Craniofacial Muscles

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16 Spastic Facial Muscle Disorders305or 300 units of Dysport ® per session; an interval of less than 3 months betweentwo injections; using the “Booster” technique where another dose is injected2–3 weeks after the fi rst injection; and use of a BoNT drug with a low intrinsicactivity. Cumulative dose, treatment time, and patient age have been excludedas risk factors. Antibody-induced therapy failure usually develops within thefi rst 2–3 years of BoNT therapy (Dressler 2002 ).The intrinsic activity of BoNT drugs is de fi ned as the number of toxin unitsper amount (nanograms) of clostridial proteins (i.e., toxin complex). At eachinjection of toxin, the administered protein mass will be greater when using atoxin with a low intrinsic activity. The toxin’s antigenic potential is probablyrelated to the total protein concentration injected (protein load). This may be amuch more relevant parameter in the development of resistance than the numberof units injected (Borodic et al. 1996 ). In patients with cervical dystonia, theoriginal formulation of Botox ® (100 units/25 ng protein) was six times morelikely to elicit the production of neutralizing antibodies than the newer formulationof Botox ® (100 units/5 ng protein). The authors conclude that the low riskof antibody formation after newer Botox ® treatment is related to lower proteinload (Jankovic et al. 2003 ).The newly FDA approved BoNT/A drug Xeomin ® may reduce antibodyinducedtherapy failure, since it contains only the pure neurotoxin (150 kDa)produced by a manufacturing process that separates it from complexing proteinssuch as hemagglutinins and other proteins in the neurotoxin complex(Frevert 2009 ; Park et al. 2011 ). Long-term comparative trials in naïve patientsbetween Xeomin ® and conventional BoNT/A drugs are required to con fi rm thelower immunogenicity of Xeomin ® (Park et al. 2011 ).(f) Systemic Toxic Effects : The LD in humans is approximately 390,000 unit/kg,50and single injection of more than 500 units may cause acute systemic toxicity.Systemic toxic effects have not been reported in the treatment of cranial dystoniabecause the amount for each treatment is relatively small.(g) Excessive Facial Weakness : In the patients with Meige’s syndrome or hemifacialspasm, injections in the mid- and lower facial muscles may induce excessivefacial weakness. Careful toxin injection of appropriate drug levels canreduce this side effect.16.8.2 PsychotherapyPsychotherapy such as behavior modi fi cation and biofeedback has been used todecrease the frequency and amplitude of spasm. The principle is based on teachingpatients to control their muscle contractions using an electromyographic recording.
306 J. Park et al.Table 16.4 Drugs used for treatment of blepharospasmAntipsychoticsAffective disorder drugsAnxiolytics (Antianxiety drugs)StimulantsSedativesMuscle relaxants (Gamma aminobutyric acid, GABA)ParasympathomimeticsAntimuscarinicsAnticholinergicsAnticonvulsants (Benzodiazepines)Serotonin antagonistsAntihistaminesPhenothiazine, butyrophenone,reserpineLithium carbonate, tetrabenazineMeprobamateAmphetaminePhenobarbitalBaclofenLecithin, choline, physostigmineTincture of belladonna, scopolamine,catecholamine synthesis inhibitorsOrphenadrine, trihexyphenidylDiazepam, clonazepam, lorazepam,oxazepamCyproheptadineDiphenhydramine hydrochloride16.8.3 Oral MedicationsMany drugs have been used for the treatment of blepharospasm and cranial dystonias(Table 16.4 ) on the basis of three hypothetical pharmacological paradigms:(1) cholinergic excess, (2) gamma-aminobutyric acid (GABA) hypofunction, and(3) dopamine excess. Even though some drug studies have reported high percentagesof favorable patient responses, including lorazepam (67% of patients), donazepam(42%), and trihexyphenidyl HCl (41%), in general, their effects are temporaryand only useful in a small number of patients. The side effects, which include sedation,may be dangerous in older individuals. Oral medications control symptoms ona long-term basis in only 25% of patients with cranial dystonia, and their long-termuse is usually limited by side effects. Thus, they are usually reserved as a secondline of treatment or adjuvant therapy for spasms that respond poorly to BoNT andin patients with middle and lower face spasms, which are dif fi cult to treat withBoNT injection.16.8.4 SurgerySurgery is not usually necessary and should be reserved for patients with severesymptoms that have failed to respond to other forms of treatment. Options includeorbicularis myectomy, during which the orbicularis oculi and other muscles used ineyelid closure are excised either surgically (Anderson et al. 1998 b) or chemically(Wirtschafter and McLoon 1998 ) , and neurectomy, a procedure in which branchesof the facial nerve are cut (Kennedy et al. 1989 ) . However, signi fi cant numbers ofpatients who undergo surgeries for blepharospasm need to continue BoNT injectiontreatment after the surgery.
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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 291 and 292: 294 J. Park et al.evident eyelid sq
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
Page 297 and 298: 300 J. Park et al.Botox ® in human
Page 299 and 300: 302 J. Park et al.Long-term effect
Page 301: 304 J. Park et al.is as high as 50%
Page 305 and 306: 308 J. Park et al.septum should be
Page 307 and 308: 310 J. Park et al.16.9 Hemifacial S
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Page 311 and 312: 314 J. Park et al.regeneration beca
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Page 315 and 316: 318 J. Park et al.Grandas F, Elston
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Page 319 and 320: Part VIIISummary and Conclusions
Page 321 and 322: 326 L.K. McLoon and F.H. Andrade17.
Page 327 and 328: 332 L.K. McLoon and F.H. AndradeDie
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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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