Signs and Symptoms

Hemifacial spasm (HFS) is a facial nerve disorder characterized by episodic involuntary ipsilateral facial muscle contraction. Patients with HFS are typically acutely aware of a painless facial contracture. Half of the patient’s face is usually seen in constant, spastic motion.1,2 The spasms often start in the upper portion of the face and progress downward, increasing in involvement and frequency.1,2 The spasms are usually brief, only lasting seconds, but ongoing and often persistent during sleep. It may be severe enough to prevent eyelid opening. Patients are often predominantly concerned with cosmetic appearance.

Hemifacial spasm frequently affects individuals age 40 to 60.1 In one study of 230 patients, 6.5% had young-onset HFS and 21.7% had older onset HFS; the remaining patients in the study were uncategorized because onset took place during the classically recognized 40 to 60 age bracket. In young-onset HFS, the mean age of onset of symptoms was 26 years, with a range of six to 30 years. The average age of onset appears to be 45 to 46 years.3,4 Eighty percent of the cases occurred in women.

Genetic, anatomic or other unidentified factors are the most likely contributors to young-onset HFS, and hypertension may be a risk factor involved in late-onset HFS.1,2 One large study failed to identify a greater incidence associated with hypertension. Stress has been noted to be the main aggravating factor and sleep the prime relieving factor.4


The motor division of the seventh cranial nerve (CN VII) is responsible for delivering the voluntary motor innervations to the muscles of facial expression and to the stapedius muscle of the inner ear (helping to dampen loud sounds).5-10 Irritation by adjacent or direct infection, infiltration, inflammation or compression of CN VII nuclei or its fascicles can produce involuntary contracture of the affected region.1,2,11-20

Lesions capable of impinging on the nerve at this level include temporal bone fractures and infections, schwannomas, neuromas (cerebellopontine angle tumors) and vascular compressions. These injuries may concomitantly produce deficits in hearing, balance, tear production and salivatory flow.6,7

There is considerable evidence that primary hemifacial spasm (HFS) is, in almost all cases, related to microvascular compression of the facial nerve at its root within the exiting region of brainstem (root exit zone).16-19 The offending vessels include the vertebral arteries, the posterior inferior cerebellar arteries, the anterior inferior cerebellar arteries and, in some circumstances, an artery of uncertain origin.16-19

Clinical and electrophysiological features suggest the presence of mechanical influences at the level of the neural fibers, demyelinating pathology and functional changes in nuclear cells, which cause them to assume a posture of hyperactivity within the facial nucleus.9,12,16 Measured lateral spread responses (LSR) elicited by excessive stimulation of the facial nerve branches testify to the existence of these electrophysiological disturbances.11,12 Although vascular compression is accepted as a main producer of HFS, facial nucleus supersensitivity is also deemed to be a cause of emphatic HFS.16


Treatment of HFS contractures is aimed at addressing the underlying cause. Detailed evaluation is mandatory in all patients with newly acquired HFS or with essential blepharospasm, with or without apraxia. Magnetic resonance imaging (MRI) and three-dimensional magnetic resonance angiography (MRA) are proven techniques for identifying causes and predicting the prognosis of HFS.21,22 When HFS spasm is produced by neoplastic compression, the area can be surgically decompressed.2,13-16 Gamma knife radiosurgery, a relatively new modality, has been recently used in a patient with HFS secondary to an intracanalicular vestibular schwannoma.10,11 The resolution of the spasm and cessation of the tumor’s growth were achieved with a single session of gamma knife radiosurgery.10

Microvascular decompression (MVD) is potentially curative.23-25 In this procedure, a sponge or other barrier is placed between a compressing vessel and the facial nerve.12 In a study of 33 patients, LSR disappeared with vascular decompression in 23 patients, with no evidence of LSR upon surgical closure.12 The other 10 patients had evidence of LSR following the surgical conclusion. The authors considered 20 of the 23 LSR-absent patients clinically cured at the three-month follow-up. Three patients continued to present with mild/moderate spasm. At the 10-month follow-up, two of the remaining LSR-absent patients were free of spasm, with only one having recurrence.12 In contradistinction, seven of the 10 LSR-present patients exhibited cure at the three-month follow-up, with all 10 meeting the criteria for cure at the 10-month evaluation. This underscores the thinking that HFS not only results from mechanical pulsations of an elongated artery positioned against the CN VII root exit zone, but also that elements of demyelination and acquired neural hyperactivity are generated by the neurovascular compression.11,12 Today, MVD is about 8% to 90% successful in relieving HFS.24-25

In extreme cases, facial nerve decompression with exposure of the facial nerve from the brainstem to the parotid gland can be accomplished without injury to the nerve, tympanic membrane, external auditory canal or other structures.14 The procedure has achieved good results for patients with facial paralysis from Bell’s palsy, herpes zoster oticus, infection, hemifacial spasm, temporal bone fracture and tumors.14 Access occurs through the mastoid, middle cranial fossa and retrolabyrinthine fossa.14

Acupuncture has shown some benefit in these cases. Appropriate needling can markedly improve the blood supply to the vertebral basilar artery, increase the cerebral blood flow, relax the spasm of the vascular smooth muscles and create the effects of resuscitating and tranquilizing the mind, dredging channels and relieving spasm and pain.15

More recently, botulinum toxin A (Botox, Allergan) injection has been used to treat HFS.3,24,26-28 Botulinum toxin A injections have been seen to be safe and well tolerated, but the effects are transient and require increased subsequent dosing. True relief seems only to be effected by MVD, though botulinum toxin A injections have no adverse effect on this procedure if done first.28

Clinical Pearls

Chronic, slowly progressive HFS with the development of or conversion to facial nerve palsy suggests a space-occupying lesion or demyelination.

The presence or a parotid mass suggests tumor of the gland.

Tardive dyskinesia (late twitching secondary to exposure to antipsychotic medications) can produce symptoms similar to HFS.

Facial synkinesis, abnormal movements created by aberrant sprouting of axons after injury (similar to the “jaw wink” phenomenon), is a separate entity.

Hemifacial spasm should be differentiated from the more common benign eyelid myokymia, which presents as a continuous contraction of the lower eyelid only and is so minor that it is not typically grossly noticeable.

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2. Nakamura T, Osawa M, Uchiyama S. Arterial hypertension in patients with left primary hemifacial spasm is associated with neurovascular compression of the left rostral ventrolateral medulla. Eur Neurol 2007;57(3):150–5.

3. Wang L, Hu X, Dong H, et al. Clinical features and treatment status of hemifacial spasm in China. Chin Med J (Engl). 2014;127(5):845-9.

4. Batla A, Goyal C, Shukla G, Hemifacial spasm: clinical characteristics of 321 Indian patients. J Neurol. 2012;259(8):1561-5.

5. Gurwood AS. The eyelid and neuro-ocular disease. In: Blaustein BH (ed.) Ocular Manifestations of Neurologic Disease, Philadelphia, Mosby, 1996:127–51.

6. Gurwood AS, Tasca JM, Kulback E. A review of cranial nerve VII palsy with emphasis on Bell’s palsy. South J Optom 1996;14(3):13–17.

7. May M, Galetta S. The facial nerve and related disorders of the face. In: Glaser JS (ed.), Neurophthalmology (2nd ed.), Philadelphia, J. B. Lippincott Co., 1990:239–77.

8. Bajandas FJ, Kline LB. Seven Syndrome of the Seventh (Facial) Nerve. In: Bajandas FJ, Kline LB (eds.), Neuro-ophthalmology Review Manual (3rd ed.), Thorofare, NJ: Slack, 1988:151–6.

9. Jowi JO, Matende J, Macharia MI, et al. Hemifacial spasm: Case report. East Afr Med J 2006 ;83(7):401–4.

10. Peker S, Ozduman K, Kiliç T, et.al. Relief of hemifacial spasm after radiosurgery for intracanalicular vestibular schwannoma. Min Invas Neurosurg 2004;47(4):235–7.

11. Sindou MP. Microvascular decompression for primary hemifacial spasm. Importance of intraoperative neurophysiological monitoring. Acta Neurochir (Wien) 2005;147(10):1019–26.

12. Hatem J, Sindou M, Vial C. Intraoperative monitoring of facial EMG responses during microvascular decompression for hemifacial spasm. Prognostic value for long-term outcome: A study in a 33-patient series. Br J Neurosurg 2001;15(6):496–9.

13. James ML, Husain AM. Brainstem auditory evoked potential monitoring: When is change in wave V significant? Neurol 2005;2265(10):1551–5.

14. Pulec JL. Total facial nerve decompression: Technique to avoid complications. Ear Nose Throat J 1996;75(7):410–5.

15. Liu Z, Fang G. Mind-refreshing acupuncture therapy for facial spasm, trigeminal neuralgia and stubborn facial paralysis. J Tradit Chin Med 2004;24(3):191–2.

16. Suthipongchai S, Chawalparit O, Churojana A, et al. Vascular loop compressing facial nerve in hemifacial spasm: demonstrated by 3D-phase contrast magnetic resonance angiography in 101 patients. J Med Assoc Thai 2004;87(3):219–24.

17. Abbruzzese G, Berardelli A, Defazio G. Hemifacial spasm. Handb Clin Neurol. 2011;100:675-80.

18. Yaltho TC, Jankovic J. The many faces of hemifacial spasm: differential diagnosis of unilateral facial spasms. Mov Disord. 2011;26(9):1582-92.

19. Chiaramonte R, Bonfiglio M, D’Amore A, Chiaramonte I. Developmental venous anomaly responsible for hemifacial spasm. Neuroradiol J. 2013;26(2):201-7.

20. Harrison AR. Chemodenervation for facial dystonias and wrinkles. Curr Opin Ophthalmol 2003;14(5):241–5.

21. Tan EK, Chan LL, Lim SH, et al. Role of magnetic resonance imaging and magnetic resonance angiography in patients with hemifacial spasm. Ann Acad Med Singapore 1999;28(2):169–73.

22. Ho SL, Cheng PW, Wong WC, et al. A case-controlled MRI/MRA study of neurovascular contact in hemifacial spasm. Neurol 1999;53(9):2132–9.

23. Zhong J, Zhu J, Sun H, et al. Microvascular decompression surgery: surgical principles and technical nuances based on 4000 cases. Neurol Res. 2014 Mar 5:1743132814Y0000000344. [Epub ahead of print]

24. Rosenstengel C, Matthes M, Baldauf J, et al. Hemifacial spasm: conservative and surgical treatment options. Dtsch Arztebl Int. 2012;109(41):667-73.

25. Miller LE, Miller VM. Safety and effectiveness of microvascular decompression for treatment of hemifacial spasm: a systematic review. Br J Neurosurg. 2012;26(4):438-44.

26. Ababneh OH, Cetinkaya A, Kulwin DR. Long-term efficacy and safety of botulinum toxin a injections to treat blepharospasm and hemifacial spasm. Clin Experiment Ophthalmol. 2013 Jul 12. doi: 10.1111/ceo.12165. [Epub ahead of print].

27. Wu CJ, Shen JH, Chen Y, Lian YJ. Comparison of two different formulations of botulinum toxin A for the treatment of blepharospasm and hemifacial spasm. Turk Neurosurg. 2011;21(4):625-9.

28. Wang X, Thirumala PD, Shah A,et al. Effect of previous botulinum neurotoxin treatment on microvascular decompression for hemifacial spasm. Neurosurg Focus. 2013;34(3):E3.