eMedicine Specialties > Physical Medicine and Rehabilitation > Stroke

Lacunar Stroke

Author: Adam B Agranoff, MD, Physiatrist and Partner, Chelsea Back Care, Chelsea Community Hospital
Coauthor(s): Edward H Wong, MB, BCh, Stroke Fellow, Department of Clinical Neurological Sciences, London Health Sciences Centre, University of Western Ontario
Contributor Information and Disclosures

Updated: Jul 16, 2008

Introduction

Background

The lacunar hypothesis proposes that (1) symptomatic lacunes present with distinctive lacunar syndromes and (2) a lacune is due to occlusion of a single deep penetrating artery generated by a specific vascular pathology. This concept is controversial because different definitions of lacunes have been used. Lacunes may be confused with other empty spaces, such as enlarged perivascular (Virchow-Robbins) spaces, in which the specific small-vessel pathology occasionally is absent. Originally, lacunes were defined pathologically, but lacunes now are diagnosed on clinical and radiological grounds. This problem is compounded by the present inability to image a single penetrating artery.¹

Lacunes may be defined as small subcortical infarcts (<15 mm in diameter) in the territory of the deep penetrating arteries; lacunes may present with specific lacunar syndromes or may be asymptomatic. Unfortunately, the 5 classical lacunar syndromes and the radiologic appearances are not specific for lacunes (see History). Lacunes occur most frequently in the basal ganglia and in the internal capsule, thalamus, corona radiata, and pons.

Much of our current knowledge of lacunar strokes is due to Fisher's prior cadaveric dissection of post-mortem stroke patients. He found that most symptomatic lacunar strokes are due to the occlusion of penetrating arteries of 200-800 μ m in diameter, whereas those with smaller-diameter penetrating artery infarcts tended to be asymptomatic.

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Pathophysiology

Lacunes are caused by occlusion of a single penetrating artery. The deep penetrating arteries are small, nonbranching end arteries (usually smaller than 500 μ m in diameter), which arise directly from much larger arteries (eg, the middle cerebral artery, anterior choroidal artery, anterior cerebral artery, posterior cerebral artery, posterior communicating artery, cerebellar arteries, basilar artery). Their small size and proximal position predispose them to the development of microatheroma and lipohyalinosis.²

Initially, lipohyalinosis was thought to be the predominant small-vessel pathology of lacunes; however, microatheroma now is thought to be the most common mechanism of arterial occlusion (or stenosis). Occasionally, atheroma in the parent artery blocks the orifice of the penetrating artery (luminal atheroma), or atheroma involves the origin of the penetrating artery (junctional atheroma).

A hemodynamic (hypoperfusion) mechanism is suggested when there is a stenosis (and not occlusion) of the penetrating artery. When no evidence of small-vessel disease is found on histologic examination, an embolic cause is assumed, either artery-to-artery embolism or cardioembolism. In one series, 25% of patients with clinical, radiologically defined lacunes had a potential cardiac cause for their strokes.

Frequency

United States

In the United States and other Western nations, lacunes account for 15-25% of all ischemic strokes. In 2 community - based studies in the United States, the annual incidence rates of lacunar strokes were 13.4 and 19.5 cases per 100,000 population.

International

Two European community-based studies found higher annual incidence rates (31.7 and 53 cases per 100,000 population). This difference in incidence rates between the US and European studies may be due in part to different definitions used in the studies.

Mortality/Morbidity

• The early (<30 d) survival rate for patients who have had a lacunar stroke is approximately 96-97%. This compares to an early survival rate of 85% for patients who have suffered a nonlacunar stroke.
• The late (1 yr) survival rates are 87% and 65-70% following lacunar and nonlacunar strokes, respectively.
• Between 70% and 80% of patients who have suffered a lacunar stroke are functionally independent at 1 year, compared with fewer than 50% of patients who have had a nonlacunar stroke.

Race

Some studies have found higher frequencies of lacunar strokes in African Americans, Mexican Americans, and Hong Kong Chinese.⁶

Sex

Some studies have indicated that there is a higher incidence of lacunar strokes in men.

Age

The incidence of lacunar strokes increases with age. The mean age of first lacunar stroke is approximately 65 years.

Clinical

History

Lacune-related symptoms may occur suddenly or may evolve in either a fluctuating (eg, the capsular warning syndrome) or a progressive manner.Each of the 5 classical lacunar syndromes has a symptom complex that is relatively specific to it. Occasionally, cortical infarcts and intracranial hemorrhages can mimic a lacunar syndrome.⁷ Cortical symptoms (eg, aphasia, neglect) and visual field defects are absent.

• Pure motor stroke/hemiparesis
  • This is the most common (33-50%) lacunar syndrome. It consists of hemiparesis or hemiplegia that typically affects the face, arm, and leg equally; however, the face or leg can be involved to a lesser extent than other regions, and occasionally only arm or leg weakness is noted.
  • Transient sensory symptoms (but not signs) may be present.
  • Dysarthria and dysphagia also may be present.
  • The lacune is usually in the posterior limb of the internal capsule, which carries the descending corticospinal and corticobulbar tracts, or the basis pontis.
• Ataxic hemiparesis
  • This is the second most frequent lacunar syndrome and features a combination of cerebellar and motor symptoms, including weakness and clumsiness, on the ipsilateral side of the body.
  • This lacunar syndrome usually affects the leg more than it does the arm; hence, it is known also as homolateral ataxia and crural paresis. The onset of symptoms is often over hours or days.
  • The most frequent sites of infarction are the posterior limb of the internal capsule, basis pontis, and corona radiata.
• Dysarthria/clumsy hand
  • Although now considered to be a variant of ataxic hemiparesis, this disorder usually still is classified as a separate lacunar syndrome. The lesion is in the pons.
  • The main symptoms are dysarthria and clumsiness (ie, weakness) of the hand, which often are most prominent when the patient is writing.
• Pure sensory stroke
  • This lacunar syndrome consists of persistent or transient numbness and/or tingling on one side of the body (eg, face, arm, leg, trunk).
  • Occasionally, patients complain of pain or burning, or of another unpleasant sensation. The infarct is usually in the thalamus.
• Mixed sensorimotor stroke
  • With this lacunar syndrome, hemiparesis or hemiplegia is noted with ipsilateral sensory impairment.
  • The infarct is usually in the thalamus and adjacent posterior internal capsule (seemingly, in the carotid and vertebrobasilar territories).

Physical

Physical examination findings differ in each of the lacunar syndromes, as follows:

• Pure motor stroke/hemiparesis - Hemiparesis or hemiplegia is noted, with hyperreflexia and Babinski sign; no involvement of any other system is observed.
• Ataxic hemiparesis - A combination of pyramidal signs (eg, hemiparesis, hyperreflexia, Babinski sign) and cerebellar ataxia on the same side of the body. Lower extremities are typically more involved than are upper extremities. Nystagmus may be present.
• Dysarthria/clumsy hand - Unilateral lower facial weakness with dysarthric speech is noted. On protrusion, the tongue may deviate to the side of facial weakness. A mild, ipsilateral hemiparesis usually is noted, but the arm is ataxic. Ipsilateral hyperreflexia and Babinski sign may be observed.
• Pure sensory stroke - Unilateral sensory loss is observed. Although the patient may complain of weakness, no weakness is found on examination.
• Mixed sensorimotor stroke - A combination of pyramidal signs (eg, hemiparesis, hyperreflexia, Babinski sign) is noted, as is sensory loss in the absence of any cortical signs.
• A different system for categorization of stroke subtypes also has been developed. The Trial of ORG 10172 in Acute Stroke Treatment (TOAST) developed a classification based on etiology. This system had a high interphysician agreement rate. The 5 subtypes of ischemic stroke in the TOAST study included the following⁸ :
  • Large-artery atherosclerosis
  • Cardioembolism
  • Small-vessel occlusion
  • Stroke of other determined etiology
  • Stroke of undetermined etiology

Causes

The cause of lacunar infarction is occlusion of a single small penetrating artery. This occlusion may be due to microatheroma and lipohyalinosis, which are associated with hypertension, smoking, and diabetes, or may result from microembolism from the heart or carotid arteries.^5,9

• Study results initially indicated that almost all patients with lacunes have hypertension. However, later studies found hypertension in only 44-75% of patients. In the setting of chronic hypertension, the penetrating arteries, which usually are not affected by atherosclerosis, may develop microatheroma and lipohyalinosis.
• Diabetes mellitus is well recognized as a risk factor for development of small-vessel disease throughout the body, including in the penetrating arteries.
• Smoking is an established risk factor for lacunes.
• Embolism (either cardioembolism or artery-to-artery embolism) traditionally was considered a rare mechanism of lacunar stroke, but a potential embolic cause is not uncommon when lacunes are defined clinicoradiologically. A potential embolic cause may be a coincidental finding only. The following treatment modalities are discussed only in passing:
  • The role of anticoagulation or carotid endarterectomy in patients with lacunes has not been fully defined.
  • Although a study showed that the benefit of endarterectomy in patients with lacunes is smaller than it is in patients with nonlacunar strokes, the procedure is superior to medical therapy.
• Atrial fibrillation and ipsilateral carotid stenosis have a stronger association with nonlacunar infarcts.¹⁰
• Data is less clear regarding a strong association between other risk factors and lacunar stroke, including alcohol consumption, elevated cholesterol, and history of prior of stroke.

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