Posterior Cerebral Artery Stroke Clinical Presentation
- Author: Christopher Luzzio, MD; Chief Editor: Denise I Campagnolo, MD, MS more...
History
Patients with posterior cerebral artery (PCA) infarcts present for neurologic evaluation with symptoms including the following:
- Acute vision loss
- Confusion[5]
- New onset posterior cranium headache
- Paresthesias
- Limb weakness
- Dizziness
- Nausea
- Memory loss
- Language dysfunction[6]
Because many individuals identify stroke with motor weakness or language loss, they may delay seeking medical care after experiencing only vision change or headache, unaware that a stroke has occurred.
Patients may report bumping into objects, hitting obstacles on the roadside, or not seeing half the printed page when reading.
- Small, homonymous visual-field cuts often are mistaken for a loss or change of vision from 1 eye attributable to a refractive error correctable with optical glasses.
- A person with a hemifield visual loss and headache also may be discharged from urgent care with a diagnosis of migraine headache rather than of PCA stroke. A computed tomography (CT) scan easily can differentiate between both conditions. Additionally, a migraine is characterized by a moving scintillating scotoma, not a fixed bilateral homonymous field cut.
- The presence of homonymous hemianopia also helps in differentiating between a middle cerebral artery and PCA stroke, as profound hemiplegia or somatosensory loss may occur in both conditions.
Physical
The most common examination finding is a homonymous visual-field cut, usually a complete hemianopia, caused by a lesion in the contralateral occipital lobe. Macular or central field sparing can occur if the occipital pole remains intact through blood supply from a branch of the middle cerebral artery. Cortical blindness results from bilateral posterior cerebral artery (PCA) infarcts.[4, 7]
- Deep or proximal PCA infarcts involve portions of the thalamus and midbrain. Thalamic lesions result in contralateral face and limb sensory loss. The midbrain cerebral peduncle carries corticospinal tract fibers that decussate caudally in the brainstem. A peduncle lesion is associated with contralateral motor weakness. Motor symptoms also are induced by thalamic edema near the internal capsule or a focal lesion in this structure. The posterior aspect of the internal capsule, variably, receives some blood from branches off the proximal PCA.
- Large or bilateral PCA infarcts that involve thalamus, temporal, and/or parietal-occipital lobes often result in a spectrum of possible findings (neuropsychologic deterioration and memory, language, or visual-cognitive dysfunction). Prosopagnosia and visual agnosia are representative examples.
Causes
Major etiologies of posterior cerebral artery (PCA) infarction include cardiac embolism, vertebrobasilar disease, and PCA atherothrombosis.[8]
- Vertebrobasilar disease includes atherosclerosis, dissection, and aneurysm, all of which may cause artery-to-artery embolic events. Less frequent causes include paradoxical embolism, migraine, hypotension, hypercoagulable state, and fibromuscular dysplasia.
- A study by de Monyé et al investigated whether the risk for ischemic stroke is higher in persons who have a PCA with a fetal origin (ie, a PCA that arises directly from the supraclinoid internal carotid artery rather than from the basilar artery).[9] Using 16–multidetector-row CT angiography, the authors studied 82 patients with a PCA infarct and/or isolated homonymous hemianopia. Thirty-two patients had a PCA with a fetal origin, 14 of whom had it on their symptomatic side and 18 of whom had it on their asymptomatic side. The study found no link between the presence of a fetal origin for PCAs and an increased ischemic stroke risk in the territory of the PCA.
Kapoor K, Singh B, Dewan LI. Variations in the configuration of the circle of Willis. Anat Sci Int. Jun 2008;83(2):96-106. [Medline].
Arboix A, Arbe G, García-Eroles L, Oliveres M, Parra O, Massons J. Infarctions in the vascular territory of the posterior cerebral artery: clinical features in 232 patients. BMC Res Notes. Sep 7 2011;4:329. [Medline]. [Full Text].
Kwon JY, Kwon SU, Kang DW, Suh DC, Kim JS. Isolated lateral thalamic infarction: the role of posterior cerebral artery disease. Eur J Neurol. Aug 5 2011;[Medline].
Brandt T, Steinke W, Thie A. Posterior cerebral artery territory infarcts: clinical features, infarct topography, causes and outcome (1). The authors dedicate this paper to Michael S Pessin, MD, who died before publication. Multicenter results and a review of the literature. In: Cerebrovasc Dis. May-Jun 2000;10(3):170-82. [Medline].
Devinsky O, Bear D, Volpe BT. Confusional states following posterior cerebral artery infarction. Arch Neurol. Feb 1988;45(2):160-3. [Medline].
Capitani E, Laiacona M, Pagani R, et al. Posterior cerebral artery infarcts and semantic category dissociations: a study of 28 patients. Brain. Mar 2 2009;[Medline].
Barbeau H, Norman K, Fung J. Does neurorehabilitation play a role in the recovery of walking in neurological populations?. Ann N Y Acad Sci. Nov 16 1998;860:377-92. [Medline].
Steinke W, Mangold J, Schwartz A. Mechanisms of infarction in the superficial posterior cerebral artery territory. J Neurol. Sep 1997;244(9):571-8. [Medline].
de Monye C, Dippel DW, Siepman TA, et al. Is a fetal origin of the posterior cerebral artery a risk factor for TIA or ischemic stroke? A study with 16-multidetector-row CT angiography. J Neurol. Feb 2008;255(2):239-45. [Medline].
Hasso AN, Stringer WA, Brown KD. Cerebral ischemia and infarction. Neuroimaging Clin N Am. Nov 1994;4(4):733-52. [Medline].
Sylaja PN, Puetz V, Dzialowski I, et al. Prognostic value of CT angiography in patients with suspected vertebrobasilar ischemia. J Neuroimaging. Jan 2008;18(1):46-9. [Medline].
Finelli PF. Neuroimaging in acute posterior cerebral artery infarction. Neurologist. May 2008;14(3):170-80. [Medline].
Kwak JH, Choi JW, Park HJ, Chae EY, Park ES, Lee DH, et al. Cerebral artery dissection: spectrum of clinical presentations related to angiographic findings. Neurointervention. Aug 2011;6(2):78-83. [Medline]. [Full Text].
Del Zoppo GJ, Saver JL, Jauch EC, et al. Expansion of the time window for treatment of acute ischemic stroke with intravenous tissue plasminogen activator. A science advisory from the American Heart Association/American Stroke Association. Stroke. May 28 2009;[Medline]. [Full Text].
Rothwell PM. Is intravenous recombinant plasminogen activator effective up to 4.5 h after onset of ischemic stroke?. Nat Clin Pract Cardiovasc Med. Mar 2009;6(3):164-5. [Medline].
Hacke W, Kaste M, Bluhmki E, et al. Thrombolysis with alteplase 3 to 4.5 hours after acute ischemic stroke. N Engl J Med. Sep 25 2008;359(13):1317-29. [Medline]. [Full Text].
Wahlgren N, Ahmed N, Davalos A, et al. Thrombolysis with alteplase 3-4.5 h after acute ischaemic stroke (SITS-ISTR): an observational study. Lancet. Oct 11 2008;372(9646):1303-9. [Medline].
Adams HP Jr, del Zoppo G, Alberts MJ, et al. Guidelines for the early management of adults with ischemic stroke: a guideline from the American Heart Association/American Stroke Association Stroke Council, Clinical Cardiology Council, Cardiovascular Radiology and Intervention Council, and the Atherosclerotic Peripheral Vascular Disease and Quality of Care Outcomes in Research Interdisciplinary Working Groups: the American Academy of Neurology affirms the value of this guideline as an educational tool for neurologists. Stroke. May 2007;38(5):1655-711. [Medline]. [Full Text].
Adams DS. Stroke rehabilitation: indications, outcomes, recent developments. J La State Med Soc. Nov 1996;148(11):498-502. [Medline].
Hanlon RE, Dobkin BH, Hadler B. Neurorehabilitation following right thalamic infarct: effects of cognitive retraining on functional performance. J Clin Exp Neuropsychol. Jul 1992;14(4):433-47. [Medline].
Hassid EI. Neuropharmacological therapy and motor recovery after stroke. Mil Med. May 1995;160(5):223-6.
Rose FD, Brooks BM, Attree EA. A preliminary investigation into the use of virtual environments in memory retraining after vascular brain injury: indications for future strategy?. Disabil Rehabil. Dec 1999;21(12):548-54. [Medline].
Middleton S, McElduff P, Ward J, et al. Implementation of evidence-based treatment protocols to manage fever, hyperglycaemia, and swallowing dysfunction in acute stroke (QASC): a cluster randomised controlled trial. Lancet. Nov 12 2011;378(9804):1699-706. [Medline].
Gustafsson D, Elg M. The pharmacodynamics and pharmacokinetics of the oral direct thrombin inhibitor ximelagatran and its active metabolite melagatran: a mini-review. Thromb Res. Jul 15 2003;109 Suppl 1:S9-15. [Medline].
Georgiadis AL, Yamamoto Y, Kwan ES. Anatomy of sensory findings in patients with posterior cerebral artery territory infarction. Arch Neurol. Jul 1999;56(7):835-8. [Medline]. [Full Text].
Ghika J, Bogousslavsky J, Henderson J. The "jerky dystonic unsteady hand": a delayed motor syndrome in posterior thalamic infarctions. J Neurol. Aug 1994;241(9):537-42. [Medline].
Takenouchi T, Shimozato S, Fujiwara H, Momoshima S, Takahashi T. Posterior cerebral artery dissection on a serial magnetic resonance angiography. Brain Dev. Jul 16 2011;[Medline].
Traversa R, Cicinelli P, Bassi A. Mapping of motor cortical reorganization after stroke. A brain stimulation study with focal magnetic pulses. Stroke. Jan 1997;28(1):110-7. [Medline].
Volpe BT, Krebs HI, Hogan N. Robot training enhanced motor outcome in patients with stroke maintained over 3 years. Neurology. Nov 10 1999;53(8):1874-6. [Medline].
Yamamoto Y, Georgiadis AL, Chang HM. Posterior cerebral artery territory infarcts in the New England Medical Center Posterior Circulation Registry. Arch Neurol. Jul 1999;56(7):824-32. [Medline]. [Full Text].
Zweifler RM. Management of acute stroke. South Med J. Apr 2003;96(4):380-5. [Medline].

