Lacunar stroke syndrome
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).
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 characterised 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 motor symptoms, including 'pyramidal' weakness, on the ipsilateral 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 or 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 characterised 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 characterised by contralateral numbness of the face, arm and leg.
This lacunar stroke syndrome is not to be confused with Déjerine and Roussy syndrome, which is a condition developed weeks or months after an initial thalamic stroke, and is characterised by severe contralateral dysaesthesia.
Mixed sensorimotor stroke
This lacunar syndrome is typically due to infarction of the thalamus and adjacent posterior limb of the internal capsule. It is characterised 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 haemorrhage, 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, an infarct of the caudate nucleus, the putamen, and the anterior limb of the internal capsule. A striatocapsular infarct is caused by either a complete proximal MCA occlusion, or a partial occlusion of the MCA origin that also blocks lateral striate artery origins. However unlike cortical infarcts that may also be due to MCA occlusion, the overlying cortex is not involved in striatocapsular infarcts due to either collateral circulation via transcortical and transdural anastomoses, or the partial MCA occlusion still allowing the MCA to be patent enough to supply blood to the cortex. In differentiating these patients from those with lacunar stroke syndromes who may have similar imaging findings, patients with striatocapsular infarcts, in the acute phase, interestingly may exhibit both cortical (e.g. aphasia, sensory neglect or extinction, apraxia) and subcortical (eg. hemiparesis) signs, despite the cortex not being directly involved in the infarction. The underlying mechanisms for these cortical signs being present in this subcortical striatocapsular infarction are unfortunately not well understood, but is thought to be due to decreased, but not absent, cortical blood flow.
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Stroke and intracranial haemorrhage
stroke and intracranial haemorrhage
- general discussions
- scoring and classification systems
- by region
- hemispheric infarcts
- frontal lobe infarct
- parietal lobe infarct
- temporal lobe infarct
- occipital lobe infarct
- internal capsule infarct
- ataxic hemiparesis syndrome: MCA perforators or basilar artery perforators
- lacunar infarct
- thalamic infarct
- cerebellar infarct
- midbrain infarct
- pontine infarct
- medullary infarct
- acute spinal cord ischaemia syndrome
- hemispheric infarcts
- by vascular territory
- anterior cerebral artery infarct
- anterior choroidal artery infarct
- anterior inferior cerebellar artery infarct
- basilar artery infarct
- middle cerebral artery infarct
- posterior cerebral artery infarct
- posterior inferior cerebellar artery infarct
- superior cerebellar artery infarct
- basal ganglia haemorrhage
- cerebellar haemorrhage
- cerebral contusions
- CTA spot sign
- haemorrhagic venous infarct
- haemorrhagic transformation of an ischaemic infarct
- hypertensive intracranial haemorrhage
- intraventricular haemorrhage (IVH)
- lobar haemorrhage
- pontine haemorrhage
- remote cerebellar haemorrhage
- extra-axial haemorrhage
- extradural haemorrhage (EDH)
- intralaminar dural haemorrhage
- subdural haemorrhage (SDH)
- subarachnoid haemorrhage (SAH)
- intra-axial haemorrhage
- ischaemic stroke