Cerebral ischaemia and infarction

Cerebral ischaemia and infarction are usually caused by sudden occlusion of an artery supplying the brain or, less often, by low flow distal to an already occluded or highly stenosed artery. Occlusion or stenosis can be the result of disease of the arterial wall; embolism from the heart; haematological disorders; and various rare, but sometimes treatable, conditions which are proportionately more common in young stroke patients (where degenerative arterial disease is unusual) but which can still be a cause of stroke in the elderly. Venous infarction is considered later. Ischaemia due to head injury, encephalitis, and other global encephalopathies is beyond the scope of this chapter.

Imaging the brain

Ischaemic stroke: the CT scan is normal immediately after onset, and if the lesion is small (less than about 0.5 cm in diameter), or in the posterior fossa, the scan may remain normal. With larger infarcts, a diffuse low-density area begins to appear, due to increasing brain water content, within a few hours. This may be accompanied by subtle effacement of sulci and loss of the normal grey–white matter differentiation, loss of the insular ribbon, loss of outline of the lentiform nucleus, and compression of the adjacent ventricle (Horowitz et al. 1991; Moulin et al. 1996). When the lesion is large, more obvious infarct swelling, brain shift, and herniation may be seen a few days after onset. Also CT can show haemorrhagic transformation, either asymptomatic or symptomatic, and although this tends to occur a few days after stroke onset in large infarcts, it can happen within hours and the haemorrhagic area can look very like a primary haemorrhage (Bogousslavsky et al. 1991).

Sometimes an acute thrombus or embolus in the middle cerebral artery, or other large intracranial artery, may be visible for a few days as a high-density streak on an unenhanced scan; this can be confused with vascular calcification but then a later scan will show persistence of the hyperdensity. An infarct may become isodense in the second and third weeks (the ‘fogging’ effect) before reappearing as a well-demarcated low-density area (Skriver and Olsen 1981).

Later there may be ipsilateral ventricular dilatation due to loss of brain substance. To some extent, the site of any low density can be related to an arterial distribution, but bearing in mind the variability between and within individuals. A small proportion of first-ever-stroke patients have focal hypodensities on CT in areas irrelevant to the present symptoms, presumably representing previous asymptomatic or undetected infarcts. Others have such widespread diffuse periventicular hypodensity that any new infarcts are difficult, if not impossible, to delineate (Chodosh et al. 1988).

Various patterns of contrast enhancement appear a few days to about 4 weeks after onset, particularly during the ‘fogging’ effect stage, due to hyperaemia and/or disruption of the blood–brain barrier (Skriver and Olsen 1982; Hornig et al. 1985). Sometimes this enhancement can cause confusion with a cerebral tumour, but the history is different, and in cases of doubt time will reveal the truth (Masdeu 1983). There is seldom any indication for intravenous contrast, except possibly if the scan is done at the stage when ‘fogging’ is likely and the unenhanced scan is therefore normal.

MRI is more sensitive but less specific than CT, so that although many more ‘lesions’ are shown, it is sometimes difficult to decide which one is relevant to the current symptoms (Edelman and Warach 1993). It shows acute infarcts best as high-intensity signal on T2-weighted images which persists; this is particularly helpful when the infarcts are small, or in the posterior fossa, and for clinico-anatomical research. T1-weighted images may be normal or show a low signal which tends to persist. Like for CT, there may be fogging in the second week or so. MRI displays swelling of oedematous infarcts. It can also show loss of normal flow voids in occluded cerebral arteries and may sometimes definitively display arterial dissection. However, MRI is less available than CT and patients have to lie still for longer, which for acute stroke makes CT the preferred immediate imaging technique, particularly since it displays intracerebral haemorrhage more reliably (Patel et al. 1996). Also, MRI is not necessarily superior to CT in detecting the very earliest signs of cerebral infarction (Mohr et al. 1995).

Diffusion-weighted MR imaging (DWI) is being increasingly improved and used. This does show lesions earlier than conventional MRI and, usefully, it also displays the new lesion(s) amongst old areas of infarction, by virtue of the reduced diffusion of water within acute infarcts (Warach et al. 1995; van Everdingen et al. 1998).

Positron emission tomography (PET) and single-photon emission tomography (SPET) are interesting research tools but, as yet, of no great clinical relevance in acute stroke.

Primary intracerebral haemorrhage (PICH) appears at once on CT as a well-demarcated high-density round or oval area, with or without rupture into the ventricles or on to the surface of the brain. Lesions as small as 0.5 cm in diameter can be picked up. Mixed-density haemorrhages, suggesting blood of different ages, is rather characteristic of amyloid angiopathy, and a blood-fluid level suggests a haemostatic defect of some sort (Pfleger et al. 1994). Within a day or so, a low-density halo appears, which may be due to oedema, ischaemic necrosis, or clot retraction. With large haemorrhages, CT may show brain shift, herniation, and hydrocephalus if the CSF pathways are obstructed. As the blood is absorbed and haemoglobin broken down, the area of high intensity shrinks and becomes less dense, then isodense with surrounding brain, and finally—in some patients—hypodense, appearing quite like an old infarct.

With small haematomas the high density may be gone in a few days, so to exclude PICH the CT must be done quickly after stroke onset, preferably within hours, if not a day or two (Dennis et al. 1987). Another reason for speed is because haemorrhagic infarcts can be indistinguishable from PICH, and such transformation can occur within a day of ischaemic stroke onset (see above). Further confusion can be caused by haemorrhagic venous infarction. Resolving haematomas may enhance after intravenous contrast, sometimes with a very marked ring effect, looking like a tumour or abscess. Enhancement may also occur in vascular malformations and their associated enlarged vessels or aneurysms.

MR images go through a series of confusing changes after the onset of PICH as the haemoglobin changes to deoxyhaemoglobin (the T2-weighted image shows a low signal, particularly in the centre of the haematoma, the T1 image is low signal too); to methaemoglobin (the T1-weighted image signal becomes high but the T2 image remains much the same); to haemosiderin in the chronic stage (the T2-weighted image becomes bright in the centre with a very dark rim, the T1 images are similar but less marked). Within the first few hours, the image may be normal or may mimic cerebral infarction with a high signal on T2-weighted images. Exactly when all these changes occur depends not just on the haematoma itself but also on the strength of the magnetic field and the scanning sequence.

MRI may also show flow voids in AVMs, haemorrhage into tumour, and dural sinus thrombosis. The PICH site may give a clue to its cause: hypertensive haemorrhages tend to be in the basal ganglia, pons, and cerebellum, while lobar haemorrhages are rather more likely to be caused by an aneurysm, vascular malformation, haemostatic defect, venous infarction, or amyloid angiopathy. Multiple haemorrhages suggest certain specific causes.

Imaging the cerebral circulation in ischaemic stroke

A patient with a mild carotid-territory ischaemic stroke should have similar imaging to patients with carotid TIAs because endarterectomy may be indicated if there is severe carotid stenosis . In more severe strokes, an early angiogram may have some medico-legal relevance if there is any suspicion of carotid or vertebral artery dissection after trauma, because it may reveal the dissection and no other cause such as atherothrombosis. But, demonstrating an occluded cerebral artery in an ischaemic stroke patient is usually of no more than academic interest, and a normal artery a few days after onset does not preclude the possibility of an occlusion which has recanalized.

The causes of cerebral ischaemia and infarction

1 Arterial wall disorders

  • Atherothromboembolism
  • Intracranial small vessel disease (lipohyalinosis, arteriolosclerosis, microatheroma)
  • Trauma
  • Dissection
  • Fibromuscular dysplasia
  • Congenital arterial anomalies
  • Moyamoya syndrome
  • Embolism from arterial aneurysms
  • Inflammatory vascular diseases
  • Leukoaraiosis
  • Irradiation
  • Infections

2 Embolism from the heart

3 Haematological disorders

4 Miscellaneous conditions

  • Pregnancy/puerperium
  • Oral contraceptives and other female sex hormones
  • Drug abuse
  • Cancer
  • Perioperative
  • Migraine
  • Inflammatory bowel disease
  • Homocystinaemia
  • Fabry's disease
  • Mitochondrial cytopathy
  • Hypoglycaemia
  • Fibrocartilaginous embolism
  • Snake bite
  • Fat embolism
  • Epidermal naevus syndrome
  • Susac's syndrome
  • Nephrotic syndrome

Causes of injury of the arteries supplying the brain

Penetrating injury

1 Missile wounds

  • Neck laceration
  • Neck surgery
  • Tonsillectomy
  • Oral trauma
  • Catheter angiography
  • Jugular vein cannulation

2 Non-penetrating injury

  • Blow to the neck
  • Carotid compression tests
  • Attempted strangulation
  • Neck injury (fracture, subluxation, dislocation)
  • Sudden neck movements (whiplash injury, ‘head-banging’, ceiling painting, head injury, head turning, minor falls)
  • Yoga
  • Neck manipulation
  • Labour
  • Tonic–clonic seizure
  • Vomiting
  • Bronchoscopy
  • Atlanto-axial dislocation
  • Occipito-atlantal instability
  • Fractured base of skull
  • Cervical rib
  • Fractured clavicle

Causes of dissection of the extra- and intracranial arteries

1 Traumatic

  • Penetrating injury
  • Non-penetrating injury

2 Spontaneous

  • Fibromuscular dysplasia
  • Cystic medial necrosis
  • Marfan's syndrome
  • Ehlers–Danlos syndrome
  • Pseudoxanthoma elasticum
  • Inflammatory arterial disease
  • Infective arterial disease (e.g. syphilis)

Inflammatory vascular diseases causing stroke

  • Giant-cell arteritis
  • Takayasu's disease
  • Systematic lupus erythematosus
  • Antiphospholipid antibody syndrome
  • Primary systematic vasculitis
  • Rheumatoid disease
  • Sjögren's syndrome
  • Behçet's disease
  • Relapsing polychondritis
  • Progressive systemic sclerosis
  • Sarcoid angiitis
  • Isolated angiitis of the central nervous system
  • Malignant atrophic papulosis
  • Acute posterior multifocal placoid pigment epitheliopathy
  • Buerger's disease

Cardiac sources of embolism (in anatomical sequence)

1 Paradoxical emoblism from the venous system

  • Atrial septal defect
  • Ventricular septal defect
  • Patent foramen ovale
  • Pulmonary arteriovenous fistula

2 Left atrium

  • Atrial fibrillation
  • Sinoatrial disease
  • Myxoma
  • Inter-atrial septal aneurysm

3 Mitral valve

  • Rheumatic stenosis or regurgitation
  • Infective endocarditis
  • Non-bacterial thrombotic (marantic) endocarditis
  • Prosthetic valve
  • Mitral annulus calcification
  • Mitral leaflet prolapse
  • Libman–Sacks endocarditis
  • Papillary fibroelastoma

4 Left ventricular mural thrombus

  • Acute myocardial infarction
  • Left ventricular aneurysm
  • Cardiomyopathy
  • Myxoma
  • Blunt chest injury
  • Mechanical artificial heart

5 Aortic valve

  • Rheumatic stenosis or regurgitation
  • Infective endocarditis
  • Non-bacterial thrombotic (marantic) endocarditis
  • Prosthetic valve
  • Calcification and/or sclerosis
  • Syphilis
  • Congenital cardiac disorders (particularly with right to left shunt)
  • Cardiac surgery, catheterization, angioplasty

5 Others

  • Primary oxalosis
  • Hydatid cyst

Haematological disorders causing ischaemic stroke

  • Polycythaemias
  • Essential thrombocythaemia
  • Leukaemia
  • Sickle-cell disease/trait and other haemoglobinopathies
  • Iron deficiency anaemia
  • Paraproteinaemias
  • Paroxysmal nocturnal haemoglobinuria
  • Thrombotic thrombocytopenic purpura
  • Disseminated intravascular coagulation
  • Thrombophilias and other causes of "hypercoagulability"

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