Ischemic syndromes refer to a variety of cerebrovascular disorders caused by inadequate cerebral circulation. Ischemic syndromes include transient ischemic attack (TIA) and ischemic stroke.
Under normal conditions, an efficient collateral circulation system guarantees an adequate blood supply to the brain: collateral circulation exists between the vertebral arteries on both sides, communication is established between the carotid and vertebral arteries through the Willis ring at the base of the skull, and collateral circulation is also present at the hemispheric level. Congenital malformations of vascular development or acquired atherosclerosis can block intracranial or extracranial arterial blood flow and impede collateral circulation, causing cerebral ischemia with secondary neurological symptoms. If blood supply can be restored quickly, brain tissue can recover and symptoms of cerebral ischemia can disappear, but if cerebral ischemia persists for more than one hour, cerebral infarction can occur and cause permanent brain damage.
Blood clots or emboli caused by atherosclerosis or other diseases (e.g., arteritis, rheumatic heart disease) usually cause ischemic arterial blockage. Atherosclerotic plaques are the basis of most thrombi and can involve any major cerebral artery (Figure 174-1). Large atherosclerotic plaques usually involve the origin of the common carotid artery and the vertebral artery, but the bifurcation of the common carotid artery in the neck is the most frequent site of emboli, resulting in ischemic stroke. Intracranial thrombosis can occur within one of the large arteries at the base of the skull, or within a deep penetrating branch artery, or within a small cortical branch artery, but the most common site of thrombosis is within the trunk of the middle cerebral artery and its branch arteries. The intracranial carotid siphon and the basilar artery located just proximal to the origin of the posterior cerebral artery are also frequently involved. The occurrence of ischemia and/or infarction depends on the compensatory efficiency of the collateral circulation; for example, the coexistence of bilateral vertebral artery stenosis can impede the collateral circulation and enhance the ischemic effects of carotid artery lesions.
Less commonly, vascular inflammation can also cause thrombotic obstruction, the latter secondary to acute or chronic meningitis, connective tissue vascular disease, or syphilis.
The emboli that cause cerebral embolism can remain temporarily or permanently in any part of the cerebral arterial system. Emboli usually arise from atherosclerotic plaques within extracranial vessels or from thrombi within the diseased heart, particularly from redundant organisms on central valves in bacterial or wasting endocarditis, from appendage thrombi after atrial fibrillation or myocardial infarction, or from clots after open-heart surgery. Rarely, there are fat emboli (from long bone fractures), air emboli (seen in diving disease), or venous clot emboli entering the left heart from the right heart through an unclosed oval orifice (paradoxical emboli). Emboli in cerebral embolism may also arise from atherosclerotic lesions in the aortic arch. Emboli may occur spontaneously or be knocked down by invasive cardiovascular manipulation (e.g., after catheter insertion in the aortic arch).
Physiologic insufficiency of blood supply is a relatively rare cause of cerebral ischemia and cerebral infarction. Cerebral perfusion deficit can occur alone or in addition to a pre-existing partial vascular obstruction. Reduced cerebral perfusion can be caused by many processes. Severe anemia or carbon monoxide poisoning (which reduces the ability of the blood to carry oxygen) and severe hemoglobinemia (which increases the viscosity of the blood) can both bring about cerebrovascular problems. Usually, only a significant and long-lasting drop in arterial blood pressure can cause a severe local impairment of cerebral blood flow, but in the presence of arterial disease or hypoxia, a less severe drop in blood pressure can cause ischemia and infarction.
The use of sympathomimetic drugs (e.g., cocaine, amphetamines) can cause cerebral ischemia, probably through a vasculitic mechanism. Oral contraceptives used in earlier years could be associated with ischemic strokes; current use of low-dose contraceptives is associated with a lower chance of ischemic stroke. In very rare cases, herniated bones of the cervical spine can cause compression of the vertebral artery.