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

Background: Posterior cerebral artery (PCA) stroke is a common cause of homonymous hemianopia and other neurologic deficits associated with more proximal ischemia in the vertebrobasilar circuit. Localization of the process can be challenging unless the symptom complex is well recognized, yet early diagnosis is critical to forestall dangerous driving and repeated stroke. We undertook this study to provide additional detail about the presenting symptoms and signs and their correlation with imaging abnormalities and stroke etiology. Methods: Retrospective study of medical records of patients presenting to a single tertiary care academic center between 2009 and 2020 with homonymous hemianopia from PCA stroke. We excerpted data on symptoms, visual and neurologic signs, incident medical procedures and diagnoses, and imaging features. We determined stroke etiology using the Causative Classification Stroke system. Results: In a cohort of 85 patients, 90% of strokes occurred without preceding symptoms. But in retrospect, 10% of strokes did have warning symptoms. In 20% of patients, strokes followed within 72 hours of a medical or surgical procedure or newly identified medical condition. In the subgroups of patients whose records contained a description of visual symptoms, 87% reported the visual sensation as negative, and 66% realized that it was located in a hemifield in both eyes. Concurrent nonvisual symptoms were present in 43% of patients, consisting commonly of numbness, tingling, and new headache. Infarction located outside the visual cortex affected primarily the temporal lobe, thalamus, and cerebellum, reflecting the widespread nature of ischemia. Nonvisual clinical manifestations and arterial cutoffs on imaging were associated with thalamic infarction, but the clinical features and location of the infarction did not correlate with the etiology of the stroke. Conclusions: In this cohort, clinical localization of the stroke was aided by the fact that many patients could lateralize their visual symptoms and had nonvisual symptoms suggestive of ischemia affecting the proximal vertebrobasilar circuit. Numbness and tingling were strongly linked to concurrent thalamic infarction. Clinical features and infarct location were not associated with the etiology of the stroke.

Original Contribution Section Editors: Clare Fraser, MD Susan Mollan, MD Presenting Symptoms and Imaging Features of Posterior Cerebral Artery Stroke Causing Homonymous Hemianopia Elaine A. Liu, BA, Sadhana Murali, MD, Roberto Rivera-de Choudens, MD, Jonathan D. Trobe, MD Background: Posterior cerebral artery (PCA) stroke is a common cause of homonymous hemianopia and other neurologic deficits associated with more proximal ischemia in the vertebrobasilar circuit. Localization of the process can be challenging unless the symptom complex is well recognized, yet early diagnosis is critical to forestall dangerous driving and repeated stroke. We undertook this study to provide additional detail about the presenting symptoms and signs and their correlation with imaging abnormalities and stroke etiology. Methods: Retrospective study of medical records of patients presenting to a single tertiary care academic center between 2009 and 2020 with homonymous hemianopia from PCA stroke. We excerpted data on symptoms, visual and neurologic signs, incident medical procedures and diagnoses, and imaging features. We determined stroke etiology using the Causative Classification Stroke system. Results: In a cohort of 85 patients, 90% of strokes occurred without preceding symptoms. But in retrospect, 10% of strokes did have warning symptoms. In 20% of patients, strokes followed within 72 hours of a medical or surgical procedure or newly identified medical condition. In the subgroups of patients whose records contained a description of visual symptoms, 87% reported the visual sensation as negative, and 66% realized that it was located in a hemifield in both eyes. Concurrent nonvisual symptoms were present in 43% of patients, consisting commonly of numbness, tingling, and new headache. Infarction located outside the visual cortex affected primarily the temporal lobe, thalamus, and cerebellum, reflecting the widespread nature of ischemia. Nonvisual clinical manifestations and arterial cutoffs on imaging were associated with thalamic infarction, but the clinical features and location of the infarction did not correlate with the etiology of the stroke. Conclusions: In this cohort, clinical localization of the stroke was aided by the fact that many patients could lateralize their visual symptoms and had nonvisual symptoms suggestive of ischemia affecting the proximal vertebrobasilar circuit. Numbness and tingling were strongly Medical Scientist Training Program (EAL), University of Michigan School of Medicine, Ann Arbor, Michigan; and Departments of Neurology (SM, JDT), Radiology (RR-dC), and Ophthalmology and Visual Sciences (JDT), University of Michigan, Ann Arbor, Michigan. The authors report no conflicts of interest. Address correspondence to Jonathan D. Trobe, MD, Kellogg Eye Center, 1000 Wall Street, Ann Arbor, MI 48105; E-mail: jdtrobe@ umich.edu Liu et al: J Neuro-Ophthalmol 2023; 43: 393-398 linked to concurrent thalamic infarction. Clinical features and infarct location were not associated with the etiology of the stroke. Journal of Neuro-Ophthalmology 2023;43:393–398 doi: 10.1097/WNO.0000000000001934 © 2023 by North American Neuro-Ophthalmology Society S troke in the distribution of the posterior cerebral artery (PCA) commonly produces homonymous hemianopia by visual cortex infarction, which lies in its distal arterial domain.1–6 The clinical diagnosis of PCA stroke presenting with homonymous hemianopia can be challenging if patients do not clearly convey that their visual disturbance has affected a hemifield or if the examiner has not elicited nonvisual symptoms. Past reports1–6 have yielded no quantitative data on these matters or on the correlation between symptoms, neurologic signs, imaging features, and stroke etiology. METHODS With permission from the Michigan Medicine (University of Michigan) Institutional Review Board, we conducted a 2009–2020 electronic medical records (Epic) search of patients with “homonymous hemianopia,” “visual fields,” and “MRI” using the university’s Electronic Medical Record Search Engine (EMERSE).7 Patients were included only if medical records disclosed a homonymous hemianopia on automated visual field examination and MRI or computed tomography documentation of an infarct in the corresponding retrogeniculate visual pathway, including the occipital lobe. Patients could have additional infarcts in other brain regions. We obtained a cohort of 85 patients. We documented whether the stroke was diagnosed within 72 hours of a medical or surgical procedure or diagnosis, and if there was a preexiting hypercoagulable disorder. We documented symptoms before and concurrent with stroke as reported by the patient or patient’s partner. We determined whether the visual disturbance was described as an absence of vision (“negative visual symptoms”) or as patterns of light (“positive visual symptoms”) and whether it affected a sector of vision on one side of visual space (“lateralizing”). If it was nonlateralizing, we 393 Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. Original Contribution noted whether the patient reported it as affecting just one eye (“monocular”), both eyes but not on one side of visual space (“binocular”), or of uncertain localization (“unsure”). In noting new-onset persistent accompanying nonvisual symptoms, we combined “numbness,” “tingling,” and “paresthesias” into “numbness/tingling,” regardless of whether those symptoms were unilateral or bilateral or affecting extremities or face. We documented persistent, new, nonvisual neurologic signs discovered on examination at the time of stroke. The etiologic diagnosis for the stroke was determined by the Causative Classification System (CCS), which uses a web-based calculator.8 Statistics were performed using Chisquare or Fisher exact test for categorical variables. Statistical significance was set at P , 0.05. Patient Description of the Visual Disturbance In 68 patients (80%), there were no pertinent new medical procedures or diagnoses preceding the stroke. There were 29 records containing adequate documentation of the patient’s activity at the time of the stroke, which included driving—6; morning awakening from sleep—6; undergoing a routine vision examination—3; awakening from an afternoon nap, watching television, walking, exiting a hot shower or bath—2 each; looking out into the garden, listening to music, bowling, exercising, eating, and as part of a falling episode—1 each. There was no time of the day that favored first awareness of the visual disturbance. The patients who first noticed its onset while driving reported that they could not see cars or the dashboard on one side. One driver was unaware of a visual disturbance until he began drifting to one side of the lane, prompting his spouse to note that he could not see objects in his right hemifield. There were 73 patients (86%) who reported a new visual disturbance. Among the 12 patients (14%) who did not report a new visual disturbance, 5 had the disturbance reported by a partner during driving, 4 had major neurologic manifestations that overshadowed the visual disturbance, and 3 had the visual disturbance detected only on routine eye examination. In 61 patients, there was sufficient documentation of the patients’ description of the nature of the visual disturbance. It was purely “negative” in 53 patients (87%), purely “positive” in 5 patients (8%), and a combination of “negative” and “positive” in 3 patients (5%). The negative symptoms were most often reported vaguely as “lost vision,” “blurred vision,” “difficulty with vision,” and “troubled vision” but also with terms like “dark vision” and “dim vision” that suggested reduced transmission, and—even more diagnostically helpful—with terms that hinted at scotomas, such as “shaded vision,” “blocked vision,” “blank areas,” “disappearing letters,” “tunnel vision,” “black bars,” “blur spot,” “gray clouds,” “cannot see cars on one side,” and “cannot see numbers on one side of the bingo card.” The 8 patients with positive symptoms reported “flashes of light,” “colored Christmas lights,” “sparkling lights,” stationary “jagged glistening C shape,” stationary “wavy lines,” “speckled vision,” “silvery chicken wire,” or “bright floaters.” The 3 patients who reported a combination of “negative” and “positive” symptoms described seeing brightness within a visual void. In 58 patients, there was sufficient documentation of how patients localized their visual disturbance. Among them, 38 (66%) reported that it affected the “right side” or the “left side” of their visual field (“lateralized”). These 38 patients reported loss of a portion of their temporal visual field on one side, but sometimes only the upper or lower sector. Only 6 patients used the term “peripheral” to describe the location of the visual disturbance and only 2 realized that the nasal field of their other eye had also lost vision. There were 20 patients (35%) whose description was “nonlateralizing.” Among them were 5 patients who described the visual disturbance as affecting 1 eye only, 7 who reported the disturbance as affecting both eyes, and 8 who were unsure of its location with respect to their eyes. Incident Medical or Surgical Conditions Nonvisual Symptoms and Signs In 17 patients (20%), the stroke followed within 72 hours of a potentially contributory procedure or newly identified medical condition (spine surgery—2, systemic hypotension—2, cardiac catheterization, cholecystectomy, thoracotomy, abdominal surgery, hysterectomy, embolectomy, carotid endarterectomy, ovarian cystectomy, evacuation of brain hematoma, knee replacement, renal dialysis, heroin overdose, posterior reversible encephalopathy syndrome—1 each). In no case was a preexisting hypercoagulable disorder identified. Among the 80 patients for whom there was adequate documentation, the visual disturbance was accompanied by nonvisual symptoms in 34 patients (43%) (Table 1) . The most common nonvisual symptoms were numbness/ tingling in 13 (face, arm, and/or leg on one side—9, perioral/tongue—3, both hands—1) and headache in 12 (periocular—7, occipital convexity—5). Examination documented pertinent new nonvisual signs in 19 patients (26%), including hemibody hyperesthesia/ RESULTS Preceding Symptoms In 76 patients (90%), the visual disturbance occurred without preceding symptoms. But 9 patients (10%) reported the following episodic symptoms in the previous days to weeks: numbness/tingling—3; headache—2; transient hemifield loss, limb weakness, diplopia, slurred speech, combination of gait imbalance, slurred speech, and memory loss—1 each. Stroke Setting 394 Liu et al: J Neuro-Ophthalmol 2023; 43: 393-398 Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. Original Contribution TABLE 1. Nonvisual symptoms and signs Number of Patients (%) Nonvisual symptoms Numbness/tingling Headache Weakness Imbalance Slurred speech Diplopia Dizziness/lightheadedness Nausea/vomiting Confusion Reduced consciousness Sweating Sensation of head motion Head tilt Incoordination Nonvisual signs Hemibody hyperesthesia/hypesthesia Hemiparesis Pure alexia Hemispatial neglect/horizontal gaze deviation Ataxia Encephalopathy Nystagmus Dorsal midbrain syndrome Topographical agnosia Visuospatial/recognition dysfunction Brachial monoparesis 34 (43%) 13 12 7 4 4 3 3 3 2 2 1 1 1 1 19 (26%) 4 4 4 3 2 2 1 1 1 1 1 hypesthesia, hemiparesis, pure alexia, hemispatial neglect, ataxia, encephalopathy, nystagmus, dorsal midbrain syndrome, topographical agnosia, and visuospatial/visual recognition dysfunction. Infarct Locations Among the 85 patients, 39 (46%) had infarcts confined to the occipital lobe, 2 of which were bilateral (Table 2). The remaining 46 patients (54%) had concurrent infarcts involving other parts of the brain. An ipsilateral fetal PCA was present in 9 patients, 2 of whom had ipsilateral carotid artery stenosis, raising the possibility that the carotid stenosis was pertinent to the posterior circulation stroke. Thalamic Infarction and Nonvisual Manifestations The presence of infarcts in the thalamus significantly correlated with the presence of nonvisual symptoms and signs (Table 3). Among 13 patients with numbness/ tingling, 6 (40%) had infarcts involving the thalamus. Thalamic Infarction and Arterial Cutoffs Among the 57 patients who had undergone vascular imaging, 30 (49%) had visible arterial cutoffs in the Liu et al: J Neuro-Ophthalmol 2023; 43: 393-398 vertebrobasilar circuit. There were 5 cutoffs in the first PCA segment (P1), 14 cutoffs in the second PCA segment (P2), 6 cutoffs in the third PCA segment (P3), and 5 cutoffs in the vertebral artery (Fig. 1). There was a significant correlation between P1, P2, or vertebral cutoffs and thalamic infarcts (P = 0.0078). There were 9 patients with imaging evidence of intracranial atherosclerosis and 4 patients with extracranial atherosclerosis. Nonvisual Manifestations and Arterial Cutoffs Among 57 patients who had vascular imaging, 54 had adequate documentation of nonvisual symptoms, and 53 had adequate documentation of nonvisual signs. P1, P2, P3, or vertebral cutoffs significantly correlated with nonvisual symptoms and signs (Table 4). Nonvisual Symptoms and Signs and Stroke Etiology There was no correlation between nonvisual symptoms and signs and the 4 stroke etiologies determined by the CCS. Similarly, there was no correlation between the location of the infarct and stroke etiology. DISCUSSION This retrospective review of 85 patients with PCA stroke causing homonymous hemianopia disclosed several clinical and imaging features relevant to diagnosis, many of which have not been previously highlighted. Preceding Symptoms Symptoms preceding the PCA strokes were uncommon (10.6%). One previous report6 indicated that TIAs had occurred in fewer than 10% of cases, but another report5 indicated a rate as high as 25%. In our series, only 1 patient described a prodromal visual symptom (hemifield loss). The remaining patients reported nonvisual symptoms mostly TABLE 2. Infarct locations (N = 85) Infarct Location Occipital lobe only Unilateral Bilateral Occipital + other* Temporal lobe Thalamus Cerebellum Frontal lobe Parietal lobe Basal ganglia Periventricular cerebral Pons Number of Patients (%) 39 (46) 37 2 46 (54) 30 (35) 20 (24) 15 (18) 9 (11) 7 (8) 2 (2) 1 (1) 1 (1) *Many patients had infarcts in multiple locations. 395 Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. Original Contribution TABLE 3. Infarct location and clinical manifestations* Infarct Location Occipital lobe only Occipital lobe and thalamus Occipital lobe and other nonthalamic Infarct Location Occipital lobe only Occipital lobe and thalamus Occipital lobe and other nonthalamic No Nonvisual Symptoms Present (N = 46) Nonvisual Symptoms Present (N = 34) P 26 (57%) 7 (15%) 13 (28%) 9 (27%) 13 (38%) 12 (35%) 0.0117† 0.0350† 0.6265† No Nonvisual Signs Present (N = 55) Nonvisual Signs Present (N = 19) P 30 (55%) 8 (15%) 17 (31%) 2 (11%) 11 (58%) 6 (32%) 0.0010† 0.0005† .0.9999† *As occipital infarcts alone are known to cause headache, we also performed an analysis by assigning headache to patients with and without nonvisual symptoms. The correlations continued to be significant. † Fisher exact test. attributable to thalamic or brainstem/cerebellar ischemia. Numbness/tingling was prominent, supporting the contention of Fisher4 that “spells of numbness” are the most common TIA symptoms in PCA stroke, affecting the face, arm, or leg. Stroke Setting Most strokes appeared to occur spontaneously and without preference for a particular time of day. However, an important minority (20%) occurred within 72 hours of a procedure or a new contributory medical condition. Published reports have provided no comparable information. Patient Description of the Visual Disturbance Patients were mostly aware of their visual deficit. Only rarely was it first identified by their partners or on routine eye examination. A minority of patients (13%) reported “positive” visual symptoms. Unlike our study, Fisher4 found that the “visual hallucinations” and “photopsias” were “common” in PCA stroke. Only 2 of the 8 patients in our study reported scintillating features that could have been mistaken for migraine, but the hallucinations did not migrate across the visual field, as they typically do in migraine. Fisher4 had affirmed that the positive visual symptoms of PCA stroke do not resemble the hallucinations of migraine. A majority of our patients reported their visual loss as segmental and lateralized, affecting either the right side or left side of visual hemispace and offering a valuable clue to localization of the stroke. Although few patients used the term “peripheral vision loss,” and even fewer recognized that the vision loss affected both eyes, clinicians could have surmised that the patient was describing either a monocular temporal defect or a homonymous defect, prompting visual field testing that would have differentiated between these possibilities. Diagnosis was more difficult in the minority of 396 patients whose visual disturbance lacked lateralizing features, especially in the small number of patients who mislocalized the disturbance to one eye. Nonvisual Symptoms Almost half of the patients had accompanying nonvisual symptoms referable to the posterior arterial circulation, a feature that was a further aid in excluding an ocular event. Numbness and/or tingling and new headache dominated the nonvisual symptoms and were associated with thalamic infarction. Earlier published reports1–5 had emphasized “sensory symptoms,” usually unilateral numbness and tingling, as the most common nonvisual symptom of PCA stroke. New headache has also been reported as an important feature.1,2,4,6 Nonvisual Signs The neurologic examinations prompted by the nonvisual symptoms disclosed persistent deficits in 26% of the cohort that underwent documented examinations. The deficits were attributable to damage to vision-related cerebral cortex, thalamus, brainstem, or cerebellum, confirming that in PCA stroke, ischemia often affects tissues in the proximal domain of the vertebrobasilar circulation.2 The presence of nonvisual symptoms and signs significantly correlated with the presence of thalamic infarction but not to infarction elsewhere. Imaging Abnormalities Intravascular arterial cutoffs in the vertebrobasilar circuit were present in 49% of those who underwent MR angiography. Comparable data from previous studies are not available, although computed tomographic angiography in one earlier study6 showed occlusion in a majority of cases. Nonvisual symptoms and signs were associated with P1, P2, or P3 cutoffs and thalamic infarction was associated with P1, P2, or vertebral cutoffs. Notably, however, the Liu et al: J Neuro-Ophthalmol 2023; 43: 393-398 Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. Original Contribution FIG. 1. Imaging abnormalities in selected patients with and without arterial cutoffs. A. Diffusion-weighted axial MRI shows high signal (restricted diffusion) in the left visual cortex indicative of an isolated infarct (left); axial CTA maximum intensity projection (MIP) shows an arterial cutoff in the left distal PCA P3 segment (white arrow, right). B. Diffusion-weighted axial MRI shows restricted diffusion in the left thalamus and visual cortex, indicative of 2 acute infarcts (left); coronal CTA MIP shows an arterial cutoff (white arrow) in the left P1 (first) PCA segment (right). C. Diffusion-weighted axial MRI shows restricted diffusion in the right thalamus and visual cortex (left); axial MRA MIP shows an arterial cutoff (white arrow) in the right P2 (second) PCA segment (right). Patients B and C had numbness/tingling as well as homonymous hemianopia. CTA indicates computed tomographic angiography; PCA, posterior cerebral artery. location of the infarcts did not correlate with the etiology of the stroke as determined by a sophisticated calculator that incorporates all pertinent data.8 Clinical and Imaging Profile The following profile of PCA stroke presenting with homonymous hemianopia emerges from this study. An important minority of PCA strokes follow incident medical or surgical procedures. These “provoked” strokes Liu et al: J Neuro-Ophthalmol 2023; 43: 393-398 lack clinical and imaging features that differentiate them from “unprovoked” PCA strokes. PCA strokes occur at all times of day and without regard to activity. Preceding symptoms are unusual, consisting mainly of numbness and/or tingling affecting the face or extremities. Patients are usually aware of their visual deficit, often reporting it as a visual void or an area of blocked vision rather than as a scintillation. Sometimes, the descriptions 397 Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. Original Contribution TABLE 4. Arterial cutoffs and clinical manifestations Cutoff Locations P1, P2, P3, or vertebral Cutoff Locations P1, P2, P3, or vertebral No Nonvisual Symptoms Present (N = 29) Nonvisual Symptoms Present (N = 25) P 8 (28%) 17 (68%) 0.0057* No Nonvisual Signs Present (N = 37) Nonvisual Signs Present (N = 16) P 13 (35%) 12 (75%) 0.0151* *Fisher exact test. suggest scotomatous vision loss. Many patients realize that the disturbance occupies one side of their visual field. This critical piece of history, when combined with the elicitation of nonvisual symptoms (especially numbness and tingling in the face and extremities and new headache), should allow clinical localization to the PCA domain. However, when headache is described as emanating from the periocular region, clinicians may be misdirected to the eye as the source. Concurrent infarcts affecting nonvisual cortex are common, highlighting the fact that ischemia often affects tissues proximal to the visual cortex. Imaging evidence of proximal PCA occlusion significantly predicts nonvisual manifestations. Thalamic infarction is especially associated with numbness and tingling. However, the etiology of PCA stroke, as determined by a sophisticated calculator, does not correlate with clinical manifestations or with the location of the infarct. Although this study replicates many previous observations, it provides new and more detailed information about presenting symptoms and signs and their correlation with imaging abnormalities and stroke location. As a singleinstitution retrospective study from an academic center, it is subject to patient accrual biases and flaws of nonstandard observations and record-keeping. For example, the inclusion of patients depended on their having homonymous hemianopia identified on neuro-ophthalmologic examination, which might have underestimated the prevalence of the more neurologically devastating midbrain infarctions in PCA stroke. Clinical information and appropriate vascular imaging data were incomplete. However, the study population was large enough to generate reliable clinical information, yet not so large as to preclude detailed extraction and analysis of neuro-ophthalmic data. This investigation updates and amplifies the Fisher study,4 which 398 contains valuable but nonquantitative neuro-ophthalmic detail and no modern correlative imaging information. STATEMENT OF AUTHORSHIP Conception and design: E. A. Liu, S. Murali, R. Rivera-de Choudens, J. D. Trobe; Acquisition of data: E. A. Liu, S. Murali, R. Rivera-de Choudens, J. D. Trobe; Analysis and interpretation of data: E. A. Liu, S. Murali, R. Rivera-de Choudens, J. D. Trobe. Drafting the manuscript: J. D. Trobe; Revising the manuscript for intellectual content: E. A. Liu, S. Murali, R. Rivera-de Choudens, J. D. Trobe. Final approval of the completed manuscript: E. A. Liu, S. Murali, R. Riverade Choudens, J. D. Trobe. REFERENCES 1. Arboix A, Arbe G, Garcia-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. 2011;4:329. 2. Brandt T, Steinke W, Thie A, Pessin MS, Caplan LR. Posterior cerebral artery territory infarcts: clinical features, infarct topography, causes and outcome. Multicenter results and a review of the literature. Cerebrovasc Dis. 2000;10:170–182. 3. Cals N, Devuyst G, Afsar N, Karapanayiotides T, Bogousslavsky J. Pure superficial posterior cerebral artery territory infarction in the Lausanne Stroke Registry. J Neurol. 2002;249:855–861. 4. Fisher CM. The posterior cerebral artery syndrome. Can J Neurol Sci. 1986;13:232–239. 5. 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