Cerebral infarction

Clinical features:

• The most common stroke is the hemiplegia caused by infarction in the internal capsule following thromboembolism of a branch of the middle cerebral artery
• There is weakness of the limbs of the opposite (contralateral) side which develops over seconds, minutes or hours
• The signs are those of an acute complete contralateral UMN lesion, including limbs and face
• Aphasia is usual when the dominant hemisphere is affected
• The affected limbs are, at first, flaccid and areflexic
• Headache is unusual and consciousness is NOT lost
• After a variable period (usually several days) the reflexes recover and become exaggerated and an extensor plantar response appears
• Weakness is maximal at first, and recovers gradually over the course of days, weeks or many months

Brainstem infarction:

Infarction in the brainstem causes complex patterns of dysfunction depending on the site of the lesion and its relationship to the cranial nerve nuclei, long tracts and brainstem connections.

Lateral medullary syndrome:

• Caused by PICA (posterior inferior cerebellar artery) or vertebral artery thromboembolism

Coma:

• Ensues when bilateral brainstem infarction damages the reticular formation

Locked-in syndrome:

• Is caused by an upper brainstem infarction
• The patient has a functioning cerebral cortex and is, thus, aware but cannot move or communicate except by vertical eye movement

Pseudobulbar palsy:

• Bilateral infarction of the lower cranial nerve nuclei
• Produces weakness and poverty of movement of the tongue and pharyngeal muscles
• Emotional lability (inappropriate laughing or crying) often accompanies pseudobulbar palsy

Features of a brainstem infarction:

Clinical feature Structure involved

Hemi/tetraparesis Corticospinal tracts

Sensory loss Medial lemniscus and Spinothalamic tracts

Facial numbness 5^th nerve nuclei

Facial weakness 7^th nerve nuclei

Nystagmus/vertigo Vestibular connections

Dysphasia/dysarthria 9^th and 10^th nerve nuclei

Horner’s syndrome Sympathetic fibres

Altered consciousness Reticular formation

Clinical signs in the lateral medullary syndrome:

Ipsilateral:

• Facial numbness (CN V)
• Diplopia (CN VI)
• Nystagmus
• Ataxia
• Horner’s syndrome
• Lesions of CNs IX and X

Contralateral:

• Spinothalamic sensory loss

Lacunar infarction:

• Lacunes are small (<1.5cm³) areas of infarction seen on MRI or at autopsy
• HT is commonly present
• Minor strokes are syndromes caused, typically, by single lacunar infarcts. Examples include:
• Pure motor stroke
• Pure sensory stroke
• Sudden unilateral ataxia
• Sudden dysarthria

• Lacunar infarction is often also ‘symptomless’

Hypertensive encephalopathy:

• This describes various neurological sequelae of severe accelerate HT with occlusion of small arteries
• Leads to:
• Severe headaches
• TIA
• CVA
• Subarachnoid haemorrhage (rarely)

Multi-infarct dementia:

• Multiple lacunes or larger infarcts cause the picture of generalized intellectual loss that is seen in patients with advanced cerebrovascular disease.
• Signs include:
• Dementia
• Pseudobulbar palsy
• Shuffling gait with small steps

Examination:

• In addition to neurological examination, particular care should be taken to find a possible source of embolus, e.g:
• Carotid bruit
• Atrial fibrillation
• Valve lesion
• Evidence of endocarditis

• One must also determine whether HT or postural hypotension is (or has been) present

Immediate management of a CVA:

• In practice, many TIAs and mild CVAs can be managed at home and specialist advice sought when necessary
• Patients admitted to stroke wards tend to fare better than those admitted to a general ward
• Thrombolytic agents (such as tissue plasminogen activator) have sometimes appeared promising in the immediate treatment of ischaemic CVA, but are not in general use

Preliminary investigations:

Test Potential yield

Urinalysis, blood glucose Diabetes mellitus

Hb, platelets Polycythaemia

WCC Infection (e.g. endocarditis)

ESR, CRP Possible arteritis

Serology for syphilis Possible neurosyphilis

CXR Neoplasm

ECG Recent infarct, dysrhythmias

Further investigations of TIA and CVA:

CT and MRI:

• Location of lesion
• Distinguishes between ischaemic and haemorrhagic lesion
• May reveal unexpected mass lesions, e.g:
• Tumour
• Subdural haematoma
• Abscess

Carotid doppler and duplex scanning:

• Screening for arterial stenosis and occlusion

Angiography:

• Very valuable in anterior circulation TIAs to diagnose surgically accessible arterial stenoses (mainly internal carotid stenoses)
• There is a high probability of finding a carotid stenosis when there is a loud localised carotid bruit in the neck

Long-term medical management:

Antihypertensive therapy:

• The control of HT is the single most important factor in the primary prevention of stroke
• If the HT is sustained, it must be lowered slowly to avoid a sudden fall in cerebral perfusion pressure

Antiplatelet therapy:

• E.g. soluble aspirin 75mg OD PO
• Inhibits COX, which converts arachidonic acid to PGs and thromboxanes
• The predominant therapeutic effect is to reduce platelet aggregation

Anticoagulants:

• Heparin and warfarin should be used when there is:
• Atrial fibrillation
• Other paroxysmal dysrhythmias
• Cardiomyopathies
• Valve lesions (non-infected)
• Are potentially dangerous in the 2 weeks following cerebral infarction because of the risk of provoking cerebral haemorrhage

Surgical approaches to stroke:

Internal carotid endarterectomy:

• This is considered in TIA or CVA patients who are shown to have internal carotid artery stenosis that narrows the arterial lumen by >70%
• In these patients, the risk of further TIA or CVA is reduced by ~75% following successful surgery
• Mortality rate of ~3%

Prognosis:

• Between 30-50% of patients who die, do so in the first month following a stroke
• A poor outcome is likely when the following triad is present:
• Coma
• A defect in conjugate gaze
• Severe hemiplegia

• Recurrent strokes are common (10% in the first year)
• In addition, many patients die subsequently from a MI
• Of initial stroke survivors, 30-40% are alive after 3 years
• Of those who survive a stroke:
• 30% return to independent mobility
• 30% have severe disability, requiring permanent institutional care