Hypoxic Encephalopathy contd Pathology

As a consequence of high metabolic demand, some areas are more susceptible than others. Vulnerability to hypoxia

Most Frontal cortex

Hippocampus, parietal/occipital cortex

Basal ganglia/cerebellum c : Least Brain stem

Damage begins in the 'watershed' areas - at the extremes of their blood supply, e.g. between the anterior cerebral and middle cerebral artery territory.

Grey matter is more vulnerable than white matter.

/ ^ Mid-temporal section

_. pQA ^ * ^¿ZZ^J ! posterior cerebral artery Occipital section *+*■-'

Microscopic changes depend upon the delay between the hypoxic event and death.

Immediate: Scattered petechial haemorrhages.

At 48 hours: Cerebral oedema associated with petechial haemorrhage.

Clinical features:

e.g. Severe hypoxia from circulatory arrest

At several days ¡weeks: Necrosis in cortical grey matter and globus pallidus with associated astrocytic proliferation. The cerebellum and brain stem may also be affected.

Inattentive (frontal)

■ >

Visual disturbance (parietal, occipital)

Inco-ordinate (cerebellar)

amnesia

Unconscious (diffuse cortical)

(hippocampus)

-!>

brain stem signs •-v

, 1 2

4 1 5

Full recovery Full recovery

Recovery + sequelae

If recovery, major deficit

Flexion or extension to pain. Death.

No recovery

Ataxia

Myoclonus Parkinsonism

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