Home 5 Conditions 5 Hemifacial Spasm

Neurovascular Compression

Hemifacial Spasm

Involuntary twitching of one side of the face — not dangerous, but treatable and often curable.

In brief

Involuntary, repetitive twitching of the muscles on one side of the face
Caused by a blood vessel irritating the facial nerve
Almost always one-sided; can cause social and functional distress
Diagnosed clinically, with MRI to identify the offending vessel
Botulinum toxin gives relief; microvascular decompression can cure it

What is Hemifacial Spasm?

Hemifacial spasm (HFS) is a neurological condition characterised by involuntary, repetitive twitching or contraction of the muscles on one side of the face. These muscles are all supplied by the facial nerve (the seventh cranial nerve), and the spasms result from abnormal, spontaneous firing of this nerve. HFS is almost always unilateral (affecting one side only) and, whilst not dangerous to physical health, can cause significant social embarrassment, psychological distress, and interference with daily activities such as reading, driving, and communication. HFS is an uncommon condition, with a prevalence of approximately 14.5 per 100,000 in women and 7.4 per 100,000 in men.1 It tends to present in middle to older age, with an average age of onset in the late forties to early fifties. It is observed across all races, though a somewhat higher prevalence has been noted in Asian populations.²

What Causes Hemifacial Spasm?

In the vast majority of cases (more than 90%), HFS is caused by a blood vessel — most commonly a branch of the anterior inferior cerebellar artery (AICA), posterior inferior cerebellar artery (PICA), or vertebral artery — pressing against the facial nerve where it exits the brainstem.³ This is known as neurovascular conflict (NVC). The pulsatile compression of the blood vessel causes localised damage and irritation of the nerve, which leads to abnormal electrical activity and involuntary muscle firing. Less common causes include:

Tumours or cysts in the cerebellopontine angle (the space at the base of the brain near the brainstem) pressing on the facial nerve
Arteriovenous malformations (abnormal tangles of blood vessels)
Very rarely, a multiple sclerosis (demyelinating) plaque within the brainstem affecting the facial nerve

In a small number of cases, no underlying cause can be identified.

What are the Symptoms?

Hemifacial spasm typically begins with intermittent, painless twitching around one eye — most commonly the lower eyelid — which can sometimes be mistaken for a benign eyelid twitch (myokymia). Over time, the spasms tend to spread and become more frequent, eventually involving the cheek, the corner of the mouth, and occasionally the neck muscles on the affected side. Unlike a benign eyelid twitch, the spasms of HFS:

Tend to be progressive over months to years
Can cause involuntary closure of the eye, which may interfere with vision
Can persist during sleep, which is a characteristic feature that helps distinguish HFS from other movement disorders
Occasionally cause a mild aching discomfort on the affected side

The spasms are almost always confined to one side of the face. They begin on one side, and only very occasionally does the other side become involved as well; when this happens, the two sides twitch independently of one another rather than together — a feature that helps distinguish hemifacial spasm from blepharospasm, in which both eyes close at the same time.⁴

A helpful diagnostic clue is the “other Babinski sign” — a brief contraction of the frontalis muscle (forehead) when the lower facial muscles are activated — which is highly specific for HFS.⁵

Some patients also notice an associated clicking sound in the ear on the affected side during spasms, caused by the stapedius muscle (a tiny muscle in the middle ear also supplied by the facial nerve) contracting. A number of patients also experience altered hearing or a sense of fullness in the affected ear, reflecting the close relationship between the facial nerve and the nearby hearing (vestibulocochlear) nerve, which the same offending blood vessel can also affect.⁶

What Conditions can be Confused with Hemifacial Spasm?

Several other conditions can resemble HFS, and accurate diagnosis is important as their management differs significantly:

Blepharospasm — involuntary eye closure affecting both eyes simultaneously (not unilateral)
Facial tics — typically suppressible voluntary movements often associated with anxiety or habit; almost always bilateral
Bell’s palsy synkinesis — co-contraction of facial muscles following recovery from Bell’s palsy; the history of prior Bell’s palsy and the pattern of movement distinguishes this from true HFS
Facial myokymia — a benign, fine rippling movement of the eyelid, not involving other facial muscles; often associated with stress, fatigue, or caffeine
Oromandibular dystonia — involuntary jaw and lower face movements, typically bilateral

How is Hemifacial Spasm Diagnosed?

HFS is diagnosed by taking a careful history and examination, looking for characteristic patterns of facial movement. However, several investigations are routinely performed:

Magnetic Resonance Imaging (MRI)

An MRI of the brain is the most important investigation. Specialised high-resolution sequences allow the neurosurgeon to visualise the facial nerve at its exit zone from the brainstem and identify whether a blood vessel is compressing it. The other important sequence is an MR angiogram, which helps to define the blood vessel responsible for the compression. MRI is also important to exclude other causes of HFS such as tumour, arteriovenous malformation, or multiple sclerosis. The quality of MRI reporting is important, as false-negative results can lead to diagnostic delays.³ It is important to understand that HFS is fundamentally a clinical diagnosis. A small blood vessel lying close to the facial nerve is a common finding on MRI in people without any symptoms, so imaging serves to support the diagnosis and to plan surgery — not to make the diagnosis on its own.³

Electromyography (EMG) and Lateral Spread Response

Electromyography (EMG) records the electrical activity of the facial muscles and can demonstrate the characteristic abnormal firing pattern seen in HFS. A specific finding called the “lateral spread response” — where stimulation of one branch of the facial nerve produces an electrical response in a different branch — is highly specific for HFS and helps confirm the diagnosis.⁴ It is particularly useful when the clinical picture is atypical or the diagnosis is uncertain.

Hearing Assessment (Pure Tone Audiometry)

Because hemifacial spasm can be associated with subtle changes in hearing on the affected side, and because microvascular decompression carries a small risk to hearing, a baseline hearing test (a pure tone audiogram) is routinely arranged before surgery is considered. This documents hearing before any intervention and helps inform the decision to operate.⁶

CT Scanning

CT scanning is generally not used for the diagnosis or follow-up of HFS, but may be performed in specific circumstances to evaluate the surrounding bony anatomy.

How is Hemifacial Spasm Treated?

There are two established treatment options for HFS: botulinum toxin injections and surgical microvascular decompression. The appropriate treatment depends on the patient’s age, overall health, severity of symptoms, personal preferences, and the underlying cause. Both options should be discussed with your treating neurosurgeon.

Oral medications — a limited role. Several oral drugs, including carbamazepine, clonazepam, baclofen, and gabapentin, have been used in HFS. Their effectiveness is generally modest and often diminishes over time, so they are not a mainstay of treatment. They are most useful as a temporary measure, or for patients who are unable or unwilling to have botulinum toxin injections or surgery.³

Botulinum Toxin Injections — First-Line Treatment

Botulinum toxin (brand names include Botox and Dysport) is a purified protein that, when injected in small doses into the affected facial muscles, temporarily blocks the nerve signals causing the spasms. It does not treat the underlying nerve compression, but provides very effective symptom control. Botulinum toxin is the first-line treatment for most patients with HFS and is the preferred option for those who are older, have significant medical comorbidities, or who do not wish to undergo surgery. Large clinical studies have demonstrated marked to significant improvement in approximately 85–95% of patients treated with botulinum toxin.7 The injections are performed in a clinic setting, are well tolerated, and do not require an anaesthetic. In Australia, botulinum toxin is subsidised through the Pharmaceutical Benefits Scheme (PBS) for hemifacial spasm, which substantially reduces the cost to the patient, although some consultation or administration fees may still apply. Results typically last 3–4 months, after which repeat injections are required. Importantly, botulinum toxin controls the symptoms but does not correct the underlying blood-vessel compression — it is not a cure, and treatment generally needs to be continued long-term, often for life. Some patients also find that the benefit wears off sooner over time and require more frequent injections. Most patients can be maintained on a regular injection programme, with a very low risk of serious side effects. Common minor side effects include temporary localised bruising, mild drooping of the eyelid (ptosis), or a slight weakness of nearby muscles, all of which resolve completely between treatment cycles. Long-term studies covering more than 15 years of treatment have confirmed a sustained, consistent response with no evidence of significant long-term adverse effects.⁸

Microvascular Decompression — The Surgical Option

Microvascular decompression (MVD) is a surgical procedure that directly addresses the underlying cause of HFS — the blood vessel compressing the facial nerve at the brainstem. It is the only potentially curative treatment for HFS.

The operation is performed under general anaesthetic and involves making a small opening in the skull behind the ear (a retrosigmoid craniotomy). Under a surgical microscope, the facial nerve is identified where it leaves the brainstem, and the offending blood vessel is gently dissected free of the nerve. Where possible, a “transposition” technique is preferred — mobilising the vessel and holding it completely away from the nerve with a small piece of Teflon and tissue glue, and occasionally a tiny clip — rather than an “interposition” technique, in which padding is simply placed between the vessel and the nerve. This relieves the compression and allows the nerve to recover its normal function. Current evidence suggests that, for hemifacial spasm, the transposition technique achieves a higher rate of complete, lasting relief, although both approaches are effective and safe.⁹

Overall, approximately 90% of patients are cured of their spasms following MVD.10 The spasms do not always settle immediately: often they take several days to weeks, and sometimes up to three months, to resolve fully. If the spasms are still present at three months, the operation is regarded as having failed. Recurrence of HFS after initially successful MVD occurs in a small proportion of patients (approximately 2–4% over the long term).11 Once the spasms have resolved, ongoing botulinum toxin injections are no longer required.

As with any major operation within this region, adjacent to the brainstem and cranial nerves, MVD carries meaningful risks that must be carefully weighed against the benefits. The main risks discussed before surgery include:

Significant hearing loss on the operated side (approximately 2.5–5%)
Facial weakness — temporary (less than 5%) or, less commonly, permanent (approximately 1–2%)
Facial numbness (less than 1%)
Damage to the 9th or 10th cranial nerves, which can cause difficulty swallowing and, in the worst case, may require a temporary feeding tube (PEG) (less than 1%)
Infection, which is sometimes delayed by several months (1–2%)
CSF (cerebrospinal fluid) leak (1–2%)
Bleeding requiring a return to the operating theatre (less than 1%)
Brainstem injury — very rare (less than 1 in 1,000) but potentially serious, and may cause weakness, numbness, or difficulty with swallowing or speech

As with any operation performed under general anaesthetic, there are additional small risks, including blood clots in the legs or lungs, heart attack, stroke, a severe allergic reaction, and — very rarely — death.

MVD should preferably be performed by a neurosurgeon with experience in cerebrovascular or skull base surgery, at a centre with the appropriate operative expertise and intraoperative neurophysiological monitoring. During the operation this monitoring serves two purposes: the lateral spread response helps confirm that the nerve has been adequately decompressed and helps predict the outcome, and — just as importantly — auditory monitoring is used to help protect hearing on the side of surgery.⁴

MVD is most appropriate for patients who are significantly affected by their HFS and are seeking a long-term solution free from ongoing injections. Medical fitness for surgery — rather than age itself — is the key consideration: with careful selection, MVD can be carried out safely in older patients who are otherwise well. It is generally less suitable for those with significant medical comorbidities, or those whose symptoms are adequately controlled with botulinum toxin. The decision to proceed with surgery should always be made collaboratively between the patient and their neurosurgeon, with a clear and detailed discussion of the risks, benefits, and alternatives specific to the individual.

What to Expect After Surgery

Microvascular decompression is carried out under general anaesthetic as a planned hospital admission. Most patients spend the first night in an intensive care unit for close monitoring before being transferred to the ward, and are usually well enough to go home a few days later. Significant headache, nausea, vomiting, and unsteadiness (poor balance) are common in the first day or two and generally settle quickly. For the first week at home, patients will need someone to help care for them. The wound is closed with self-dissolving sutures, which are visible but should not be removed — including by the GP. We recommend seeing your GP about 7 to 10 days after surgery to check the wound and confirm that recovery is progressing normally. Most patients are reviewed in the rooms at around six weeks. Normal daily activities can usually be resumed within one to two weeks, but most people need at least six weeks off work, and sometimes longer.

What Happens if Hemifacial Spasm is Left Untreated?

HFS is not a life-threatening condition, and for patients who are well controlled on botulinum toxin injections or who have mild symptoms, conservative management is entirely appropriate. HFS does not shorten life expectancy and does not damage the brain. Without treatment, the condition tends to persist and may slowly worsen over time, though it can occasionally remain stable for long periods. The spasms often fluctuate and may ease for a time, but lasting spontaneous resolution is uncommon.⁷ For some patients — particularly those with mild or intermittent symptoms — choosing simply to monitor the condition, without active treatment, is an entirely reasonable approach.

References

Helpful links

Microvascular decompression (MVD) — procedure animation A short medical animation of how the operation works



Hemifacial Spasm — patient information sheet PDF · prepared by Mr Jeremy Russell

Download PDF

Content on this page is for education and information only and is not a substitute for advice from your doctor. Medically reviewed by Mr Jeremy Russell.