325:
toxin is expensive, the cost of even prolonged courses of injections compares favourably with the cost of surgery. Patients with HFS should be offered a number of treatment options. Sometimes as a temporary measure, medical treatment can be offered to patients with very mild cases or those who are reluctant to have surgery or botulinum toxin injections. In young and fit patients, microsurgical decompression and botulinum injections should be discussed as alternative procedures. In the majority of cases, and especially in the elderly and the unfit, botulinum toxin injection is the treatment of first choice. Imaging procedures should be done in all unusual cases of hemifacial spasm and when surgery is contemplated.
276:
138:
280:
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283:
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112:
of the eyelid, which can result in forced closure of the eye which gradually spreads to the muscles of the lower part of the face (Typical form- See Image). In atypical form the spasms start in the cheekbone area and spreads to the eyelid. Ultimately, all the muscles on that side are affected, nearly
375:
of hemifacial spasm and location of the abnormality have been debated for more than a century. Surgical treatment for hemifacial spasm in the early 20th century included neurolysis (destruction of nerve tissue), stretching the facial nerve (seventh cranial nerve), and high-pressure irrigation of the
337:
The incidence of hemifacial spasm is approximately 0.8 per 100,000 persons. Hemifacial spasm is more prevalent among females over 40 years of age. The estimated prevalence for women is 14.5 per 100,000 and 7.4 per 100,000 in men. Prevalence for hemifacial spasm increases with age, reaching 39.7 per
358:
or infection. The study found that 77% of cases were primary and 23% secondary. The study also found that the two sets of patients shared a similar age at onset, male to female ratios, and similar affected side. In another study of 2050 patients who had presented with hemifacial spasm between 1986
329:
hyperhidrosis (excessive sweating). BTX-A was later approved for the treatment of excessive underarm sweating. This is technically known as severe primary axillary hyperhidrosis – excessive underarm sweating with an unknown cause which cannot be managed by topical agents (see focal hyperhidrosis).
324:
is safe and effective in the treatment of hemifacial spasm with success rates of between 76–100%. The injections are administered as an outpatient or office procedure. Although side effects do occur, these are never permanent. Repeated injections over the years remain highly effective. Whilst the
246:
Studies have shown that the most effective method of hemifacial spasm screening is MRI. In one study, only 25% of the CT scans showed the abnormality in hemifacial spasm patients, whilst more than half of the MRI imaging demonstrated a vascular anomaly. MRI imaging is recommended as the initial
328:
Patients with hemifacial spasm were shown to have decreased sweating after botulinum toxin injections. This was first observed in 1993 by Khalaf
Bushara and David Park in the first demonstration of nonmuscular use of BTX-A. Bushara further showed the efficacy of botulinum toxin in treating
299:
appears to be the most popular surgical treatment at present. Microvascular decompression relieves pressure on the facial nerve, which is the cause of most hemifacial spasm cases. Excellent to good results are reported in 80% or more cases with a 10% recurrence rate. In the present series
77:, then progresses up to the orbicularis oculi muscle in the eyelid as time progresses. The most common form is the typical form, and atypical form is only seen in about 2–3% of patients with hemifacial spasm. The incidence of hemifacial spasm is approximately 0.8 per 100,000 persons.
288:
Endoscope-assisted microvascular decompression in hemifacial spasm with a teflon bridge. Source: Rhomberg, T., Eördögh, M., Lehmann, S. et al. Endoscope-assisted microvascular decompression in hemifacial spasm with a teflon bridge. Acta
Neurochir 166, 239 (2024).
279:
415:
Additional advances in understanding the etiology and improving treatments for hemifacial spasm did not occur until the mid-seventies. In 1977, 47 cases of hemifacial spasm underwent microvascular decompression of the facial nerve using the
214:
in genes related to vascular change causing compression of blood vessels did not show an association with hemifacial spasm. Clarifying the role of genetic susceptibility in hemifacial spasm may help to better understand the
300:
approximately 10% had previously failed surgery. Serious complications can follow microsurgical decompressive operations, even when performed by experienced surgeons. These include cerebellar haematoma or swelling,
814:
Caces F; Chays A; Locatelli P; Bruzzo M; Epron JP; Fiacre E; Magnan J (1996). "Neuro-vascular decompression in hemifacial spasm: anatomical, electrophysiological and therapeutic results apropos of 100 cases".
73:
area. The reverse process of twitching occurs in atypical hemifacial spasm; twitching starts in orbicularis oris muscle around the lips, and buccinator muscle in the cheekbone area in the
845:
Lee SH; Rhee BA; Choi SK; Koh JS; Lim YJ (2010). "Cerebellopontine angle tumors causing hemifacial spasm: types, incidence, and mechanism in nine reported cases and literature review".
454:
compression of the facial nerve was the primary cause of hemifacial spasm, and proposed a specific region of the facial nerve where the effects of longstanding compression results in
125:
at the spot where it leaves the patient's brain stem, sometimes there is no known cause. When the affected individual is younger than 40, doctors suspect an underlying cause such as
1119:
Piatt JH; Wilkins RH (1984). "Treatment of tic douloureux and hemifacial spasm by posterior fossa exploration: therapeutic implications of various neurovascular relationships".
187:
is accepted to be the general cause of hemifacial spasm. Less than 1% of cases are caused by tumor. Hemifacial spasm is much more common in some Asian populations.
312:
and intracerebral infarction (blockage of blood flow to the brain). Death or permanent disability (hearing loss) can occur in 2% of patients of hemifacial spasm.
1602:
1287:
Tan E-K; Fook-Chong S; Lum S-Y; Lim E (16 January 2004). "Botulinum toxin improves quality of life in hemifacial spasm: validation of a questionnaire (HFS-30)".
108:
The first sign of hemifacial spasm is typically muscle movement in the patient's eyelid and around the eye. It can vary in intensity. The intermittent
1598:
704:
267:(an anticonvulsant drug). Microsurgical decompression and botulinum toxin injections are the current main treatments used for hemifacial spasm.
1631:
168:
The third theory or "Kindling theory" involves increased excitability of the facial nerve nucleus due to feedback from a damaged facial nerve.
227:
There are several tests available to diagnose a case of hemifacial spasm. Diagnosis begins with a complete neurological exam, including an
1343:
113:
all the time. This sometimes causes the mouth to be pulled to the side. Experts have linked hemifacial spasm to facial nerve injury,
771:
Jarrahy R; Cha ST; Eby JB; Berci G; Shahinian HK (2002). "Fully endoscopic vascular decompression of the glossopharyngeal nerve".
891:
Yaltho TC; Jankovic J (1 August 2011). "The many faces of hemifacial spasm: differential diagnosis of unilateral facial spasms".
485:
231:(EMG: a test that measures and records electrical activity generated in muscle at rest and in response to muscle contraction),
184:
320:
Observational data from studies (the updated review in 2020 did not find any randomized controlled trials) indicates that
180:
338:
100,000 for those aged 70 years and older. One study divided 214 hemifacial patients based on the cause of the disease:
664:"Etiology and definitive microsurgical treatment of hemifacial spasm. Operative techniques and results in 47 patients"
635:
385:
149:
Three theories exist to explain the facial nerve dysfunction found in hemifacial spasm. The first proposed theory is
360:
153:
transmission, which is electrical activity crossing from one demyelinated neuron to another resulting in a false
424:) to be located at the root exit zone of the facial nerve in all cases. The root exit zone is where the central
1195:
Duarte GS; Rodrigues FB; Castelão M; Marques RE; Ferreira J; Sampaio C; Moore AP; Costa J (November 19, 2020).
1156:"Serious complications of microvascular decompression operations for trigeminal neuralgia and hemifacial spasm"
211:
377:
172:
1606:
1457:
Auger RG; Whisnant JP (1990). "Hemifacial spasm in
Rochester and Olmsted County, Minnesota, 1960 to 1984".
708:
296:
232:
1252:
Loeser JD; Chen J (1982). "Hemifacial spasm: treatment by microsurgical facial nerve decompression".
1568:
Jannetta PJ (1975). "Trigeminal neuralgia and hemifacial spasm--etiology and definitive treatment".
239:(CT scan: a type of x-ray that uses a computer to make pictures of structures inside the head), and
100:, or it may have no apparent cause. Individuals with spasm on both sides of the face are very rare.
58:
308:(ischemic stroke resulting from a disturbance in the blood vessels supplying blood to the brain),
934:
Zappia JJ; Wiet RJ; Chouhan A; Zhao JC (1997). "Pitfalls in the diagnosis of hemifacial spasm".
446:
of the root exit zone demonstrated degeneration of axons, denuded axis cylinder and interrupted
350:
hemifacial spasm, where the patients had peripheral facial palsy or nerve lesion due to tumors,
371:
The earliest descriptions about hemifacial spasm is by
Shultze in 1875 and Gowers in 1899. The
343:
195:
620:
Fukushima T (1995). "Microvascular decompression for hemifacial spasm: Result in 2890 cases".
176:
27:
417:
8:
1470:
1070:"Endoscope-assisted microvascular decompression in hemifacial spasm with a teflon bridge"
305:
236:
31:
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309:
235:(MRI: a test that uses magnetic waves to make pictures of structures inside the head),
199:
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38:) on one side (hemi-) of the face (-facial). The facial muscles are controlled by the
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243:(an x-ray exam of the blood vessels when they are filled with a contrast material).
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228:
62:
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114:
1330:
Wang A; Jankovic J (1998). "Hemifacial spasm: clinical findings and treatment".
206:, and except for a younger age at onset, the clinical features overlap with the
190:
Several families with hemifacial spasm have been reported, suggesting a genetic
1086:
1067:
982:
Lorentz IT (April 1995). "Treatment of hemifacial spasm with botulinum toxin".
751:
734:
680:
663:
548:
498:
1510:
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171:
It is generally accepted as compression of the facial nerve by vessels of the
46:
and exits the skull below the ear where it separates into five main branches.
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351:
290:
264:
162:
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10.1002/(SICI)1097-4598(199812)21:12<1740::AID-MUS17>3.0.CO;2-V
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93:
39:
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707:. National Institute of Neurological Disorders and Strokes. Archived from
591:
583:
556:
1194:
1038:
689:
380:. The medical regimens of that time involved injection of the nerve with
247:
screening procedure in the assessment of patients with hemifacial spasm.
240:
81:
49:
This disease takes two forms: typical and atypical. In typical form, the
702:
207:
203:
904:
1025:
Alexander GE; Moses H (1982). "Carbamazepine for hemi facial spasm".
425:
301:
121:. Although the most frequent cause is a blood vessel pressing on the
70:
43:
661:
137:
88:
women more frequently. Hemifacial spasm is much more common in some
570:
Ryu H; Yamamoto S; Miyamoto T (1998). "Atypical hemifacial spasm".
451:
405:
372:
191:
161:
at the facial nerve root end zone secondary to compressive damage/
813:
401:
397:
381:
154:
85:
933:
638:. National Institute for Neurological Disorders and Stroke. 2018
80:
This disorder occurs in both men and women, although it affects
1494:"A comparative study of primary and secondary hemifacial spasm"
1286:
447:
443:
435:
263:
Mild cases of hemifacial spasm may be managed with sedation or
61:. As time progresses, it spreads to the whole lid, then to the
54:
1068:
T. Rhomberg; M. Eördögh; S. Lehmann; H.W.S. Schroeder (2024).
1491:
662:
Jannetta PJ; Abbasy M; Maroon JC; Ramos FM; Albin MS (1977).
455:
450:. The results of the experiment strengthened the theory that
432:
118:
109:
97:
50:
35:
770:
535:
Jannetta PJ (1998). "Typical or atypical hemifacial spasm".
428:
393:
158:
89:
74:
844:
179:
by a dolichoectatic (a distorted, dilated, and elongated)
569:
735:"Hemifacial Spasm - A Reversible Pathophysiologic State"
1603:
National
Institute of Neurological Disorders and Stroke
1197:"Botulinum toxin type A therapy for hemifacial spasm"
420:. The results illustrated nerve-vessel conflicts (or
346:
in the facial nerve at the end of the brainstem; and
304:
infarction (blood vessel of the brain stem blocked),
1456:
1414:Kemp LW; Reich SG (June 2004). "Hemifacial spasm".
1375:"Hemifacial spasm and involuntary facial movements"
1372:
1024:
890:
255:There is no known way to prevent hemifacial spasm.
1118:
202:pattern of inheritance in these families with low
157:. The second theory involves abnormal activity of
1533:Wilkins RH (1991). "Hemifacial spasm: a review".
1153:
732:
42:(seventh cranial nerve), which originates at the
1623:
1329:
1413:
1251:
1280:
657:
655:
653:
481:"Hemifacial spasm: a neurological perspective"
478:
270:
703:Office of Communications and Public Liaison.
1561:
1567:
1201:The Cochrane Database of Systematic Reviews
650:
619:
534:
530:
528:
526:
359:and 2009, only nine cases were caused by a
342:hemifacial spasm, where the patients had a
1532:
1492:Colosimo C; Bologna M; Lamberti S (2006).
981:
615:
613:
611:
609:
291:https://doi.org/10.1007/s00701-024-06142-7
92:populations. It may be caused by a facial
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1228:
1171:
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1085:
977:
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973:
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884:
750:
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705:"NINDS Hemifacial Spasm Information Page"
679:
506:
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274:
136:
30:characterized by irregular, involuntary
606:
486:Journal of Korean Neurosurgical Society
1624:
970:
881:
840:
838:
723:
474:
472:
470:
198:in some cases. There appears to be an
1632:Extrapyramidal and movement disorders
766:
764:
762:
431:insulation of the nerve ends and the
103:
1471:10.1001/archneur.1990.00530110095023
1289:Journal of the Neurological Sciences
628:
185:posterior inferior cerebellar artery
1599:"Hemifacial Spasm Information Page"
835:
773:The Journal of Craniofacial Surgery
636:"Hemifacial Spasm Information Page"
624:. New York: McGraw Hill: 1133–1145.
467:
181:anterior inferior cerebellar artery
96:, compression by a blood vessel, a
13:
1605:. October 11, 2011. Archived from
1591:
759:
388:, application of toxic compounds (
315:
14:
1643:
404:) as well as medications such as
1373:Tan NC; Chan LL; Tan EK (2002).
1266:10.1227/00006123-198308000-00006
1173:10.1227/00006123-198802000-00012
1133:10.1227/00006123-198404000-00012
984:Journal of Clinical Neuroscience
948:10.1097/00005537-199704000-00007
785:10.1097/00001665-200201000-00021
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1485:
1450:
1407:
1366:
1323:
1245:
1188:
1147:
1112:
1061:
1018:
927:
817:Rev Laryngol Otol Rhinol (Bord)
807:
361:cerebellopontine angle syndrome
332:
212:single-nucleotide polymorphisms
175:. In detail compression of the
1213:10.1002/14651858.CD004899.pub3
696:
563:
1:
461:
258:
250:
1547:10.1016/0090-3019(91)90087-P
1154:Hanakita J; Kondo A (1988).
996:10.1016/0967-5868(95)90005-5
733:Gardner WJ; Sava GA (1962).
440:The Obersteiner-Redlich zone
222:
65:muscle around the lips, and
53:usually starts in the lower
7:
297:Microvascular decompression
271:Microvascular decompression
145:(The Seventh Cranial Nerve)
10:
1648:
1087:10.1007/s00701-024-06142-7
752:10.3171/jns.1962.19.3.0240
681:10.3171/jns.1977.47.3.0321
549:10.3171/jns.1998.89.2.0346
499:10.3340/jkns.2007.42.5.355
366:
233:magnetic resonance imaging
1511:10.1001/archneur.63.3.441
1428:10.1007/s11940-004-0009-4
1416:Curr Treat Options Neurol
1301:10.1016/j.jns.2004.01.010
859:10.1007/s00701-010-0796-1
479:Kong D-S; Park K (2007).
438:begins, this is known as
378:lactate ringer's solution
363:, an incidence of 0.44%.
132:
59:orbicularis oculi muscle
739:Journal of Neurosurgery
668:Journal of Neurosurgery
537:Journal of Neurosurgery
1392:10.1093/qjmed/95.8.493
386:electrical stimulation
293:
146:
1570:Trans Am Neurol Assoc
847:Acta Neurochir (Wien)
622:Neurovascular Surgery
584:10.1007/s007010050233
287:
210:cases. Evaluation of
177:seventh cranial nerve
173:posterior circulation
140:
28:neuromuscular disease
1609:on December 28, 2011
1074:Acta Neurochirurgica
1039:10.1212/wnl.32.3.286
418:operating microscope
711:on 28 December 2011
306:cerebral infarction
237:computed tomography
32:muscle contractions
16:Neurologic disorder
1535:Surgical Neurology
893:Movement Disorders
436:axonal myelination
310:subdural haematoma
294:
200:autosomal dominant
147:
127:multiple sclerosis
104:Signs and symptoms
1465:(11): 1233–1234.
1338:(12): 1740–1747.
905:10.1002/mds.23692
853:(11): 1901–1908.
578:(11): 1173–1176.
390:nitrate of silver
285:
219:of this disease.
67:buccinator muscle
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1332:Muscle and Nerve
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1320:
1295:(1–2): 151–155.
1284:
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1242:
1232:
1207:(11): CD004899.
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936:The Laryngoscope
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899:(9): 1582–1592.
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433:peripheral nerve
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229:electromyography
63:orbicularis oris
20:Hemifacial spasm
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1592:Further reading
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322:botulinum toxin
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316:Botulinum toxin
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1541:(4): 251–277.
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1504:(3): 441–444.
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1422:(3): 175–179.
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1385:(8): 493–500.
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1260:(2): 141–146.
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1166:(2): 348–352.
1146:
1127:(4): 462–471.
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1033:(3): 286–287.
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990:(2): 132–135.
969:
942:(4): 461–465.
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834:
823:(5): 347–351.
806:
758:
745:(3): 240–247.
722:
695:
674:(3): 321–328.
649:
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572:Acta Neurochir
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543:(2): 346–347.
522:
493:(5): 355–362.
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376:nerve with
344:compression
241:angiography
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1613:January 6,
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462:References
259:Treatments
251:Prevention
208:idiopathic
204:penetrance
75:lower face
1576:: 89–91.
1221:1469-493X
1027:Neurology
408:or other
348:secondary
302:brainstem
223:Diagnosis
110:twitching
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444:Biopsies
406:Dilantin
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373:etiology
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151:ephaptic
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