Apoplexy and Stroke – Characteristics and History
The old, very popular, and quite international term apoplexy (or its equivalents “apoplectic attack,” “apoplectic ictus,” and “ictus”) today generally means stroke. The word “apoplexy” comes from the Greek meaning “stroke” and “to strike.” To define apoplexy is therefore to relate the history of the word and its different successive significations. This is followed by the medical details of stroke.
In the Hippocratic corpus, “apoplexy” appears as an obviously clinical term. For many centuries after Galen’s writings of the second century A.D., it was thought that apoplexy involved brain matter, whereas epilepsy represented a disturbance of brain function. From the invention of the printing press to the late nineteenth century, several hundred monographs were de-voted to apoplexy.
The first autopsies involving examination of the brain were performed in the seventeenth century. In 1761, Giovanni Battista Morgagni reported numerous cases of postmortem examinations of apoplexy, which he separated into “serous apoplexy” (apoplexia serosa) and “sanguineous apoplexy” (apoplexia sanguinea).
In 1820, John Cooke wrote that he considered hemorrhagic lesions the commonest and that other types of lesions (e.g., tumors, suppuration, cysts) were questionable cases of apoplexy. In a book published in 1812, John Cheyne thought that apoplexy might be “serous” or “sanguineous,” but he was skeptical of the former entity. Periodic apnea, now known as Cheyne-Stokes respiration, was first described by Cheyne in 1818. For John Abercrombie, writ-ing in 1828, the cerebral lesion of apoplexy might be either a hemorrhage or a serous ef-fusion, but sometimes there seemed to be no apparent anatomic lesions.
Jean Cruveilhier, professor of morbid anatomy in Paris, used the word “apoplexy” as a synonym for “hemorrhage” (in its anatomic, pathological meaning). He distinguished “apoplexy without loss of consciousness” from “apo-plexy with loss of consciousness” and wrote of pontine or spinal apoplexies as well as cerebral ones. This pathological point of view was strengthened by Richard Bright, who described and illustrated under the term “apoplexy” several cases of cerebral hemorrhage. This association of apoplexy with hemorrhage in the central nervous system led gradually to the use of apoplexy as a synonym for hemorrhage and to the creation of expressions such as “spinal apoplexy” (in place of “spinal hemorrhage”), “pulmonary apoplexy” (in place of “hemorrhagic pulmonary infarct”), “abdominal apoplexy” (in place of “massive abdominal hemorrhage”), “renal apoplexy” (in place of “renal hemorrhage”), “splenic apoplexy” (in place of “hemorrhage of the spleen”), and so forth.
From the second half of the nineteenth century to the early twentieth century, the semantic confusion between apoplexy and hemorrhage continued. Russell Reynolds, for example, in 1866 stated that an apoplectic attack could result from congestion, hemorrhage, tumor, uremia, or vascular obstruction. But A. Trousseau, a professor in Paris, had attacked this problem of confusion in 1865, and French neurologist J. Charcot later emphasized that apoplexy was a clinical syndrome that unfortunately was often used synonymously with cerebral hemorrhage.
Thus, Trousseau and Charcot, along with others, concluded that apoplexy could arise from conditions other than intracerebral hemorrhage, and that the use of the term should be restricted to the clinical syndrome that involved a sudden loss of brain functions. Surprisingly, in 1921 J. Lhermitte nonetheless persisted in the use of apoplexy as a synonym for hemorrhage and opposed “hemiplegy of the apoplexy” and “hemiplegy of the infarctus.”
The term “apoplexy” has since become obsolete and disappeared from most contemporary textbooks and from the usual vocabulary of the modern physician. Nevertheless, it remains widely used in popular language and literature. Its proper use, however, should be restricted to the history of medicine, from Hippocrates to the beginning of the twentieth century. In present medical vocabulary, the term “apoplexy” must be replaced by either “stroke” or “hemorrhage,” according to the context.
Characteristics of Stroke
According to the World Health Organization, a stroke consists of “rapidly developing clinical signs of focal (at times global) disturbance of cerebral function, lasting more than 24 hours or leading to death with no apparent causes other than that of vascular origin.” “Global” refers to patients in deep coma and those with subarachnoid hemorrhage. This definition excludes transient ischemic attacks (TIAs), a condition in which signs last less than 24 hours.
Strokes are the most common life-threatening neurological disease and the third leading cause of death, after heart disease and cancer, in Europe and the United States. Death rates from strokes vary with age and sex; for example, in the United States, the rates for males are 11.9 per 100,000 for those aged 40–44 and 1,217 per 100,000 for those aged 80–84. For females, the respective rates are 10.9 and 1,067. Large differences in cerebrovascular disease (CVD) mortality have been noted among races. For example, in the United States, mortality is 344 per 100,000 for nonwhites but 124 per 100,000 for whites. Among countries, differences in mortality from stroke ranged from 70 per 100,000 in Switzerland to 519 per 100,000 in Japan.
Decline in CVD deaths has occurred in all developed countries since 1915, and the decline accelerated in recent decades. The acceleration seems related to a decline in incidence. Strokes, however, are more disabling than lethal: 20– 30 percent of survivors become permanently and severely handicapped. Moreover, recurrent strokes are observed in 15–40 percent of stroke survivors.
Apart from age, the most important risk fac-tor for CVD is arterial hypertension. Control of severe and moderate, and even mild, hypertension has been shown to reduce stroke occurrence and stroke fatality. Cardiac impairment ranks third, following age and hypertensive dis-ease. At any level of blood pressure, people with cardiac disease, occult or overt, have more than twice the risk of stroke. Other risk factors are cigarette smoking, increased total serum cholesterol, blood hemoglobin concentration, obesity, and use of oral contraceptives.
Strokes are a heterogeneous entity caused by cerebral infarction or, less commonly, cerebral hemorrhage. Cerebral infarction accounts for the majority of strokes. When perfusion pres-sure falls in a cerebral artery below critical levels, brain ischemia (deficiency of blood) develops, progressing to infarction if the effect persists long enough. In most cases, ischemia is caused by occlusion of an intracerebral artery by a thrombus or an embolus arising from extracranial artery disease or a cardiac source. The main cause of ischemic strokes is atherosclerotic brain infarction, the result of either intra-cerebral artery thrombosis or embolism arising from stenosed (narrowed or restricted) or occluded extracranial arteries.
Lacunar infarction (14 percent of ischemic strokes) is a small, deep infarct in the territory of a single penetrating artery, occluded by the parietal changes caused by hypertensive dis-ease. Cerebral embolism from a cardiac source (15–30 percent of ischemic strokes) is mainly caused by atrial fibrillation related to valvular disease or ischemic heart disease. Other causes of cerebral infarction are multiple, resulting from various diseases, hemopathies, or coagulation abnormalities. However, in 20 percent of cases, the cause of cerebral infarction remains undetermined.
Intracranial hemorrhage (ICH) accounts for 37 percent of strokes. The main cause of ICH is the rupture of miliary aneurysms that have developed in the walls of interior arteries be-cause of hypertensive disease. Nonhypertensive causes of ICH are numerous.
Clinical manifestations of strokes depend on both the nature of the lesion (ischemic or hemorrhagic) and the part of the brain involved. In the 1960s, a classification of strokes according to temporal profile was proposed to promote common terminology in discussion of history and treatment.
The term “incipient stroke” (also TIA) was defined as brief (less than 24 hours), intermittent, and focal neurological deficits from cerebral ischemia, with the patient normal between at-tacks. The term “reversible ischemic neurological deficit” was coined for entirely reversible deficits occurring over more than 24 hours. The term “progressing stroke” (stroke-in-evolution) is applied to focal cerebral deficits observed by the physician to progress in severity of neurological deficit over a period of hours or, occasionally, a few days.
The term “completed stroke” is used when neurological signs are stable and no progression has been noted over 18–72 hours. “Major stroke” is applied when immediate coma or massive neurological deficit occurs. In these cases, chances of recovery and effective treat-ment are minimal. “Minor stroke,” by contrast, is applied to cases where deficits relate to only a restricted area of a cerebral hemisphere, or where the symptoms experienced are of only moderate intensity. With minor strokes, diagnosis and institution of treatment should be rapidly combined to avoid further deterioration and, if possible, facilitate the regression of deficit.
These definitions contain some obvious un-certainties, particularly in categorizing a stroke during the early hours. However, they under-score the fact that the management of a stroke often depends more on its temporal profile and on the severity of neurological deficit than on the nature of the lesion.