barcode reader in java source code is usually much less prominent than that seen in FSHD Muscle weakness is slowly progressive in Objective-C

Encoding Data Matrix ECC200 in Objective-C is usually much less prominent than that seen in FSHD Muscle weakness is slowly progressive

is usually much less prominent than that seen in FSHD Muscle weakness is slowly progressive
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The serum CK levels can be normal or moderately abnormal The motor and sensory nerve conductions are normal aside from a reduced CMAP in the more severely affected muscles211,212,214,216 Needle electromyography may demonstrate sparse brillation potentials and myopathic units
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Histopathology
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Muscle biopsies reveal nonspeci c myopathic features including ber size variation with atrophic and hypertrophic bers, split bers, necrotic and regenerating bers, and increased endomysial connective tissue214,216,217 Some biopsies demonstrate inclusions typical of MFM215
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Scapuloperoneal muscular dystrophy is an autosomaldominant disorder There is no linkage to chromosome
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4q35 in scapuloperoneal muscular dystrophy; therefore, the disorder is not allelic to FSHD217 The kinship originally described by Kaeser212 has been found to be caused by mutations in the desmin gene on chromosome 2q35 and is thus a form of MFM (discussed later) Another family with scapuloperoneal syndrome and cardiomyopathy has been linked to chromosome 12215
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Treatment
There are no reported studies regarding medical therapy in scapuloperoneal muscular dystrophy Hopefully, studies being performed on patients with DMD and FSHD will apply to those with scapuloperoneal muscular dystrophy Ankle foot orthoses are bene cial in patients with ankle dorsi exor weakness Surgery to stabilize the scapula may improve arm function in some patients
X-LINKED EDMD Clinical Features
EDMD is characterized by (1) early contractures of the Achilles tendons, elbows, and posterior cervical muscles; (2) slowly progressive muscle atrophy and weakness, with a predominantly humeroperoneal distribution in early stages; and (3) cardiomyopathy with conduction defects49,218 220 Prominent contractures are evident in early childhood or in the teenage years, with an inability to fully extend the elbows secondary to elbow exion contractures (Fig 24 18) Patients may toe walk due to early heal cord contractures There is reduced mobility of the spine such that EDMD is in the differential diagnosis of the so-called rigid spine syndrome 221 Patients have dif culty exing their neck and trunk Importantly, the contractures of the Achilles tendons, elbows, and paraspinal muscles are evident before there is any signi cant weakness, which helps distinguish EDMD from other the types of dystrophies associated with contractures Patients with EDMD usually appear normal at birth Some children develop mild weakness The characteristic pattern of muscle involvement helps distinguish EDMD from most other forms of dystrophy There is an early predilection for weakness and atrophy affecting the humeroperoneal muscles (ie, biceps brachii, triceps, anterior tibial, and peroneal muscles) Pes cavus deformities of the feet are common Weakness is slowly progressive, and eventually the shoulder- and pelvic-girdle muscles can become involved Most affected individuals are able to ambulate into the third decade Unlike many of the LGMDs, which it may be confused with, there is no calf hypertrophy Muscle stretch re exes are diminished or absent early in the disease Importantly, EDMD is associated with potentially lethal cardiac arrhythmias by the end of the second or beginning of the third decade Conduction defects range
Figure 24 18 Emery Dreifuss muscular dystrophy (EDMD) Posterior view of a patient with EDMD demonstrate atrophy of the triceps musculature, left more than right, and early contractures of the elbows (patient is unable to straighten the arms down at the side) There is also mild scapular winging
from rst-degree A-V block to complete heart block Syncope and sudden cardiac death can occur Although female carriers do not manifest muscle weakness or contractures, they may develop the cardiopathy
Laboratory Features
The serum CK levels may be normal or moderately elevated EKG frequently reveal sinus bradycardia, prolongation of the PR interval, or more severe degrees of conduction block Motor and sensory nerve conduction studies are typically normal in these patients EMG reveals myopathic MUAPs
Histopathology
The muscle biopsy ndings can be quite varied, depending on the degree of weakness of the biopsied muscle222 There is usually muscle ber size variation with type 1 ber atrophy There can be a predominance of either type 1 or type 2 muscle bers Muscle ber splitting, increased central nuclei, and endomysial brosis may be seen Immunohistochemistry reveals the absence of emerin as well as abnormal lamin A/C and lamin B2 on the nuclear membrane24,25 Ultrastructural
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