Synopsis
Recognise the classic lacunar phenotypes, distinguish a small deep infarct from cortical and non-vascular mimics, and connect cerebral small-vessel imaging findings with acute stroke care and long-term vascular prevention.
- Lacunar infarcts are small subcortical infarctions, usually caused by disease of a penetrating arteriole supplying structures such as the internal capsule, thalamus, basal ganglia, corona radiata or pons.
- The five useful bedside patterns are pure motor stroke, pure sensory stroke, sensorimotor stroke, ataxic hemiparesis and dysarthria–clumsy hand syndrome; real presentations can be incomplete or overlap.
- A convincing lacunar syndrome lacks cortical signs: aphasia, neglect, gaze deviation, visual field loss and a clear cortical sensory deficit should prompt consideration of a cortical or larger-vessel lesion.
- Small-vessel disease is broader than an acute lacune and includes white-matter hyperintensities, old lacunes, cerebral microbleeds, enlarged perivascular spaces and small-vessel-related brain atrophy on MRI.
- Do not assume that a mild deficit or a deep clinical pattern excludes a treatable proximal occlusion; thrombolysis and thrombectomy decisions depend on current imaging, time and eligibility criteria.
- Hypertension, ageing, diabetes, smoking, dyslipidaemia and chronic kidney disease increase small-vessel injury, but unusual age or imaging distribution should widen the differential to inherited, inflammatory or toxic arteriopathies.
- An acute non-cardioembolic lacunar infarct generally enters the same antiplatelet and vascular-risk pathway as other ischaemic strokes after intracranial haemorrhage has been excluded.
- The burden of apparently silent small-vessel disease matters: it predicts future stroke, gait impairment, cognitive decline, mood disorder and reduced resilience to other cerebral insults.
Key red flags
Unilateral face, arm and leg weakness without aphasia, neglect, hemianopia or a primary sensory deficit suggests a compact corticospinal or corticobulbar lesion, classically in the internal capsule or pons.
Abrupt numbness or altered sensation affecting the contralateral face and body, without weakness or cortical sensory dysfunction, is compatible with a thalamic lacunar infarct after mimics are considered.
Ipsilateral limb weakness with disproportionate incoordination can follow a lesion in the pons, internal capsule or corona radiata; cerebellar and posterior-circulation alternatives still require urgent imaging.
Prominent dysarthria, facial weakness and impaired fine hand movement with little limb weakness is a recognised perforator syndrome, but dysphagia and airway safety must be assessed rather than dismissed as minor.
Investigation priorities
Exclude intracranial haemorrhage and major structural mimics before acute antithrombotic or reperfusion decisions.
Management branches
Any new, persistent focal deficit compatible with a lacunar syndrome.
- 1. Record onset or last-known-well time, perform ABCDE, check capillary glucose and quantify the deficit with the local stroke assessment.
- 2. Activate urgent stroke imaging, including arterial imaging when the pathway requires it, without waiting for a presumed small-vessel diagnosis.
- 3. Assess thrombolysis or thrombectomy eligibility with the stroke team; symptom severity and disability are judged clinically rather than from the word lacunar.
- 4. After haemorrhage is excluded, start acute antithrombotic and supportive measures at the timing specified by the national and local stroke protocol.