Finding the culprit in long-standing ptosis and diplopia

Take Home

In difficult neuro-ophthalmology cases, selecting the correct imaging tools and trusting the skill of the radiologist are highly important.

By Lynda Charters; Reviewed by Rod Foroozan, MD

Houston-Neuro-ophthalmologists can often experience cases that are difficult to diagnose. One such case had a patient who experienced ocular symptoms for a decade that abated and then began to progress. A detailed clinical history can provide valuable information. However, choosing the correct imaging tools is extremely important for arriving at a correct diagnosis, as well as trusting the radiologist.

Rod Foroozan, MD, presented the case of a 46-year-old man who had had ptosis of the left upper eyelid and diplopia for 10 years. Initially, the patient had undergone a computed tomography (CT) scan of the brain that was performed 1 year after the onset of his symptoms. Five years after the diplopia began, the patient underwent an unspecified strabismus surgery and the results showed that the diplopia had improved temporarily. However, the diplopia recurred and later worsened over the 5 years before he presented to Dr. Foroozan, associate professor of ophthalmology, Baylor College of Medicine, Houston.

The patient’s medical history showed that he had hyperlipidemia and hypertension about 5 years before presentation to Dr. Foroozan and no other ocular problems. The patient had been taking simvastatin (Zocor, Merck) and lisinopril (Zestril, AstraZeneca Pharmaceuticals), and the patient’s father had glaucoma.

The examination

The ocular examination showed that the visual acuity was 20/20 bilaterally. The right pupil (3 mm) had a brisk response to light and the left pupil (4 mm) was slightly sluggish, while the anisocoria was slightly greater in the light. The rest of the examination was normal, according to Dr. Foroozan.

During examination of the patient, he observed incomplete ptosis, an incomplete supraduction deficit, an incomplete adduction deficit, and an incomplete infraduction deficit on the left side. There was no change in the pupillary size in gaze position and no abnormality in the left eyelid position.

An old left third nerve palsy was a consideration because the left pupil was slightly larger than the right pupil and sluggish in response to light, suggesting involvement of the pupillary pathway in the pathologic process. In addition, the diplopia improved in response to strabismus surgery and progressed again 5 years later.

Considering the progression of the case, a compressive lesion of the left third nerve can be suspected, Dr. Foroozan said.

How to proceed

In a patient who presents with a recent ocular deficit with symptoms like those in the current patient, the first imaging choice may include a CT or CT angiogram because of the possibility of an aneurysm. However, in a patient with a 10-year duration of symptoms, an aneurysm is unlikely, but an aneurysm localized to the left cavernous sinus is possible. However, this would be unusual in the absence of a left Horner syndrome. Magnetic resonance imaging (MRI) or MR angiography should be the testing of choice to well visualize the tissue around the left third nerve and the nerve itself.

In the patient under discussion, neuro-ophthalmologists are advised to look for a compressive lesion, but not a vascular lesion. Because of the long duration of the symptoms, the possibilities are a slow-growing cavernous sinus meningioma or a lesion of the third nerve, such as a schwannoma.

MRI images of this patient showed a small abnormality of the left cavernous sinus. The medial rectus muscle was seen to be atrophic with a signal that suggested fatty replacement with atrophy from a longstanding left cranial nerve palsy. The patient ultimately was considered to have a schwannoma.

A challenge for neuro-ophthalmologists is ascertaining the skill of the clinicians reading the neuro-images. Even when the appropriate tests are ordered, serious conditions, such as aneurysms, can be missed. Radiologists in some institutions may have no training in neuroradiology. In a case such as that under discussion, vascular causes of cranial nerve palsies are rare and these patients do not present frequently. In addition, the ordering neuro-ophthalmologist should request the radiologist to look for a specific pathology in a specific location.

Rod Foroozan, MD

E: foroozan@bcm.edu

Dr. Foroozan has not financial interest in any aspect of this report.

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