know that a TIA has the same causes as a cerebral infarction, and when the causes remain untreated,
there is high risk of recurrence. 8,9

8. Mayfield Brain & Spine: Stroke. © Mayfield Clinic; 1998-2018; 1-6 [cited 2019 April 21]. Available from: https://d3djccaurgtij4.cloudfront.net/pe-stroke.pdf 9. What is stroke. National Stroke association® [cited 2019 April 12]. Available from:
https://www.stroke.org/understand-stroke/what-is-stroke/ 14. Easton DJ, Saver JL, Albers GW et al. Definition and evaluation of transient Ischemic attack a scientific statement for healthcare professionals from the American Heart
Association/American Stroke Association stroke council; Council on cardiovascular surgery and anesthesia; council on cardiovascular radiology and intervention; council on cardiovascular nursing; and the interdisciplinary council on peripheral
vascular disease. Stroke. 2009;40:2276-2293.
Aetiology and Pathogenesis of Cerebral Infarct
Stroke can be classified at different levels and, indeed, this is essential for patient admission. A stroke can generally be
subdivided by clinical syndromes, aetiology, pathogenesis, time response, severity, localisation and morphology (Table
2).15 There are other classifications developed from Adams et al., 1993, during the “Trial of Org 10172 in Acute Stroke
Treatment (TOAST)”.16 This classification tool is useful to assess the aetiology of stroke.16 TOAST criteria are based on
imaging and angiological findings and observe the aetiology and pathogenesis of stroke (Table 1). This is often used in
clinical practice; handling is simple and distinguishes five groups.15,16

The topographic diagnosis of a cerebral ischaemia is based on the clinical examination, and even for acute therapy,
magnetic resonance imaging (MRI) is essential.16
TABLE 1: TOAST CLASSIFICATION
(Assessment of the aetiology of stroke, adapted from Amarenco, 2009)

1 Cerebrosclerosis
2 Cardioembolic infarct
3 Small artery occlusion (lacune)
4 Stroke of other determined aetiology
5 Stroke of undetermined aetiology
15. Amarenco P, Bogousslavsky J, Caplan LR et al. Classification of stroke subtypes. Cerebrovascular disease 2009;27:493-501. 16. Adams HP, Bendixen BH et al. Classification of subtype of acute ischemic stroke definitions for use
in a multicenter clinical trial. Stroke 1993;24(1):35-41.
Classification of Stroke
TABLE 2: CLASSIFICATION OF STROKE
CLINICAL SYNDROMES FOCAL ISCHAEMIC STROKE
AETIOLOGY17 Artherosclerosis
Cardiac embolism
PATHOGENESIS17 Embolic
Thrombotic
Small vessel disease
Inherited diseases (dermatitis)
TIME REPONSE17 Reversible result
Irreversible result
SEVERITY17 Minor vs. major stroke

LOCALISATION16 Cortical
Subcortical
MORPHOLOGY17 Without lesion → reversible ischaemic
disorder with lesion → cerebral infarct
16. Adams HP, Bendixen BH et al. Classification of subtype of acute ischemic stroke definitions for use in a multicenter clinical trial. Stroke 1993;24(1):35-41. 17. Gund BM, Jagtap PN, Ingale VB et al. Stroke: A brain attack. Journal of Pharmacy
2013;3(8):1-23.
How are strokes classified?
A STROKE CAN BE DUE TO A BLOCKAGE IN ONE OF THE ARTERIES (ISCHAEMIC STROKE) OR
BLEEDING IN THE BRAIN (HAEMORRHAGIC STROKE)8

TRANSIENT ISCHAEMIC ATTACK


ISCHAEMIC STROKE8,9 HAEMORRHAGIC STROKE8,9
(TIA)8,14
THE BLOOD SUPPLY TO AN AREA OF THE
BRAIN BLEEDING IN THE BRAIN PREVENTS
THE BLOOD SUPPLY TO AN AREA OF THE
IS TEMPORARILY INTERRUPTED BUT IS THE NORMAL FLOW OF BLOOD TO THE
BRAIN IS COMPLETELY BLOCKED, CAUSING
RESTORED WITHIN 60 MIN AND THE PATIENT TISSUE BEYOND THE DAMAGE AND CAUSES
TISSUE DEATH AND NEUROLOGICAL DAMAGE
RETURNS NEUROLOGICAL SYMPTOMS
TO NORMAL

ISCHAEMIC STROKE IS THE


COMMONEST FORM OF STROKE9

8. Mayfield Brain & Spine: Stroke. © Mayfield Clinic; 1998-2018; 1-6 [cited 2019 April 21]. Available from: https://d3djccaurgtij4.cloudfront.net/pe-stroke.pdf 9. What is stroke. National Stroke association® [cited 2019 April 12].
Available from: https://www.stroke.org/understand-stroke/what-is-stroke/14. Easton DJ, Saver JL, Albers GW et al. Definition and evaluation of transient Ischemic attack a scientific statement for healthcare professionals from
the American Heart Association/American Stroke Association stroke council; Council on cardiovascular surgery and anesthesia; council on cardiovascular radiology and intervention; council on cardiovascular nursing; and the
interdisciplinary council on peripheral vascular disease. Stroke. 2009; 40:2276-2293.
Stroke types and incidence18,45

Cardiac embolism
20 %

Cryptogenic
30 %
Small vessel

87
disease “lacunes”
25 %

Other
Atherosclerotic 5%
cerebrovascular disease Haemorrhagic
20 % 13 %

18. Albers GW, Amarenco P, Easton D et al. Antithrombotic and thrombolytic therapy for ischemic stroke. The seventh ACCP conference on antithrombotic and thrombolytic therapy. Chest 2004; 126: 438S–512S. 45. Mozaffarian D,
Benjamin EJ, Go AS et al. Heart disease and stroke statistics—2016 update. A report from the American Heart Association. Circulation 2015;133:e38-e360 .
Symptoms, Diagnosis & Differential Diagnosis
ISCHAEMIC SYNDROMES
As mentioned earlier, in the case of an ischaemic stroke, the blood supply to parts of the brain is decreased, which
leads to dysfunction of the brain tissue in that area. Recognising the pattern of stroke syndromes would be helpful in
localising the lesion, but can also suggest treatment, identify the underlying cause and provide help with
prognostication. The main syndromes are lacunar, embolic and artherosclerotic.19
The lacunar syndrome results in a lack of cortical signs and symptoms distinguishing them from large vessel syndromes.
Syndromes are: 19
1. Ataxic Hemiparesis resulting in isolated unilateral weakness and ataxia. The lesion is along the corticospinal and
cerebellar pathways.
2. Pure motor stroke/hemiparesis resulting in isolated unilateral weakness of the face, arm, or leg, the lesion is mostly
in posterior limb of the internal capsule or the basic pontis.
3. Pure sensory stroke resulting in isolated unilateral numbness, pain or paraesthesia. The lesion is mostly in the
contralateral thalamus.
4. Mixed sensorimotor stroke resulting in hemiparesis or sensory impairment. The lesion is typically in the thalamus
and adjacent posterior internal capsule.
5. Clumsy hand-dysarthria resulting in unilateral mild weakness/clumsiness of the hand and dysarthia with face and
tongue weakness. The lesion is mainly in the basis pontis.

19. Torbey MT, Selim MH. The stroke book. 2nd edition. Cambridge University press. 2013.
Symptoms, Diagnosis & Differential Diagnosis

Emboli occur in the circulatory system where they enter the cerebral circulation and lodge in and occlude brain blood
vessels. If an embolus is large, occlusion of an intracranial artery may occur. If it is small, it can become struck in a
smaller segment of an artery. Signs are: 19
1. Seizure: simple focal or focal-onset
2. Cortical signs: aphasia, neglect, dyspraxia, hemianopia and agraphesthesia
3. Discrete focal signs: isolated hand weakness, isolated aphasia.

Atherosclerotic Stenosis (extracranial or intracranial) can render cerebral tissue receptive to ischaemia from
hypoperfusion and oligaemia or embolisation. Transient examples are: 19
1. Amaurosis fugax (transient monocular blindness) from the ophthalmic artery or internal carotid stenosis.
2. Limb-shaking transient ischaemic attack (TIA): repeated brief episodes of contralateral arm weakness from cervical
or intracranial carotid stenosis/occlusion.

19. Torbey MT, Selim MH. The stroke book. 2nd edition. Cambridge University press. 2013.
Symptoms, Diagnosis & Differential Diagnosis
HAEMORRHAGIC SYNDROMES
Haemorrhagic strokes result in tissue injury by causing compression of tissue from a growing hematoma or hematomas. This can
distort and injure tissue and the pressure can lead to a loss of blood supply to the affected tissue, resulting in an infarction. It appears
that the blood released by brain haemorrhage has direct toxic effects on brain tissue and vasculature. Intracerebral haemorrhage (ICH)
symptoms are often clinically indistinguishable from ischaemic stroke syndromes. Ischaemic and haemorrhagic strokes produce focal
deficits of acute onset. Nevertheless, the blood within the cranial vault can lead to: Headache, nausea and vomiting, decreased level of
consciousness. 9,19

The symptoms of an ischaemic stroke syndrome can be exposed as a transient ischaemic attack while ICH symptoms persist and are
likely to worsen. Identifying the location of haemorrhage can help predict the underlying cause. The haemorrhage can be intracerebral
or subarachnoidal. 9,19
CEREBROVASCULAR EMERGENCY SYNDROMES
In individual cases there is a need to separate cerebrovascular emergency syndromes that look like stroke syndromes:20
• Todd’s paresis after epilepsy
• seizure with focal motor symptoms
• aura in migraine
• aphasic disturbances in herpes simplex encephalitis
• functional disorders
• In contrast to blood clot in the basilar artery: altered consciousness of another origin
• In contrast to the vertebrobasilar stroke, peripheral vertigo causes
9. What is stroke. National Stroke association® [cited 2019 April 12]. Available from: https://www.stroke.org/understand-stroke/what-is-stroke/19. Torbey MT, Selim MH. The stroke book. 2nd edition. Cambridge University
press. 2013. 20. Fernandes PM, Whiteley WN, Hart SR et al. Strokes: mimics and chameleons. Practical Neurology 2013;13:21-28.
Common stroke mimics20,21,22

ALCOHOL CEREBRAL METABOLIC NEUROPATHY


INTOXICATION INFECTION DISORDERS (BELL’S PALSY)

SEIZURES AND
BRAIN POST-SEIZURE
MIGRAINE
TUMOURS STATES, TODD’S
PARALYSIS

DRUG
HYPO- EPIDURAL HYPERTENSIVE
OVERDOSE /
GLYCAEMIA HAEMATOMA ENCEPHALOPATHY
TOXICITY

20. Fernandes PM, Whiteley WN, Hart SR et al. Strokes: mimics and chameleons. Practical Neurology 2013;13:21-28. 21. Summers D, Leonard A, Wentworth D et al. Comprehensive overview of nursing and interdisciplinary care of
the acute ischemic stroke patient: A scientific statement from the American Heart Association. Stroke 2009;40:2911-2944. 22. Hatzitolios A, Savopoulos C, Ntaios G et al. Stroke and conditions that mimic it: a protocol secures a safe
early recognition. Hippokratia 2008;12(2):98-102.
Time is brain tissue7

PENUMBRA
(SALVAGEABLE
BRAIN AREA)23

ISCHAEMIC CORE
(BRAIN TISSUE
DESTINED TO DIE)23

AN UNTREATED PATIENT LOSES


APPROXIMATELY REPERFUSION OFFERS THE
1,9 MILLION NEURONS EVERY MINUTE IN POTENTIAL TO REDUCE THE EXTENT OF
THE ISCHAEMIC AREA7 ISCHAEMIC INJURY24

7. Saver JL. Time is brain- Quantified. Stroke 2006;37:263-266. 23. Gonzalez RG. Imaging-guided acute ischemic stroke therapy:From “time to brain” to “physiology is brain”. American Journal of Neuroradiology 2006;27:728-735. 24.
Kidwell CS, Alger JR, Saver JL. Evolving paradigms in neuroimaging of the ischemic penumbra. Stroke 2004;35(11):2662-5.
Regions of Ischaemia25,26

25. Donnan GA, Baron JC, Ma H et al. Penumbral selection of patients for trials of acute stroke therapy. Lancet Neurology 2009;8:261–69. 26. Moustafa RR, Baron JC. Review: Pathophysiology of ischaemic stroke: insights from
imaging, and implications for therapy and drug discovery. British Journal of Pharmacology 2008;153:S44–S54
Time is brain!
In a typical ischaemic stroke:

Every minute the brain loses:7


▪ 1,9 million neurons
▪ 14 billion synapses
▪ 12 km myelinated fibers
Every minute counts!
7. Saver JL. Time is brain- Quantified. Stroke 2006;37:263-266.
Symptoms, Diagnosis & Differential Diagnosis
It is important to recognise stroke symptoms and react as fast as possible in order to ensure best medical
treatment in time. Since effective stroke treatment is very time critical, people have to be aware of the
criteria for identifying a stroke. Below is the face arm speech test (FAST), which can be used to remember the
warning signs, act FAST and call for medical help.27,28

TABLE 3: FAST CRITERIA28


(WARNING SIGNS OF STROKE, NATIONAL STROKE ASSOCIATION)

F Face drooping
(asymmetry when asked to smile)

A Arm weakness
(difficulty when raising arms)

S Speech difficulties
(fuzzy articulation of simple sentences)

T Time
(time to call emergency)

27. Jauch EC, Saver JL, MD, HP Adams et al. Guidelines for the early management of patients with acute ischemic stroke: A guideline for healthcare professionals from the American Heart Association/American Stroke Association.
Stroke 2013;44:870-947. 28. Stroke symptoms: FAST. American Stroke Association; 2019 [cited 2019 April 12]. Available from https://www.strokeassociation.org/en/about-stroke/stroke-symptoms
Symptoms, Diagnosis & Differential Diagnosis
STROKE SYMPTOMS STROKE SYMPTOMS

The most common symptom of stroke is a sudden weakness of the face, arm or legs, most often on
one side of the body. But, there are other symptoms, including the sudden onset of:8,27,28

• numbness of the face, arms or legs


• confusion, difficulty speaking or understanding speech
• difficulty seeing with one or both eyes
• difficulty walking, dizziness, loss of balance or coordination
• severe headache with no known cause
• fainting or unconsciousness

8. Mayfield Brain & Spine: Stroke. © Mayfield Clinic; 1998-2018; 1-6 [cited 2019 April 21]. Available from: https://d3djccaurgtij4.cloudfront.net/pe-stroke.pdf 27. Jauch EC, Saver JL, MD, HP Adams et al. Guidelines for the early management
of patients with acute ischemic stroke: A guideline for healthcare professionals from the American Heart Association/American Stroke Association. Stroke 2013;44:870-947. 28. Stroke symptoms: FAST. American Stroke Association; 2019
[cited 2019 April 12]. Available from https://www.strokeassociation.org/en/about-stroke/stroke-symptoms
How do I know if someone is having a stroke?
BE SUSPICIOUS OF A STROKE IF ANY OF THE FOLLOWING SYMPTOMS OCCUR8,27,28

CONFUSSION
AND/OR
DROOPING OF
SEVERE, SUDDEN- PROBLEMS
UNCONCIOUSNESS THE MOUTH ON
ONSET HEADACHE UNDERSTANDING
ONE SIDE
WHAT IS BEING
SAID

WEAKNESS
OR COMPLETE
LOSS OF MOVEMENT
DIZZINESS
AND/OR SENSATION
IN ONE OR MORE
LIMBS

DIFFICULTY VISUAL
TALKING, DISTURBANCE OR
FORMING WORDS LOSS OF SIGHT IN
OR SLURRING ONE OR BOTH
WORDS EYES

IMPORTANT
NOTE THE TIME AT WHICH THESE SYMPTOMS STARTED AND
CALL THE EMERGENCY SERVICES IMMEDIATELY
8. Mayfield Brain & Spine: Stroke. © Mayfield Clinic; 1998-2018; 1-6 [cited 2019 April 21]. Available from: https://d3djccaurgtij4.cloudfront.net/pe-stroke.pdf 27. Jauch EC, Saver JL, MD, HP Adams et al. Guidelines for the early management
of patients with acute ischemic stroke: A guideline for healthcare professionals from the American Heart Association/American Stroke Association. Stroke 2013;44:870-947. 28. Stroke symptoms: FAST. American Stroke Association; 2019
[cited 2019 April 12]. Available from https://www.strokeassociation.org/en/about-stroke/stroke-symptoms
What to look out for28,29

IS HS

• Sudden numbness of the face, arm, or leg, especially on one side of the body; X X
• Sudden confusion, trouble speaking or understanding speech; X X

• Sudden trouble seeing in one or both eyes; X X

• Sudden trouble walking, dizziness, loss of balance or coordination X X

• Sudden severe headache with no known cause X X


• In addition, neck pain29 X
• In addition, nausea / vomiting29 X
• In addition, loss of consciousness29 X

28. Stroke symptoms: FAST. American Stroke Association; 2019 [cited 2019 April 12]. Available from https://www.strokeassociation.org/en/about-stroke/stroke-symptoms 29. Ahmed J, Blakeley C, Sakar R et al. Acute neck
pain, an atypical presentation of subarachnoid haemorrhage. Emergency Medical Journal 2007;24:e23
Signs and Symptoms – FAST Test27,28

Facial drooping: A section of the face, usually only on one


side, that is drooping and hard to move

Arm weakness: The inability to raise one's arm fully

Speech difficulties: An inability or difficulty to


understand or produce speech

Time: Time is of the essence when having a stroke


– Record time of symptoms onset and treat quickly
27. Jauch EC, Saver JL, MD, HP Adams et al. Guidelines for the early management of patients with acute ischemic stroke: A guideline for healthcare professionals from the American Heart
Association/American Stroke Association. Stroke 2013;44:870-947. 28. Stroke symptoms: FAST. American Stroke Association; 2019 [cited 2019 April 12]. Available from
https://www.strokeassociation.org/en/about-stroke/stroke-symptoms
Reducing Risk of Stroke
The best way to reduce the risk of getting a stroke is to minimise the risk factors.
The risk factors of stroke can be classified into:30,31

• Therapeutically non-influenceable risk factors


• Therapeutically influenceable risk factors

The risk factors that can be influenced are treatable with drugs, interventional treatments or through lifestyle
changes.32

In 2010, a standardised case-control study entitled “INTERSTROKE” offered much information about the risk factors for
stroke in different regions of the world. It revealed that five risk factors could explain more than 80 % of the global risk
of strokes: hypertension, smoking, diet, abdominal obesity and physical activity. 33

30. Mackay J, Mensah GA. The atlas of heart disease and stroke. World health organization and center for disease control and prevention. 2004. [cited 2019 April 26]. Available from:
http://www.who.int/cardiovascular_diseases/resources/atlas/en 31. Romero JR, Morris J, Pikula A. Stroke prevention: mofifying risk factors. Therapeutic advances in cardiovascular diseases 2008;2(4):287-303 32. Hankey G. The global
and regional burden of stroke. Lancet 2013;1:e239-e240. 33. O‘Donnell MJ, Xavier D, Liu L et al. Risk factors for ischaemic and intracerebral haemorrhagic stroke in 22 countries (the INTERSTROKE study): a case-control study. Lancet
2010;376:112-123.
Non - Modifiable Risk Factors
Age is the most important independent risk factor for stroke. The risk of stroke doubles every decade after age 55.30,34

The incidence rates are higher in men than in women, but more women die from stroke as they tend to live longer.35

A positive family history of stroke means approximately 1,5 times higher risk of suffering a stroke. In addition, there are
single mutations to consider, especially at a young age. There is an increased risk of stroke if a first-degree blood
relative has had a stroke before.30,36,37

Low-income and middle-income countries, as well as populations with a low socioeconomic status in high-income
countries are disproportionally affected by stroke. This does not only apply to stroke risk but also to short-term and
long-term outcome. These effects are based on increased individual risk factors, such as hypertension, hyperlipidaemia,
excessive alcohol intake, smoking obesity, and lack of access to good quality hospital and rehabilitation care.32

The risk of getting a stroke is three times higher for African Americans as it is for Caucasian Americans. In Asia, the risk
of getting a stroke or a cerebral haemorrhage is higher than in Western Europe and North America.30,38,39

30. Mackay J, Mensah GA. The atlas of heart disease and stroke. World health organization and center for disease control and prevention. 2004. [cited 2019 April 26]. Available from:
http://www.who.int/cardiovascular_diseases/resources/atlas/en 32. Hankey G. The global and regional burden of stroke. Lancet 2013;1:e239-e240. 34. Feigin VL, Forounzafar H, Krishnamuthi R et al. Global and regional burden of stroke
during 1990-2010: findings from the global burden of disease study 2010. Lancet 2014;383:245-255. 35. Turtzo LC, McCullough LD. Sex differences in stroke. Cerebrovascular Disease 2008;26:462–474. 36.Markus H. Genes for stroke. Journal
of neurology, neurosurgery and psychiatry. 2004;75(1):1229-1231. 37. Lindgren A. Stroke genetics: A review and update. Journal of stroke 2014;16(3):114-123. 38. Howard G, Labarthe DR, Hu J et al. Regional differences in African Americans’
high risk for stroke: The remarkable burden of stroke for Southern African Americans. Annals of epidemiology 2007;17(9):689-696. 39 . Sun Z, Zheng L, Detrano R et al. An epidemiological survey of stroke among rural Chinese adults results
from Liaoning province. Research 2013;8:701-706.
Non - Modifiable Risk Factors
AGE30,34 ADVANCED
GENDER35
RISK OF STROKE MORE THAN DOUBLES IN EACH SUCCESSIVE
INCREASED RISK OF STROKE IN WOMEN
DECADE AFTER 55 YEARS

PROBABLY RELATED TO PREGNANCY, GESTATIONAL DIABETES, ORAL


THE RISK OF STROKE DOUBLES EVERY DECADE AFTER 55 YEARS OF AGE
CONTRACEPTIVE USE, HORMONE-REPLACEMENT THERAPY & SMOKING

FAMILY HISTORY36 ADVANCED


RACE30,38

RISK MAY BE HIGHER WITH A POSITIVE FAMILY HISTORY INCREASED RISK OF STROKE IN AFRICAN-AMERICANS

PROBABLY DUE TO INCREASED RISK OF HYPERTENSION,


SOME CAUSES ARE HEREDITARY, E.G. CADASIL**
DIABETES & OBESITY

** CADASIL, cerebral autosomal dominant arteriopathy with sub-cortical infarcts and leukoencephalopathy

30. Mackay J, Mensah GA. The atlas of heart disease and stroke. World health organization and center for disease control and prevention. 2004. [cited: 2019 April 26]. Available from:
http://www.who.int/cardiovascular_diseases/resources/atlas/en 34. Feigin VL, Forounzafar H, Krishnamuthi R et al. Global and regional burden of stroke during 1990-2010: findings from the global burden of disease study 2010. Lancet
2014;383:245-255. 35. Turtzo LC, McCullough LD. Sex differences in stroke. Cerebrovascular Disease 2008;26:462–474. 36.Markus H. Genes for stroke. Journal of Neurology, Neurosurgery and Psychiatry. 2004;75(1):1229-1231. 37. Lindgren A.
Stroke genetics: A review and update. Journal of stroke 2014;16(3):114-123. . 38. Howard G, Labarthe DR, Hu J et al. Regional differences in African Americans’ high risk for stroke: The remarkable burden of stroke for Southern African
Americans. Annals of Epidemiology 2007;17(9):689-696.
Modifiable Risk Factors

Diabetes mellitus is one of the major risk factors for stroke.30

The uncertainty interval around the global estimate of adults with diabetes was estimated to range from 7,2 % to
11,4 % (339 – 536 million). This means that while the International Diabetes Federation estimates the prevalence
of diabetes to be 415 million (IDF Diabetes Atlas 7th edition, 2015) the true figure could lie between 339 and
536 million.40

The incidence rate is rising. It is estimated that by 2040, one adult in ten will have diabetes (642) million.40

30. Mackay J, Mensah GA. The atlas of heart disease and stroke. World health organization and center for disease control and prevention. 2004. [cited 2019 April 26]. Available from:
http://www.who.int/cardiovascular_diseases/resources/atlas/en 40. © International Diabetes Federation. IDF diabetes atlas, 7th edition. Brussels, Belgium. [cited 2019 April 26]. Available from:
www.diabetesatlas.org/component/attachments/?task=download&id=180
Modifiable Risk Factors
Cholesterol is essential for the formation of cell membranes and the synthesis of steroid hormones and
vitamin D. It can be found in the bloodstream and in all cells of the body. In particular, low-density
lipoproteins (LDL) and high-density lipoproteins (HDL) play a role in the transport and metabolism of
cholesterol and triglycerides.41

Carotid artery stenosis is the narrowing of the carotid arteries,


which are the two main blood vessels in the neck that supply
blood to the brain (Figure 7). Artherosclerotic plaques lead to
stenosis of the carotid arteries and can be the reason for
subsequent emboli. Hypertension, smoking, diabetes mellitus,
and hyperlipidaemia are major risk factors for the
development of atherosclerotic disease.42

Smoking significantly increases the risk of heart disease


and stroke. Smokers are two to four times more likely to
have a stroke than non-smokers. The more you smoke, the Figure 7: Intracranial stenosis.42

more the risk increases.30,43

30. Mackay J, Mensah GA. The atlas of heart disease and stroke. World health organization and center for disease control and prevention. 2004. [cited 2019 April 26]. Available from:
http://www.who.int/cardiovascular_diseases/resources/atlas/en 41. National Stroke Association. Cholesterol fact sheet. [cited 2019 April 26] Available from:
file:///C:/Users/Helen/AppData/Local/Packages/Microsoft.MicrosoftEdge_8wekyb3d8bbwe/TempState/Downloads/Cholesterol_Fact-Sheet.pdf 42. Mayfield Brain & Spine: Intracranial artery stenosis. © Mayfield Clinic; 1998-
2018; 1-4 [cited 2019 April 26]. Available from: https://d3djccaurgtij4.cloudfront.net/pe-intracranialstenosis.pdf 43. Shah RS, Cole W. Smoking and stroke: the more you smoke the more you stroke. Expert Review of Cardiovascular
Therapy 2010;8(7):917–932.
Modifiable Risk Factors
The definition and classification of blood pressure
according to the updated guidelines, show that there is a
manifest arterial hypertension when the blood pressure
shows > 130/80 mmHg.44

Elevated blood pressure is the most common treatable


reason for vascular events. Arterial hypertension is the
strongest risk factor for a stroke; this applies to cerebral
haemorrhage as well as to brain infarcts.33

With increasing blood pressure, the risk of getting a


stroke rises exponentially. Normalising high blood
pressure is the most effective way to prevent a stroke.30

30. Mackay J, Mensah GA. The atlas of heart disease and stroke. World health organization and center for disease control and prevention. 2004. [cited 2019 April 26]. Available from:
http://www.who.int/cardiovascular_diseases/resources/atlas/en 33. O‘Donnell MJ, Xavier D, Liu L et al. Risk factors for ischaemic and intracerebral haemorrhagic stroke in 22 countries (the INTERSTROKE study): a case-control study.
Lancet 2010;376:112-123. 44. Whelton PK, Carey RM, Aronow WS et al. 2017 ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ ASPC/NMA/PCNA Guideline for the prevention, detection, evaluation, and management of high blood pressure
in adults: Executive summary a report of the American College of Cardiology/American Heart Association task force on clinical practice guidelines. Hypertension 2018;71:1269-1324.
Modifiable Risk Factors
Atrial fibrillation is an eminent risk factor for suffering a cerebral infarction even if you exclude the risk factors like age and
hypertension, which mostly accompany AF. The relative stroke risk increases about fivefold in the presence of atrial fibrillation. The size
of this risk is strongly related to the age group of affected individuals.45

The average age of patients with this condition is between 67 (men) and 75 (woman) years and it is expected to rise in the future.46
Validated scores for the prediction of stroke risk such as CHADs2 and CHA2DS2VASc, can be useful tools in the assessment of patients.47

The CHADS2 score can be calculated from the table by adding the relevant points (Table 4).47

TABLE 4: CHADS2 SCORE TO ESTIMATE THE ANNUAL RISK OF STROKE IN PATIENTS WITH AF
CONDITION POINTS
C Congestive heart failure 1 Point
H (Hypertension) Blood pressure consistently above 140/90 mmHg (or treated 1 Point
hypertension on medication)
A (Age) ≥ 75 years 1 Point
D (Diabetes) Diabetes mellitus 1 Point
S (Stroke) Prior Stroke, TIA or Thromboembolism 2 Point

45. Mozaffarian D, Benjamin EJ, Go AS et al. Heart disease and stroke statistics—2016 update. A report from the American Heart Association. Circulation 2015;133:e38-e360 . 46. Roger VL, Go AS, Lloyd-Jones DM et al. Heart Disease and
Stroke Statistics—2012 Update a report from the American Heart Association. Circulation. 2012;125:e2-e220. 47. Gage BF, Waterman AD, Shannon W et al. Validation of clinical classification schemed for predicting stroke. Results from
the national registry of atrial fibrillation. The Journal of the American Medical Association 2001;285(22):2864-2870.
Modifiable Risk Factors30,31,33

HIGH BLOOD HEART LACK OF


PRESSURE DIABETES
DISEASE EXERCISE
(HYPERTENSION)

ATRIAL ALCOHOL
FIBRILLATION INTAKE

HIGH
SMOKING OBESITY STRESS
CHOLESTEROL

30. Mackay J, Mensah GA. The atlas of heart disease and stroke. World health organization and center for disease control and prevention. 2004. [cited 2019 April 26]. Available from:
http://www.who.int/cardiovascular_diseases/resources/atlas/en 31. Romero JR, Morris J, Pikula A. Stroke prevention: mofifying risk factors. Therapeutic advances in cardiovascular diseases 2008;2(4):287-303 33. O‘Donnell MJ,
Xavier D, Liu L et al. Risk factors for ischaemic and intracerebral haemorrhagic stroke in 22 countries (the INTERSTROKE study): a case-control study. Lancet 2010;376:112-123.
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