55% increase in stroke in people in their 50s

Need a free and open discussion on the possible causes.

This is the video I have just recorded on this topic with data from England.

Hospital admissions for strokes rise by 28% since 2004 – as NHS urges the public to ‘Act FAST’

(Face, Arms, Speech, Treatment)

This is the paper from NHS England.

The number of people being admitted to hospital following a stroke has risen by 28% in the last 20 years, new NHS analysis has found.

17^th November 2024

https://www.england.nhs.uk/2024/11/hospital-admissions-for-strokes-rise-by-28-since-2004-as-nhs-urges-the-public-to-act-fast/

https://www.nhs.uk/conditions/stroke/symptoms/

These following notes are taken from the NHS paper and discussed in the video.

NHS England data

Stroke admissions in England in 2023/24

111,137 stroke admissions

Stroke admissions in England in 2004/05

87,069 stroke admissions

(driven in part by an ageing population and the impacts of lifestyle factors on the nation’s cardiovascular health)

Stroke admissions among people aged 50-59, 2023/24

12,533

Stroke admissions among people aged 50-59, 2004/05

8,063

That is a 55% rise in admissions among people aged 50-59

Stroke admissions among people aged 60-69

42% increase

Stroke admissions among people aged 70-79

25% increase

NHS launched a major campaign

999 immediately

Struggling to smile (Face)

Raise an arm          (Arms)

Slurring their words (Speech)

England’s top doctor

figures show that strokes “are not just a risk for older people”

Experts say

(increase in admissions among ages 50-59)

Better detection and reporting

Hypertension

Obesity

Poor diet

Lack of exercise

Signs Symptoms

Face weakness

Arm weakness, weakness or numbness in 1 arm

Speech problems, slur words or sound confused

Other symptoms of a stroke

Weakness or numbness down 1 side of body

Blurred vision or loss of sight in 1 or both eyes

Finding it difficult to speak or think of words

Confusion and memory loss

Feeling dizzy or falling over

A severe headache

Feeling or being sick (nausea or vomiting)

After reporting on this video I gave an introduction to the pathophysiology of stroke based on my textbook, Campbell’s Pathophysiology Notes.

Available for free download here,

https://drjohncampbell.co.uk

Cerebrovascular accident (Stroke)

Stroke is defined as a focal neurological deficit due to a vascular lesion which

lasts for more than 24 hours. Stroke is the third most common cause of death

in most developed countries, after heart disease and cancer. It is also the major

cause of disability in adults.

Thromboembolic pathophysiology

There are two main types of stroke; thromboembolic and haemorrhagic. As the

name implies thromboembolic stroke is caused by an occlusion of the normal

blood supply by thrombosis or embolism. This cause of stroke is most common

accounting for about 85% of cases. Thromboembolic stroke occurs mostly as a

compilation of atherosclerosis with atheroma leading to thrombus formation.

As in other forms of arterial disease a thrombus will develop on a ruptured

plaque of atheroma. The presence of a thrombus will occlude an arterial lumen

and so fully or partly cut off the blood supply to an area of the brain. Parts of

a thrombus may break away from the main clot generating emboli. When an

embolus reaches a vessel it is too large to pass through, the embolus becomes

jammed, occluding blood flow. Thromboembolic pathology may arise from

the heart and large extracranial arterial vessels supplying blood to the brain or

from smaller intracerebral vessels.

Extracranial emboli

Emboli may arise from thrombus formation in the heart. Emboli from the left

side of the heart can pass into the cerebral circulation via the aorta and account

for about 20% of thromboembolic strokes. Emboli may be generated in the

heart as a complication of atrial fibrillation, endocarditis or from a mural

thrombus which may complicate myocardial infarction.

The most common cause of stroke is emboli which arise from thrombus

development in the extracranial arteries such as the aorta, carotid or vertebral

arteries. These vessels transport blood from the left ventricle to the cerebral

arteries in the brain. The most common cerebral artery which becomes

occluded as a result of embolism is the middle cerebral artery. This artery

carries high volumes of blood from the circle of Willis to large areas of the

brain. As a result any thromboembolic occlusion of this vessel will potentially

deprive a significant area of brain of its normal blood supply resulting in a large

cerebral infarction.

Disease in intracerebral arteries

A further 20% of infarctions are due to disease within the smaller

intracerebral arterial vessels within the brain. These small penetrating arterial

branches carry blood from the larger vessels, such as the middle, posterior

or anterior cerebral arteries into the brain tissue. Disease in these smaller

vessels is most likely to develop in patients with diabetes and hypertension.

When one of these arteries becomes occluded it will infarct a small area of

the brain giving rise to a highly localised stroke. For example, the patient

may present with only loss of motor or sensory function, as opposed to

most strokes when both are lost in the same area of the body. The relatively

small lesions generated by disease of these penetrating vessels are termed

lacunar infarcts. Because they do not involve a large area of the brain they

are unlikely to cause impairment of cognition, memory, speech, or level of

consciousness. Despite only affecting relatively small areas of the brain the

effects of a small infarct can be significant, especially as they may affect the

nerve fibres within the internal capsule.

There is an internal capsule in both hemispheres of the brain. These capsules

carry nerve fibres between the cerebral cortex and brain stem. All of the motor

fibres from the motor cortex pass through this capsule. All of the sensory fibres

travelling to the sensory cortex also pass through the internal capsule.

These nerve pathways carry on through the brain stem and down the spinal

cord to the body. This means that if part of the blood supply to the internal

capsule is occluded, many nerve fibres can be infarcted which will no longer be

able to carry nerve impulses. As a result sensory information will not be able to

pass from the body to the sensory cortex and motor impulses will be unable to

pass from the cortex to the body.

Haemorrhagic pathophysiology

Haemorrhage is the other main cause of stroke. Haemorrhagic stroke caused by

intracerebral (within the cerebrum) bleeds account for about 10% of cases.

Bleeds may occur as a result of a ruptured aneurysm, which is a weakness in the

wall of a blood vessel. The explosive entry of blood into the tissues of the brain

immediately prevents the normal function of the neurones in the affected area.

The haematoma caused by the haemorrhage may be reabsorbed over time and

there may be varying degrees of patient recovery. Large bleeds may lead to raised

intracranial pressure, shifting of intracranial contents and death from coning.

In addition to cerebral haemorrhage causing stroke it is also possible for a

thromboembolic stroke to be complicated by haemorrhage. Ischaemia or

infarction caused by an arterial occlusion may damage the walls of blood vessels

as well as neurological tissue. Bleeding may then occur through this damaged

vascular wall leading to haemorrhage into the infarcted area. This is referred to

as haemorrhagic transformation.

The remaining strokes which are not thromboembolic or haemorrhagic may

be caused by cerebral hypoperfusion, subarachnoid haemorrhage and subdural

or extradural haematoma.

Aetiology and Prevention

As stroke is most commonly caused by underlying arterial disease, the risk factors

are the same as those for the development of atherosclerosis. People should be

given all of the health education advice and treatments necessary for the

prevention of atherosclerosis. In particular, hypertension is a significant risk

factor for stroke. This is important to know as high blood pressure can usually

be effectively managed, therefore reducing the risk. If heart disease is present

this should be treated as far as possible. If atrial fibrillation is an ongoing problem

then anticoagulants are important to reduce the risk of thrombi developing in

the atria.

Clinical features of stroke

There will be a sudden onset (over a few minutes) of focal neurological deficit.

Features may continue to develop over the next few hours; this is called a

stroke in evolution. Usually the clinical features reach a maximum after about

6 hours when the stroke is said to be completed.

As most nerve fibres cross over at the level of the medulla oblongata, a

stroke affecting the left side of the brain will cause neurological deficit on the

right side of the body. Likewise a stroke in the right side of the brain will affect

the left side of the body. Therefore limbs on the opposite side to the cerebral

lesion become weak and may be completely paralysed. In severe cases there may

be a complete hemiplegia (paralysis of one side of the body). Other cases may

show a hemiparesis (muscular weakness on one side of the body). Often the

facial muscles on one side will be paralysed giving rise to a droop.

Sensation is also usually lost; the patient is unable to feel affected areas of

the body. Indeed the situation is often more extreme than this, patients neglect,

or even fail to acknowledge the existence of one side of the body. Some patients

may try to push their hand out of bed because they do not believe it belongs to

them.

Centres which generate speech are usually located in the dominant cerebral

hemisphere. In right handed people the dominant hemisphere is the left. This

means that if the left hemisphere is involved the speech centres may no longer

function normally. An impaired ability to generate speech is termed a dysphasia

and a complete loss of speech as aphasia. Other patients know what they want

to say but find it difficult to articulate words as a result of loss of motor function.

This feature is described as dysarthria. There may also be involvement of the

parts of the brain that facilitate the understanding of language, described as

receptive dysphasia. Dysphagia (difficulty in swallowing) is also common after

stroke. If the occipital lobes or tracts are involved there may be a sudden

deterioration of vision in one or both eyes.

Most patients remain conscious during a stroke making it a very frightening

experience. Confusion is possible but loss of consciousness usually indicates a

large lesion or the involvement of the brain stem. While severe headache and

vomiting at the onset of a stroke are possible indicators of a haemorrhagic

cause, brain imaging is needed to diagnose thromboembolic as opposed to

haemorrhagic strokes.

Prognosis

Patients have very varied recovery after a stroke. Initial recovery may be rapid

for a few days. This initial recovery can be explained by the existence of a zone

of ischaemia and inflammation around the cerebral infarction. This area of

ischaemia and inflammation, caused by the stroke, can be severe enough to

prevent normal electrical activity in the cells involved, but not severe enough to

cause them to necrose. Short term adaptations in the circulation can allow the

ischaemic area to regain an adequate level of blood perfusion and so result in a

restoration of function. If an area of brain recovers, the motor and sensory

function will be restored to the represented parts of the body. Following this

initial period, most patients show a gradual improvement and some recovery

may continue for 2-3 years. Overall about a third of patients make a good

recovery, a third are likely to die and the final third are left permanently disabled.

Management principles

Initial management must pay careful attention to maintenance of a clear airway.

Swallowing must also be assessed to prevent aspiration of saliva, food or drink

into the airway. Specialist stroke units now give thrombolysis to suitable patients

as soon as a diagnosis of thromboembolic stroke is confirmed, usually by CT

or MRI. Clearly, if a stroke has a haemorrhagic component thrombolysis would

be contraindicated. CT and MRI scanning can readily distinguish between a

haemorrhagic or thromboembolic stroke. In thromboembolic stroke aspirin

started within 48 hours has been demonstrated to improve long term outcome.

This reduces platelet aggregation and so reduces the likelihood of thrombus or

emboli formation in future. Lowering blood pressure reduces the risk of recurrent

stroke. Statins should be given to lower high plasma cholesterol and are

associated with improved outcomes. Rehabilitation is often a long process in

stroke management but can be very rewarding. Speech therapists, physiotherapists

and occupational therapists all have an important role in addition to good

nursing.

Transient ischaemic attack (TIA)

This refers to the clinical features generated by an episode of cerebral ischaemia.

Once blood flow and oxygen delivery fall below a minimum threshold neurones

will be unable to generate normal electrical activity. At this reduced level of

blood flow the neurones remain viable so infarction will not develop. Function

will recover as blood flow increases after the ischaemic episode. Traditionally a

TIA has been defined as neurological deficits which resolve within 24 hours.

The neurological deficit is caused by reduced blood flow through a partly

occluded vessel or a small thromboembolic event. While recovery is complete,

the patient should be regarded as being at risk of a future stroke.

Diagram 13.10

Sources of emboli which may enter the cerebral circulation and so lead to stroke. In atrial fibrillation there are stagnant areas of blood which may clot, mural thrombosis may complicate myocardial infarction and the arch of the aorta and carotid arteries are both common sites of atheroma formation. Emboli from extracranial vessels are the most common cause of cerebrovascular accidents. Arrows indicate the direction of emboli travel towards the brain.

Diagram 13.11

Thromboembolic stroke caused by occlusion in a large arterial

vessel. This diagram shows a large area of infarct in the left

cerebral hemisphere affecting the parietal and frontal lobes. The

cause is a thromboembolic occlusion of the middle cerebral artery.

Motor loss will occur on the right side of the body as a result of

involvement of the left motor cortex in the frontal lobe. Sensory loss

on the right side can be explained by involvement of the sensory

cortex in the left parietal lobe. It is also likely that this patient will

be aphasic as the speech centre is usually in the left hemisphere.

Diagram 13.12

From the cerebral cortex (including the motor and sensory areas) numerous fibres

pass down into the white matter of the brain. Collectively these fibres are called

the projection tracts (they are also called the corona radiata). These fibres are

all collected together in an internal capsule to be carried through the brain

to the brain stem. Most nerve fibres cross over at the level of the of the medulla

oblongata, before communicating with the body via the spinal cord.