Case 2: Posterior communicating artery aneurysm
Given the patient’s high BP, ruling out a hypertensive emergency with CT was the first priority. TNP caused by microvascular ischemia is not uncommon in the elderly. However, her pupil involvement and persistent headache called for an MRI to better evaluate the soft tissues and to rule out possible vascular pathologies. Left posterior communicating artery aneurysm was discovered with MRI, and urgent cerebral angiography and coiling was performed successfully.
Incidence. One report of 1400 patients with TNP confirmed that aneurysm was the cause in 10% of cases, with posterior communicating artery aneurysm accounting for the greatest number, 119 (25.7%).10 Of these cases of posterior communicating artery aneurysm, pupillary involvement was detected in 108 (90.8%). The oculomotor nerve lies adjacent to the posterior communicating artery as it passes through the subarachnoid space of the basal cisterns, where it is susceptible to compression.3
A high index of suspicion for posterior communicating artery aneurysm is crucial for early detection and lifesaving treatment. The patient in this case did well after the coiling. Her ptosis resolved at 2 months, although she had residual left eye exotropia.
Case 3: Viral infection
We chose CTA of the brain instead of contrast CT to rule out the possibility of intracranial aneurysm. CTA has been shown to be an adequate first-line study to detect aneurysms, particularly those greater than 4 mm in diameter.2,11 One study demonstrated an 81.8% sensitivity for aneurysms smaller than 3 mm when performed on a 320-slice CT.12
Additional imaging selection. We also selected MRA to rule out berry aneurysm, which is often asymptomatic. We decided against MRI because of its higher cost and longer acquisition time. It is usually reserved for patients with a negative initial work-up with CT or cerebral angiography if suspicion of a possible aneurysm remains.11 The MRA finding in this case was negative, and we made a presumptive diagnosis of TNP secondary to viral infection.
Isolated TNP following viral infection is a clinical diagnosis of exclusion. In 1 reported case, a 39-year-old man developed a superior division palsy after a common cold without fever, underwent no serologic study, and recovered spontaneously 6 weeks later.13 A 5-year-old boy who experienced a superior division palsy immediately after a common cold with fever was found on serologic examination to have an increased titre of influenza A virus. His palsy resolved in 4 months.14
The exact mechanism of viral-induced palsy is unknown. The possibility of postinfectious cranial neuropathy has been postulated, as most reported cases following a flu-like illness resolved within a few months.15 Although the pathogenesis remains speculative, an autoimmune process might have been involved.16 Our patient recovered fully in 1 month following a short course of oral prednisolone 30 mg/d for 5 days.
Case 4: Trauma
Trauma accounts for approximately 12% of all TNP cases.17 Traumatic TNPs are usually sustained in severe, high-speed, closed-head injuries, and are often associated with other CN injuries and neurologic deficits. The damage may be caused indirectly by compression, hemorrhage, or ischemia, or directly at certain vulnerable points including the nerve’s exit from the brainstem and the point at which it crosses the petroclinoid ligament.17 In our case, despite the patient having complete TNP, there was no sign of localized orbital trauma on the CT other than the presence of subarachnoid hemorrhage at the right frontotemporal region.
In a similar reported case, the patient had a right traumatic isolated TNP and was found to have left frontal subarachnoid hemorrhage with no sign of orbital trauma.18 However, the mechanisms of isolated TNP caused by traumatic brain injury are not clear. Possible causes include rootlet avulsion, distal fascicular damage, stretching of the nerve (including the parasellar segment), and decreased blood supply.18
It has been suggested that TNP is more frequently observed in cases of frontal region injury. As orbitofrontal regions are predominantly affected by cortical contusions, the risk for ocular involvement increases.19
Keep these fundamentals in mind
The diagnosis and management of isolated TNP are guided by the patient’s age, by the degree to which each of the oculomotor nerve’s 2 major functions—pupillomotor and oculomotor—are affected, and by the circumstances preceding the onset of TNP.2 Cases 1 and 3 in our series presented with partial TNP, while Cases 2 and 4 exhibited complete TNP. Pupillary involvement was detected only in Case 2. Nevertheless, radiologic imaging was ordered for all 4 cases after the diagnosis of TNP was made, to exclude the most worrying neurologic emergencies. The choice of imaging modality depends on not only the availability of the services but also the clinical signs and symptoms and presumptive clinical diagnosis. A tailored and thoughtful approach with consideration of the anatomy and varied pathologies help clinicians to skillfully discern emergencies from nonurgent cases.
CORRESPONDENCE
Lott Pooi Wah, MSOphth, FRCOphth, Department of Ophthalmology, Faculty of Medicine, Universiti Malaya, 50603 Kuala Lumpur, Malaysia; lottpw@yahoo.com Orcid no: 0000-0001-8746-1528