Introduction

Within the first few days after hemispheric stroke, mortality is mainly determined by the extent and location of space-occupying postischemic brain edema which leads to intracranial hypertension, brain tissue shifts, and tentorial herniation (Hacke et al., 1996). Medical complications and co-morbidity are the predominant causes of death in those patients who survive this critical time period of approximately 1 week.

Until a few years ago, large hemispheric strokes were commonly accepted as an untreatable disease with a uniformly poor prognosis. However, recent developments in diagnosis and pathophysiology have led to new monitoring and treatment strategies which may improve mortality and lead to a better functional outcome of the surviving patients.

In this chapter we will review the basic diagnostic and therapeutic approach to patients with large life-threatening hemispheric infarcts. We define hemispheric infarcts as ‘large’ when more than 50% of the MCA territory is affected and as ‘panhemispheric’ when the ACA or PCA territory is infarcted in addition to a large MCA territory stroke. Brainstem and cerebellar infarcts will not be discussed here.

Epidemiology and etiology

Because the infarct size was not considered in most epidemiological stroke studies, the incidence of large hemispheric infarcts according to our definition is not known exactly. As a rough estimate, 5–10% of all ischemic strokes are taken to meet the above-mentioned criteria of large or panhemispheric strokes (Hacke et al., 1996; Krieger et al., 1999; Wijdiks & Diringer, 1998).

The vast majority of large infarcts are embolic in origin. The main source of embolism is the heart, with atrial fibrillation as the most common cause, followed by artery-to-artery embolism after dissection of the internal carotid artery.

Introduction

Dissection of a cervico-cerebral artery (CAD) occurs by a rupture within the arterial wall leading to an intramural hematoma. A possible consequence is an acute obstruction of the vessel inducing a high risk for local thrombus formation and cerebral embolism. The clinical spectrum of CAD varies considerably from local pain in the neck or unusual unilateral headaches and a Horner's syndrome to life-threatening complete hemispheric or brainstem infarction. Symptomatic dissections of the carotid and vertebral arteries have been diagnosed more frequently since the introduction of Doppler sonography and magnetic resonance imaging (MRI) (Saver et al., 1992; Rother et al., 1993; Steinke et al., 1994; Sturzenegger, 1995). Among young and middle-aged patients, CADs are now recognized as an important cause of stroke (Bogousslavsky et al., 1987; Caplan & Tettenborn, 1992; Saver et al., 1992; Kristensen et al., 1997; Brandt et al., 1998). Bogousslavsky found an incidence of 2.5% in 1200 consecutive first stroke patients (Bogousslavsky et al., 1987). Under the age of 45 years the incidence of CAD is much higher at 10–20% and CAD are the second leading cause of stroke in the younger age group (Bogousslavsky & Pierre, 1992; Gautier et al., 1989; Livosky & Rousseau, P., 1991). The mean age of the patients with CAD is 40 to 45 years (Gautier et al., 1989; Schievink et al., 1994b; Brandt et al., 1998).

The true incidence of CAD is unknown: an estimation for ICA dissection on the basis of a community study has been 2.6 per 100000 per year (Schievink et al., 1993b).