Facial Spasms in a Man Recently Released From the Hospital

Muthunivas Muthuraj; Shailesh Rajguru, DO


May 05, 2022

A TIA was also considered owing to this patient's acute presentation of vision changes and left temporal headache. Because a TIA is a strokelike condition involving a temporary blockage of blood flow to one of the cerebral arteries, its presentation can resemble that of a stroke.[4] Noncontrast CT should be ordered immediately to determine whether a patient is experiencing a stroke; this test is especially useful for determining whether a hemorrhagic stroke has occurred. The noncontrast CT findings will be unremarkable in a patient with a TIA because the blockage of blood flow in the cerebral arteries is temporary. Patients typically recover from these events within 1 hour and return to baseline function. Patients who have these events should be regularly monitored, however, because a history of a TIA increases the risk for stroke.[4] In view of this patient's acute headache, vision changes, and prior history of hypertension and smoking, an immediate noncontrast CT of the head was ordered upon admission to the emergency department to assess for stroke; however, the results were unremarkable.

To narrow the differential diagnoses in this case further, this patient's current and past medical history was evaluated. His history of hemifacial spasms, hypertension, and hypercholesterolemia did not appear to play a significant role in his acute presentation of headache and diplopia. However, these symptoms could be secondary to his type 2 diabetes, which can result in CN III palsy through a process called nonenzymatic glycosylation (NEG). In NEG, free amino groups of proteins are glycated because the patient is in a hyperglycemic state.[5] This results in the accumulation of glycated proteins in blood vessels and nerves, which is the main culprit in the microvascular and neuropathic changes that are seen among patients with diabetes.

Given that this patient was steadily recovering from his diplopic symptoms and had no other symptoms, CN III palsy was diagnosed clinically. On average, the annual incidence of CN III palsy is 4 per 100,000 population. Persons older than 60 years are at greater risk for CN III palsy; the incidence is 12.5 per 100,000. In persons younger than 60 years, the incidence of CN III palsy is lower: 1.7 per 100,000.[6] CN III palsy has a multitude of causes, including idiopathic, congenital, hemorrhagic, neoplastic, traumatic, and ischemic.[6] Diseases such as diabetes and hypertension are the most common systemic causes and can lead to ischemic changes in the blood supply of the cranial nerves innervating the eyes.

The CN III nucleus sits at the midbrain. The fibers of CN III travel through the interpeduncular fossa and pass between the posterior cerebral artery and the superior cerebellar artery to eventually reach the cavernous sinus. An aneurysm between these two arteries can often lead to CN III palsy.[6] Tumors within the cavernous sinus may also cause CN III palsy. From the cavernous sinus, the nerve enters the superior orbital fissure. Once in the superior orbital fissure, the nerve supplies the superior rectus, inferior rectus, medial rectus, inferior oblique, and levator palpebrae superioris muscles of the eyes. CN III also innervates the sphincter pupillae muscles, which allow the pupils to constrict or dilate.

Any changes in the blood supply or compression of the third cranial nerve can lead to CN III palsy. Clinical features of CN III palsy include ptosis, ocular deviation, pupillary dilation, and diplopia.[6] Figure 2 shows a different patient with CN III palsy. Note that this photograph is not representative of the patient in this case but illustrates how a complete CN III palsy presents. This image highlights the ptosis that is evident in the right eye, along with a slight ocular deviation and pupillary dilation. The patient's CN III palsy most likely was a result of diabetic ischemic changes; however, compression of the nerve could be a possibility as well owing to the pupillary dilation.

Figure 2.


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