In general, hemodynamic changes in the retinal or cerebral circulation make their appearance when the lumen of the internal carotid artery is reduced to 2.0 mm or less (normal diameter, 7.0 mm; range, 5 to 10 mm, lower part of this range in women). This corresponds to a reduction in cross-sectional area of the vessel of more than 95 percent compared to the normal cross-sectional area of a more distal part of the carotid artery. The exact degree of stenosis that may cause TIAs and the risk of stroke with mild and moderate degrees of stenosis are controversial and are addressed further on.
In some cases of presumed embolism, the neurologic state fluctuates from normal to abnormal repeatedly for as long as 36 h, giving the appearance of TIAs (“stuttering TIAs”); in others, a deficit of several hours’ duration occurs, fulfilling the traditional (now discarded duration of 24 hours) criterion for TIAs. As already noted, the same sequence of events can precede lacunar infarction and seem far more likely in that instance to be the result of locally reduced blood flow than to recurrent emboli.
Ophthalmoscopic observations of the retinal vessels made during episodes of transient monocular blindness may infrequently show either an arrest of blood flow in the retinal arteries and breaking up of the venous columns to form a “boxcar” pattern or scattered bits of white material temporarily blocking the retinal arteries. These observations indicate that in some cases of ischemic attacks involving the retinal vessels, a temporary, complete, or relatively complete cessation of blood flow occurs locally. Whether this is a result of platelet or fibrin emboli or of platelet aggregation in situ because of decreased perfusion pressure remains unsettled.
TIAs that occur with exercise or the assumption of upright posture are particularly suggestive of stenosis of aortic branches, as occurs in Takayasu disease (see further on) and in dissection of the carotid artery or aortic arch. TIAs induced by hyperventilation are said to be characteristic of moyamoya disease, a progressive stenosis of intracranial vessels discussed in a later section.
In states of severe anemia, polycythemia, thrombocythemia, extreme hyperlipidemia, hyperviscosity from macroglobulinemia, sickle cell anemia, and extreme hyperor hypoglycemia, there may be transient neurologic deficits related to rheologic or other changes in blood. In some of these cases, the metabolic or rheologic change appears to have brought out symptoms of stenosis in a large or small vessel but just as often, the vasculature is normal. Patients with antiphospholipid antibodies may have TIAs, the mechanism of which is undefined.
Some cases of TIA that occur after the carotid artery has become occluded are probably due to embolism from the thrombus, usually acute, in the lumen of the vessel distal to the thrombus. In other instances, it has been hypothesized by Barnett and colleagues (1978) that a TIA occurring after the carotid artery has been occluded by thrombus may even arise from the proximal end of the thrombus. In this case, the embolic material is posited to enter the cerebral vessels through the external carotid artery and retrograde through the ophthalmic artery. He called this “stump embolism,” a term which has been often inadvertently used to describe embolism from the distal part of the occluded vessel.
Differential Diagnosis of TIA