It has been recognized that strokes caused by occlusion of small penetrating vessels of the brain—lacunes—have a propensity to be intermittent (“stuttering”) at their onset and occasionally to allow virtually complete restitution of function between discrete episodes. Whether this constitutes a “lacunar TIA” has been debated, but it seems to us that the more important problem is our inability to distinguish a transitory occlusion of a small vessel from that of a larger vessel. Donnan and colleagues (1993) speak of a “capsular warning syndrome,” which we have seen a number of times, consisting of escalating episodes of weakness in the face, arm, and leg and culminating in a capsular lacunar stroke. Nevertheless, the basic pattern of a small deep stroke remains identifiable in mild form; partial syndromes that simulate cortical TIA are less common. Lacunar stroke is discussed extensively further on.
In the transient ischemic attack of the eye, transient monocular blindness (also called amaurosis fugax or TMB) is the usual symptom. Most of the visual episodes evolve swiftly, over 5 to 30 s, and are described as a horizontal shade falling (or rising) smoothly over the visual field until the eye is completely but painlessly blind. The attack clears slowly and uniformly. Sometimes the attack takes the form of a wedge of visual loss, sudden generalized blurring, or, a gray or bright light obscuring vision. Transient attacks of monocular blindness are usually more stereotyped with repeated episodes than are hemispheric attacks. TIAs consisting of a homonymous hemianopia should suggest a stenosis of the posterior cerebral artery but it is often difficult for the patient to make the distinction from monocular blindness.
The implications of amaurosis fugax have been evaluated by several investigators and found not to be as ominous as those of hemispheral TIAs (such as hemiparesis, hemisensory symptoms, aphasia), particularly in younger patients. As pointed out by Benavente and colleagues, the risk of stroke over the 3 years following an attack is as low as 2 percent if there are no other issues such as diabetes, but it may be as high as 24 percent in older patients with risk factors for atherosclerosis. It is evident that particularly in younger patients a mechanism other than atherosclerosis is operative, such as migraine or an antiphospholipid antibody (discussed further on).
It is perhaps not surprising that the risk of stroke after transient monocular blindness is lower than for cerebral TIAs from carotid atherosclerotic disease. The size of particulate material that occludes the ophthalmic and its branches’ vessels is so small that a similar event in the cerebral hemispheres would be less likely to produce symptoms. Furthermore, ischemia of the retina produces symptoms that are hard for the patient to ignore. While there are other underlying causes of TMB, these notions taken together could explain a large part of the difference in risk between conventional TIA and TMB.
Mechanism of Transient Ischemic Attacks
The likely causes of TIA are reduced blood flow or embolic particles. It has become clear that many instances of single transient attacks have an embolic mechanism. In contrast, repetitive TIAs, repeatedly producing the same or similar clinical syndrome are in most cases related to vascular stenosis with reduced blood flow to a limited region of the brain. It is also the case that single TIAs can result from vascular stenosis and, of course, on the occurrence of a first TIA it is generally not possible to determine the source. In support of the concept of embolism as a cause of TIAs, almost one-fifth of anterior circulation (carotid territory) TIAs in the series of Pessin and colleagues (1977), and a somewhat larger proportion of cases reported by Ueda and coworkers, had neither stenosis nor ulceration of the carotid arteries. These ischemic attacks, presumably from the heart or great vessels including the aortic arch, exceeded 1 h in duration, suggesting embolism; but there were also a small number of brief ischemic attacks that were unexplained even after arteriography.