Lacunar stroke syndrome (LACS) is a description of the clinical syndrome that results from a lacunar infarct.
Each of the five classical lacunar syndromes has a relatively distinct symptom complex. Symptoms may occur suddenly, progressively, or in a fluctuating manner (e.g. the capsular warning syndrome, see transient ischemic attack).
Unlike cortical strokes, patients with lacunar stroke syndromes do not exhibit any cortical signs such as aphasia, agnosia, sensory neglect or extinction, apraxia, visual field defects, or cortical sensory loss (e.g. agraphaesthesia, loss of two-point discrimination, loss of joint position sense, astereognosis).
The five classic syndromes are as follows.
Pure motor stroke/hemiparesis
This is the most common (33-50%) lacunar syndrome and usually occurs with infarction of the posterior limb of the internal capsule, which carries the descending corticospinal and corticobulbar tracts, or the basis pontis. It is characterized by contralateral hemiparesis that typically affects the face, arm, or leg in approximately equal measure. A 'pyramidal' pattern of weakness may also be present.
This is the second most common lacunar syndrome and usually occurs with infarction of the posterior limb of the internal capsule, basis pontis, or corona radiata. It displays a combination of cerebellar and pyramidal hemiparesis on the contralateral side of the body. It usually affects the foot and leg more than it does the hand and arm; hence, it is known also as 'homolateral ataxia and crural paresis'.
Dysarthria-clumsy hand syndrome
This is sometimes considered a variant of ataxic hemiparesis (above), but is usually still classified as a distinct lacunar stroke syndrome. The infarct is of the basis pontis or the genu of the internal capsule. The syndrome is characterized by dysarthria and contralateral 'clumsiness' (i.e. weakness) of the hand, which is often most prominent when the patient is writing.
Pure sensory stroke
This syndrome is due to an infarct of the ventral posterolateral (VPL) nucleus of the thalamus. It is characterized by contralateral numbness of the face, arm and leg.
This lacunar stroke syndrome is not to be confused with Déjerine-Roussy syndrome, which is a condition developed weeks or months after an initial thalamic stroke, and is characterized by severe contralateral dysesthesia.
Mixed sensorimotor stroke
This lacunar syndrome is typically due to infarction of the thalamus and adjacent posterior limb of the internal capsule. It is characterized by contralateral hemiparesis and sensory impairment of the face, arm and leg.
Occasionally, it may be difficult to differentiate a cortical stroke, due to either cortical infarct or intracranial hemorrhage, from a lacunar stroke syndrome. It is important to recall that unlike cortical strokes, patients with lacunar infarcts and associated lacunar stroke syndromes will not have cortical signs. Additionally, what may initially appear to be a lacunar stroke syndrome, may actually be a 'warning sign' of a larger deep territory infarction of MCA, PCA, or basilar artery territories.
Another differential diagnosis that may be considered is the striatocapsular infarct, a comma-shaped infarct of the caudate nucleus, the putamen, and the anterior limb of the internal capsule. These subcortical infarctions are caused by either a either a complete or partial proximal MCA occlusion, but can clinically manifest similar to lacunar stroke syndromes. The main two differentiating factors are:
- in the acute phase, patients with striatocapsular infarcts may exhibit both cortical (e.g. aphasia, sensory neglect or extinction, apraxia) and subcortical (eg. hemiparesis, dysarthria) signs, despite the cortex not being directly involved in the infarction
- radiographically, the infarction is larger than a lacune, having a size of at least 30 mm in length and 10 mm in width.
- 1. Davis SM, Donnan GA. Why lacunar syndromes are different and important. Stroke. 2004;35 (7): 1780-1. doi:10.1161/01.STR.0000131929.98486.54 - Pubmed citation
- 2. Henry JL, Lalloo C, Yashpal K. Central poststroke pain: an abstruse outcome. Pain Res Manag. 2008;13 (1): 41-9. Free text at pubmed - Pubmed citation
- 3. Fisher CM. Lacunar strokes and infarcts: a review. Neurology. 1982;32 (8): 871-6. Pubmed citation
- 4. Donnan GA, Bladin PF, Berkovic SF et-al. The stroke syndrome of striatocapsular infarction. Brain. 1991;114 ( Pt 1A): 51-70. Pubmed citation
- 5. Shukir Muhammed Amin O, Aziz Abdullah A, Xaznadar A et-al. Striatocapsular infarction; a single institutional experience. Acta Inform Med. 2012;20 (2): 106-12. doi:10.5455/aim.2012.20.106-112 - Free text at pubmed - Pubmed citation
- 6. Fisher CM. Ataxic hemiparesis. A pathologic study. (1978) Archives of neurology. 35 (3): 126-8. Pubmed
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- treatment options
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- basal ganglia hemorrhage
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- cerebral contusions
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- hemorrhagic venous infarct
- hemorrhagic transformation of an ischemic infarct
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