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298 Chapter 7: Nervous system
include weakness, numbness, and transient monocular of the perfusion pressure; however, a low oxygen concen-
loss of vision (amaurosis fugax) or other visual distur- tration or a blood pressure outside the range will result
bance. Evidence of vascular disease such as bruits, valvu- in tissue damage. Shorter periods or less severe episodes
lar heart disease, and other risk factors such as hyper- lead to ‘watershed infarction’ of the junctional areas be-
tension, arrhythmias, hypercholestrolaemia or diabetes tween the cerebral arteries, in particular the visual cortex
mellitus should be sought. Important differentials in- and cerebellum. The hippocampus is also at risk of dam-
clude hypoglycaemia, focal epilepsy (usually with a pre- age as it has a high metabolic demand.
ceding jerking of one or more limbs, and a post-ictal
phase) and migraine (symptoms may precede or follow
Clinical features
the onset of headache). Mild cases tend to have an impaired intellect with mem-
ory loss and cortical blindness. Severe cases have a pro-
Investigations longed comatose state with variable outcome including
Theseareasforstroke.CTheadmaydistinguishbetween the persistent vegetative state.
TIA, stroke and haemorrhage. However, <24 hours after
astroke, the CT may still be normal.
Macroscopy
There is loss of cortical mass mainly from the white mat-
Management
ter leading to an atrophic brain. Neurones are replaced
All patients should be on an antiplatelet agent such as as-
with gliosis by astrocytes.
pirin. Other treatments include antihypertensives, statin
cholestrol lowering agents, and management of cardiac
arrhythmias, heart disease or diabetes mellitus. Management
InpatientswithsymptomaticTIAswithanunderlying The underlying cause requires rapid identification and
significant carotid stenosis (>70%), surgery is indicated management to limit the extent of necrosis. Long term
with carotid endarterectomy (see above). carerequiresmultidisciplinaryinputandmaynecessitate
ongoing residential care.
Prognosis
Five years after a transient ischaemic attack
Intracerebral haemorrhage
1in6patients will have had a stoke.
1in4 patients will have died usually from a stroke or Definition
heart disease. Spontaneoushaemorrhagemayoccurwithininthebasal
ganglia, internal capsule, cerebellum or pons presenting
Hypoxic ischaemic brain injury as a stroke.
Definition
Incidence
Theglobalbraindamageresultingfromafailureoftissue
Accounts for 15% of strokes.
perfusion.
Age
Aetiology
Generalised failure of blood flow or oxygenation may Occurs most commonly in the elderly.
result from cardiac or respiratory arrest, severe hypogly-
caemia, drowning or carbon monoxide poisoning. Aetiology/pathophysiology
Prolonged uncontrolled hypertension is the most
Pathophysiology commoncause.Pseudoaneurysmsformonfineperfo-
The generalised loss of perfusion results in diffuse death rating arteries, these have a tendency to rupture lead-
of neurones. The blood flow through the brain is subject ing to haemorrhage.
to autoregulation. Within the range of 80–170 mmHg Arteriovenous malformations may haemorrhage es-
systolic pressure the cerebral blood flow is independent pecially in younger patients.