Pathophysiology of Neurologic Damage

When a cerebral aneurysm ruptures, arterial blood is forced from the higher pressure in cerebral arteries into the lower pressure subarachnoid space. Hemorrhaging blood spreads through the CSF, across the surface of the brain, collecting and clotting in cisterns and aqueducts.

Blood in the CSF is associated with a decreased cerebral perfusion. Of course, perfusion distal to the rupture is decreased, but the presence of blood in CSF may cause vasospasm and hydrocephalus which can reduce perfusion throughout the brain

Vasospasm is the leading cause of death and morbidity after a subarachnoid hemorrhage. Blood irritates the meninges and causes subarachnoid blood vessels to constrict. The greater the hemorrhage volume, the greater the likelihood of vasospasm. More vasospasm means less perfusion.

Acute hydrocephalus can occur following hemorrhage. The cranium can't expand and the brain does not compress, therefore, the intracranial pressure (ICP) can rise rapidly. As the ICP approaches mean arterial pressure, cerebral perfusion is reduced by compression of both venous and arterial vessels. Subacute or chronic hydrocephalus can also result following SAH. The presence of blood in the CSF can obliterate the arachnoid villi and block flow between ventricles, cisterns and the spinal cord. Hydrocephalus results when CSF is not absorbed through the arachnoid villi, into the venous circulation. Hydrocephalus may require emergency vetriculostomy to relieve intracranial pressure.

A change in level of consciousness occurs when the ruptured aneurysm results in decreased cerebral perfusion. Stroke syndrome can develop rapidly. The individual patient's signs and symptoms depend on the location of the SAH, the duration and amount of vasospasm and the degree of increased ICP.


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