Craniofacial Muscles

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16 Spastic Facial Muscle Disorders297the drug history includes drugs which can cause tardive dystonia (Mauriello et al.1998a ). Treatment consists of withdrawing the offending agent, sometimes combinedwith the use of botulinum neurotoxin (BoNT) injections in refractory cases.16.8 TreatmentSpeci fi c treatment may be not necessary until patients with blepharospasm or othercranial dystonia are disabled by the abnormal movements. Any potentially exacerbatingocular disease such as dry eye or blepharitis must be treated fi rst. Dry eyesymptoms can be treated symptomatically with arti fi cial tears and punctal occlusion.Tinted lenses also have been recommended to ameliorate photophobia in patientswith blepharospasm (Adams et al. 2006 ; Herz and Yen 2005 ) .The treatment of choice in patients with debilitating blepharospasm, Meige’ssyndrome, and hemifacial spasm is localized injections of botulinum neurotoxintype A ( BoNT / A ) around the eyelids to weaken the orbicularis oculi and other musclesinvolved in eyelid closure and facial movements (Aramideh 1996 ; Aramideh1995 ; Osako and Keltner 1991 ; Price and O’Day 1994 ; Defazio et al. 2002 ; Duttonand Fowler 2007 ) . Greater than 90% of patients report a marked decrease in thesqueezing action of the eyelids and twitching in lower part of the face (Osako andKeltner 1991 ; Elston 1987 ; Engstrom et al. 1987 ; Dutton and Buckley 1988 ;Kennedy et al. 1989 ; Mauriello et al. 1996 ; Anderson et al. 1998b ). Some patientswith apraxia of eyelid opening bene fi t from BoNT injection depending on howmuch of their eyelid closure is spastic. Most need higher doses of toxin and morefrequent injections.16.8.1 BoNT InjectionBoNT injections were fi rst used to treat strabismus in 1977 by Alan Scott, a pediatricophthalmologist, (Dressler 2000 ) and subsequently used to treat blepharospasm inthe early 1980s by Frueh et al. ( 1984 ) and Scott et al. ( 1985 ) . Since then, BoNT hasbeen highly effective and well tolerated in the symptomatic treatment of a verybroad range of conditions involving either muscle hyperactivity such as blepharospasmand hemifacial spasm, or cholinergic hyperactivity such as hyperhidrosis andhypersalivation (Jankovic 2009 . Recently, BoNT has been approved for the treatmentof glabellar rhytids and chronic migraine headaches (Harrison 2003 ) .The various strains of the anaerobic bacteria Clostridium botulinum produceseven distinct serotypes of BoNT, of which fi ve are pharmacologically active inhumans (A, B, E, F, and G) and two are inactive (C and D) (Brin and Blitzer 1993 ) .In all naturally occurring serotypes of BoNT (types A~G) and commercially availableBoNT preparations, the active neurotoxin (150 kDa; 100 kDa of a heavy chain;and 50 kDa of a light chain) is noncovalently associated with a set of nontoxic and
298 J. Park et al.Fig. 16.1 Contents of botulinum neurotoxin preparationinactive complexing proteins (hemagglutinins (HA) and nonhemagglutinins (NHA))and thus forms high molecular toxin complexes (Hasegawa et al. 2007 ; Hambleton1992 ) (Fig. 16.1 ). The molecular weight of the toxin complex ranges between 230and 900 kD, depending on the serotype (Daniele Ranoux 2007 ) .Today, two serotypes are used in therapeutics, BoNT type A (BoNT/A) and typeB (BoNT/B). Among the seven distinct exotoxins, BoNT/A is the most powerful,followed by type B and type F (Huang et al. 2000 ) . BoNT/A has been most commonlyused in the studies of eye movement disorders because this bacterial strainretains its toxigenicity well, and it can be crystallized in a stable form. Comparedwith BoNT/A, BoNT/B seems to have a quicker onset and greater diffusion in thetissues. Also, its dosage is signi fi cantly different from that of type A, and its durationof action is shorter. Patients treated with BoNT/B generally experience morediscomfort at injection, and their ultimate satisfaction rates are lower. Therefore,BoNT/B is considered as an alternative only for patients who show decreased clinicalresponse or who fail to respond to initial treatment with BoNT/A (Baumann andBlack 2003 ; Alster and Lupton 2003 ) .There are 3 type A and 1 type B brands of BoNT preparations currently availablein the United States (Table 16.3 ): Botox®(onabotulinum toxin A; Allergan Inc,Irvine, CA, USA), Dysport ® (abobotulinum toxin A; Ipsen Ltd, Slough, Berks, UK),Myobloc ® (rimabotulinum toxin B; Solstice Neurosciences Inc, Malvern, PA, USA),and newly FDA approved Xeomin ® (incobotulinum toxin A; Merz PharmaceuticalsGmbH, Frankfurt, Germany) (Albanese 2011 ; Frevert 2009 ) . The potency (toxicity)of the BoNT preparations is expressed in units, but each preparation has its ownmeasurement. For example, 1 unit of Botox ® is de fi ned as the weight of intraperitoneallyinjected toxin required to kill 50% of a group Swiss-Webster mice weighing18–20 g (Harrison 2003 ; Schantz and Johnson 1990 ) . The mean lethal dose of
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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 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%
Page 303 and 304: 306 J. Park et al.Table 16.4 Drugs
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Page 307 and 308: 310 J. Park et al.16.9 Hemifacial S
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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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