Homonymous visual field (VF) defects impair visual function and frequently preclude driving (1-4). Stroke is the most common cause of homonymous hemianopia (HH) and approximately 10% of patients with stroke are found to have a HH, which may affect their functional neurologic outcome (1-5). Interestingly, a large number of these patients are not aware of their VF defect and most are still driving (4). Most of our knowledge of HH in stroke is based on relatively few small series (1-3,6-14). However, these reports have not always been supported by brain imaging. This study describes the characteristics of HH caused by stroke in a large number of cases.
We reviewed the medical records of all patients with HH seen in our unit between 1989 and 2004 as detailed in another report (15). All patients with a HH, detailed clinical information, and results of brain CT or MRI were included. Patients with a diagnosis of neglect were not included. Demographic characteristics, clinical features, characteristics of VF defects, causes of VF defects, neuroradiologic definition of lesion location, and associated neurologic deficits were recorded. Cases with bilateral HH were recorded twice so that each HH (right and left) could be analyzed separately. All patients had a HH confirmed by Goldmann visual field testing (GVF), Humphrey visual field testing (HVF), or confrontation visual field examination. Humphrey visual fields were performed on the 24-2 or 30-2 full threshold program until the year 2000 and on the SITA-fast or SITA-standard programs after 2000. All GVF tests were performed in a standardized way by the same experienced technician. All confrontation visual field examinations were performed by an experienced neuro-ophthalmologist (NJN and VB) using hand movement, finger counting, and color comparison (red saturation across the vertical meridian). Reliability of HVFs was determined based on the number of fixation loss, false-positive and false-negative responses. Patients with unreliable HVF were tested with GVF. Reliability of GVF was determined by our technician and was based on accuracy of fixation and consistence of responses.
HHs were classified into “complete” and “incomplete,” the latter including homonymous quadrantanopia (superior and inferior homonymous visual field defects respecting both the vertical and horizontal meridians), partial HH (incomplete HH not respecting the horizontal meridian), HH with macular sparing (homonymous visual field defect sparing the central 5-25° of visual field on the affected side), homonymous scotomatous defects, and homonymous sectoranopia as detailed in another report (15). Congruency was defined as visual field defects identical in size and shape in both eyes. The location of brain lesion was determined based on the head CT or brain MRI report (15).
HHs were divided into two groups according to cause as stroke and non-stroke. The stroke group was further divided into infarction and primary intraparenchymal hemorrhage.
The mean and the standard deviation or the median, 25th percentile, and 75th percentile were obtained for continuous variables; the percentages in the categories along with the standard errors were obtained for categorical variables. The demographic, clinical, and visual field characteristics were compared using a t test or Wilcoxon rank sum test (for continuous variables) and a χ2 test (for categorical variables).
Among the 904 HHs included in our study, 629 (69.7%) resulted from stroke and 273 HHs (30.3%) from other conditions, including 123 from head trauma, 102 from brain tumor, 22 from neurosurgical procedures, 13 from multiple sclerosis, 13 from miscellaneous causes, and 2 from undetermined causes (Table 1) (15). Formal visual field testing was obtained in 864 HHs, including 714 GVF, 115 HVF, and 35 with both GVF and HVF testing. Forty HHs were diagnosed by confrontation visual field testing only. Among these 40 HHs, 24 were complete and 16 were incomplete; all 16 were classified as partial HH. The 629 HHs caused by stroke included 531 HHs (84.4%) caused by cerebral infarction and 98 HHs (15.6%) caused by primary intraparenchymal hemorrhage.
As shown in Table 1, HH resulting from stroke occurred in older patients, was more often bilateral and congruous and was more often unaccompanied by other neurologic manifestations (“isolated”) than HH resulting from other causes. Occipital lesions were more common in stroke than in non-stroke cases (P < 0.0001).
There were no significant differences in the frequencies of the different configurations of HH in patients with stroke and non-stroke patients. The time from injury to initial visual field test tended to be shorter among stroke cases.
Compared with primary intraparenchymal hemorrhage, infarction occurred more often in older patients (60 ± 17 years vs 50 ± 18 years, P < 0.0001), was more often responsible for bilateral HH (40 vs 0, P = 0.001), and involved the occipital lobes more often relative to optic radiations (56% occipital vs 45% occipital and 30% optic radiations vs 47% optic radiations, respectively, P < 0.05).
The configuration of the HH did not reliably predict the location of the responsible lesion within the retrochiasmal visual pathway (Fig. 1).
This report is the largest series of HHs secondary to stroke. All patients were referred to our service for VF testing either because they had visual complaints or because the treating physician thought the brain lesion could produce visual impairment. Although most patients were sent to us late, the median time was significantly lower for patients with stroke than for patients with other brain lesions (Table 1). This may reflect better awareness of VF defects in the setting of stroke or possibly better outcome of patients with stroke (whose HH was more often isolated) than of non-stroke patients.
Previous studies have emphasized that most HH is caused by stroke and that most stroke HH is secondary to an occipital infarct (1-3). In these studies, the diagnosis of stroke was based mostly on clinical evaluation and not all patients had undergone brain imaging. Our study, which included neuroimaging in all cases, confirms these results. Previous studies have emphasized that the nature of the lesion may be suggested by the presumed lesion location and the characteristics of the VF defect (1-3). Indeed, macular sparing is considered to result from occipital lesions, specifically occipital infarctions in the distribution of the posterior cerebral artery (1-3,6-8,10,13,14). Our study showed that macular sparing was not only caused by lesions other than stroke, but also resulted from strokes involving the anterior portions of the visual pathways such as the optic tract. Similar findings were observed for homonymous scotomatous defects. Indeed, it has been previously suggested that one of the causes of macular sparing is incomplete damage to the anterior portions of the retrochiasmal visual pathways (3,16). Homonymous scotomatous VF defects have been reported in patients who with lesions of the optic tract after pallidotomy for Parkinson disease (17). These VF defects have been attributed to the particular anatomic fiber organization within the optic tract (17-19).
This study confirms that stroke is the commonest cause of HH. The long delay between stroke onset and the recognition of HH suggests that HH is often overlooked in patients with stroke. Because HH can interfere with rehabilitation and is associated with a worse functional outcome in patients with stroke, VF testing should be systematically performed in all patients after a stroke involving the cerebral hemispheres. Finally, HH often precludes driving and should be investigated before allowing patients with stroke to drive.
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