Posterior Circulation Stroke Syndromes

The posterior cerebral circulation — vertebral arteries, basilar artery, posterior cerebral arteries (PCA), and their major branches (PICA, AICA, SCA) — supplies the brainstem, cerebellum, occipital lobes, posterior thalamus, and medial temporal lobes. Posterior circulation strokes are clinically diverse and often missed at first presentation: they can produce isolated vertigo (mimicking peripheral disease), bilateral occipital lesions (mimicking psychiatric or visual disease), or thalamic findings (mimicking metabolic encephalopathy). The recognition of posterior circulation stroke syndromes is one of the more challenging — and consequential — exercises in stroke neurology. This page covers the major posterior circulation stroke syndromes.

The Posterior Circulation

Vertebral Arteries

• Arise from subclavian arteries.
• Ascend through the foramina transversaria of the cervical vertebrae.
• Enter cranium through foramen magnum.
• Join at the pontomedullary junction to form the basilar artery.
• Each vertebral gives off PICA before joining.

Basilar Artery

• Runs anterior to pons.
• Gives off AICA, then SCA branches, then bifurcates into two PCAs.
• Paramedian pontine perforators supply medial pons.

Posterior Cerebral Arteries

• Supply occipital lobe, medial/inferior temporal lobe (including hippocampus), posterior thalamus.
• P1 segment gives perforators to midbrain and thalamus (thalamoperforator arteries).
• P2 segment gives thalamogeniculate arteries.
• Posterior choroidal arteries supply pulvinar, LGN, posterior thalamus.

PCA Stroke Syndromes

Cortical PCA Infarct

• Contralateral homonymous hemianopia with macular sparing: characteristic — dual blood supply to occipital pole spares the macular representation.
• Memory impairment: if hippocampus involved.
• Alexia without agraphia: left PCA, with splenium of corpus callosum involvement.
• Visual hallucinations / agnosias: extrastriate cortex.
• Color naming deficits: lingual gyrus.

Bilateral PCA Infarct

• Cortical blindness: bilateral occipital infarction. Pupils still react.
• Anton syndrome: cortical blindness with denial of blindness.
• Dense memory impairment: bilateral hippocampal involvement.
• Balint syndrome: if extending to parieto-occipital.

Top of the Basilar Syndrome

Embolic occlusion of distal basilar artery → infarction of rostral midbrain, bilateral thalami, occipital lobes, sometimes cerebellum. Features:

• Altered consciousness: ARAS, paramedian thalami.
• Vertical gaze palsy: midbrain.
• Pupillary abnormalities: midbrain, pretectal.
• Visual abnormalities: hemianopia, cortical blindness, hallucinations.
• Memory disturbance: bilateral hippocampi.
• Behavioral changes: agitation, confusion, abulia.
• Limb findings: variable.

Artery of Percheron Infarct

Single artery from one PCA P1 supplies BILATERAL paramedian thalami plus rostral midbrain.

• Sudden altered consciousness: often misdiagnosed as metabolic.
• Vertical gaze palsy.
• Memory impairment: persistent.
• Bilateral thalamic infarcts on MRI: characteristic.

Basilar Artery Occlusion

Basilar Tip Occlusion

Discussed above (top of the basilar syndrome).

Basilar Trunk Occlusion (Mid-Basilar)

• Bilateral pontine infarction.
• Locked-in syndrome: quadriplegia, mutism, with preserved consciousness and vertical eye movements.
• Pinpoint reactive pupils: descending sympathetic interruption.
• High mortality.
• Emergent thrombectomy if recognized in window — life-saving.

Proximal Basilar Occlusion

Variable: can extend caudally to cause medullary involvement, or rostrally to cause pontine involvement.

Vertebral Artery Stroke Syndromes

Vertebral Artery Occlusion

• Most commonly produces Wallenberg syndrome (lateral medullary).
• Can produce medial medullary syndrome (anterior spinal artery territory).
• Can produce cerebellar infarct (PICA territory).

Vertebral Artery Dissection

• Especially in younger patients after neck trauma, manipulation, sports.
• Neck pain often preceding stroke.
• Wallenberg syndrome (lateral medullary) is the most common stroke.
• Image with MRA, CTA, or conventional angiography.
• Treatment: anticoagulation or antiplatelet; intervention if recurrent ischemia.

Brainstem Stroke Syndromes (Crossed Patterns)

Discussed in detail in the Brainstem Localization pages. Key examples:

Cerebellar Stroke Syndromes

PICA Cerebellar Stroke

• Inferior cerebellum and lateral medulla.
• Vertigo, vomiting, ipsilateral limb ataxia.
• Lateral medullary findings if medullary branches involved (Wallenberg).
• Large infarcts can produce mass effect → brainstem compression.

AICA Cerebellar Stroke

• Inferolateral cerebellum + lateral lower pons + labyrinth.
• Vertigo, hearing loss (ipsilateral), ipsilateral facial palsy, ipsilateral ataxia, contralateral pain-temp loss.

SCA Cerebellar Stroke

• Superior cerebellum + parts of upper lateral pons.
• Ipsilateral limb ataxia, dysarthria, sometimes nausea/vomiting.
• Sometimes Horner.

Special Considerations

Vertigo as the Sole Presenting Symptom

Acute cerebellar stroke can present with isolated acute vestibular syndrome and mimic vestibular neuritis. In appropriately selected patients — acute continuous vertigo or dizziness, with spontaneous or gaze-evoked nystagmus, nausea/vomiting, head-motion intolerance, and unsteady gait — a HINTS / HINTS+ examination performed by a trained clinician can help distinguish central from peripheral causes:

• Head Impulse: normal in central (paradoxical); abnormal (catch-up saccade) in peripheral.
• Nystagmus: direction-changing in central; unidirectional in peripheral.
• Test of Skew: skew deviation suggests central.
• Hearing (the “+”): bedside finger rub; new unilateral hearing loss in acute vestibular syndrome increases concern for AICA / labyrinthine ischemia even when the other three components look peripheral.

HINTS / HINTS+ outperforms early MRI for distinguishing central from peripheral causes in the acute vestibular syndrome, and the SAEM GRACE-3 (2023) recommendations endorse it as the bedside framework for AVS. Missing a posterior circulation stroke in this setting is one of the most consequential diagnostic errors in emergency neurology.

Scope caution. HINTS / HINTS+ should be applied only to acute vestibular syndrome with nystagmus, by a trained clinician. It should not be applied to brief episodic vertigo, triggered positional vertigo (use Dix-Hallpike), nonspecific lightheadedness, or unselected dizziness without nystagmus. Outside the AVS context, a “negative” HINTS does not exclude central disease.

Cerebellar Edema

Large cerebellar infarcts can produce edema → brainstem compression → herniation. Suboccipital decompression is life-saving for selected patients. ICU monitoring critical.

Thrombectomy for Basilar Occlusion

Basilar artery occlusion historically had high mortality. Recent trials demonstrate substantial benefit from thrombectomy. Time window for posterior circulation thrombectomy is somewhat more permissive (up to 24 hours by some criteria), but earlier intervention better. Recognition is the key — locked-in syndrome and altered mental status should prompt urgent imaging and intervention.

Imaging

• Non-contrast CT: less sensitive for posterior fossa; can miss early ischemic changes.
• CT angiography: identifies large vessel occlusion. Important for basilar, vertebral imaging.
• MRI with DWI: most sensitive for posterior circulation strokes. Image promptly if posterior stroke suspected and CT negative.
• MRA or CTA neck and brain: vertebral artery dissection, atherosclerosis, large vessel occlusion.

Recognizing Posterior Circulation Stroke at the Bedside

The “5 D’s” plus the “5 N’s”:

• Diplopia
• Dysarthria
• Dysphagia
• Dizziness / Vertigo
• Dysmetria / Ataxia

• Numbness (perioral or hemibody)
• Nausea
• Nystagmus
• (plus other brainstem signs)

Patients with any combination of these symptoms — especially if multiple — warrant urgent posterior circulation imaging. Pure vertigo, pure dysarthria, or pure visual disturbance can each be posterior circulation stroke and must not be dismissed.

Common Posterior Circulation Stroke Patterns

🔍 Did You Know?

The phrase “locked-in syndrome” was coined to describe patients with ventral pontine infarction from basilar artery occlusion. The patients are conscious and aware — the dorsal pontine tegmentum (with the reticular activating system) is spared — but they cannot move any muscle except for vertical eye movements and eyelid blinking, because the ventral pontine corticospinal and corticobulbar pathways are destroyed bilaterally. Patients can hear, understand, recognize family, and feel pain and emotion — all while appearing utterly unresponsive. The diagnosis can be missed if the examiner does not specifically test vertical eye movements: asking the patient to “look up” or “look down” or “blink twice” reveals consciousness. The clinical implications are profound. The recognition allows the patient to communicate (often slowly, by blinks or eye movements), changes the way caregivers speak around the patient, and most importantly may prompt emergent thrombectomy — basilar artery occlusion has remarkable potential for good outcome with thrombectomy if recognized early. The recent positive trials of basilar artery thrombectomy (BAOCHE, ATTENTION trials) have transformed expectations: a patient who was previously expected to die or remain locked-in for life can now sometimes have a good functional outcome. The lesson: any patient with altered consciousness and limb weakness without obvious cause should have their vertical eye movements tested — finding them preserved is potentially life-saving.

Pitfalls and Pearls

• Posterior circulation strokes are often initially missed: vertigo, isolated visual disturbance, isolated dysarthria, isolated ataxia.
• Vertigo + any other neurologic finding → posterior circulation stroke until proven otherwise.
• HINTS / HINTS+ battery for acute vestibular syndrome with nystagmus: distinguishes peripheral from central better than early MRI. Not for triggered or episodic dizziness.
• PCA infarct + macular sparing: hallmark — dual blood supply to occipital pole.
• Bilateral PCA infarct: cortical blindness (pupils still react); Anton syndrome if denial.
• Top of the basilar syndrome: altered consciousness + visual disturbance + vertical gaze palsy + memory.
• Locked-in syndrome: ventral pontine infarct from basilar occlusion. Conscious; test vertical eye movements.
• Basilar thrombectomy: potentially curative if recognized early. Expanded time window.
• Wallenberg syndrome: vertebral artery dissection in younger patients.
• Cerebellar stroke + mass effect: suboccipital decompression life-saving.
• Artery of Percheron infarct: bilateral paramedian thalamic infarcts — often mistaken for metabolic encephalopathy.
• AICA infarct: vertigo + hearing loss + facial palsy + ataxia + contralateral pain-temp loss.
• Pinpoint reactive pupils + quadriplegia: think pontine hemorrhage or basilar artery occlusion.
• Alexia without agraphia: left PCA (left occipital + splenium of corpus callosum).

References

1. Brazis PW, Masdeu JC, Biller J. Localization in Clinical Neurology. 7th ed. Wolters Kluwer; 2017.
2. Caplan LR. Caplan’s Stroke: A Clinical Approach. 5th ed. Cambridge University Press; 2016.
3. Jovin TG, Li C, Wu L, et al. Trial of thrombectomy 6 to 24 hours after stroke due to basilar-artery occlusion (BAOCHE). N Engl J Med. 2022;387(15):1361-1372.
4. Tao C, Li R, Zhu Y, et al. Trial of endovascular treatment of acute basilar-artery occlusion (ATTENTION). N Engl J Med. 2022;387(15):1373-1384.
5. Newman-Toker DE, Kerber KA, Hsieh YH, et al. HINTS outperforms ABCD2 to screen for stroke in acute continuous vertigo and dizziness. Acad Emerg Med. 2013;20(10):986-996.
6. Gerlach OHH, Edlow JA, Carpenter CR, et al. Guidelines for reasonable and appropriate care in the emergency department 3 (GRACE-3): acute dizziness and vertigo in the emergency department. Acad Emerg Med. 2023;30(5):442-486.
7. Ropper AH, Samuels MA, Klein JP, Prasad S. Adams and Victor’s Principles of Neurology. 11th ed. McGraw-Hill; 2019.