Craniofacial Muscles

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16 Spastic Facial Muscle Disorders313carbamazepine, baclofen, and clonazepam have been found to be useful in smallnumbers of patients, but have generally proven much less effective than BoNTinjections or surgical decompression in controlling the spasms in both the typicaland post-paralytic form.16.9.5.3 Surgery(a) Neurosurgical decompression ( MVD , Janetta i ): Placing a sponge prosthesissuch as expanded polytetra fl uoroethylene (ePTFE, Gore-Tex ® ), between thefacial nerve and the offending vessel to prevent future compression was fi rstsuccessfully demonstrated by Janetta ( 1983 ). The reported success rate for thisprocedure varies and ranges from 50–90%. Other surgical options, such asorbicularis myectomy, CNVII neurectomy, crushing the facial nerve at its exitfrom the stylomastoid foramen, percutaneous fractional thermolysis, alcoholinjections, and anastomosis of the facial nerve with the CNXI or CNX11 arerarely indicated because of high complication rates, limited bene fi t, and onlyprovide temporary relief.Although MVD of CNVII may be curative in hemifacial spasm and produce betterspasm reduction compared to other surgical treatments, there is always an operativerisk. This was estimated at 2% (Jannetta 1983 ; Jannetta et al. 1977 ) with permanentsequelae: facial paralysis, deafness, or vestibular disorders, which aremore debilitating than the facial spasm. Reported potential complications includeinfection in 1%, hematoma in 0.5%, CSF leak in 3%, facial nerve palsy in 1.4%,ipsilateral hearing loss in 0.86%, and stroke in less than 0.5% (Kalkanis et al.2003 ). Therefore, it seems reasonable to treat patients fi rst with BoNT injectionsand resort to surgery only if these injections fail or if the patient is not satis fi edwith the results.16.9.6 Other Precipitating FactorsAberrant Regeneration of the Facial Nerve (Facial synkinesia , Facial nerve misdirection, Post-Bell ’s palsy syndrome ): If the facial nerve is damaged, it might regenerateaberrantly, with misdirection to other facial muscles on the ipsilateral side orwith cross-innervation to the contralateral side. The abnormal regeneration of CNVIIcan result in synkinesis of facial muscles, which in turn can cause unwanted facialmovements during normal facial expressions (Osako and Keltner 1991 ) . The abnormalsynkinetic innervation can develop after facial palsy or facial nerve injury. Itcauses unilateral synkinetic facial movements mimicking blepharoptosis, orbicularismyokymia, or hemifacial spasm. Hemifacial spasm is often accompanied by aberrant
314 J. Park et al.regeneration because the irritation at the facial nerve root causing hemifacial spasmcan evoke nerve injury and consequently aberrant regeneration (Nerad et al. 2008 ) .The aberrant regeneration also can result, albeit rarely, as a primary phenomenonfrom a slow-growing tumor compressing or in fi ltrating the facial nerve.The abnormal movements in hemifacial spasm are seen most commonly in themiddle-aged but can occur in childhood. Abnormal reinnervation patterns can beginseveral months after an acute facial palsy as motor function recovers. It is mostcommonly manifested as ipsilateral narrowing of the palpebral fi ssure with movementsof the mouth such as smiling, chewing, and speaking. In addition, uncontrolledtearing when eating or in anticipation of food (crocodile tears) occurs whennerve fi bers destined to supply the salivary glands are misdirected to the lacrimalgland. Abnormal sweating of face while eating (gustatory sweating or Frey syndrome)can be seen in the parotid gland area, which is caused by aberrant fi bersinnervating sweat glands.BoNT injection provides reasonably effective control for synkinetic facialspasms, and the treatment regimen is similar to that of the typical form of hemifacialspasm (Putterman 1990 ; Armstrong et al. 1996 ) . BoNT injection into the lacrimalgland may help reduce or prevent involuntary tearing (Boroojerdi et al. 1998 ) .16.10 Myokymia and NeuromyotoniaMyokymia is the spontaneous, fi ne fascicular contractions of muscle in the absenceof muscular atrophy or weakness. Facial myokymia is characterized by small, continuousunilateral contractions of the facial muscles. When associated with ipsilateralfacial contracture and weakness (spastic-paretic facial contracture), a pontinelesion rostral to the facial nerve nucleus in the brainstem should be considered.Multiple sclerosis and brain stem tumors are also typical etiologies (Jacobs et al.1994 ) . Other causes of facial myokymia include stroke, hypoxic injury, meningitis,hydrocephalus, acoustic neuroma, syringobulbia, and Guillain–Barre syndrome.Eyelid myokymia (ocular or orbicularis myokymia), which is small, annoyingtwitches of an eyelid unilaterally, mainly affect the lower lid, and are very commonin young adults. It tends to be precipitated by fatigue, stress, alcohol, nicotine, orexcessive caffeine consumption.It is benign and usually idiopathic. Contractions may last for seconds and recurseveral times daily over a period of weeks or months. Most patients require onlyreassurance and avoidance of precipitating factors because eyelid myokymia usuallyresolves spontaneously. Neuroimaging may be necessary only if the twitchesspread to involve other facial muscles. Benzodiazepines or BoNT injection into theaffected parts of twitching muscle can be applied for persistent cases (Pane et al.2007 ; Banik and Miller 2004 ) .Facial neuromyotonia, which is similar to myokymia but is de fi ned as a delay inmuscle relaxation after a voluntary contraction, has been reported as a complicationof radiation and responds to carbemazepine (Marti-Fabregas et al. 1997 ) .
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Craniofacial Muscles
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EditorsLinda K. McLoonDepartment of
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viContents8 Masticatory Muscle Resp
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viiiContributorsMark Lewis School o
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Chapter 1The Craniofacial Muscles:
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1 The Craniofacial Muscles: Argumen
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1 The Craniofacial Muscles: Argumen
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Chapter 2Head Muscle DevelopmentIta
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2 Head Muscle Development132.3 Head
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2 Head Muscle Development15Fig. 2.3
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2 Head Muscle Development17normal h
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2 Head Muscle Development19to specu
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2 Head Muscle Development21as Islet
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2 Head Muscle Development232.10 Sum
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2 Head Muscle Development25Hirsinge
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2 Head Muscle Development27Rudnicki
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Part IIIExtraocular Muscles
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32 L.K. McLoon et al.Fig. 3.1 Diagr
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34 L.K. McLoon et al.Fig. 3.4 Speci
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36 L.K. McLoon et al.3.4 Unusual Ch
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38 L.K. McLoon et al.Fig. 3.7 Longi
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40 L.K. McLoon et al.Fig. 3.8 Co-ex
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42 L.K. McLoon et al.Fig. 3.9 An ex
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44 L.K. McLoon et al.Fig. 3.10 Use
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46 L.K. McLoon et al.3.9 SummaryIn
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48 L.K. McLoon et al.Fuchs AF, Bind
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50 L.K. McLoon et al.Tajbakhsh S, R
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52 V.E. DasFig. 4.1 Initial studies
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54 V.E. DasFig. 4.2 Schematic view
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56 V.E. DasFig. 4.3 Top panel —co
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58 V.E. Das4.3 Motor Control of Con
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60 V.E. DasFig. 4.6 Schematic showi
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62 V.E. DasFR: fi ring rateD t : ne
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64 V.E. Dasresponses of abducens ne
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66 V.E. Dasend (Buttner-Ennever et
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68 V.E. Dascontrolled by appropriat
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70 V.E. Das4.6 SummaryThe oculomoto
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72 V.E. DasHoerantner R, Kaltofen T
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74 V.E. DasTweed DB, Haslwanter TP,
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76 F. Pedrosa Domellöfcompletely d
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78 F. Pedrosa DomellöfFig. 5.2 NMJ
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80 F. Pedrosa DomellöfHowever, bec
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82 F. Pedrosa Domellöfadhesions be
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84 F. Pedrosa Domellöfshown that (
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86 F. Pedrosa DomellöfReferencesAg
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88 F. Pedrosa DomellöfMori M, Kuwa
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Chapter 6Masticatory Muscle Structu
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6 Masticatory Muscle Structure and
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112 B.J. Sessle et al.zygomaticus m
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114 B.J. Sessle et al.Fig. 7.1 ( a
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116 B.J. Sessle et al.Most of the m
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118 B.J. Sessle et al.lie immediate
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120 B.J. Sessle et al.(Dubner et al
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122 B.J. Sessle et al.Fig. 7.3 An e
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124 B.J. Sessle et al.that each out
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126 B.J. Sessle et al.2010 ; Plowma
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128 B.J. Sessle et al.activities. S
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130 B.J. Sessle et al.Moayedi M, We
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132 S.L. Hebert et al.type 3 and cr
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134 S.L. Hebert et al.This early de
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136 S.L. Hebert et al.that EMG valu
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138 S.L. Hebert et al.Newton JP, Ab
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Chapter 9Structure and Function of
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9 Structure and Function of the Lar
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Chapter 10Motor Control and Biomech
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10 Motor Control and Biomechanics o
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186 J.C. Stemple et al.established
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188 J.C. Stemple et al.of protein d
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190 J.C. Stemple et al.the depictio
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192 J.C. Stemple et al.Fig. 11.2 Ul
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194 J.C. Stemple et al.11.6 Larynge
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196 J.C. Stemple et al.Neurapraxia,
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198 J.C. Stemple et al.of the preci
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200 J.C. Stemple et al.Gardner GM,
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202 J.C. Stemple et al.Rhee HS, Luc
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Part VITongue Musculature
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208 A. Sokoloff and T. BurkholderTh
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210 A. Sokoloff and T. BurkholderFi
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212 A. Sokoloff and T. Burkholder12
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214 A. Sokoloff and T. Burkholderou
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216 A. Sokoloff and T. Burkholderbe
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218 A. Sokoloff and T. Burkholderel
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220 A. Sokoloff and T. BurkholderFi
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222 A. Sokoloff and T. BurkholderCo
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224 A. Sokoloff and T. BurkholderAn
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226 A. Sokoloff and T. BurkholderOl
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Chapter 13Tongue Biomechanics and M
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Fig. 13.1 Retrogradely labeled enti
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13 Tongue Biomechanics and Motor Co
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Chapter 14Tongue Muscle Responseto
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14 Tongue Muscle Response to Neurom
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Page 261 and 262: Part VIIFacial Muscles
Page 263 and 264: 266 A.O. Grobbelaar and A.C.S. Wool
Page 285 and 286: 288 J. Park et al.Table 16.1 Disord
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Page 293 and 294: 296 J. Park et al.Focal motor seizu
Page 295 and 296: 298 J. Park et al.Fig. 16.1 Content
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Page 299 and 300: 302 J. Park et al.Long-term effect
Page 301 and 302: 304 J. Park et al.is as high as 50%
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Page 305 and 306: 308 J. Park et al.septum should be
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Page 319 and 320: Part VIIISummary and Conclusions
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Page 331 and 332: IndexAAbducens nucleusvs. lateral r
Page 333 and 334: Index339Embryonic myosin heavy chai
Page 335 and 336: IndexLLagophthalmos , 304, 308Lamin
Page 337 and 338: Indexmuscular dystrophy , 187-190my
Page 339: Index345hydrostat mass reduction ,
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