Three degrees of completeness can be recognized: transient ischemic attack (TIA), stroke-in-evolution, and completed stroke. A TIA is an episode of temporary focal cerebral dysfunction occurring on a vascular basis. It typically resolves within minutes but may last up to 24 hours. A new definition was proposed and accepted when it was recognized that a significant percentage of patients whose deficits last up to 24 hours have minor stroke, not TIA. The new definition states TIA to be an acute vascular neurological deficit that is reversible within 60 minutes with no evidence of infarction on CT or MRI. A stroke-in-evolution is a neurovascular event that worsens over several hours to several days. In a completed stroke, the deficit remains fixed for at least 24 hours in the carotid system and for up to 72 hours in the vertebral-basilar system.

Two broad clinical anatomic categories of ICVD syndromes are recognized, based on division of the cerebrovascular supply into those areas supplied by the carotid system (anterior circulation) and those supplied by the vertebral-basilar system (posterior circulation).

Symptoms commonly encountered in carotid system disease include aphasia, monoparesis or hemiparesis, monoparesthesias or hemiparesthesias, binocular visual field disturbance (hemianopia), or monocular visual loss. Symptoms that may be seen in vertebral-basilar system disease include hemianopia, cortical blindness, diplopia, vertigo, dysarthria, ataxia, and limb paresis or paresthesias, frequently with ipsilateral involvement of cranial nerve functions, and contralateral body involvement. Loss of consciousness or isolated vertigo rarely occurs without other vertebral-basilar symptoms. Other isolated symptoms, such as diplopia, amnesia, dysarthria, and light-headedness, usually do not serve as a basis for the diagnosis of vertebral-basilar disease; however, association with other brainstem symptoms may support this diagnosis [1].

Acute ICVD can be categorized as large vessel thrombosis, small vessel thrombosis, cardioembolism, or stroke of
undetermined etiology. Large vessel atherothrombotic occlusion is due to atherosclerosis in the carotid or vertebral-basilar arteries and is a common cause of acute ICVD. The pattern and severity of the neurologic deficit depend on the arterial territory, completeness of occlusion, and collateral flow [1]. Small vessel occlusion occurs due to lipohyalinosis of the lenticulostriate arteries or basilar penetrators, and results in a small area of cerebral infarction called a lacune (Fig. 173.1). If a lacune is strategically placed in the internal capsule, thalamus, or basis pontis, substantial neurologic deficits occur. The most common lacunar syndromes are pure motor hemiparesis, pure sensory loss, ataxic hemiparesis, and dysarthria-clumsy hand syndrome [2].

The typical presentation of a cardioembolic stroke is with maximal deficit at onset, although a small minority may have a stuttering clinical course. Diagnosis may be difficult if the patient has coexistent large arterial lesions; as many as one third of patients with a cardiac embolic source have another potential explanation for their strokes [3]. The most common cardiac sources associated with cerebral embolic events are outlined in Table 173.1. Nonvalvular embolic source with atrial fibrillation is associated with a stroke risk of 4% to 5% per year, increasing with advancing age, the presence of paroxysmal/chronic atrial fibrillation, and an enlarged left atrium [4]. Transmyocardial infarction, atrial fibrillation, and mechanical valves are associated with a high risk, while the risk is lower in patients with bioprosthetic valves. Patent right-to-left cardiac shunts have been recognized by contrast echocardiography with increasing frequency in younger stroke patients. In the absence of a hypercoagulable state or atrial septal aneurysm, a patent foramen ovale (PFO) is not a significant risk factor for cardioembolic stroke, as up to 5% of the healthy population have a small PFO [5].

Watershed infarction is due to globally diminished cerebral blood flow resulting from cardiac arrest or systemic hypotension, with focal infarction and deficits occurring in well-described patterns in the endarterial distribution between major vessels [6] (Fig. 173.2). In the carotid circulation, watershed infarcts occur between the distribution of the middle cerebral artery and either the anterior or posterior cerebral arteries. The usual anterior infarction causes contralateral weakness and sensory loss sparing the face; in posterior watershed infarcts, homonymous hemianopia with little or no weakness is most common. Quadriparesis, cortical blindness, or bilateral arm weakness (the “man-in-the-barrel” syndrome) may also be seen.

Stroke prevention has improved as risk factors have been identified and treatments developed [18]. The treatment of hypertension and smoking cessation are helpful in the prevention of stroke. Systolic blood pressure reduction by 5 to 10 mm Hg may reduce relative risk of ischemic stroke by 20% to 25%. Angiotensin-converting enzyme inhibitors and angiotensin receptor blockers may offer additional protection against first or recurrent ischemic stroke. Patients with hyperglycemia should be aggressively treated to maintain euglycemic control (fasting blood glucose of less than 100 mg per dL). Use of HMG CoA reductase inhibitors (statins) reduces the risk of ischemic stroke by 25% to 30% in patients with underlying ischemic heart disease and possibly improves the outcome after AIS. The American College of Chest Physicians and American Stroke Association guidelines recommend starting all in-patients with hyperlipidemia (low-density lipoprotein [LDL] greater than 100 mg per dL) on statins. More recent trials of statins suggest that reducing LDL cholesterol to 70 mg per dL is safe and may have a plaque stabilization effect [19]. Patients with TIA have a substantial risk of stroke and should be completely investigated before discharge from the hospital. This is especially true for patients older than 60 years, those presenting with aphasia, motor deficits, or with associated diabetes. Patients with symptomatic carotid artery stenosis of greater than 70% benefit from carotid endarterectomy, provided the combined mortality and morbidity of the surgical procedure in the treating institution is less than 5.65% [20]. In nonsurgical TIA patients, antiplatelet therapy with aspirin, aspirin and extended-release dipyridamole (25/200 mg) twice daily, clopidogrel 75 mg once daily, or ticlopidine 250 mg twice daily is beneficial [21,22]. Indirect comparison of newer antiplatelet agents as compared to aspirin suggests that aspirin/extended-release dipyridamole (25/200 mg) (ERDP/ASA) twice daily is 23% more effective than aspirin alone, while clopidogrel offers no advantage over aspirin. However, the recently completed head-to-head comparative trial of clopidogrel vs ERDP/ASA failed to demonstrate a significant difference between the two medications. The combination of ERDP/ASA was associated with nonsignificantly fewer ischemic events, but with a greater number of intra- and extracerebral hemorrhages. On the other hand, there was a nonsignificant trend toward less congestive heart failure with this combination [23]. Atrial fibrillation with or without valvular heart disease is associated with a high stroke risk. Anticoagulation using warfarin reduces the absolute recurrent stroke relative risk by 8% in patients with nonvalvular atrial fibrillation. The annual risk of symptomatic hemorrhage is 1%, which can be minimized by keeping the international normalized ratio (INR) between 2 and 3 [15]. Ximelagatran, a thrombin inhibitor, in a head-to-head study with warfarin, failed to show noninferiority in reducing ischemic recurrent events and did not require INR monitoring, but the drug was not approved by the U.S. Food and Drug Administration (FDA) because of concerns of significant hepatic toxicity [24].