Lacunar infarction

Clinical manifestations
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By Catalina Ionita MD

A lacunar infarct comes on abruptly within 3 hours stepwise in one third or gradually over 2 to 3 (up to 6) days in one third; it is preceded by a transient ischemic attack within 24 hours in one third (Fisher 1991). Transient ischemic attacks preceding a lacunar infarct tend to be stereotypic and to occur in the days immediately prior to the stroke. Many lacunar infarcts are silent, and most silent infarctions are lacunar infarcts.

Because of their small size, lacunar infarcts tend to cause restricted neurologic signs, which have been categorized into “lacunar” syndromes. There are 5 “classical” lacunar syndromes (See Table 1) and at least 70 other (miscellaneous) clinical lacunar syndromes (See Table 2) (Pullicino et al 1993; Adams et al 2001). A small proportion of lacunar infarctions can present with an atypical lacunar syndrome, most frequently with isolated dysarthria or dysarthria facial paresis (Arboix et al 2006). Lacunar syndromes can be produced by nonlacunar infarctions (large artery or cardioembolic) or occasionally by nonvascular lesions (tumor, multiple sclerosis). In a patient presenting with a lacunar syndrome, one cannot assume the presence of a lacunar infarct, and it is important to establish the underlying pathogenesis by investigation.

Pure motor stroke is the most frequent lacunar syndrome. The hemiparesis may be complete with face, arm, and leg equally involved, or there may be a partial brachiocrural motor deficit, isolated central facial palsy, or isolated monoplegia. Twenty-eight percent of cases with pure motor stroke have an associated dysarthria. Eighty-five percent of pure motor strokes are caused by a lacunar infarct and by other stroke subtypes in 15% of cases. The second most frequent lacunar syndrome is sensorimotor stroke. This can be classified into 4 types according to the nature and the extent of the sensory loss: (1) all sensory modalities affected, (2) only nociceptive deficits present, (3) only proprioceptive deficits present, and (4) only 1 limb involved. Each of these types can be qualified into 2 groups: (A) submaximal motor or sensory deficit and (B) total paralysis or total sensory loss in at least 1 limb. Pure sensory stroke may involve nociceptive deficits, proprioceptive deficits, or both. The deficit may involve face, arm, and leg (83%) (cheiro-oral-pedal syndrome, 88% of which are caused by a lacunar infarct); face and arm (7%) (cheiro-oral syndrome, 35% caused by lacunar infarct); or arm and leg (8%). Partial pure sensory deficits include an isolated oral sensory loss and restricted acral sensory loss. Fractional anisotropy maps can make a more accurate diagnosis of lacunar infarction subtype. Sensorimotor syndromes are caused mostly by thalamic lacunes (50%), whereas pure motor hemiparesis is caused by lacunar infarctions in internal capsule and corona radiate (91%) or basal ganglia (83%) (Jeong 2005).

Due to associated cerebral small vessel disease, lacunar infarcts are no less likely to affect cognition than large cortical infarcts. A meta-analysis involving more than 7000 patients with different stroke subtypes comparing the prevalence of dementia and minimal cognitive impairment occurring during 4-year follow-up after stroke reported similar rates after lacunar (n=2860) and nonlacunar infarcts (n=6478) (Makin et al 2013). Cognitive impairment associated with lacunar infarcts is less selective than previously thought, affecting all major cognitive domains: executive function, memory, language, attention, visuospatial abilities, and global cognition (Edwards et al 2013). Lacunar infarcts may cause dementia in different ways. At one end of the spectrum is the classical lacunar state with multiple small deep infarcts and traditional clinical findings: (1) pseudobulbar syndrome (dysarthria, dysphagia, and emotional lability); (2) small stepped gait (marche á petit pas); (3) parkinsonian-like rigidity; (4) hyperreflexia; (5) Babinski sign; (6) dementia, gait imbalance, and urinary incontinence; (7) variable motor and sensory focal signs. At the other end of the spectrum is a single strategically located lacunar infarct, causing persistent cognitive deficits. Lacunar infarcts in several locations can impair cognition: paramedian thalamic, anterior thalamic, and genu of the internal capsule. Lacunar infarcts in the internal capsule, corona radiata, putamen, or caudate nuclei can also cause subtle cognitive impairments or emotional disturbances. Positron emission tomography has demonstrated reduction of glucose metabolism throughout the whole brain in patients with deeply located lacunar infarcts, showing that the functional loss exceeds that attributable to the anatomical lesion. Dementia in patients with lacunar infarction often represents a combination of lacunes with diffuse microvascular disease. These patients tend to have frontal signs on clinical examination. Cerebral blood flow and cerebral reactivity may be significantly decreased in patients with multiple lacunar infarctions and leukoaraiosis, causing cognitive impairment not related to the extent of tissue loss or anatomical location of lesions.

Table 1. Classical Lacunar Syndromes

Pure motor stroke (absent sensory and visual symptoms, absent aphasia)

  Clinical deficit

 

• Contralateral hemiparesis

• Brachiocrural deficit

• Facial weakness ± dysarthria

• Dysarthria-lingual paresis

• Isolated limb paresis

• Bilateral pure motor stroke

  Most frequent localization

 

• Internal capsule (posterior limb)

• Pons

• Cerebral peduncle

• Corona radiata

• Centrum semiovale

• Medulla

• Bilateral capsular or medullary

 

Sensorimotor stroke

  Clinical deficit

 

• Contralateral hemiparesis

• Hemisensory loss

  Most frequent localization

 

• Thalamocapsular

• Pons

• Medulla

• Paramedian medulla

• Corona radiata

• Internal capsule (anterior or posterior limb)

 

Pure sensory stroke (absent motor weakness, visual symptoms, or neuropsychological balance)

  Clinical deficit

 

• Contralateral numbness with sensory loss (all modalities or dissociated), cheiro-oral-pedal, cheiro-oral, or oral

  Most frequent localization

 

• Lateral thalamus

• Posterior corona radiata

• Pons

 

Ataxic hemiparesis (homolateral ataxia and crural paresis ± hypesthesia)

  Clinical deficit

 

• Pyramidal (weakness)

• Cerebellar signs on the same side

  Most frequent localization

 

• Pons

• Internal capsule (anterior limb, posterior limb)

• Thalamocapsular

• Corona radiata

 

Dysarthria-clumsy hand syndrome

  Clinical deficit

 

• Dysarthria and clumsiness of 1 hand ± central facial paralysis

• Dysphagia

• Tongue deviation

  Most frequent localization

 

• Upper basis pontis

• Corona radiata

• Internal capsule (genu)

Table 2. Miscellaneous Lacunar Syndromes

Lacunar syndromes with oculomotor palsies

  Clinical deficits

 

• Pure hemiplegia + oculomotor nerve palsy

• Pure hemiplegia + abducens nerve palsy

• Pure hemiplegia + horizontal gaze palsy

• Pure hemiplegia or ataxic hemiparesis + one-and-a-half syndrome

• Pure hemiplegia + bilateral ptosis and upgaze palsy

Oculomotor nerve palsy ± contralateral limb ataxia

• (Claude) or involuntary movements (Benedikt) syndrome

  Most frequent localization

 

• Midbrain

• Pons (ventral)

• Pons (tegmentum)

• Pons (dorsal tegmentum)

• Posterior limb of the internal capsule (right side)

 

Lacunar syndromes with isolated eye movements

  Clinical deficit

 

• Isolated ocular nerve palsy

• Internuclear ophthalmoplegia

• Vertical gaze palsy

• Pseudoabducens palsy (Pullicino 2000)

  Most frequent localization

 

• Midbrain

• Pons, midbrain

• Rostral midbrain

• Thalamus

• Midbrain-diencephalic junction

 

Lacunar syndromes with movement disorders

  Clinical deficit

 

• Chorea

• Athetosis

• Ballism

• Dystonia

Asterixis ± hemiataxia and hypesthesia

• Parkinsonism

  Most frequent localization

 

• Deep striatum

• Subthalamic nucleus

• Thalamus, striatum

• Thalamus, midbrain (rostral)

• Bilateral basal ganglia

 

Lacunar syndromes with neuropsychological disturbances

  Clinical deficit

 

• Acute perseverative behavior

• Aphasia

• Apathia

• Abulia

• Confusion

• Coma

• Verbal amnesia

• Visual memory deficit

• Akinesia

• Frontal signs

  Most frequent localization

 

• Thalamus (anterior nuclei)

• Bilateral paramedian thalamic

• Caudate and internal capsule (anterior limb)

 

In This Article

Introduction
Historical note and nomenclature
Clinical manifestations
Etiology
Pathogenesis and pathophysiology
Epidemiology
Prevention
Differential diagnosis
Diagnostic workup
Prognosis and complications
Management
Pregnancy
References cited
Contributors