Can a Lacunar Infarct in the Left Putamen Present with Left-Sided Facial Numbness and Blurring of Vision?
No, a lacunar infarct in the left putamen would not typically present with ipsilateral (left-sided) facial numbness and blurring of vision—this presentation is anatomically inconsistent with the expected clinical syndrome and should prompt investigation for alternative diagnoses.
Anatomical and Clinical Reasoning
Expected Presentation of Left Putamen Lacunar Infarct
Lacunar infarcts are subcortical strokes measuring <1.5 cm in diameter caused by small vessel disease affecting penetrating arteries, and patients typically present with one of the classical lacunar syndromes 1, 2.
A left putamen infarct would be expected to produce contralateral (right-sided) motor or sensory deficits, most commonly presenting as pure motor hemiparesis or sensorimotor stroke affecting the right face, arm, and leg 1, 2.
The putamen is supplied by lenticulostriate arteries (penetrating branches), and infarction here typically affects the adjacent internal capsule, producing contralateral motor findings rather than ipsilateral symptoms 3.
Why the Described Presentation is Atypical
Ipsilateral facial numbness (left-sided with left putamen lesion) violates basic neuroanatomical principles, as sensory pathways decussate before reaching the putamen level, meaning a left hemisphere lesion should produce right-sided symptoms.
Blurring of vision is not a feature of classical or atypical lacunar syndromes 2. Visual symptoms suggest either:
- Posterior circulation involvement (occipital cortex, thalamus, or brainstem)
- Retinal or ophthalmic artery pathology
- A cortical rather than subcortical process
Alternative Diagnoses to Consider
Retinal or Ophthalmic Artery Occlusion
Visual symptoms, particularly monocular vision loss or blurring, should raise suspicion for retinal artery occlusion (RAO) or ophthalmic artery occlusion (OAO), which can be the initial manifestation of systemic embolic disease 4.
The American Heart Association recommends that patients presenting with symptomatic RAO undergo critical initial systemic evaluation at an acute stroke-ready hospital, as stroke risk associated with newly diagnosed OAO, CRAO, or BRAO may be as high as 25% 4.
Fundoscopy should be performed to look for retinal emboli, vascular "boxcarring," cotton wool spots, or retinal hemorrhages 4.
Cortical Stroke or Large Vessel Disease
The presence of visual symptoms and atypical sensory distribution suggests a cortical or larger vessel stroke rather than a lacunar infarct 1.
To confirm lacunar etiology, potential sources of cardioembolism and ipsilateral large-artery stenosis (>50% stenosis of relevant vessels) must be excluded 1, 5.
Susac Syndrome
In younger patients presenting with visual symptoms (particularly retinal artery abnormalities), vestibulocochlear symptoms, and white matter lesions involving the corpus callosum, Susac syndrome should be considered 4.
This autoimmune condition presents with a triad of hearing loss, central nervous system lesions (especially corpus callosum), and branch retinal artery occlusions 4.
Diagnostic Approach
Neuroimaging
MRI is more sensitive than CT for detecting lacunar infarcts and can distinguish them from perivascular spaces using T2 FLAIR imaging 4.
MRI findings of lacunar infarcts include small (<1.5 cm) subcortical lesions that are hyperintense on T2-weighted sequences, typically located in the basal ganglia, internal capsule, thalamus, or deep white matter 3.
Ophthalmologic Evaluation
Given the visual symptoms, urgent ophthalmologic examination including fundoscopy, visual acuity testing, and assessment for relative afferent pupillary defect is warranted 4.
Color fundus photography and optical coherence tomography (OCT) can document retinal findings if retinal artery occlusion is suspected 4.
Vascular Imaging
CT angiography (CTA) or MR angiography (MRA) of the head and neck should be performed to detect large vessel stenosis, occlusions, or dissection 4.
Carotid ultrasound can detect vascular hypertrophy or asymptomatic atherosclerosis 4.
Management Considerations if Lacunar Infarct is Confirmed
Acute Management
- Standard acute stroke protocols apply, with consideration for thrombolysis or thrombectomy if within appropriate time windows and large vessel occlusion is identified 1.
Secondary Prevention
Aggressive blood pressure control to <130/80 mmHg using diuretics combined with ACE inhibitors is the cornerstone of lacunar stroke management 5.
Antiplatelet therapy with aspirin 75-100 mg daily should be initiated 5.
Statin therapy should be started for all patients regardless of baseline cholesterol levels (Class I, Level A evidence) 5.
For diabetic patients, target HbA1c <7% with tight glycemic control, as diabetes is a strong determinant for multiple lacunar infarcts 4, 5, 6.
Common Pitfalls to Avoid
Do not assume all small subcortical lesions are benign lacunar infarcts—atypical presentations warrant investigation for alternative etiologies including cardioembolism, large vessel disease, or vasculitis 1.
Do not overlook visual symptoms as "non-localizing"—they provide critical diagnostic information pointing away from typical lacunar syndromes 4.
Do not underestimate the long-term risk of lacunar infarcts—while short-term prognosis is favorable (85% survival at 2 years), there is increased long-term risk of recurrent stroke, dementia, and cardiovascular death 2, 7.