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Muscle biopsies reveal nonspeci c myopathic features including variability in ber size, increased internal nuclei, type 1 ber predominance, and moth-eaten bers and lobulated bers on NADH-TR stains Some cases are associated with multiple minicores Cytoplasmic bodies, Mallory bodies, increased desmin expression, and sarcoplasmic and intranuclear tubulo lamentous inclusions may also be present similar to myo brillar myopathy181 Endomysial brosis is apparent, particularly in axial muscles (ie, rectus abdominus and paraspinal muscles) Immunostains for dystrophin, sarcoglycans, and the dystroglycans are normal

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Some cases of autosomal-recessive RSMD have been linked to mutations in the gene that encodes for selenoprotein N1 located on chromosome 1p35 36126,180,183 Mutations in this gene have also been shown in some patients with multi/minicore myopathy and MFM184 Selenoprotein N1 is an endoplasmic reticulum glycoprotein The function of this protein is not known

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Facioscapulohumeral muscular dystrophy (FSHD) is an autosomal-dominant disorder, with an incidence of approximately 4 per million and a prevalence of roughly 50 per million185,186 There is a variable degree of penetrance of clinical ndings within families, while around 30% of affected family members are unaware of their de cits Thus, it is very important to examine family members of patients suspected of having FSHD Onset of weakness is usually appreciated between 3 and 44 years, although onset as late as 75 years has also been reported187 191 As the name suggests, FSHD is characterized by muscle weakness and wasting in a rather speci c distribution The muscles of facial expression, particularly the orbicularis oculi, zygomaticus, and orbicularis oris muscles, are affected early Patients may be unable to fully close their eyes against resistance and may sleep with incomplete eyelid closure On examination of forced eye closure, many individuals demonstrate prominent Bell phenomena (visible sclera with eye closure) Affected persons can have a horizontal smile and weak puckering of the lips Facial weakness may be strikingly asymmetric, mimicking a seventh nerve palsy The muscles of mastication and the external ocular muscles are typically spared The scapula-stabilizer muscles (serratus anterior, rhomboid, middle trapezius, and, to some degree, latissimus dorsi muscles) are also weak and atrophic early in the course Weakness of these muscles lead to upward and lateral rotation of the shoulder blades with scapular winging and the appearance of a trapezius hump, which often is mistaken for muscle hypertrophy (Fig 24 15) Although the deltoids are relatively spared during the early course of the disease, the sternocostal head of the pectoralis major is often atrophic and weak

This code sets the rightmost bit of myShort to 0, no matter what its current value. It might help to think of 0xFFFE as 1111111111111110 in binary. This line of code, based on the &= operator, does the exact same thing:

var var var var var meteorNum:Number = 0; meteorInterval:Number; meteorInit:Object = new Object(); score:Number; pointsToWin:Number = 10;

Figure 24 15 Facioscapulohumeral muscular dystrophy (FSHD) Characteristic appearance of a patient diagnosed with FSHD On attempted forward exion of the arms at the shoulders the scapulae elevates and laterally deviates off the posterior rib cage under the trapezius musculature, giving the false impression of very muscular individual Palpation reveals the bone underlying the muscle tissue

modalities, and the re exes are usually absent or diminished commensurate with the degree of muscle wasting Some patients with FSHD appear to experience a late exacerbation of muscle weakness They may only have mild weakness for years and then suddenly have a marked increase of weakness in the typical distribution over the course of several years Affected individuals usually have a normal life span; however, severe progressive respiratory muscle weakness has been reported in approximately 1% of large series of patients with FSHD193 Severe extremity weakness, wheelchair dependency, and kyphoscoliosis appear to be risk factors for respiratory failure Further, rare patents develop cardiac involvement manifesting as conduction defects, supraventricular, or ventricular arrhythmias that may require pacemaker implantation194 Infantile-onset FSHD is associated with severe weakness presenting in the rst 2 years of life185,195 A wheelchair is required to maintain mobility by the time the patient is 9 or 10 years of age Another form of FSHD involves a combination of facioscapulohumeral weakness, profound sensorineural hearing loss, and retinal telangiectasias (Coats disease) Some infants present with profound facial diplegia mimicking Mobius syndrome196

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