lacunar infarct

Introduction

Infarction following atherothrombotic or lipohyalonic occlusion of one of the penetrating branches of the circle of Willis, middle cerebral artery stem, vertebral artery or basilar artery.

Etiology

• hypertension is the principal risk factor
• left ventricular hypertrophy is an associated risk factor

Epidemiology

• lacunar infarcts account for 20% of strokes

Pathology

• atherothrombotic or lipohyalonic occlusion of one of the penetrating branches of the circle of Willis, middle cerebral artery stem, or vertebral artery or basilar artery
• the middle cerebral artery, arteries comprising the circle of Willis, & the vertebral artery & basilar artery all give rise to 100-300 uM diameter branches that penetrate deep gray & white matter of the cerebrum & brainstem
• each of these small branches can be thrombosed by either atherothrombotic disease at its origin or by lipohyalonic thickening
• thrombosis of these vessels results in small infarcts (lacunes) which may range in size from 3-4 mm to 1-2 cm

Genetics

• early-onset lacunar infarcts associated with defects in CECR1

Clinical manifestations

• general
  • usually evolve over hours or longer
  • transient ischemic attacks (TIA's) may herald a lacunar infarct; they may occur several times a day & last only a few minutes
  • when infarction occurs, it usually causes a sudden deficit, but it may evolve progressively over a period of days
  • recovery often begins within hours or days after the infarct & may continue over weeks or months, or result in minimal residual deficit
• common lacunar syndromes:
  • pure motor hemiparesis
    • results from an infarct in the internal capsule, corona radiata, base of the pons or pyramidal tract within the medulla oblongata
    • lenticulostriate artery from the middle cerebral artery or basilar artery penetrating artery
    • the face, arm, leg, foot, & toes are almost always involved
    • weakness may be intermittent (TIA)
    • progress in a step-like fashion or may occur abruptly
    • progression to complete paralysis or improvement may occur
  • pure sensory stroke
    • results from an infarct in the ventrolateral thalamus
    • inferolateral artery from posterior cerebral artery involved
  • sensorimotor
    • results from infarct in the thalamus, internal capsule, caudate &/or putamen
    • middle cerebral artery & posterior cerebral artery penetrating arteries
  • ataxic hemiparesis
    • result from infarction of the base of the contralateral pons or genu of the internal capsule
    • basilar artery penetrating artery (pons) or lenticulostriate artery from the middle cerebral artery (internal capsule) involved
  • dysarthria clumsy hand syndrome
    • results from infarction of the anterior limb of the internal capsule
    • lenticulostriate artery from the middle cerebral artery involved
  • hemiballism, dystonia & other movement disorders
    • results from basal ganglia infarction
    • lenticulostriate artery from the middle cerebral artery involved
  • eye movement disorder with other focal neurologic deficits
    • results from brainstem infarction
    • basilar artery penetrating artery involved
  • pure motor hemiparesis with motor aphasia
    • results from occlusion of a lenticulostriate branch originating from the stem of the middle cerebral artery supplying the genu & anterior limb of the internal capsule & adjacent white matter of the corona radiata.
• other lacunar syndromes include:
  • anarthric pseudobulbar palsy
    • due to bilateral infarctions of the internal capsule
    • results from occlusion of the lenticulostriate arteries
  • occlusion of the penetrating arteries of the basilar artery may result in ipsilateral ataxia & leg paresis, pure motor hemiparesis with horizontal gaze palsy
  • lower basilar branch occlusion may result in sudden internuclear ophthalmoplegia, horizontal gaze palsy, & appendicular cerebral ataxia
  • vertebral branch occlusion may result in pure motor hemiparesis sparing the face.
  • occlusion of vessels supplying the lateral pons & medulla may result in vertigo, vomiting, facial weakness, Horner's syndrome, ipsilateral trigeminal numbness, & contralateral spinothalamic sensory loss.
• residual subtle cognitive impairment may occur

Laboratory

• EEG is usually normal in a lacunar infarct, but abnormal in a cortical infarct

Radiology

• computed tomography (CT) scan demonstrates most supratentorial lacunar infarcts
• magnetic resonance imaging (MRI) demonstrates supratentorial & infratentorial lacunar infarcts > 5 mm (not affected by radio-opacity of the base of the skull)
  • cognitive impairment correlates with MRI hyperintensities in putamen & thalamus & with cortical atrophy

Complications

• prior to the advent of antihypertensive therapy, multiple lacunar infarcts often resulted in pseudobulbar palsy, with emotional liability, a slowed abulic state & bilateral pyramidal signs; this syndrome is now uncommon
• cognitive impairment

Management

• acute reduction in blood pressure may worsen symptoms
• antihypertensive therapy is begun after the patient's symptoms have become stable
  • calcium channel blocker
  • ACE inhibitor (losartan) lowers risk 25% (NOT in blacks)
  • thiazide diuretic
  • see risk factors for & prevention of ischemic stroke for long-term post ischemic stroke blood pressure control
• antiplatelet therapy
  • clopidogrel plus aspirin no better than aspirin alone
    • dual therapy results in
      • more hemorrhages
      • higher mortality
• anticoagulation therapy is at best controversial
• statins are effective for secondary prevention of ischemic strokes

More general terms

• ischemic stroke

Additional terms

• cerebral arterial circle of Willis
• dysarthria clumsy hand syndrome
• pseudobulbar palsy (spastic bulbar palsy, supranuclear palsy)
• transient ischemic attack (TIA)