Transient neurological symptoms often present a difficult diagnostic dilemma. It is often difficult to tell if the transient symptoms were due to ischemia or due to something else (see Chapter 1). Usually, by the time the physician sees the patient, the neurological exam has returned to normal. On the other hand, it is critically important not to miss the diagnosis of transient ischemic attack (TIA). TIAs may provide an opportunity for physicians to intervene and prevent an ischemic stroke and subsequent disability, and must be taken seriously. The search for an etiology must be done expeditiously. Just as angina may serve as a warning for future myocardial infarction, a TIA is often a warning sign of an impending stroke.

As acute stroke therapies have developed, the context in which stroke care is provided has become more important. Creating and maintaining the organization of stroke care within a region or even a hospital requires much commitment and effort. High-quality stroke care requires coordination and communication between multiple stakeholders in the prehospital and in-hospital settings in what the American Heart Association (AHA) and American Stroke Association (ASA) term the “stroke chain of survival” (Table 14.1).

It is never too early to begin to educate the patient and family about lifestyle changes and medical treatments to prevent another stroke. These need to be reinforced throughout the hospital and rehabilitation stay, and in the outpatient stroke clinic.

After a major stroke, both the family and the patient go through a grief reaction that at first includes denial and disbelief, and sometimes anger. In particular, the need to insert a PEG is often a crisis point when the family finally comes to terms with the severe disability and prolonged recovery that lies ahead. At this stage, which is usually when the patient is in the acute stroke unit, mainly supportive measures are indicated.

In this chapter, we discuss mainly secondary prevention for stroke, although many of the measures, especially control of risk factors and lifestyle changes such as not smoking, controlling blood pressure, etc., are also important measures to avoid a first stroke.

Initially, we discuss a tailored diagnostic work-up, then general measures for secondary prevention of ischemic stroke, and finally recommendations for specific conditions that are associated with a high risk of recurrent stroke.

The following initial measures apply to all stroke patients. They are necessary to stabilize and assess the patient, and prepare for definitive therapy. All current and, probably, future stroke therapies for both ischemic and hemorrhagic stroke are best implemented as fast as possible, so these things need to be done quickly. This is the general order to do things, but in reality, in order to speed the process, these measures are usually dealt with simultaneously. They are best addressed in the ED, where urgent care pathways for stroke should be established and part of the routine (see Chapter 14).

This chapter covers the diagnosis and management of spontaneous subarachnoid hemorrhage due to rupture of intracranial aneurysms. At the end of the chapter we also discuss unruptured intracranial aneurysms. Much SAH management is not based on good-quality evidence. Much of what is recommended here comes from published practice guidelines and what is commonly practiced. Options for therapy might be limited by the availability and experience of persons performing surgery, endovascular therapy, and neurointensive care.

In this chapter, we consider spontaneous hemorrhage into the brain parenchyma and ventricles (intracerebral hemorrhage, ICH). Non-traumatic bleeding into the subarachnoid space (subarachnoid hemorrhage, SAH) is covered in Chapter 13. Traumatic subdural and epidural hemorrhages are not covered in this book.

Intracerebral hemorrhage is associated with very high morbidity and mortality. It is important to realize that, as with acute ischemic strokes, time is of the essence in ICH. The reason for this is that the blood accumulates rapidly, and the volume of the hematoma is the most important determinant of outcome.

Cerebral venous sinus thrombosis (CVST) is the thrombosis of dural venous sinuses and/or cerebral veins. It accounts for 0.5% of all strokes. It occurs predominantly in the younger population (usually < 50 years old, median age of 37). Female-to-male ratio is 3 to 1, likely secondary to sex-specific thrombogenic states including pregnancy, puerperium, oral contraceptive pill use, and hormonal therapy.

When used alone, intravenous and intra-arterial thrombolysis have yielded low recanalization rates of proximal large-vessel occlusions (LVO). The endovascular trials utilizing first-generation devices such as the Merci retriever and the Penumbra aspiration system were essentially neutral and failed to demonstrate superiority of mechanical thrombectomy over IV tPA (MR RESCUE, SYNTHESIS, IMS-III). In 2015, however, six trials – MR CLEAN, EXTEND-IA, SWIFT PRIME, ESCAPE, REVASCAT, and THRACE – led to a fundamental shift in how we acutely manage LVOs today. All six trials compared endovascular thrombectomy (EVT) to IV tPA alone and demonstrated clear superiority of thrombectomy in patients presenting within 6 hours from the time they were last known well (LKW) if they met specific imaging criteria.

This chapter discusses the four main components of acute ischemic stroke care. The sections on prevention of complications, and recovery and rehabilitation, are applicable to both ischemic and hemorrhagic stroke patients.

Although, classically, stroke symptoms are maximal at onset and patients gradually recover over days, weeks, and months, patients sometimes deteriorate. People have termed the phenomenon stroke progression, stroke in evolution, stroke deterioration, and symptom fluctuation. There is no consistent terminology. The phenomenon occurs from different causes and is incompletely understood. Although the typical definition of a significant neurological deterioration in trials has been a gain of ≥ 1 point on item 1a (level of consciousness) or ≥ 4 points in the motor items of the NIHSS, any detectable deterioration should prompt careful assessment and a tailored work-up.

Most strokes are caused by the mechanisms already described, i.e., cardioembolism, atherosclerosis, and small-vessel disease, but at least 20% are due to other mechanisms. This is even more likely in younger patients (< 40 years old), and in older patients without atherosclerotic risk factors. The following is our approach to stroke diagnosis in younger patients and older patients in whom the cause remains obscure after the usual evaluation of the heart for sources of emboli and cerebral vessels for atherosclerosis, or who continue to have strokes despite standard treatment with antithrombotic agents and control of risk factors.