In a 38‑year‑old man with intermittent involuntary left facial muscle contractions, which is the most likely cause—herpes zoster reactivation, brainstem demyelination, microvascular compression of the facial nerve, pontine glioma, or stroke—and what MRI findings would be expected?

Hemifacial Spasm: Microvascular Compression is the Most Likely Cause

In a 38-year-old man with intermittent involuntary left facial muscle contractions (hemifacial spasm), microvascular compression of the facial nerve is by far the most likely etiology, and MRI should demonstrate a vascular loop (typically an ectatic artery) contacting the facial nerve at or near its root exit zone from the brainstem. 1, 2

Why Microvascular Compression is the Answer

The clinical presentation described—intermittent involuntary contractions rather than weakness or paralysis—is the hallmark of hemifacial spasm, not facial palsy. 1 This distinction is critical:

• Hemifacial spasm = unilateral hyperactivity/spasm of facial muscles 1
• Facial palsy = weakness or paralysis of facial muscles 1

The overwhelming majority of hemifacial spasm cases result from pulsatile vascular compression of the facial nerve (CN VII), specifically within the centrally (oligodendrocyte) myelinated portion of the nerve at the root exit zone. 1, 2 This occurs in 83-100% of cases on high-quality imaging. 2

The most common offending vessels are the posterior inferior cerebellar artery (PICA) or anterior inferior cerebellar artery (AICA), though vertebral or basilar arteries can also be causative. 3, 4, 5

Why the Other Options Are Wrong

Herpes Zoster Reactivation

• Herpes zoster (Ramsay Hunt syndrome) causes facial weakness/paralysis, not involuntary contractions or spasm 6
• It presents with vesicular rash, pain, and facial droop—not the intermittent spasms described here 6

Brainstem Demyelination

• Multiple sclerosis or other demyelinating lesions affecting the facial nucleus in the pons cause facial weakness, not spasm 1
• These lesions are typically accompanied by additional neurologic symptoms (diplopia, ataxia, sensory changes), which are not mentioned in this case 1
• While demyelination can rarely cause secondary hemifacial spasm, it represents a tiny minority of cases 4

Pontine Glioma

• Brainstem tumors cause facial weakness/paralysis, not spasm 1
• A pontine glioma in a 38-year-old would present with progressive neurologic deficits, cranial nerve palsies, and likely other brainstem signs 1
• Tumors in the cerebellopontine angle (schwannomas, meningiomas, epidermoid cysts) account for only 0.3-2.5% of hemifacial spasm cases 7

Stroke

• Brainstem or cortical infarction causes facial weakness, not spasm 1
• Isolated facial nerve palsy from stroke is rare and would present acutely with weakness, not intermittent contractions 1

Expected MRI Findings

The diagnostic imaging of choice is high-resolution MRI with 3D heavily T2-weighted sequences and MRA. 1, 2, 8 This protocol demonstrates:

• Vascular loop (typically an ectatic vessel) in direct contact with the facial nerve at the root exit zone from the brainstem 1, 2, 8
• The compression typically occurs at the pontomedullary junction where the facial nerve exits the brainstem 1
• Neurovascular contact is identified in 83-100% of cases on high-quality imaging 2
• 3T and volumetric imaging provide superior visualization of the facial nerve and surrounding perineural vascular plexus 1, 8

Important Imaging Caveats

• Both false-positive and false-negative studies occur—MRI findings should be considered supportive rather than diagnostic when selecting candidates for microvascular decompression 1, 2
• The imaging correlates well with surgical findings but must be interpreted in the clinical context 1, 2, 8
• High-resolution temporal bone CT is complementary to MRI for characterizing osseous anatomy, particularly useful for presurgical planning 1, 8

Clinical Algorithm for This Patient

1. Confirm the diagnosis clinically: Hemifacial spasm typically starts around the eye (orbicularis oculi) and progresses inferiorly to involve the cheek, mouth, and sometimes neck muscles 3

2. Order MRI brain with dedicated facial nerve protocol: 3D heavily T2-weighted sequences plus MRA to identify neurovascular compression 1, 2, 8

3. Exclude secondary causes: While microvascular compression is overwhelmingly likely, the MRI will also exclude cerebellopontine angle tumors, brainstem lesions, or temporal bone pathology 1, 2

4. Treatment planning: If vascular compression is confirmed and symptoms are bothersome, microvascular decompression surgery is the only curative treatment, with 77-86% immediate symptom resolution 3, 5