# Posterior Communicating Artery Configuration and Laterality of Thalamic and Lenticulostriate Infarction

**Authors:** Junpei Nagasawa, Masamichi Hozumi, Tatsuhiro Yokoyama, Makiko Ogawa, Junya Ebina, Mari Shibukawa, Takehisa Hirayama, Osamu Kano

PMC · DOI: 10.3390/neurolint18030061 · Neurology International · 2026-03-22

## TL;DR

This study found that variations in the posterior communicating artery do not influence the side of brain infarction in patients with lacunar strokes.

## Contribution

The study provides new evidence that PCoA configuration does not affect infarct laterality in lacunar stroke.

## Key findings

- PCoA presence was similar on infarcted and non-infarcted hemispheres in both LSA and thalamic infarction groups.
- No significant association was found between PCoA configuration and infarct laterality.
- Local small-vessel disease appears more important than PCoA anatomy in lacunar stroke development.

## Abstract

Background: Anatomical variations in the posterior communicating artery (PCoA) are common, but their association with ischemic stroke remains unclear. In this study, we investigated the relationship between PCoA configuration and the localization of perforator infarction. Methods: We conducted a single-center, retrospective observational study of consecutive patients admitted with acute ischemic stroke between April 2016 and July 2023. Patients with a single, unilateral lacunar infarction confined to the thalamic or lenticulostriate artery (LSA) territory were included. PCoA configuration was assessed using time-of-flight magnetic resonance angiography and dichotomized as present (normal PCoA or fetal-type posterior cerebral artery) or absent (hypoplastic or aplastic PCoA). Using a within-patient, hemisphere-based approach, the presence of PCoA on the infarcted side was directly compared with that on the contralateral side. McNemar’s test with continuity correction was used for laterality analysis. Results: A total of 64 patients met the inclusion criteria, including 45 with LSA infarction and 19 with thalamic infarction. The prevalence of PCoA presence on the infarcted hemisphere was 20.0% in the LSA group and 26.3% in the thalamic group, identical to that observed on the contralateral hemisphere in each group. Within-patient comparisons revealed no significant difference in PCoA presence between infarcted and non-infarcted hemispheres in either territory (all p > 0.05). Conclusions: In patients with unilateral perforator infarction involving the thalamic or LSA territories, PCoA configuration was not associated with infarct laterality. These findings suggest that variations in PCoA anatomy have a limited influence on hemispheric vulnerability to perforator infarction, supporting the predominant role of local small-vessel pathology rather than proximal collateral anatomy in the development of lacunar stroke.

## Linked entities

- **Diseases:** ischemic stroke (MONDO:1060198)

## Full-text entities

- **Diseases:** TIA (MESH:D002546), injury to (MESH:D014947), sleep apnea syndrome (MESH:D012891), cardioembolic stroke (MESH:D000083262), ischemic stroke (MESH:D002544), carotid occlusive disease (MESH:D002340), antiphospholipid antibody syndrome (MESH:D016736), aplasia (MESH:C536482), coagulation disorders (MESH:D001778), Acute Stroke (MESH:D020521), ischemic (MESH:D002545), dyslipidemia (MESH:D050171), CKD (MESH:D012080), large-artery disease (MESH:D002539), artery occlusive disease (MESH:D001157), atrial fibrillation (MESH:D001281), Hypoplasia (MESH:D000080344), arterial dissection (MESH:D000094665), hypotension (MESH:D007022), Thalamic infarction (MESH:D007238), PCA (MESH:D020762), proximal large-artery disease (MESH:D004194), arterial stenosis (MESH:D012078), leukoaraiosis (MESH:D049292), large (MESH:D018287), embolic (MESH:D004617), ICA stenosis or occlusion (MESH:D016893), stenosis (MESH:D003251), heart failure (MESH:D006333), hypertension (MESH:D006973), Lacunar infarction (MESH:D059409), microangiopathy (MESH:D014652), vasculitis (MESH:D014657), small-vessel disease (MESH:D059345), aplasia or hypoplasia of the ipsilateral PCoA (MESH:D002532), diabetes mellitus (MESH:D003920), atherosclerosis (MESH:D050197), ischemia (MESH:D007511), hypoplastic (MESH:D000741), neurological deterioration (MESH:D009422), ischemic injury (MESH:D017202), chronic kidney disease (MESH:D051436), atheromatous disease (MESH:D058226)
- **Chemicals:** ORG (-)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

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## References

18 references — full list in the complete paper: https://tomesphere.com/paper/PMC13029242/full.md

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Source: https://tomesphere.com/paper/PMC13029242