Page 896 - Textbook of Pathology, 6th Edition

880 fall of systemic arterial systolic pressure below this critical cortex; the loss of pyramidal cell layer is more severe than
value results in rapid fall in cerebral perfusion pressure and that of granular cell layer producing laminar necrosis.
eventual ischaemic encephalopathy. Such types of medical Longer duration: Use of modern ventilators has led
emergencies occur at the time of cardiac arrest followed by to maintenance of cardiorespiratory function in the
relatively delayed resuscitation, severe episode of hypo- presence of total brain necrosis unassociated with vital
tension, carbon monoxide intoxication and status epilepticus. reaction.
Hypoxic encephalopathy may be followed by a post-
ischaemic confusional state and complete recovery or a state
of coma and even a persistent vegetative life and brain death. Cerebral Infarction
Depending upon the proneness of different cells of the Cerebral infarction is a localised area of tissue necrosis caused
brain to the effects of ischaemia-hypoxia, three types of lesion by local vascular occlusion—arterial or venous. Occasionally,
may occur: it may be the result of non-occlusive causes such as
1. Selective neuronal damage: Neurons are most vulnerable compression on the cerebral arteries from outside and from
to damaging effect of ischaemia-hypoxia and irreversible hypoxic encephalopathy. Clinically, the signs and symptoms
injury. In particular, oligodendroglial cells are most associated with cerebral infarction depend upon the region
susceptible, followed by astrocytes while microglial cells and infarcted. In general, the focal neurologic deficit termed
vascular endothelium survive the longest. The reason for stroke, is present. However, significant atherosclerotic
undue vulnerability of neurons to hypoxia can be explained cerebrovascular disease may produce transient ischaemic
by various factors: attacks (TIA).
i) Different cerebral circulatory blood flow. 1. Arterial occlusion. Occlusion of the cerebral arteries by
ii) Presence of acidic excitatory neurotransmitters called either thrombi or emboli is the most common cause of
excitotoxins. cerebral infarction. Thrombotic occlusion of the cerebral
iii) Excessive metabolic requirement of these neurons. arteries is most frequently the result of atherosclerosis, and
iv) Increased sensitivity of neurons to lactic acid. rarely, from arteritis of the cranial arteries. Embolic arterial
2. Laminar necrosis: Global ischaemia of cerebral cortex occlusion is commonly derived from the heart, most often
results in uneven damage because of different cerebral from mural thrombosis complicating myocardial infarction,
vasculature which is termed laminar or pseudolaminar from atrial fibrillation and endocarditis. The size and shape
necrosis. In this, superficial areas of cortical layers escape of an infarct are determined by the extent of anastomotic
damage while deeper layers are necrosed. connections with adjacent arterial branches as under:
SECTION III
3. Watershed infarcts: Circulatory flow in the brain by Circle of Willis provides a complete collateral flow for
anterior, middle and posterior cerebral arteries has internal carotid and vertebral arteries.
overlapping circulations. In ischaemia-hypoxia, perfusion of Middle and anterior cerebral arteries have partial
overlapping zones, being farthest from the blood supply, anastomosis of their distal branches. Their complete
suffers maximum damage. This results in wedge-shaped occlusion may cause infarcts.
areas of coagulative necrosis called watershed or borderzone Small terminal cerebral arteries, on the contrary, are end-
infarcts. Particularly vulnerable is the border zone of the arteries and have no anastomosis. Hence, occlusion of these
cerebral cortex between the anterior and middle cerebral branches will invariably lead to an infarct.
arteries, producing para-sagittal infarction.
2. Venous occlusion. Venous infarction in the brain is an
MORPHOLOGIC FEATURES. The pathologic appear- infrequent phenomenon due to good communications of the
Systemic Pathology
ance of the brain in hypoxic encephalopathy varies cerebral venous drainage. However in cancer, due to
depending upon the duration and severity of hypoxic increased predisposition to thrombosis, superior sagittal
episode and the length of survival.
thrombosis may occur leading to bilateral, parasagittal,
Survival for a few hours: No pathologic changes are multiple haemorrhagic infarcts.
visible.
3. Non-occlusive causes. Compression of the cerebral arte-
Survival 12-24 hours: No macroscopic change is ries from outside such as occurs during herniation may cause
discernible but microscopic examination reveals early cerebral infarction. Mechanism of watershed (border zone)
neuronal damage in the form of eosinophilic cytoplasm cerebral infarction in hypoxic encephalopathy has already
and pyknotic nuclei, so called red neurons.
been explained above.
After 2-7 days: Grossly, there is focal softening. The In any case, the extent of damage produced by any of the
area supplied by distal branches of the cerebral arteries above causes depends upon:
suffers from the most severe ischaemic damage and may i) rate of reduction of blood flow;
develop border zone or watershed infarcts in the junctional ii) type of blood vessel involved; and
zones between the territories supplied by major arteries. iii) extent of collateral circulation.
Microscopically, the nerve cells die and disappear and
are replaced by reactive fibrillary gliosis. There are minor MORPHOLOGIC FEATURES. Grossly, cerebral infarcts
variations in the distribution of neuronal damage to the may be anaemic or haemorrhagic. An anaemic infarct