Transient focal neurologic symptoms are ubiquitous in neurologic practice. They may be a result of seizures, migraine (see the analysis of late life migraine accompaniments by Fisher, 1980), syncope, or other conditions such as transient global amnesia (see Chap. 20), and they occur occasionally in patients with multiple sclerosis and with certain systemic metabolic disorders such as severe hyperglycemia. The clinical setting in which they occur assists in making clear the nature of the attack. Furthermore, transient and reversible episodes of focal cerebral symptoms, indistinguishable from TIAs, are known to occur in patients with meningioma, glioblastoma, metastatic brain tumors situated in or near the cortex, and even with subdural hematoma. Although infrequent, these attacks are important mainly because the use of anticoagulants is relatively contraindicated in some of these circumstances. We have seen these episodes mainly with meningiomas and subdural hematomas; they have consisted of transient aphasia or speech arrest lasting from 2 min to several hours, but sensory symptoms with or without spread over the body, arm weakness, and hemiparesis have also been reported. Some remarkable cases of meningioma have involved repeated transient attacks for decades. Seizures are always suspected in these cases but are rarely proved. It has been speculated that a local vascular disturbance of some kind is operative, but the mechanism is not understood. As far as we can determine, mass lesions have not caused episodes that simulate posterior circulation TIAs.
The issue of the uncertainty regarding vertigo alone as a manifestation of a TIA referable to the basilar or vertebral artery was addressed in Chap. 14. There are occasional cases in which multiple brief episodes of vertigo, lasting perhaps a minute or less and fluctuating in intensity, may be interspersed with additional signs of brainstem ischemia. Careful questioning of the patient usually settles the question but imaging may be necessary in cases where uncertainty remains. Even then, more instances of vertigo than are justified are attributed to stenosis of the posterior circulation vessels. In some patients, the complaint of non-vertiginous “dizziness” will prove, however infrequently, to be part of a carotid TIA. According to Ross Russell, so-called drop attacks (see Chap. 6) have been recorded in 10 to 15 percent of patients with vertebrobasilar insufficiency but we have never observed such attacks as a recurrent ischemic phenomenon or a manifestation of other forms of cerebrovascular disease and the syndrome has usually been due to syncope, seizure, or has been of obscure origin.
Pathophysiology of Ischemic Infarction
Cerebral infarction basically comprises two pathophysiologic processes: one, a loss of the supply of oxygen and glucose secondary to vascular occlusion, and the other, an array of changes in cellular metabolism consequent to the collapse of energy-producing processes, ultimately with disintegration of cell structures and their membranes, a process subsumed under the term necrosis. Of potential therapeutic importance are the observations that some of the cellular processes leading to neuronal death are not irrevocable and may be reversed by early intervention, either through restoration of blood flow, by prevention of the influx of calcium into cells, or by interdicting intermediary processes involved in cell death.
At the center of an ischemic stroke is a zone of infarction. The necrotic tissue swells rapidly, mainly because of excessive intracellular water content (cytotoxic edema). Because anoxia also causes necrosis and swelling of cerebral tissue, oxygen lack must be a factor common to both infarction and anoxic encephalopathy. The effects of ischemia, whether functional and reversible or structural and irreversible, depend on its degree and duration. The margins beyond the infarct are hyperemic, being supplied by meningeal collaterals, and here there is only minimal or no parenchymal damage.