Stroke

Stroke

Definition and classification

Definition

Stroke is the sudden onset of a focal neurological deficit, lasting more than 24hr or leading to death, caused by a vascular problem.

Infarction: emboli, in situ thrombosis or low flow
Haemorrhage: spontaneous (not associated with trauma). Excludes subdural and extradural haematomas, but includes spontaneous subarachnoid haemorrhage

Use of the term cerebrovascular accident is now discouraged.

Transient ischaemic attacks are focal neurological deficits (including monocular visual loss) due to inadequate blood supply that last <24hr (in reality, most TIAs last just minutes).

Infarction and TIAs have the same pathogenesis, and the distinction is likely to become less helpful with time. Both stroke and TIA need urgent treatment, and as it is impossible to distinguish TIA from stroke in the first few minutes and hours, the distinction becomes less relevant. Waiting to see if the focal neurology resolves causes neuronal loss at a rate of 1.9 million per minute. The term ‘brain attack’ is being used to describe the full spectrum of disease severity from TIA to fatal stroke, where early intervention to save brain tissue has parallels with approaches to myocardial salvage in coronary syndromes.

Stroke burden

Incidence of first ever stroke is about 200 per 100 000 per year
Prevalence is around 5-12 per 1000 population, depending on the age of the sample
It is a disease of older people (over 2/3rds of cases occur in the over 65s, less than 15% occur in under 45s)
Globally it is the third most common cause of death (after coronary heart disease and all cancers)
In England and Wales it accounts for 12% of all deaths and is the commonest cause of severe disability among community dwellers

Classification

Various methods including;

Infarct or haemorrhage (also haemorrhagic infarcts)
Pathogenesis—large vessel, small vessel, cardioembolic (AF or LV mural thrombus), valve disease, infective endocarditis, non-atheromatous arterial disease (vasculitis, dissection), blood disorders
Vessel affected—anterior circulation (mainly middle cerebral artery), lacunar (deep small subcortical vessels), posterior circulation (vertebral and basilar arteries)
Bamford’s classification—clinical features to define likely stroke territory. Used in major trials and gives prognostic information about each group (see Table 8.1).

Table 8.1 Bamford’s classification

Total anterior circulation stroke (TACS)
Features	Hemiparesis and hemisensory loss
	Homonymous hemianopia
	Cortical dysfunction (dysphasia, visio-spatial or perceptual problems)
Infarction (TACI)	85%
Haemorrhage	15%
Causes	Occlusion of the internal carotid artery or proximal middle cerebral artery
	Emboli from heart, aortic arch or carotids, in situ thrombosis
Prognosis at 1 year	Dead	60%
	Dependent	35%
	Independent	5%
Partial anterior circulation stroke (PACS)
Features	Two of the three listed in this table above OR cortical dysfunction alone
Infarction (PACI)	85%
Haemorrhage	15%
Causes	Occlusion of the anterior or middle cerebral artery
Prognosis at 1 year	Dead	15%
	Dependent	30%
	Independent	55%
Lacunar stroke (LACS)
Features	Hemiparesis
OR	Hemi-sensory loss
OR	Hemi-sensorimotor loss
OR	Ataxic hemiparesis (with NO cortical dysfunction)
Infarction (LACI)	95%
Haemorrhage	5%
Causes	Small perforating arteries microatheroma
	Hypertensive small vessel disease
Prognosis at 1 year	Dead	10%
	Dependent	30%
	Independent	60%
Posterior circulation stroke (POCS)
Features	Brainstem symptoms and signs (diplopia, vertigo, ataxia, bilateral limb problems, hemianopia, cortical blindness, etc.)
Infarction (POCI)	85%
Haemorrhage	15%
Causes	Occlusion of vertebral, basilar or posterior cerebral artery
	Emboli from heart, aortic arch or vertebrobasilar artery
Prognosis at 1 year	Dead	20%
	Dependent	20%
	Independent	60%

Predisposing factors

Fixed

Age: stroke risk increases with age (this is the strongest risk factor)
Sex: males > females
Ethnicity: higher risk in Blacks and Asians than Whites living in the West. Probably due to increased obesity, hypertension, and diabetes
Family history: positive family history increases risk. Not simple inheritance—complex genetic/environmental interaction
Previous stroke/TIA: risk of recurrence is about 10-16% in the first year, highest in the acute phase
Other vascular disease: presence of any atheromatous disease (coronary, peripheral arterial etc) increases risk of stroke

Modifiable by lifestyle change

Smoking: causal and dose related. Risk diminishes 5 years after quitting
Alcohol: Conflicting evidence with some studies suggesting any alcohol consumption increases risk, while others suggest heavy drinking is a risk factor, but moderate intake is protective
Obesity: Increased risk of all vascular events in obesity—confounded by increase in other risk factors (hypertension, diabetes) but probably weak independent factor, especially central obesity
Physical inactivity: Increased stroke in less active—again confounded by presence of other risk factors in the inactive; to date limited evidence that increased activity lowers risk
Diet: Healthy eaters have lower risk, but may have healthier lifestyles in general. Low salt, high fruit and vegetable, high fish and antioxidant diets are likely to be protective, but trials have failed to show an effect from dietary interventions
Oestrogens: the oral contraceptive confers a slightly increased risk of stroke and should be avoided in the presence of other risk factors. Postmenopausal hormone replacement therapy has been shown to increase risk of ischaemic stroke, but not TIA or haemorrhagic stroke

Medically modifiable

Hypertension: clear association between increasing BP and increased stroke risk across all population groups. Risk doubles with each 5-7 mmHg increase in diastolic blood pressure. Also increases with systolic rises and even isolated systolic hypertension
AF: Risk of stroke significantly increased in AF (see ‘Atrial fibrillation’, p.276)
Diabetes: risk factor independent of hypertension
High cholesterol: weaker risk factor than in heart disease—likely due to diversity of stroke aetiologies
Carotid stenosis: risk increases with increasing stenosis and with the occurrence of symptoms attributable to the stenosis
Other comorbidity: Increased risk in some conditions, such as sickle-cell anaemia, blood diseases causing hyperviscosity and vasculitides

Acute assessment

Due to the development of new acute treatments (eg thrombolysis and carotid endarterectomy) the focus for modern stroke management in hospital has shifted towards rapid and accurate diagnosis during the first few hours/days.

History

Is it a focal neurological deficit?
Did it come on ‘at a stroke’ or is there a hint of progression (simple stroke may worsen over several days, but think of alternative diagnoses, eg tumour)
Is there headache or drowsiness? (haemorrhage more likely)
Was there a fall or other head trauma?

Think subdural and request urgent scan.

What are the vascular risk factors?
What was the premorbid state?
What are the comorbidities? (Increases chance of poor outcome)
What are the medications? (Call GP surgery if unknown)
Where do they live, and with whom? Who are the significant family members?

Examination

GCS (see Appendix, ‘Glasgow Coma Scale’, p.696). A standardized measure to assess neurological deterioration. Unconsciousness or deteriorating GCS suggests haemorrhage, large infarct with oedema or brainstem event.
NIH Stroke Scale (NIHSS). Clinical evaluation instrument with documented reliability and validity. Used to assess severity of initial stroke (when making a thrombolysis decision), outcome and degree of recovery in stroke. Grades the following areas: consciousness, orientation, obeying commands, gaze, visual fields, facial weakness, motor function in the arm and leg, limb ataxia, sensory, language, dysarthria and inattention.

General examination

General inspection (head trauma, signs of fitting—incontinence or tongue biting, frailty, and general condition, eg skin)
Temperature (especially after a long lie)
Cardiovascular examination (pulse rate and rhythm, blood pressure, cardiac examination for source of cardiac emboli, carotid bruits)
Respiratory examination (aspiration pneumonia or pre-existing respiratory conditions)
Abdominal examination (palpable bladder, organomegaly)
Neurological examination (may need to be adapted if patient drowsy)
Cranial nerves: especially visual fields and visual inattention (if difficulty with compliance, test blink response to threat, and look for a gaze preference which may occur with hemianopia or neglect), assess swallow (see ‘HOW TO … Manage swallow after stroke’, p.189)
Limbs: tone (may be diminished acutely), any weakness (grade power for later comparison). Is the distribution pyramidal—arm flexors stronger than extensors, leg extensors stronger than flexors? If weakness subtle, assess for pyramidal/pronator drift and fine movements of both hands—(dominant should be better), coordination (limited if power is diminished), sensation (gross testing by touching both sides with eyes closed), also sensory inattention, reflexes (initially may be absent, then become brisker with time). Plantars extensor on affected side
Gait: assess in less severe stroke—is it safe? If not safe can the patient sit unaided?
Speech: dysarthria (trouble enunciating because of, eg facial weakness or posterior circulation stroke) or dysphasia (cortical disruption of speech—may be receptive and/or expressive):
- Receptive dysphasia is an inability to understand language— test with one-stage commands—‘close your eyes’ and progress to more complex tasks ‘put your left hand on your right ear’. Don’t do the action yourself or the patient will copy you—a test of mimicry rather than dysphasia. If comprehension intact, reassure the patient that you know they can understand, but are having difficulty finding the right words
- Expressive dysphasia—problems producing speech. May be fluent (lots of words that make no sense), or non-fluent (unrecognizable words). Nominal dysphasia is part of an expressive dysphasia and is tested by asking the patient to name increasingly rare objects, eg watch, hand, second hand)

HOW TO … Assess for inattention

Occurs with parietal cortex damage, where there are errors in awareness of self—the patient’s ‘automatic pilot’ has gone wrong.

In extreme cases, the patient will not recognize their own arm, and only wash half of their body. Lesser degrees are more common, and complicate the rehabilitation process, as the patient must constantly be reminded of the existence of the affected side. Can affect vision or whole of one side of body—most commonly non-dominant hemispheric (ie right hemisphere, left neglect)

To test:

Establish that sensory input is present bilaterally, ie check that the patient can feel a touch to each hand individually and does not have a hemianopia (may be hard to establish where extreme gaze preference exists)
Provide two stimuli at once (touch both hands together, or move fingers in both sides of the visual field) and see if the patient preferentially notices the sensory input on the good side. If so, there is inattention of the bad side

Even if formal testing does not reveal inattention, sometimes it will become apparent during rehabilitation, often noted by therapists.

Investigations (Table 8.2)

Table 8.2 The rationale for investigations in acute stroke

Test	Rationale
FBC	Anaemic or polycythaemic
	Elevated white count suggestive of sepsis
	High or low platelet count
Urea and electrolytes	Look for evidence of dehydration, and assess fluid replacement
LFTs	Baseline assessment
	Evidence of comorbidity
CK	Evidence of muscle breakdown (if prolonged lie on floor)
Glucose	Diabetic—old or new diagnosis (elevated sugars initially may represent hyperglycaemic stress response)
	Hypoglycaemia may mimic stroke
Cholesterol	Vascular risk factor
ESR	Elevation in vasculitis or sepsis (including endocarditis)
CRP	Any evidence of sepsis (eg aspiration pneumonia)
Blood cultures	Consider if sepsis or new heart murmur heard (endocarditis)
Urinalysis	Diabetic, vasculitis, urinary infection
ECG	Assess rhythm (look for AF)
	Evidence of IHD/MI or previous hypertension
CXR	Often useful screening test—look for any sign of aspiration, what is the heart size, etc.
CT brain	Guidelines advise scan within 24hr for all strokes, or sooner (<1hr) if:
	Thrombolysis candidate
	<GCS 13 or fluctuating neurology
	Severe headache at onset On warfarin Papilloedema, neck stiffness or fever
	CT will distinguish stroke from non-stroke, eg tumour, identify whether bleed or an infarct, the likely cause of the event — carotid territory infarcts from stenosis, multiple infarcts from cardiac emboli
	Blood appears white in early CT; infarcts may not show acutely (first few hours), develop into low-density areas after a few days
	Small infarcts may never be seen, and the diagnosis is made clinically or on MR scan
	A normal CT does not exclude a stroke
Carotid Doppler	Request in carotid territory events with good recovery where the patient is a candidate for endarterectomy
Echocardiogram	Consider where multiple (? cardio embolic) infarcts, in AF, after recent MI (looking for thrombus) or where there is a murmur