What are the signs and symptoms of a right posterior communicating artery (PCOM) infarction?

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Last updated: September 22, 2026 • View editorial policy

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Right PCOM Infarct: Signs and Symptoms

A right posterior communicating artery (PCOM) infarct most commonly presents with ipsilateral third nerve palsy featuring pupillary involvement, along with contralateral motor and sensory deficits affecting the left side of the body.

Primary Clinical Manifestations

Cranial Nerve Findings (Ipsilateral - Right Side)

The right PCOM courses adjacent to the third cranial nerve in the subarachnoid space, making third nerve palsy the hallmark presentation 1, 2:

  • Pupillary involvement (dilated right pupil) - critical distinguishing feature suggesting compression from aneurysm or ischemia
  • Complete ptosis of the right eyelid
  • Ophthalmoplegia with inability to adduct, elevate, or depress the right eye
  • Eye positioned "down and out" at rest
  • Diplopia when ptosis is lifted

Critical distinction: Pupil-involving third nerve palsy in the context of PCOM pathology raises urgent concern for posterior communicating artery aneurysm and requires immediate neuroimaging with MRA or CTA 1, 2.

Contralateral Motor and Sensory Deficits (Left Side)

PCOM perforators supply critical structures including the thalamus, hypothalamus, and portions of the midbrain 3, 4:

  • Left-sided weakness (hemiparesis) - particularly if cerebral peduncle involvement
  • Left-sided sensory loss or paresthesias - from thalamic involvement
  • Left hemibody numbness/tingling 5, 6

Visual Field Deficits

When PCOM infarction extends to involve PCA territory 6, 7:

  • Left homonymous hemianopia (loss of left visual field in both eyes)
  • Patients typically describe this as a negative visual phenomenon (darkness, blackness) rather than positive symptoms
  • 66% of patients can correctly lateralize the deficit to a hemifield 6

Associated Neurological Features

Thalamic Involvement

The PCOM gives rise to thalamogeniculate and premammillary perforators 3, 4:

  • Sensory deficits (most prominent feature with lateral thalamic infarction) 5, 7
  • Slight motor weakness (typically reversible) 7
  • Neuropsychological deficits: attention impairment, memory dysfunction 4
  • Altered level of consciousness if bilateral thalamic involvement 3

Midbrain Involvement

If infarction affects the midbrain (precommunal segment involvement):

  • Ipsilateral cerebellar ataxia (superior cerebellar peduncle) 1, 2
  • Ipsilateral flapping hand tremor (red nucleus) 1, 2
  • Contralateral hemiplegia (cerebral peduncle) 1, 2
  • Decreased consciousness - indicates severe proximal involvement 7

Presenting Symptoms

Acute Onset Features

  • Unilateral headache (ipsilateral to the lesion) - common presenting symptom 7
  • Dizziness (47% in posterior circulation strokes) 5
  • Nausea/vomiting (27-41% in posterior circulation ischemia) 8, 5
  • Sudden onset in 90% of cases without preceding warning 6

Warning Symptoms (10% of cases)

May have preceding transient symptoms before complete infarction 6

Anatomical Correlation

The right PCOM connects the right internal carotid artery to the right posterior cerebral artery, supplying:

  • Perforators to the ipsilateral thalamus (thalamogeniculate artery)
  • Premammillary artery territory
  • Hypothalamus
  • Portions of the midbrain
  • Runs immediately adjacent to the third cranial nerve 1, 2

Clinical Pitfalls

  1. Pupil-sparing vs. pupil-involving: Pupil-sparing third nerve palsy suggests microvascular ischemia (diabetes, hypertension), while pupil involvement with PCOM pathology mandates urgent aneurysm evaluation 1, 2

  2. Bilateral infarctions possible: Despite unilateral PCOM occlusion, bilateral thalamic infarctions can occur via compromised circuminfundibular plexus 3

  3. Fetal-type PCOM anatomy: When the PCA is predominantly supplied by a fetal-type PCOM (hypoplastic P1 segment), PCOM occlusion causes more extensive ischemia including lateral thalamus, medial temporal lobe, and occipital cortex 4

  4. Delayed recognition: Visual field deficits may not be immediately apparent if complete ptosis is present, as patients cannot see the deficit until the lid is elevated 1

Diagnostic Urgency

Immediate neuroimaging with MRI/MRA or CT/CTA is mandatory to:

  • Rule out posterior communicating artery aneurysm (especially with pupil involvement) 1, 2
  • Identify extent of infarction
  • Assess for hemorrhagic transformation
  • Evaluate Circle of Willis anatomy and collateral flow 9

The combination of ipsilateral third nerve palsy with pupillary involvement plus contralateral motor/sensory deficits should immediately trigger consideration of right PCOM pathology requiring emergent neurovascular imaging.

References

Research

Presenting Symptoms and Imaging Features of Posterior Cerebral Artery Stroke Causing Homonymous Hemianopia.

Journal of neuro-ophthalmology : the official journal of the North American Neuro-Ophthalmology Society, 2023

Research

Posterior communicating artery hypoplasia as a risk factor for acute ischemic stroke in the absence of carotid artery occlusion.

Journal of clinical neuroscience : official journal of the Neurosurgical Society of Australasia, 2008

Professional Medical Disclaimer

This information is intended for healthcare professionals. Any medical decision-making should rely on clinical judgment and independently verified information. The content provided herein does not replace professional discretion and should be considered supplementary to established clinical guidelines. Healthcare providers should verify all information against primary literature and current practice standards before application in patient care. Dr.Oracle assumes no liability for clinical decisions based on this content.