A 36-year-old female with a recently treated sinus infection presents with an 18-hour history of severe right-sided headache and new-onset diplopia. Examination reveals the finding pictured below. Aside from tenderness on palpation over the frontal and maxillary sinuses, the remainder of her physical and neurologic exam is unremarkable. TH
Patient looking to her right.
What is the physical exam finding?
a) Anisocoria;
b) Facial nerve palsy;
c) Horner Syndrome;
d) Abducens palsy; or
e) Intranuclear ophthalmoplegia.
Discussion
The answer is D: Abducens palsy, or isolated right cranial nerve VI palsy. Extraocular muscle dysfunction results from insults to the muscle itself or from lesions of the motor nerve innervating the muscle. In this case, the lesion responsible is a cranial nerve VI palsy.
Cranial nerve VI innervates the lateral rectus muscle, which is responsible for eye abduction, or temporal gaze. Patients with dysfunction of the sixth cranial nerve complain of horizontal, binocular diplopia. Impaired abduction often indicates an ipsilateral cranial nerve VI lesion.
The sixth cranial nerve arises from the pons and courses through the subarachnoid space until it ascends the clivus and enters the cavernous sinus before exiting to the lateral rectus muscle. Palsies of the sixth cranial nerve may result from lesions anywhere along the anatomic course of the nerve. The most common cause of isolated sixth cranial nerve palsy in adults is ischemic injury—most often related to hypertension and/or diabetes. This is particularly true for older adults. In younger adults and children, it often occurs as a post-viral manifestation.
Isolated cranial nerve VI palsies occurring in adults over 50 require workup for ischemic vascular diseases or temporal arteritis. In patients younger than 50, MRI imaging is necessary to rule out intracranial processes. The majority of cranial nerve VI palsies that arise from ischemic or idiopathic causes will resolve spontaneously over a course of several months.
In this case, the cranial nerve VI palsy was caused by cavernous sinus thrombosis secondary to extension of a pre-existing sinus infection. Contents of the cavernous sinus include cranial nerves III, IV, and VI; the ophthalmic and maxillary divisions of cranial nerve V; and the internal carotid artery. Cavernous sinus thrombosis is usually the result of the extension of dental, sinus, or orbital infections, with the most common causative organism being Staphylococcus aureus, followed by anaerobes, Streptococcus species, and fungi.
Headache is the most common presenting symptom of cavernous sinus thrombosis, with later complaints including fever and cranial nerve involvement. Cavernous sinus thrombosis is a medical emergency requiring aggressive antimicrobial therapy and early surgical involvement. Patients with sinus infections may require urgent debridement of infected sinuses by ear, nose, and throat surgeons. The role of anticoagulation in cavernous sinus thrombosis is somewhat controversial, though it may be implemented to prevent clot propagation.
Although it is somewhat unusual for patients with cavernous sinus thrombosis to present with a mononeuropathy instead of multiple cranial nerve deficits, cavernous sinus thrombosis should be suspected in any patient complaining of a unilateral headache and horizontal diplopia, particularly in the setting of a sinus or dental infection. TH