Optic chiasmal syndrome can be caused by a variety of lesions, including tumors and carotid artery aneurysms1; however, reports of bitemporal field loss from compression by an abnormal vessel are rare.2We describe a patient with a nonprogressive bitemporal hemianopia in whom there appeared to be compression of the optic chiasm by an elongated right anterior cerebral artery (ACA).
A bitemporal hemianopia was found in a 65-year-old woman with no vascular risk factors during a routine eye examination in 2003. Magnetic resonance imaging (MRI) results were normal. One year later, the bitemporal field defect was still present and a second MRI again showed no evidence of a compressive or infiltrative process.
The patient was subsequently referred to us for an assessment. On examination, her visual acuity was 20/20 OU with normal color vision and pupillary responses. The fundi appeared normal with no evidence of tilted optic discs or retinoschisis. A bitemporal hemianopic scotoma was detected by kinetic perimetry (Figure 1A), and static perimetry revealed a bitemporal hemianopic defect, denser inferiorly than superiorly, with a pattern and severity unchanged from the examination performed 20 months earlier (Figure 1B). Multifocal electroretinography results were normal, but visual evoked potentials showed a mild bilateral delayed response. It was noted that the 2 previous MRIs had been performed without magnification and did not consist of thin sections.
A, Kinetic perimetry showing a bitemporal hemianopic scotoma. B, Static perimetry with Swedish interactive threshold algorithm fast 24-2 strategy showing a bitemporal hemianopia that is denser inferiorly than superiorly. MD indicates mean deviation; PSD, pattern standard deviation.
A repeat MRI with thin-slice and magnified views of the optic chiasm was obtained and showed a vessel indenting the optic chiasm superiorly (Figure 2A). A computed tomographic angiogram confirmed an elongated right ACA that dipped inferiorly, compressing the superior aspect of the optic chiasm before looping anteriorly (Figure 2B). The ACA loop was thought to be the cause of the patient's bitemporal hemianopia. We decided against neurosurgical intervention but recommended that the patient be evaluated at regular intervals.
A, T2-weighted coronal magnetic resonance imaging showing impingement and downward displacement of the optic chiasm (asterisk) by a vessel (arrow). B, Reconstructed coronal computed tomographic angiography shows an elongated right anterior cerebral artery that curves downward, forming a loop (arrow) that corresponds to the point of contact with the optic chiasm. The opposite anterior cerebral artery has a normal structure.
Vascular compression of the optic chiasm causing a bitemporal field defect is most often due to an aneurysm of the ACA, internal carotid artery, or anterior communicating artery.1Rare cases of dolichoectatic and atherosclerotic ACAs that cause bitemporal hemianopia have been reported, but direct chiasmal impingement has not been described. The field defect in such cases is thought to result from traction on small perforating vessels causing a chiasmal infarction.2In addition, although Bergaust3reported a patient with a bitemporal hemianopia that was thought to be caused by compression of the inferior aspect of the optic chiasm by an anomalous internal carotid artery, we are unaware of any cases of presumed vascular compression of the chiasm with production of a bitemporal field defect by a vascular loop.
Our case highlights the importance of not only obtaining appropriate neuroimaging studies but also specifying the region of interest. The presence of a bitemporal hemianopia in the absence of optic nerve or retinal pathology suggested a process involving the optic chiasm. By obtaining thin-sectioned, magnified views of this region, we were able to identify an anomalous loop of the right ACA, which appeared to be compressing and causing downward displacement of the chiasm, presumably causing the bitemporal defect. A computerized tomographic angiogram further clarified the process.
Although surgery can be performed in this setting,4surgical manipulation may disrupt the small perforating vessels supplying the optic chiasm and result in worsening of a preexisting visual field defect or even complete blindness. Thus, unless there is clear evidence of progression, it is probably best to follow up in patients with this rare condition.
Correspondence:Dr Miller, Wilmer Eye Institute, Johns Hopkins Hospital, Maumenee 127, 600 N Wolfe St, Baltimore, MD 21287 (email@example.com).
Financial Disclosure:None reported.
Chen CS, Gailloud P, Miller NR. Bitemporal Hemianopia Caused by an Intracranial Vascular Loop. Arch Ophthalmol. 2008;126(2):274-276. doi:10.1001/archophthalmol.2007.60