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Lacunar Strokes: Current Concepts Kent W J Am Board Fam Pract: first published as 10.3122/jabfm.1.1.57 on 1 January 1988. Downloaded from Lacunar Strokes: Current Concepts Kent W. Davidson, M.D. Abstract: Lacunar strokes result from occlusion of course of lacunar strokes. Recently, it has been penetrating arteries in the deeper, subcortical parts of demonstrated that lacunar strokes may be embolic the cerebrum and brain stem. Approximately 19 or hemorrhagic in causation, are not invariably percent of all strokes are of the lacunar variety associated with hypertension, and may be larger with lacunar strokes representing the most common and associated with neurological manifestations that cerebrovascular complication of chronic hyperten- do not conform to the classic patterns. In most sion. Four major clinical syndromes are pure motor instances, however, recognition of the characteristic hemiparesis, pure sensory stroke, ataxic hemipare- clinical presentation and confirmation of the diagno- sis, and the dysarthria-clumsy hand syndrome. The sis with noninvasive studies spare many patients advent of computed tomography (CT) has allowed unnecessary risks associated with anticoagulation, the antemortem study of lacunar disease and has arteriography, or vascular surgery. (JABFP 1988; shed new light on the pathogenesis and clinical 1:57-62.) It has been estimated that 19 percent of all strokes mid-1960~.~Due to the small size of the infarcts result from occlusion of penetrating arteries in the and the lack of appropriate imaging equipment deeper, subcortical parts of the cerebrum and available at the time, Fisher's work was done brain stem.' These cerebrovascular events are through meticulous brain dissection. Although termed lacunar strokes in reference to the small Fisher's contribution was considerable, several cavities or lacunae that are left behind after infarc- gaps in the understanding of lacunar disease re- tion of brain tissue with subsequent ~avitation.~ sulted from the inherent shortcomings of post- The size of the infarct is generally small, in the mortem histologic study. With the advent of range of 2 to 15 mm in diameter. The most com- computed tomography (CT), which facilitated mon sites for lacunar infarction include the puta- the antemortem study of lacunar strokes, a men, caudate, thalamus, pons, internal capsule, new body of data has accumulated regarding the and convolutional white matter.%Lacunar disease pathogenesis and the clinical features of lacunar is a common neurological sequela of chronic hy- disease. This new information has augmented pertension and frequently produces characteristic rather than refuted Fisher's work and has pro- http://www.jabfm.org/ clinical syndromes. In many instances, through vided a clearer understanding of lacunar disease recognition of the characteristic clinical presenta- and its management. tion and confirmation of the lacunar stroke with noninvasive studies, patients may be spared the unnecessary risk associated with anticoagulation, Pathophysiology arteriography, or vascular surgery.j The pathological lesions responsible for lacunar on 26 September 2021 by guest. Protected copyright. Although the occurrence of lacunar infarctions strokes vary depending on the size of the vessel was noted as early as 1901,4 years passed until the involved and the size of the resulting infarct. In- pathological processes underlying the lesions and farcts in the range 3-7 mm in diameter involve the clinical features of lacunar strokes were inten- arteries 400 to 200 pm in diameter. The patho- sively investigated. The greatest contribution to logical process responsible for these tiny infarcts is modern understanding of lacunar strokes was called segmental arterial disorganization or lipo- made by Fisher and colleagues beginning in the hyalinosis and is thought to be the result of long- standing hyperten~ion.~,'These vascular lesions result from thickening of the arterial wall through From the Department of Family and Community Medicine, replacement of the normal muscular and elastic College of Medicine, University of Arkansas for Medical Sci- elements with connective tissue and giant macro- ences, Little Rock. Address reprint requests to Kent W. David- phages. Eventually, the arterial lumen is oc- son, M.D.,'Department of Family and Commu~~ityMedicine, College of Medicine, University of Arkansas for Medical Sci- cluded, and infarction occurs. Because of the ences, 4301 W. Markham-Slot X530. Little Rock, AR 72205. small size of the lacunae resulting from this proc- Lacunar Strokes 57 J Am Board Fam Pract: first published as 10.3122/jabfm.1.1.57 on 1 January 1988. Downloaded from ess, many of these infarcts are thought to remain ported the incidence of hypertension with lacunar asymptomatic.' infarction in only 57' percent to 65 percent of A second pathological process that involves Reports noting higher associations be- larger arteries in the 400 to 900 pm range also tween lacunar infarction and hypertension in- results from chronic hyperten~ion.',~Atheromata volve primarily patients with one of the classically that develop in the cerebral vessels of normoten- described syndromes with limited neurological in- sive individuals usually occur in the extracranial volvement and small deep infarcts.I6 Infarction in distribution of the carotid and basilar arteries. In these cases was due to lipohyalinosis or micro- individuals with chronic hypertension, the ather- atheroma in a penetrating artery. In series with a omata are more widespread and, additionally, in- lower association between hypertension and lacu- volve intracranial arteries and arterioles. lo When nar infarction, one usually finds larger lacunae these vessels become occluded due to atheroscle- with more complex neurological events and a rotic plaque, infarction results. Infarcts occurring higher frequency of emboli responsible for the in- via this process are generally larger and more farct or hypoperfusion due to extensive extra- symptomatic. cranial atherosclerosis. 14,' A third mechanism involves the obstruction of the penetrating artery due to atherosclerosis of the parent artery. Atherosclerotic plaques block- Clinical Features ing the penetrating arteries from the middle cere- As noted earlier, many lacunar strokes are asymp- bral and basilar arteries have been document- tomatic. This is because the vessels involved are of ed.".12 As would be expected, these infarcts are extremely small size, the area of infarcted tissue is generally larger because the entire region of the small, and the infarction occurs in a relatively si- brain supplied by the involved penetrating artery lent part of the brain. When lacunar strokes are is affected. symptomatic, however, they are often distinctive In Fisher's work, the possibility of embolic phe- in their clinical presentations. Fisher originally de- nomena from the heart or carotid systems causing scribed four clinical syndromes, referred to as la- lacunar strokes was postulated.' Additional data cunar syndromes, that he thought were specific to obtained through the study of patients with deep these infarcts. Subsequent to Fisher's original de- cerebral lesions utilizing CT scanning have con- scriptions, there have been several other neuro- firmed this ass~ciation.'~,~~It is thought the em- logical syndromes described that have been attrib- boli block the origin of the penetrating arteries uted to lacunar infarction, although these cases are few in number and in some instances not con- after lodging in their parent arteries and produce http://www.jabfm.org/ larger and more symptomatic lesions. This is simi- fined to the deeper, noncortical parts of the brain. lar to the third mechanism previously described. There are a number of clinical features that are This mechanism is generally thought to be less common to all of the lacunar syndromes. Lacunar common than the other three in the pathophysiol- stroke syndromes characteristically evolve in a ogy of classic lacunar stroke syndromes. "leisurely" fashion, with as many as 30 percent In each instance, obliteration of the lumen developing over a period up to 36 hours.lh Lacu- results in infarction of adjacent brain tissue. Mac- nar syndromes characteristically do not embody on 26 September 2021 by guest. Protected copyright. rophages eliminate the infarcted tissue, and certain neurological manifestations, including vis- the characteristic cavity or lacuna remains. In gen- ual field defects, aphasia, stupor, coma, loss of eral, the smaller lacunae, 3-7 pL, result from consciousness, or seizures." In only approxi- segmental arterial disorganization and lipohyalin- mately 30 percent of patients with one of the lacu- osis, whereas the larger lacunae, 1-2 cc, are the nar syndromes, the stroke will be preceded by a result of atheromatous or embolic occlusion of a transient ischemic attack. penetrating vessel. The larger lacunae are usually symptomatic, whereas smaller lacunae may be asymptomatic unless situated in a sensory or Pure Motor Hemiparesis motor tract. The most common lacunar syndrome involves At one time, lacunar strokes were thought to be pure motor hemiparesis of the face, arm, and leg virtually always associated with longstanding hy- on one side of the body." The stroke may involve pertension. Fisher reported a 97 percent incidence various combinations of these three body parts, of hypertension in &%e ~eries.~Others have re- and the extent of the paralysis is variable. Dys- 58 The Journal of the American Board of Family Practice-Vol. I No. 1 J Am Board Fam Pract: first published
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