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Why has this otherwise healthy 37-year-old been seeing double for the past year, and what caused his left eyelid to droop? That's the diagnostic challenge described by Newman Cheng, MBBS, of the National Neuroscience Institute in Singapore, in .

The man had no known medical conditions nor was he using any drugs. The vertical diplopia was not associated with pain, and he believed it had developed after the left eye ptosis emerged. He told clinicians he was feeling well, with no joint pain, headaches, loss of sensation, or droop affecting his face. He had no difficulties swallowing or speaking clearly, and was not experiencing any numbness or weakness affecting his limbs.

On neurological examination, clinicians reported "a nonfatigable partial left-eyelid ptosis, left-eye hypotropia at primary position, and impaired left eye supraduction with a nonreactive left pupil on direct and consensual light reflexes." The patient showed no evidence of other cranial nerve deficits. Results of tests revealed normal limb reflexes, motor and sensory functioning, and flexor plantar responses.

Laboratory tests indicated that his fasting serum glucose level, thyroid function, and erythrocyte sedimentation rate were all normal. As well, results of tests for anti–double-stranded DNA, antinuclear antibodies, and HIV were negative. He maintained a normal response to repetitive nerve stimulation, and was negative for anti-acetylcholine receptor antibodies.

Clinicians performed a CT angiography of the circle of Willis and a routine brain MRI, without detecting any aneurysms, infarcts, or masses. Lumbar puncture results were acellular with normal glucose and protein levels, and results of several microbiological tests were negative.

Clinicians determined that the patient's symptoms were due to neurovascular conflict of the oculomotor nerve. They performed a detailed MRI constructive interference in steady-state sequence with fine cuts of the midbrain. This showed that the oculomotor nerve was indented by both the left posterior cerebral artery (PCA) and left superior cerebellar artery (SCA), with resultant displacement. There was no evidence of intracranial aneurysms.

"An oculomotor nerve palsy with pupil involvement is often due to extrinsic compression by posterior communicating artery (PCoA) aneurysms. This is because when the nerve exits the midbrain, its cisternal course passes between the PCA and SCA and is accompanied by the PCoA before running in an anteromedial-lateral direction to reach the cavernous sinus," Cheng explained. External compression of the pial vessels causes pupil dilation, impairs functioning of the parasympathetic fibers, and causes paralysis of the sphincter pupillae.

In contrast to more common neurovascular compression syndromes, such as trigeminal neuralgia and hemifacial spasms, oculomotor nerve palsy occurring in the absence of an aneurysm is relatively unusual, he observed.

In a population-based of 145 cases of acquired third nerve palsy in Olmsted County, Minnesota, diagnosed over 37 years, the most common causes were presumed microvascular (42%), followed by trauma (12%, but most common in children and young adults), compression from neoplasm (11%), post-neurosurgery (10%), and compression from aneurysm (6%).

Those authors noted that 16% of the patients with microvascular third nerve palsies presented with pupil involvement, compared with 64% of those with compressive third nerve palsies. However, they cautioned that "compressive third nerve palsies, even from aneurysm, can sometimes present without pupil involvement. Therefore, anisocoria alone cannot definitively differentiate microvascular from compressive third nerve palsies."

Cheng noted that given the increasing accuracy of high-resolution in determining the extent of neurovascular compression and related symptoms, the modality has a clinically significant role in the differential .

In citing the Olmsted county study, Cheng pointed out that a tendency to label cases with extensive negative workup as idiopathic or due to microvascular causes often means these patients are managed with observation only. However, there are numerous for oculomotor nerve palsy caused by neurovascular conflict, ranging from steroid treatment to microvascular decompression. In light of the long-term persistence of this patient's symptoms, he received microvascular decompression, which significantly improved the ptosis and ophthalmoparesis.

Cheng concluded that this case demonstrated the diagnostic value of high-resolution MRI in cases of oculomotor nerve palsy with pupillary involvement that may be due to neurovascular conflict, "especially when no other cause has been found."

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