Hemifacial Spasm

Our Specialists for Hemifacial Spasm

Hemifacial spasm is a high-volume, high-stakes operation: the facial nerve sits millimeters from the hearing nerve and the brainstem, and the difference between a cure and a complication comes down to microsurgical experience and intraoperative monitoring. The UChicago team performs microvascular decompression with real-time brainstem auditory and lateral spread response monitoring on every case.

Peter Christian Warnke, M.D.

Section Chief, Functional Neurosurgery & Epilepsy

Dr. Warnke is an international leader in functional neurosurgery and has performed over 6,000 stereotactic surgeries and more than 3,000 brain tumor surgeries. He is only the second neurosurgeon worldwide to perform laser hemispherotomy, and he has completed over 400 laser ablation surgeries since arriving at UChicago. He is funded by four NIH grants including the BRAIN Initiative, and he directs the NAUTILUS trial for thalamic stimulation in drug-resistant epilepsy. Dr. Warnke directs functional and stereotactic neurosurgery at UChicago and is one of the surgeons who performs microvascular decompression for hemifacial spasm with continuous brainstem auditory and lateral spread response monitoring — the same technique pioneered by Jannetta and validated in large long-term series (J Neurosurg, 1995). If you have hemifacial spasm and you're considering surgery at UChicago, he is likely your surgeon.

Peleg Horowitz, M.D., Ph.D.

Co-Director, Pituitary & Neuroendocrine Disorders Program

Dr. Horowitz is a skull base and neuro-oncology surgeon who also serves as Director of Quality and Associate Program Director for the Neurological Surgery residency. His laboratory research has identified novel genes driving meningioma and pediatric glioma formation, with work published in Nature Genetics and PNAS, and is funded by the DoD Neurofibromatosis Research Program. He holds a PhD in neuroscience from Northwestern and completed residency at Brigham and Women's/Boston Children's with a skull base fellowship at MD Anderson. Dr. Horowitz is a skull-base and microsurgical neurosurgeon at UChicago whose practice includes neurovascular compression syndromes at the cerebellopontine angle, where millimeter-level dissection around the facial and vestibulocochlear nerves is the whole ballgame. For hemifacial spasm patients, his focus is on a complete decompression with hearing preservation and a single, definitive operation.

What Is Hemifacial Spasm?

Hemifacial spasm is a condition in which the muscles on one side of your face start contracting on their own — without warning, without your control, and often without any obvious trigger. It usually begins as a subtle flutter around the eye, and over months to years it spreads downward to involve the cheek, the corner of the mouth, and sometimes the platysma muscle in the neck.

Unlike a tic, you cannot suppress it. Unlike a facial tremor, it doesn't go away when you relax. And unlike Bell's palsy or stroke, the face isn't weak — it's overactive. The twitching often gets worse with fatigue, stress, or concentration, and it can continue even when you sleep.

Hemifacial spasm is uncommon but not rare — population studies estimate roughly 11 cases per 100,000 people, with women affected about twice as often as men, and most patients are diagnosed between ages 40 and 70. It rarely goes away on its own, but it is treatable, and in many cases it is curable.

The reason the face is twitching is almost always the same: somewhere deep near the brainstem, a small blood vessel is pulsing against the facial nerve (cranial nerve VII) at the exact spot where the nerve leaves the brainstem — an area called the root exit zone. Each pulse slowly wears away the nerve's insulation. Once the insulation is thin enough, the electrical signals inside the nerve start short-circuiting, and the muscles of the face fire when they shouldn't.

What Does It Feel Like?

Hemifacial spasm follows a fairly predictable pattern. In nearly every patient, it starts small and gets bigger — both in the area of face involved and in the intensity of the spasms.

Early symptoms

• Intermittent twitching of the lower eyelid on one side — often mistaken for fatigue or caffeine
• Brief, involuntary closure of the eye on the affected side
• Twitching that comes and goes over days or weeks, then becomes more frequent

As it progresses

• The spasms spread downward to the cheek, the corner of the mouth, and the chin
• Sustained contractions that pull the mouth sideways or force the eye shut for several seconds at a time
• Twitching that continues during sleep — a clue that distinguishes hemifacial spasm from a simple tic
• Fatigue, bright light, reading, public speaking, and stress often make it worse
• Some patients develop a clicking sound in the ear on the affected side (from contraction of the stapedius muscle, which is also supplied by CN VII)
• Mild weakness of the face between spasms in long-standing cases

Hemifacial spasm is almost always one-sided. If both sides of your face are twitching, or if the twitching jumps from one side to the other, the diagnosis is probably something else — blepharospasm, a facial tic disorder, or a movement disorder — and your workup will look different.

How Is It Diagnosed?

Hemifacial spasm is primarily a clinical diagnosis — an experienced neurologist or neurosurgeon can usually recognize it on sight, especially if they can watch the spasms in the office. But imaging and electrical testing matter, because they confirm the mechanism and rule out other causes.

High-resolution MRI

We order a dedicated MRI of the brain with thin-slice sequences through the brainstem — specifically high-resolution T2-weighted imaging (CISS or FIESTA) combined with MR angiography. These sequences are fine enough to show the facial nerve as it exits the brainstem and to identify the specific artery pressing on it. In most patients the culprit is the anterior inferior cerebellar artery (AICA), though the posterior inferior cerebellar artery (PICA) or vertebral artery can also be responsible. MRI also rules out the rarer secondary causes — a small tumor, an AVM, multiple sclerosis, or a post-Bell's-palsy change — that can mimic hemifacial spasm.

Electromyography (EMG) and the lateral spread response

In selected cases we confirm the diagnosis electrically. When the facial nerve is normal, stimulating one branch (for example, the branch to the forehead) produces a response only in the muscles that branch supplies. In hemifacial spasm, the signal "spreads" abnormally to muscles supplied by a different branch — a phenomenon called the lateral spread response (LSR). LSR is highly specific to hemifacial spasm, and it becomes one of the most important tools we use during surgery.

Ruling out mimics

Before we commit to any treatment, we make sure we're treating the right problem. Blepharospasm (bilateral eyelid spasm), facial tics, focal dystonia, post-facial-palsy synkinesis, and psychogenic facial movements can all look similar at first glance. A careful history and exam — combined with MRI and EMG when needed — almost always sorts them out.

How Is It Treated?

There are two treatments for hemifacial spasm that actually work: botulinum toxin injections and microvascular decompression surgery. Everything else — anticonvulsants, muscle relaxants, acupuncture — has been tried and found wanting. The choice comes down to whether you want to manage the symptom or fix the cause.

Botulinum toxin — a bridge, not a cure

Small injections of botulinum toxin type A (Botox, Dysport, Xeomin) into the overactive muscles will quiet the spasms for roughly three to four months at a time. It works in about 85-95% of patients and is extremely safe. For patients who aren't ready for surgery, who can't have surgery, or who want to see how things evolve, it is an excellent option.

But botulinum toxin has important limits. It wears off. It requires lifetime injections every few months. Side effects — temporary lid droop, weakness of the corner of the mouth, dry eye — are common. And crucially, it doesn't fix the underlying problem: the artery is still pulsing against the nerve, and the nerve continues to deteriorate over the years. For a younger patient with many decades ahead of them, botulinum toxin is a holding pattern, not a destination.

Microvascular decompression — the curative operation

Microvascular decompression (MVD) is a microsurgical procedure that addresses the cause directly: we find the offending blood vessel, lift it off the facial nerve, and place a small Teflon pad between them so it can never touch again. The operation was pioneered in the 1960s and 70s by Peter Jannetta at the University of Pittsburgh, whose landmark 1995 series of 782 operations established it as a safe, definitive cure for hemifacial spasm.

Here's what happens the day of surgery:

• You're placed under general anesthesia and positioned on your side. A small patch of hair is shaved behind the ear.
• A roughly silver-dollar-sized opening is made in the bone behind the ear — a retromastoid craniotomy.
• Using an operating microscope, the surgeon gently opens the arachnoid membrane and works along the cerebellum to reach the facial nerve at the brainstem.
• The offending artery — usually AICA, sometimes PICA or a small vein — is identified and carefully mobilized off the nerve.
• A small piece of shredded Teflon felt is tucked between the vessel and the nerve. The vessel keeps its normal position and blood flow; it just no longer touches the nerve.
• The bone and scalp are closed. Most patients go home in 2-3 days.

Intraoperative monitoring — the reason experience matters

Every hemifacial spasm operation at UChicago is done with continuous neurophysiological monitoring. Two signals matter most:

• Brainstem auditory evoked responses (BAER) — we stimulate the ear with clicks and watch the electrical response travel up the hearing nerve and brainstem. Any change warns us to adjust retraction or approach before hearing is lost.
• Lateral spread response (LSR) — the same abnormal electrical signal used to confirm the diagnosis. When the offending vessel is successfully lifted off the facial nerve, the LSR disappears in real time on the monitor. It is the closest thing in cranial-nerve surgery to a "cure confirmed" signal from the operating room.

Stereotactic radiosurgery?

Unlike trigeminal neuralgia, hemifacial spasm is not a good target for Gamma Knife or other stereotactic radiosurgery. Radiation to the facial nerve carries a meaningful risk of facial weakness, and the published results don't match what MVD achieves. Botulinum toxin remains the non-surgical option of choice.

What Are the Outcomes?

Microvascular decompression for hemifacial spasm is one of the most effective operations in functional neurosurgery. Across decades and multiple centers, the data are remarkably consistent: the operation works, it lasts, and in experienced hands it is safe.

A few things are worth emphasizing. First, the cure is durable: Barker and Jannetta's long-term series followed patients for up to 20 years and found that virtually all failures declared themselves within the first two years. If you're spasm-free at two years, you are very likely spasm-free for life. Second, the outcomes are strongly correlated with surgeon volume and the use of intraoperative monitoring. The published complication rates above come from high-volume centers; results at low-volume hospitals are not the same. Third, botulinum toxin and MVD are complementary, not competing: many patients use botulinum toxin for a year or two while they decide about surgery, and it does not affect MVD results.

If you have hemifacial spasm and you are otherwise healthy, the expected outcome at a center like UChicago is a one-time operation that ends the twitching for good.

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