Neurovascular Compression of the Optic Nerve Causing Peripheral Vision Loss

Authors:
Mohan Satish, MS, and Paul Sliskovich, MS
Creighton University School of Medicine, Omaha, Nebraska

Shailendra Saxena, MD, PhD
Department of Family Medicine, Creighton University Medical Center, and Creighton University School of Medicine, Omaha, Nebraska

An 85-year-old man presented to an outpatient clinic with concern for a progressive loss of peripheral vision in his left eye.

History. The patient’s history was remarkable for hypertension, hyperlipidemia, aortic valve stenosis, and cataracts. The patient has no history of alcohol, tobacco or drug use. He was currently on aspirin, benazepril, and simvastatin.

Physical examination. Physical examination findings were prominent for a left carotid bruit but were otherwise unremarkable. Likewise, neurological examination findings were unremarkable. However, considering the possibility for a cerebrovascular accident, carotid Doppler ultrasonography was ordered, followed by magnetic resonance imaging (MRI) of the brain and the orbit with and without contrast.

Diagnostic tests. Carotid Doppler ultrasonography findings were unremarkable for blockage or severe stenosis bilaterally. Brain MRI showed cortical atrophy and mild white-matter T2 signal changes that were consistent with mild chronic small-vessel ischemic disease, but findings were otherwise normal.

MRI of the orbit was significant for a flattening of the left optic nerve anterior to the optic chiasm, with a prominent flow void from the left anterior cerebral artery (ACA) crossing over the superior aspect of the nerve. Additionally, a mild mass effect was seen inferiorly from the internal carotid artery (ICA), contributing to the compression of the left optic nerve (Figures 1-3).

Figure 1. Thickened left ACA crossing on top of the optic nerve, obliterating its visualization. The red circle notes compression.

Figure 2. Harder to appreciate, the ICA was also compressing the optic nerve inferiorly. The red circle notes compression.

Figure 3. Prominent flow void from the left ACA crossing over the superior aspect of the optic nerve.

Follow-up. The results of the workup were discussed with the patient at a follow-up visit, during which his peripheral vision loss was attributed to pressure from the left ACA on his left optic nerve. Prior to the follow-up visit, based on the results of the orbit MRI, a consultant neurosurgeon advised against intervention due to the increased risk of an iatrogenic stroke secondary to a stiff ACA. The patient declined an offer of a referral for a second opinion. At this follow-up visit, the possibility of worsening vision loss without intervention was discussed with the patient.

NEXT: Discussion

Authors:
Mohan Satish, MS, and Paul Sliskovich, MS
Creighton University School of Medicine, Omaha, Nebraska

Shailendra Saxena, MD, PhD
Department of Family Medicine, Creighton University Medical Center, and Creighton University School of Medicine, Omaha, Nebraska

An 85-year-old man presented to an outpatient clinic with concern for a progressive loss of peripheral vision in his left eye.

History. The patient’s history was remarkable for hypertension, hyperlipidemia, aortic valve stenosis, and cataracts. The patient has no history of alcohol, tobacco or drug use. He was currently on aspirin, benazepril, and simvastatin.

Physical examination. Physical examination findings were prominent for a left carotid bruit but were otherwise unremarkable. Likewise, neurological examination findings were unremarkable. However, considering the possibility for a cerebrovascular accident, carotid Doppler ultrasonography was ordered, followed by magnetic resonance imaging (MRI) of the brain and the orbit with and without contrast.

Diagnostic tests. Carotid Doppler ultrasonography findings were unremarkable for blockage or severe stenosis bilaterally. Brain MRI showed cortical atrophy and mild white-matter T2 signal changes that were consistent with mild chronic small-vessel ischemic disease, but findings were otherwise normal.

MRI of the orbit was significant for a flattening of the left optic nerve anterior to the optic chiasm, with a prominent flow void from the left anterior cerebral artery (ACA) crossing over the superior aspect of the nerve. Additionally, a mild mass effect was seen inferiorly from the internal carotid artery (ICA), contributing to the compression of the left optic nerve (Figures 1-3).

Figure 1. Thickened left ACA crossing on top of the optic nerve, obliterating its visualization. The red circle notes compression.

Figure 2. Harder to appreciate, the ICA was also compressing the optic nerve inferiorly. The red circle notes compression.

Figure 3. Prominent flow void from the left ACA crossing over the superior aspect of the optic nerve.

Follow-up. The results of the workup were discussed with the patient at a follow-up visit, during which his peripheral vision loss was attributed to pressure from the left ACA on his left optic nerve. Prior to the follow-up visit, based on the results of the orbit MRI, a consultant neurosurgeon advised against intervention due to the increased risk of an iatrogenic stroke secondary to a stiff ACA. The patient declined an offer of a referral for a second opinion. At this follow-up visit, the possibility of worsening vision loss without intervention was discussed with the patient.

NEXT: Discussion