Hemifacial spasm (HFS) is a neurological condition characterized by involuntary muscle contractions on one side of the face. These spasms typically begin around the eye as subtle twitches before gradually spreading to affect the cheek, mouth, and sometimes the neck muscles on the same side. The contractions are unpredictable, persistent, and can range from mild to severe, often interfering with daily activities and quality of life. HFS is considered a chronic disorder, making reliable medical intervention necessary for management. Treatment involves addressing either the symptom directly or the underlying structural cause.
The Root Cause of Hemifacial Spasm
Understanding the origin of hemifacial spasm is necessary for understanding why certain treatments are effective. The condition is overwhelmingly classified as a neurovascular compression syndrome, meaning a blood vessel is pressing on a nerve. The facial nerve (Cranial Nerve VII) is compressed by an adjacent artery or, less commonly, a vein near its exit point from the brainstem.
This critical site of compression is called the root exit zone, where the nerve transitions from central to peripheral nervous system myelin. The pulsatile pressure from the blood vessel, typically the Anterior Inferior Cerebellar Artery (AICA) or Posterior Inferior Cerebellar Artery (PICA), damages the nerve’s protective sheath. This demyelination causes a short-circuiting effect, leading to the nerve becoming hyperexcitable and generating the erratic electrical signals that result in facial muscle spasms.
The primary form of HFS is caused by this vascular compression and accounts for the vast majority of cases. A small percentage of patients may have secondary HFS, where the spasms are caused by other factors like a tumor, a cyst, or multiple sclerosis. Chronic hypertension is also thought to contribute to the risk of primary HFS, as high blood pressure can lead to arterial vessel widening, increasing the likelihood of nerve contact.
Managing Spasms with Botulinum Toxin Injections
For most patients, Botulinum Toxin (BoNT) injections are the first-line and least invasive method to manage and stop the involuntary muscle contractions. This approach is symptomatic, meaning it treats the effect of the condition rather than the underlying cause. The toxin works by temporarily blocking the release of acetylcholine, a neurotransmitter that signals muscles to contract.
By injecting small, precise doses of the toxin into the affected facial muscles, the treatment induces localized, temporary muscle paralysis or weakening. This controlled weakening halts the uncontrolled spasms. The most common injection sites include the orbicularis oculi (around the eye), the frontalis (forehead), and muscles around the mouth and neck on the affected side.
The efficacy of BoNT injections is high, with success rates for symptom control ranging from 73% to over 98% of patients. Following an injection session, the therapeutic effect usually begins within three to six days. Relief is not permanent; the mean duration of symptom improvement is typically around 12 to 15 weeks (three to four months).
Because the nerve terminals eventually regenerate, the treatment must be repeated several times a year to maintain spasm control. The standard dose of Onabotulinumtoxin A for HFS is generally between 10 and 34 units per session, adjusted based on the severity and spread of the spasms.
While generally considered safe, the injections can produce temporary side effects related to the muscle-weakening action of the toxin. The most common temporary adverse effects include facial weakness or paresis, eyelid droop (ptosis), and dry eye. These side effects are mild and resolve naturally as the toxin’s effect wears off, generally within a few weeks.
Curative Treatment Through Microvascular Decompression
Microvascular Decompression (MVD) surgery represents the only known treatment that directly addresses and aims to cure the root cause of hemifacial spasm. This intricate neurosurgical procedure is performed under general anesthesia by a skilled neurosurgeon. The goal of MVD is to permanently separate the offending blood vessel from the facial nerve to relieve the destructive pulsatile compression.
The procedure involves making a small incision behind the ear and creating a small opening in the skull (a craniotomy) to access the facial nerve and the brainstem area. Once the vascular compression site is located, the surgeon carefully moves the artery away from the nerve. A small, inert surgical sponge—most commonly Teflon felt—is then placed between the nerve and the blood vessel to act as a permanent cushion, preventing re-compression.
MVD has a high success rate, with over 85% of patients experiencing complete, lasting relief from their spasms. Success rates have been reported as high as 91.6% after the initial surgery. Many patients experience the cessation of spasms immediately, while others notice a gradual resolution over a few days or weeks.
The recovery period for MVD is relatively short for an intracranial surgery; patients are typically discharged from the hospital within two to three days. Most individuals are able to return to their normal daily activities within two to four weeks. Although it is a highly effective procedure, MVD carries risks that must be considered.
Potential complications include a small risk of hearing loss on the side of the operation due to the proximity of the auditory nerve, reported in about 4.8% of cases. Transient facial weakness or palsy is also a possibility, though permanent facial paralysis is extremely rare, occurring in less than 1% of patients. The risk of the spasms recurring after a successful MVD is low, estimated at up to 10% of cases.