Historical Background

During the seventeenth and eighteenth centuries, physicians and morphologists (Wepfer, Willis, Morgagni, Cheyne, and others) recognized that the brains of patients who died of apoplexy often contained hemorrhages and softenings and that brain damage could result from either bleeding or deprivation of the vital blood supply. [ii , y During the nineteenth and early twentieth centuries, physicians became interested in correlating the neurological symptoms and signs found in stroke patients during life with the anatomical region of damage in the brain found after death. Various eponymic syndromes such as those of Wallenberg, Babinski-Nageotte, Weber, Millard Gubler, among others, described the neurological findings in patients with lesions at various brain stem sites. Anatomical-clinical correlations culminated in the work of Charles Foix and his Paris colleagues who, in the mid-1920s, defined the territories of supply of the various vessels within the anterior and posterior brain circulations and noted the findings in patients with infarcts in the territories of the various arteries. y

During the middle years of the twentieth century, clinicians became interested in the clinical findings in patients with brain hemorrhages and infarcts. In 1935, Aring and Merritt analyzed the clinical findings in patients who died at the Boston City Hospital from large strokes and tried to separate the signs of embolism, thrombosis, and brain hemorrhage.^ Kubik and Adams, in 1946, reported the first detailed clinicopathological analysis of a stroke syndrome--occlusion of the basilar artery. [5 In 1951, Miller Fisher described the clinical findings in patients who had internal carotid artery occlusions in the neck. y Fisher emphasized that warning spells, which he dubbed transient ischemic attacks (TIAs), often preceded strokes in his patients and that the causative vascular disease was located in the neck, where it could theoretically be repaired by surgeons, rather than intracranially in the middle cerebral arteries (MCAs), where most of the prior literature had indicated that the usual vascular lesions were located. Shortly thereafter, Hutchinson and Yates showed that patients with posterior circulation infarcts and TIAs also often had occlusive disease in the neck,[7 at the origins of the extracranial vertebral arteries, rather than in the head. Wallenberg and Kubik and Adams had identified the vascular pathology. In 1961, Miller Fisher described the clinical findings in patients with large fatal brain hemorrhages located in the putamen, thalamus, pons, and cerebellum.y

Stimulated by these seminal reports and their own clinical experiences, physicians became more interested in the clinical features of stroke, brain ischemia, and cerebrovascular disease. Unfortunately, during the third quarter of the twentieth century (1951-1975), few neurologists had much interest in stroke, and most patients were cared for by non-neurologists. Furthermore, few investigations were available that could be performed safely during life and could also clarify the nature, location, and extent of strokerelated brain damage or the causative cardiac and cerebrovascular lesions. Physicians during this era turned to classifications based solely on the temporal features of symptoms. The terms TIAs, reversible ischemic neurological deficit (RIND), stroke-in-evolution, progressing stroke, and completed stroke became popular and were used as a basis for treatment. These terms were arbitrarily and variously defined and proved unpredictive of the presence of

brain infarction, prognosis, and stroke mechanism; they are now obsolete and of historical interest only. y , [ioi TIA is the only term that remains useful, mainly for ease in communication but not as a guide to diagnosis or treatment.

During the last quarter of the twentieth century, an explosion of technical advances in brain imaging (computed tomography [CT] and later magnetic resonance imaging [MRI]) and technology occurred that could give information about the cervicocranial arteries (subtraction angiography, magnetic resonance angiography [MRA], computed tomography angiography [CTA], and extracranial and transcranial ultrasound). Knowledge of the role of blood cells and coagulation factors in causing or contributing to thromboembolism also advanced. During this time, potential treatments also proliferated; these included agents that modify platelet functions; standard anticoagulants including heparin, heparinoids, low-molecular-weight heparins, and warfarin (Coumadin); endarterectomy and surgical bypass of stenotic or occluded arteries; thrombolytic treatment; angioplasty; and neuroprotective drugs aimed at increasing the brain's tolerance of ischemia. Treatment should now be based mainly on the nature, location, and severity of the causative cardiac, vascular, and hematological disorder; the pathogenesis of the stroke; and the state of the brain (normal, stunned, infarcted, or containing a hematoma). The newer available diagnostic technologies now make it possible to collect these data safely and quickly in most stroke patients.


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