ࡱ> 35,-./012q` 0bjbjqPqP .::AAAA$B,cE>NNNNNNNnbpbpbpbpbpbpb$dhfbONNOObNNcRRRONNnbROnbRRRNE P?cAP.RS\c0cR}gP}gR}gRNLjN6RN,NNNNbbRNNNcOOOO=AA MUSCULAR DYSTROPHIES  The muscular dystrophies are a heterogeneous group of inherited disorders, often beginning in childhood, that are characterized clinically by progressive muscle weakness and wasting. Histologically, the advanced cases are characterized by the replacement of muscle fibers by fibrofatty tissue. This feature distinguishes dystrophies from myopathies (described later), which also present with muscle weakness.  X-Linked Muscular Dystrophy (Duchenne Muscular Dystrophy and Becker Muscular Dystrophy)  The two most common forms of muscular dystrophy are X-linked: Duchenne muscular dystrophy (DMD) and Becker muscular dystrophy (BMD). DMD is the most severe and the most common form of muscular dystrophy, with an incidence of about 1 per 3500 live male births. HYPERLINK "http://www.robbinspathology.com/passthru/linktopage.cfm?showtab=toc&xrefID=R027049" \o "Go here now" \t "body" 49 DMD becomes clinically manifest by the age of 5 years, with weakness leading to wheelchair dependence by 10 to 12 years of age, and progresses relentlessly until death by the early twenties. Although BMD involves the same genetic locus, it is less common and much less severe than DMD.  Pathogenesis and Genetics. DMD and BMD are caused by abnormalities in a gene that is located in the Xp21 region and encodes a 427-kDa protein termed dystrophin. Deletions appear to represent a large proportion of the genetic abnormalities, with frameshift and point mutations accounting for the rest. HYPERLINK "http://www.robbinspathology.com/passthru/linktopage.cfm?showtab=toc&xrefID=R027011" \o "Go here now" \t "body" 11 Approximately two-thirds of the cases are familial, and the remainder represent new mutations. In the affected families, females are carriers; they are clinically asymptomatic but often have elevated serum creatine kinase and show minimal histologic abnormalities on muscle biopsy. Female carriers are at risk for developing dilated cardiomyopathy later in life.  Dystrophin is a cytoplasmic protein located adjacent to the sarcolemmal membrane in myocytes ( HYPERLINK "http://www.robbinspathology.com/content/" \o "View now" Fig. 27-10). The dystrophin molecule concentrates at the plasma membrane over Z-bands, where it forms a strong mechanical link to cytoplasmic actin. Thus, dystrophin and the dystrophin-associated protein complex form an interface between the intracellular contractile apparatus and the extracellular connective tissue matrix. The role of this complex of proteins in transferring the force of contraction to connective tissue has been proposed to be the basis for the myocyte degeneration that occurs in the absence of dystrophin HYPERLINK "http://www.robbinspathology.com/passthru/linktopage.cfm?showtab=toc&xrefID=R027050" \o "Go here now" \t "body" 50 or various other proteins that interact with dystrophin (see later). Muscle biopsy specimens from patients with DMD show minimal evidence of dystrophin by both staining and Western blot analysis. HYPERLINK "http://www.robbinspathology.com/passthru/linktopage.cfm?showtab=toc&xrefID=R027050" \o "Go here now" \t "body" 50 BMD patients, who also have mutations in the dystrophin gene, have diminished amounts of dystrophin, usually of an abnormal molecular weight, reflecting mutations that allow synthesis of the protein ( HYPERLINK "http://www.robbinspathology.com/content/" \o "View now" Fig. 27-11B).  page 1336 INCLUDEPICTURE "http://www.robbinspathology.com/images/pixel.gif" \* MERGEFORMATINET page 1337  HYPERLINK "http://www.robbinspathology.com/content/"  INCLUDEPICTURE "http://www.robbinspathology.com/content/0721601871/graphics/thumbnails/S01871-027-f010.jpg" \* MERGEFORMATINET  HYPERLINK "http://www.robbinspathology.com/content/lightbox.cfm?action=add&ImgID=F027010&ImgBody=graphics/S01871-027-f010.jpg&ID=iBox" Add to lightbox  Morphology. Histopathologic abnormalities common to DMD and BMD include (1) variation in fiber size (diameter) due to the presence of both small and enlarged fibers, sometimes with fiber splitting; (2) increased numbers of internalized nuclei (beyond the normal range of 3% to 5%); (3) degeneration, necrosis, and phagocytosis of muscle fibers; (4) regeneration of muscle fibers; and (5) proliferation of endomysial connective tissue ( HYPERLINK "http://www.robbinspathology.com/content/" \o "View now" Fig. 27-11A). DMD cases also often show enlarged, rounded, hyaline fibers that have lost their normal cross-striations, believed to be hypercontracted fibers; this finding is rare in BMD. Both type 1 and type 2 fibers are involved, and no alterations in the proportion or distribution of fiber types are evident. Histo-chemical reactions sometimes fail to identify distinct fiber types in DMD. In later stages, the muscles eventually become almost totally replaced by fat and connective tissue. Cardiac involvement, when present, consists of interstitial fibrosis, more pro minent in the subendocardial layers. Despite the clinical evidence of CNS dysfunction in DMD, no consistent neuropathologic abnormalities have been described. Figure 27-10 Diagram showing the relationship between the cell membrane (sarcolemma) and the sarcolemmal associated proteins. Dystrophin, an intracellular protein, forms an interface between the cytoskeletal proteins and a group of transmembrane proteins, the dystroglycans and the sarcoglycans. These transmembrane proteins have interactions with the extracellular matrix, including the laminin proteins. Dystrophin also interacts with dystrobrevin and the syntrophins, which form a link with neuronal-type  HYPERLINK "http://www.robbinspathology.com/content/" \o "View drug information" nitric oxide INCLUDEPICTURE "http://www.robbinspathology.com/images/linkdrug.gif" \* MERGEFORMATINET  synthetase (nNOS) and caveolin. Mutations in dystrophin are associated with the X-linked muscular dystrophies, mutations in caveolin and the sarcoglycan proteins with the autosomal limb girdle muscular dystrophies, and mutations in the 2-laminin (merosin) with a form of congenital muscular dystrophy.  INCLUDEPICTURE "http://www.robbinspathology.com/images/pixel.gif" \* MERGEFORMATINET   HYPERLINK "http://www.robbinspathology.com/content/"  INCLUDEPICTURE "http://www.robbinspathology.com/content/0721601871/graphics/thumbnails/S01871-027-f011a.jpg" \* MERGEFORMATINET  HYPERLINK "http://www.robbinspathology.com/content/lightbox.cfm?action=add&ImgID=F027011&ImgBody=graphics/S01871-027-f011a.jpg&ID=iBox" Add to lightbox   HYPERLINK "http://www.robbinspathology.com/content/"  INCLUDEPICTURE "http://www.robbinspathology.com/content/0721601871/graphics/thumbnails/S01871-027-f011b.jpg" \* MERGEFORMATINET  HYPERLINK "http://www.robbinspathology.com/content/lightbox.cfm?action=add&ImgID=F027011&ImgBody=graphics/S01871-027-f011b.jpg&ID=iBox" Add to lightbox  Figure 27-11 A, Duchenne muscular dystrophy (DMD) showing variation in muscle fiber size, increased endomysial connective tissue, and regenerating fibers (blue hue). B, Western blot showing absence of dystrophin in DMD and altered dystrophin size in Becker muscular dystrophy (BMD) compared with control (Con). (Courtesy of Dr. L. Kunkel, Children's Hospital, Boston, MA.) page 1337 INCLUDEPICTURE "http://www.robbinspathology.com/images/pixel.gif" \* MERGEFORMATINET page 1338 Clinical Course. Boys with DMD are normal at birth, and early motor milestones are met on time. Walking, however, is often delayed, and the first indications of muscle weakness are clumsiness and inability to keep up with peers. Weakness begins in the pelvic girdle muscles and then extends to the shoulder girdle. Enlargement of the calf muscles associated with weakness, a phenomenon termed pseudohypertrophy, is an important clinical finding. The increased muscle bulk is caused initially by an increase in the size of the muscle fibers and then, as the muscle atrophies, by an increase in fat and connective tissue. Pathologic changes are also found in the heart, and patients may develop heart failure or arrhythmias. Although there are no well-established structural abnormalities of the central nervous system, cognitive impairment appears to be a component of the disease and is severe enough in some patients to be considered mental retardation. HYPERLINK "http://www.robbinspathology.com/passthru/linktopage.cfm?showtab=toc&xrefID=R027051" \o "Go here now" \t "body" 51 Serum creatine kinase is elevated during the first decade of life but returns to normal in the later stages of the disease, as muscle mass decreases. Death results from respiratory insufficiency, pulmonary infection, and cardiac decompensation. Gene therapy has received a great deal of attention in DMD, with some initial success in experimental animals with genetically similar disorders. HYPERLINK "http://www.robbinspathology.com/passthru/linktopage.cfm?showtab=toc&xrefID=R027050" \o "Go here now" \t "body" 50 The principal obstacle has been the introduction of a single large gene targeted into all muscle cells without initiation of an immune response to the new gene product.  Boys with BMD develop symptoms at a later age than those with DMD. The onset occurs in later childhood or in adolescence, and it is accompanied by a slower and more variable rate of progression, although there is considerable variation between pedigrees. Many patients have a nearly normal life span. Cardiac disease is frequently seen in these patients.  Autosomal Muscular Dystrophies  Other forms of muscular dystrophy share many features of DMD and BMD but have distinct clinical and pathologic characteristics. Some of these muscular dystrophics affect specific muscle groups, and the specific diagnosis is based largely on the pattern of clinical muscle weakness ( HYPERLINK "http://www.robbinspathology.com/passthru/linktopage.cfm?showtab=toc&xrefID=T027004" \o "Go here now" \t "body" Table 27-4). Several autosomal muscular dystrophies, however, affect the proximal musculature of the trunk and limbs, similar to the X-linked muscular dystrophies, and are termed limb girdle muscular dystrophies.  Limb girdle muscular dystrophies are inherited in either an autosomal-dominant (type 1) or an autosomal-recessive (type 2) pattern ( HYPERLINK "http://www.robbinspathology.com/passthru/linktopage.cfm?showtab=toc&xrefID=T027005" \o "Go here now" \t "body" Table 27-5). Six subtypes of the dominant dys trophies (1A to 1F) and ten subtypes of the recessive limb girdle dystrophies (2A to 2J) have been identified. Mutations of the sarcoglycan complex of proteins have been identified in four of the limb girdle muscular dystrophies HYPERLINK "http://www.robbinspathology.com/passthru/linktopage.cfm?showtab=toc&xrefID=R027052" \o "Go here now" \t "body" 52 (2C, 2D, 2E, and 2F). These membrane proteins interact with dystrophin through another transmembrane protein, -dystroglycan ( HYPERLINK "http://www.robbinspathology.com/content/" \o "View now" Fig. 27-10).  Myotonic Dystrophy  Myotonia, the sustained involuntary contraction of a group of muscles, is the cardinal neuromuscular symptom in this disease. HYPERLINK "http://www.robbinspathology.com/passthru/linktopage.cfm?showtab=toc&xrefID=R027053" \o "Go here now" \t "body" 53 Patients often complain of "stiffness" and have difficulty in releasing their grip, for instance, after a handshake. Myotonia can often be elicited by percussion of the thenar eminence.   Table 27-4. Other Muscular Dystrophies Disease and InheritanceGene and LocusClinical FindingsPathologic FindingsFacioscapulohumeral muscular dystrophy; autosomal-dominantType 1A-deletion of variable number of 3.3-kB subunits of a tandemly arranged repeat (D4Z4) on 4q35 Type 1B (FSHMD1B)-locus unknownVariable age at onset (most commonly 10-30 years); Weakness of muscles of face, neck, and shoulder girdleDystrophic myopathy, but also often including inflammatory infiltrates of muscle.Oculopharyngeal muscular dystrophy; autosomal-dominantPoly(A)-binding protein-2 (PABP2) gene; 14q11.2-q13Onset in midadult life; ptosis and weakness of extraocular muscles; difficulty in swallowingDystrophic myopathy, but often including rimmed vacuoles in type 1 fibersEmery-Dreifuss muscular dystrophy; X-linked (mostly)Emerin (EMD1) gene; Xq28Variable onset (most commonly 10-20 years); prominent contractures, especially of elbows and anklesMild myopathic changes; absent emerin by immunohistochemistryCongenital muscular dystrophies; autosomal-recessive (Also called muscular dystrophy, congenital, subtypes MDC1A, MDC1B, MDC1C)Type 1A (merosin-deficient type)-laminin 2 (merosin) gene; 6q22-q23 Type 1B-locus at 1q42; gene unknown Type 1C; fukutin-related protein gene; 19q13.3Neonatal hypotonia, respiratory insufficiency, delayed motor milestonesVariable fiber size and extensive endomysial fibrosis  page 1338 INCLUDEPICTURE "http://www.robbinspathology.com/images/pixel.gif" \* MERGEFORMATINET page 1339  Table 27-5. Limb Girdle Muscular Dystrophies TypeInheritanceLocusGeneClinicopathologic Features1AAutosomal-dominant5q31MyotilinOnset in adult life with slow progression of limb weakness, but sparing of facial muscles; dysarthric speech1BAutosomal-dominant1q21Lamin A/COnset before the age of 20 years in lower limbs, progression during many years with cardiac involvement1CAutosomal-dominant3p25Caveolin-3 (M-caveolin)Onset before the age of 20, clinically similar to type 1B1DAutosomal-dominant7pUnknownLimb girdle muscle weakness, adult onset2AAutosomal-recessive15q15.1-21.1Calpain 3Onset in late childhood to middle age; slow progression during 20-30 years2BAutosomal-recessive2p13.3-q13.1DysferlinMild clinical course with onset in early adulthood2CAutosomal-recessive13q12-SarcoglycanSevere weakness during childhood, rapid progression; dystrophic myopathy on muscle biopsy2DAutosomal-recessive17q21-Sarcoglycan (adhalin)Severe weakness during childhood, rapid progression; dystrophic myopathy on muscle biopsy2EAutosomal-recessive4q12-SarcoglycanOnset in early childhood, with Duchenne-like clinical course2FAutosomal-recessive5q33-SarcoglycanEarly onset and severe myopathy; dystrophic myopathy on muscle biopsy2GAutosomal-recessive17q11-q12TelethoninDistal weakness with limb-girdle weakness in late childhood to adulthood; rimmed vacuoles in muscle cells2HAutosomal-recessive9q31-q34.1Tripartite motif-containing protein 32 (TRIM32)Limb-girdle and facial weakness with onset in childhood, mild, slowly progressive course  Pathogenesis. Inherited as an autosomal-dominant trait, the disease tends to increase in severity and appear at a younger age in succeeding generations, a phenomenon termed anticipation. Myotonic dystrophy is associated with a trinucleotide CTG repeat expansion on chromosome 19q13.2-13.3. This expansion affects the mRNA for the dystrophila myotonia-protein kinase (DMPK). HYPERLINK "http://www.robbinspathology.com/passthru/linktopage.cfm?showtab=toc&xrefID=R027054" \o "Go here now" \t "body" 54 In normal subjects, fewer than 30 repeats are present; disease develops with expansion of this repeat, and in severely affected individuals, several thousand repeats may be present. HYPERLINK "http://www.robbinspathology.com/passthru/linktopage.cfm?showtab=toc&xrefID=R027054" \o "Go here now" \t "body" 54 The mutation is not stable within a pedigree; with each generation, more repeats accumulate, and this appears to correspond to the clinical feature of anticipation. Expansion of the trinucleotide repeat influences the eventual level of protein product.  The pathologic features of the disease relate only in part to altered DMPK function. RNA that contains trinucleotide repeat expansions can directly affect splicing of other RNAs, including those for the ClC-1 chloride channel. HYPERLINK "http://www.robbinspathology.com/passthru/linktopage.cfm?showtab=toc&xrefID=R027055" \o "Go here now" \t "body" 55 A second form of myotonic dystrophy is associated with untranslated CCTG expansion in a gene called ZNF9 on chromosome 3. HYPERLINK "http://www.robbinspathology.com/passthru/linktopage.cfm?showtab=toc&xrefID=R027056" \o "Go here now" \t "body" 56  Morphology. Skeletal muscle may show variation in fiber size. In addition, there is a striking increase in the number of internal nuclei, which on longitudinal section may form conspicuous chains. Another well-recognized abnormality is the ring fiber, with a subsarcolemmal band of cytoplasm that appears distinct from the center of the fiber. The rim contains myofibrils that are oriented circumferentially around the longitudinally oriented fibrils in the rest of the fiber. The ring fiber may be associated with an irregular mass of sarcoplasm (sarcoplasmic mass) extending outward from the ring. These sarcoplasmic masses stain blue with hematoxylin and eosin, red with Gomori trichrome, and intensely blue with the nicotinamide adenine dinucleotide-tetrazolium reductase (NADH-TR) histochemical reaction. Histochemical techniques have demonstrated a relative atrophy of type 1 fibers early in the course of the disease in some cases. Of all the dystrophies, only myotonic dystrophy shows pathologic changes in the intrafusal fibers of muscle spindles, with fiber splitting, necrosis, and regeneration.  INCLUDEPICTURE "http://www.robbinspathology.com/images/pixel.gif" \* MERGEFORMATINET  Clinical Course. The disease often presents in late childhood with abnormalities in gait secondary to weakness of foot dorsiflexors and subsequently progresses to weakness of the hand intrinsic muscles and wrist extensors. Atrophy of muscles of the face and ptosis ensue, leading to the typical facial appearance. Cataracts, which are present in virtually every patient, may be detected early in the course of the disease with slit-lamp examination. Other associated abnormalities include frontal balding, gonadal atrophy, cardiomyopathy, smooth muscle involvement, decreased plasma immunoglobulin G, and an abnormal  HYPERLINK "http://www.robbinspathology.com/content/" \o "View drug information" glucose INCLUDEPICTURE "http://www.robbinspathology.com/images/linkdrug.gif" \* MERGEFORMATINET  tolerance test response. Dementia has been reported in some cases.  ION CHANNEL MYOPATHIES (CHANNELOPATHIES)  The ion channel myopathies, or channelopathies, are a group of familial diseases characterized clinically by myotonia, relapsing episodes of hypotonic paralysis (induced by vigorous exercise, cold, or a high-carbohydrate meal), or both. Hypotonia variants associated with elevated, depressed, or normal serum potassium levels at the time of the attack are called hyperkalemic, hypokalemic, and normokalemic periodic paralysis, respectively.  Pathogenesis. As their name indicates, at the molecular level these diseases are caused by mutations in genes that encode ion channels. HYPERLINK "http://www.robbinspathology.com/passthru/linktopage.cfm?showtab=toc&xrefID=R027057" \o "Go here now" \t "body" 57, HYPERLINK "http://www.robbinspathology.com/passthru/linktopage.cfm?showtab=toc&xrefID=R027058" \o "Go here now" \t "body" 58 Hyperkalemic periodic paralysis results from mutations in the gene that encodes a skeletal muscle sodium channel protein (SCN4A), which regulates the entry of sodium into muscle during contraction. The gene for hypokalemic periodic paralysis encodes a voltage-gated calcium channel.  page 1339 INCLUDEPICTURE "http://www.robbinspathology.com/images/pixel.gif" \* MERGEFORMATINET page 1340  Table 27-6. Congenital Myopathies Disease and InheritanceGene and LocusClinical FindingsPathologic FindingsCentral core disease; autosomal-dominantRyanodine receptor-1 (RYR1) gene; 19q13.1Early-onset hypotonia and nonprogressive weakness; associated skeletal deformities; may develop malignant hyperthermiaCytoplasmic cores are lightly eosinophilic and distinct from surrounding sarcoplasm; Found only in type 1 fibers, which usually predominate, best seen on NADH stainNemaline myopathy; autosomal-dominant or autosomal-recessiveAutosomal-dominant (NEM1)-Tropomyosin 3 (TPM3) gene; Autosomal-recessive (NEM2)-nebulin (NEB) gene; 2q22 Autosomal-dominant or recessive-skeletal muscle actin,  chain (ACTA1) gene; 1q42.1Weakness, hypotonia, and delayed motor development in childhood; may also be seen in adults; usually nonprogressive; involves proximal limb muscles most severely; skeletal abnormalities may be presentAggregates of subsarcolemmal spindle-shaped particles (nemaline rods); occur predominantly in type 1 fibers; derived from Z-band material (-actinin) and best seen on modified Gomori stainMyotubular (centronuclear) myopathy; X-linked (MTM1), autosomal-recessive, or autosomal-dominantX-linked-myotubularin (MTM1) gene; Xq28 Autosomal-dominant- myogenic factor 6 (MYF6) gene; 12q21 Autosomal-recessive-locus and gene unknownX-linked form presents in infancy with prominent hypotonia and poor prognosis; autosomal forms have limb weakness and are slowly progressive; autosomal-recessive form is intermediate in severity and prognosisAbundance of centrally located nuclei involving the majority of muscle fibers; central nuclei are usually confined to type 1 fibers, which are small in diameter, but can occur in both fiber types  Malignant hyperpyrexia (malignant hyperthermia) is a rare clinical syndrome characterized by a dramatic hypermetabolic state (tachycardia, tachypnea, muscle spasms, and later hyperpyrexia) triggered by the induction of anesthesia, usually with halogenated inhalational agents and succinylcholine. The clinical syndrome may also occur in predisposed individuals with hereditary muscle diseases, including congenital myopathies, dystrophinopathies, and metabolic myopathies. The only reliable method of diagnosis is contraction of biopsied muscle on exposure to anesthetic. Mutations in different genes have been identified in families with susceptibility to malignant hyperthermia, including genes encoding a voltage-gated calcium channel (lq32), an L-type voltage-dependent calcium channel (7q21-q22), and a ryanodine receptor (19q13.1). HYPERLINK "http://www.robbinspathology.com/passthru/linktopage.cfm?showtab=toc&xrefID=R027059" \o "Go here now" \t "body" 59  CONGENITAL MYOPATHIES  The congenital myopathies are a group of disorders defined largely on the basis of the pathologic findings within muscle. HYPERLINK "http://www.robbinspathology.com/passthru/linktopage.cfm?showtab=toc&xrefID=R027060" \o "Go here now" \t "body" 60 Most of these conditions share common clinical features, including onset in early life, nonprogressive or slowly progressive course, proximal or generalized muscle weakness, and hypotonia. Those affected at birth or in early infancy may present as "floppy babies" because of hypotonia or may have severe joint contractures (arthrogryposis); however, both hypotonia and arthrogryposis may also be caused by other neuromuscular dysfunction.   HYPERLINK "http://www.robbinspathology.com/content/"  INCLUDEPICTURE "http://www.robbinspathology.com/content/0721601871/graphics/thumbnails/S01871-027-f012.jpg" \* MERGEFORMATINET  HYPERLINK "http://www.robbinspathology.com/content/lightbox.cfm?action=add&ImgID=F027012&ImgBody=graphics/S01871-027-f012.jpg&ID=iBox" Add to lightbox  Figure 27-12 A, Nemaline myopathy with numerous rod-shaped, intracytoplasmic inclusions (dark purple structures). B, Electron micrograph of subsarcolemmal nemaline bodies, showing material of Z-band density. page 1340 INCLUDEPICTURE "http://www.robbinspathology.com/images/pixel.gif" \* MERGEFORMATINET page 1341 The best-characterized congenital myopathies are listed in  HYPERLINK "http://www.robbinspathology.com/passthru/linktopage.cfm?showtab=toc&xrefID=T027006" \o "Go here now" \t "body" Table 27-6.  HYPERLINK "http://www.robbinspathology.com/content/" \o "View now" Figure 27-12 shows the structural characteristics of nemaline ("rod body") myopathy, one of the most distinctive types.  MYOPATHIES ASSOCIATED WITH INBORN ERRORS OF METABOLISM  Many of the myopathies associated with metabolic disease are found in the setting of disorders of glycogen synthesis and degradation ( HYPERLINK "http://www.robbinspathology.com/passthru/linktopage.cfm?showtab=toc&xrefID=C00501871" \o "Go here now" \t "body" Chapter 5). Combinations of clinical, pathologic, and molecular information are used to arrive at a specific diagnosis. HYPERLINK "http://www.robbinspathology.com/passthru/linktopage.cfm?showtab=toc&xrefID=R027061" \o "Go here now" \t "body" 61 Myopathies can also result from disorders of mitochondrial function.  Lipid Myopathies  Abnormalities of the carnitine transport system or deficiencies of the mitochondrial dehydrogenase enzyme systems can lead to the accumulation of lipid droplets within muscle (lipid myopathies). HYPERLINK "http://www.robbinspathology.com/passthru/linktopage.cfm?showtab=toc&xrefID=R027062" \o "Go here now" \t "body" 62 To undergo -oxidation, cytoplasmic fatty acyl coenzyme A (acyl-CoA) esters are (1) transesterified with carnitine through the action of an outer membrane carnitine palmitoyltransferase (CPT I), (2) transported across the inner mitochondrial membrane, (3) re-esterified to acyl-CoA esters by an inner membrane mitochondrial CPT (CPT II), and (4) catabolized to acetyl-CoA units by the acyl-CoA dehydrogenases. In different patients with lipid myopathy, the defect may involve carnitine, acyl-CoA dehydrogenase, or CPT enzymes. HYPERLINK "http://www.robbinspathology.com/passthru/linktopage.cfm?showtab=toc&xrefID=R027063" \o "Go here now" \t "body" 63, HYPERLINK "http://www.robbinspathology.com/passthru/linktopage.cfm?showtab=toc&xrefID=R027064" \o "Go here now" \t "body" 64  Morphology. In all of these lipid myopathies, the principal morphologic characteristic is accumulation of lipid within myocytes. HYPERLINK "http://www.robbinspathology.com/passthru/linktopage.cfm?showtab=toc&xrefID=R027062" \o "Go here now" \t "body" 62 The myofibrils are separated by vacuoles that stain with oil red O or Sudan black and have the typical appearance of lipid by electron microscopy. The vacuoles occur predominantly in type 1 fibers, and they are dispersed diffusely throughout the fiber.  INCLUDEPICTURE "http://www.robbinspathology.com/images/pixel.gif" \* MERGEFORMATINET  Mitochondrial Myopathies (Oxidative Phosphorylation Diseases)  Approximately one-fifth of the proteins involved in mitochondrial oxidative phosphorylation are encoded by the mitochondrial genome (mtDNA); additionally, this circular  genome encodes 22 mitochondrial-specific tRNAs and 2 rRNA species. HYPERLINK "http://www.robbinspathology.com/passthru/linktopage.cfm?showtab=toc&xrefID=R027066" \o "Go here now" \t "body" 66, HYPERLINK "http://www.robbinspathology.com/passthru/linktopage.cfm?showtab=toc&xrefID=R027067" \o "Go here now" \t "body" 67 The remainder of the mitochondrial enzyme complexes are encoded in the nuclear genome. Mutations in both nuclear and mitochondrial genes cause the so-called mitochondrial myopathies. Diseases that involve the mtDNA show maternal inheritance, since only the oocyte contributes mitochondria to the embryo. There is a high mutation rate for mtDNA compared with nuclear DNA. HYPERLINK "http://www.robbinspathology.com/passthru/linktopage.cfm?showtab=toc&xrefID=R027068" \o "Go here now" \t "body" 68 The mitochondrial diseases may present in young adulthood and manifest with proximal muscle weakness, sometimes with severe involvement of the muscles that move the eyes (external ophthalmoplegia). The weakness may be accompanied by other neurologic symptoms, lactic acidosis, and cardiomyopathy, so this group of disorders is sometimes classified as mitochondrial encephalomyopathies ( HYPERLINK "http://www.robbinspathology.com/passthru/linktopage.cfm?showtab=toc&xrefID=C02801871" \o "Go here now" \t "body" Chapter 28).  Morphology. The most consistent pathologic finding in skeletal muscle is aggregates of abnormal mitochondria that are demonstrable only by special techniques. HYPERLINK "http://www.robbinspathology.com/passthru/linktopage.cfm?showtab=toc&xrefID=R027067" \o "Go here now" \t "body" 67, HYPERLINK "http://www.robbinspathology.com/passthru/linktopage.cfm?showtab=toc&xrefID=R027069" \o "Go here now" \t "body" 69, HYPERLINK "http://www.robbinspathology.com/passthru/linktopage.cfm?showtab=toc&xrefID=R027070" \o "Go here now" \t "body" 70 These occur under the subsarcolemma in early stages; but with severe involvement, they may extend throughout the fiber. The abnormal mitochondria impart a blotchy red appearance to the muscle fiber on the modified Gomori trichrome stain. Since they are also associated with distortion of the myofibrils, the muscle fiber contour becomes irregular on cross-section, and the descriptive term ragged red fibers has been applied to them ( HYPERLINK "http://www.robbinspathology.com/content/" \o "View now" Fig. 27-13A). HYPERLINK "http://www.robbinspathology.com/passthru/linktopage.cfm?showtab=toc&xrefID=R027067" \o "Go here now" \t "body" 67 The electron microscopic appearance is often distinctive: There are increased numbers of, and abnormalities in, the shape and size of mitochondria, some of which contain paracrystalline parking lot inclusions or alterations in the structure of cristae HYPERLINK "http://www.robbinspathology.com/passthru/linktopage.cfm?showtab=toc&xrefID=R027067" \o "Go here now" \t "body" 67, HYPERLINK "http://www.robbinspathology.com/passthru/linktopage.cfm?showtab=toc&xrefID=R027069" \o "Go here now" \t "body" 69 ( HYPERLINK "http://www.robbinspathology.com/content/" \o "View now" Fig. 27-13B). Cytochrome oxidase activity can be determined in muscle biopsy specimens using histochemistry, and cytochrome oxidase negative fibers may be present in a number of mitochondrial myopathies.  INCLUDEPICTURE "http://www.robbinspathology.com/images/pixel.gif" \* MERGEFORMATINET   HYPERLINK "http://www.robbinspathology.com/content/"  INCLUDEPICTURE "http://www.robbinspathology.com/content/0721601871/graphics/thumbnails/S01871-027-f013a.jpg" \* MERGEFORMATINET  HYPERLINK "http://www.robbinspathology.com/content/lightbox.cfm?action=add&ImgID=F027013&ImgBody=graphics/S01871-027-f013a.jpg&ID=iBox" Add to lightbox   HYPERLINK "http://www.robbinspathology.com/content/"  INCLUDEPICTURE "http://www.robbinspathology.com/content/0721601871/graphics/thumbnails/S01871-027-f013b.jpg" \* MERGEFORMATINET  HYPERLINK "http://www.robbinspathology.com/content/lightbox.cfm?action=add&ImgID=F027013&ImgBody=graphics/S01871-027-f013b.jpg&ID=iBox" Add to lightbox  Figure 27-13 A, Mitochondrial myopathy showing an irregular fiber with subsarcolemmal collections of mitochondria that stain red with the modified Gomori trichrome stain (ragged red fiber). B, Electron micrograph of mitochondria from biopsy specimen in A showing "parking lot" inclusions. page 1341 INCLUDEPICTURE "http://www.robbinspathology.com/images/pixel.gif" \* MERGEFORMATINET page 1342 Clinical Course and Genetics. The relationship between clinical course in the mitochondrial disorders and the genetic alterations is not entirely clear; however, three general categories have been defined. HYPERLINK "http://www.robbinspathology.com/passthru/linktopage.cfm?showtab=toc&xrefID=R027069" \o "Go here now" \t "body" 69 One set of mutations consists of point mutations in mtDNA. These disorders tend to show a maternal pattern of inheritance, and some examples include myoclonic epilepsy with ragged red fibers (MERRF), Leber hereditary optic neuropathy (LHON), and mitochondrial encephalomyopathy with lactic acidosis and strokelike episodes (MELAS). A second set of mutations involves genes encoded by nuclear DNA and shows autosomal-dominant or autosomal-recessive inheritance. Some cases of subacute necrotizing encephalopathy (Leigh syndrome), exertional myoglobinuria, and infantile X-linked cardioskeletal myopathy (Barth syndrome) are due to mutations in nuclear DNA. The final subset of mitochondrial myopathies is caused by deletions or duplications of mtDNA. Examples include chronic progressive external ophthalmoplegia, characterized by a myopathy with prominent weakness of external ocular movements. Kearns-Sayre syndrome, another myopathy in this group, is also characterized by ophthalmoplegia but, in addition, includes pigmentary degeneration of the retina and complete heart block. HYPERLINK "http://www.robbinspathology.com/passthru/linktopage.cfm?showtab=toc&xrefID=R027067" \o "Go here now" \t "body" 67  INFLAMMATORY MYOPATHIES  There are three subgroups of inflammatory muscle diseases: infectious, noninfectious inflammatory, and systemic inflammatory diseases that involve muscle along with other organs. Infectious myositis ( HYPERLINK "http://www.robbinspathology.com/passthru/linktopage.cfm?showtab=toc&xrefID=C00801871" \o "Go here now" \t "body" Chapter 8) and systemic inflammatory diseases ( HYPERLINK "http://www.robbinspathology.com/passthru/linktopage.cfm?showtab=toc&xrefID=C00601871" \o "Go here now" \t "body" Chapter 6) are discussed elsewhere.  Noninfectious Inflammatory Myopathies  Noninfectious inflammatory myopathies are a heterogeneous group of disorders that are probably immunologically mediated and are characterized by injury and inflammation of skeletal muscle. Three relatively distinct disorders, dermatomyositis, polymyositis, and inclusion body myositis, are included in this category. HYPERLINK "http://www.robbinspathology.com/passthru/linktopage.cfm?showtab=toc&xrefID=R027062" \o "Go here now" \t "body" 62, HYPERLINK "http://www.robbinspathology.com/passthru/linktopage.cfm?showtab=toc&xrefID=R027071" \o "Go here now" \t "body" 71 These may occur as an isolated myopathy or as one component of an immune-mediated systemic disease, particularly systemic sclerosis ( HYPERLINK "http://www.robbinspathology.com/passthru/linktopage.cfm?showtab=toc&xrefID=C00601871" \o "Go here now" \t "body" Chapter 6). The clinical features of each disorder are presented first to facilitate discussion of pathogenesis and morphologic changes.  Dermatomyositis. As the name implies, patients with dermatomyositis have an inflammatory disorder of the skin as well as skeletal muscle. It is characterized by a distinctive skin rash that may accompany or precede the onset of muscle disease. The classic rash takes the form of a lilac or heliotrope discoloration of the upper eyelids with periorbital edema ( HYPERLINK "http://www.robbinspathology.com/content/" \o "View now" Fig. 27-14A). It is often accompanied by a scaling erythematous eruption or dusky red patches over the knuckles, elbows, and knees (Grotton lesions). Muscle weakness is slow in onset, is bilaterally symmetric, is often accompanied by myalgias, and typically affects the proximal muscles first. As a result, tasks such as getting up from a chair and climbing steps become increasingly difficult. Fine movements controlled by distal muscles are affected only late in the disease. Dysphagia resulting from involvement of oropharyngeal and esophageal muscles occurs in one-third of the patients. Extramuscular manifestations, including interstitial lung disease, vasculitis, and myocarditis, may be present in some cases. Compared to the normal population, patients with dermatomyositis have a higher risk of developing visceral cancers. According to several studies, nearly 40% of adult patients with dermatomyositis have cancer. HYPERLINK "http://www.robbinspathology.com/passthru/linktopage.cfm?showtab=toc&xrefID=R027072" \o "Go here now" \t "body" 72   HYPERLINK "http://www.robbinspathology.com/content/"  INCLUDEPICTURE "http://www.robbinspathology.com/content/0721601871/graphics/thumbnails/S01871-027-f014.jpg" \* MERGEFORMATINET  HYPERLINK "http://www.robbinspathology.com/content/lightbox.cfm?action=add&ImgID=F027014&ImgBody=graphics/S01871-027-f014.jpg&ID=iBox" Add to lightbox  Figure 27-14 A, Dermatomyositis. Note the rash affecting the eyelids. B, Dermatomyositis. The histologic appearance of muscle shows perifascicular atrophy of muscle fibers and inflammation. C, Inclusion body myositis showing a vacuole within a myocyte. (Courtesy of Dr. Dennis Burns, Department of Pathology, University of Texas Southwestern Medical School, Dallas, TX.) page 1342 INCLUDEPICTURE "http://www.robbinspathology.com/images/pixel.gif" \* MERGEFORMATINET page 1343 Juvenile dermatomyositis has a similar onset of rash and muscle weakness but more often is accompanied by abdominal pain and involvement of the gastrointestinal tract. Mucosal ulceration, hemorrhage, and perforation may occur as the result of the dermatomyositis-associated vasculopathy. Calcinosis, which is uncommon in adult dermatomyositis, occurs in one third of patients with juvenile dermatomyositis. HYPERLINK "http://www.robbinspathology.com/passthru/linktopage.cfm?showtab=toc&xrefID=R027071" \o "Go here now" \t "body" 71, HYPERLINK "http://www.robbinspathology.com/passthru/linktopage.cfm?showtab=toc&xrefID=R027073" \o "Go here now" \t "body" 73  Polymyositis. In this inflammatory myopathy, the pattern of symmetric proximal muscle involvement is similar to that seen in dermatomyositis. It differs from dermatomyositis by the lack of cutaneous involvement and its occurrence mainly in adults. Similar to dermatomyositis, there may be inflammatory involvement of heart, lungs, and blood vessels.  Inclusion Body Myositis. In contrast with the other two entities, inclusion body myositis begins with the in volvement of distal muscles, especially extensors of the knee (quadriceps) and flexors of the wrists and fingers. Furthermore, the weakness may be asymmetric. It is an insidiously developing disorder that typically affects indi viduals over the age of 50 years. Most cases are sporadic, but familial cases have been recognized as "inclusion body myopathy." HYPERLINK "http://www.robbinspathology.com/passthru/linktopage.cfm?showtab=toc&xrefID=R027074" \o "Go here now" \t "body" 74  Etiology and Pathogenesis. The cause of inflammatory myopathies is unknown, but the tissue injury seems to be mediated by immunologic mechanisms. HYPERLINK "http://www.robbinspathology.com/passthru/linktopage.cfm?showtab=toc&xrefID=R027062" \o "Go here now" \t "body" 62, HYPERLINK "http://www.robbinspathology.com/passthru/linktopage.cfm?showtab=toc&xrefID=R027071" \o "Go here now" \t "body" 71 In dermatomyositis, capillaries seem to be the principal targets. The microvasculature is attacked by antibodies and complement, resulting in foci of ischemic myocyte necrosis. The deposition of antibodies and complement in capillaries precedes inflammation and destruction of muscle fibers. B cells and CD4+ T cells are present within the muscle, but there is a paucity of lymphocytes within the areas of myofiber injury. The perifascicular distribution of myocyte injury also suggests a vascular pathogenesis.  In contrast, polymyositis appears to be caused by cell-mediated injury of myocytes. CD8+ cytotoxic T cells and macrophages are seen near damaged muscle fibers, and the expression of HLA class I and class II molecules is increased on the sarcolemma of normal fibers. Similar to other immune-mediated diseases, ANAs are present in a variable number of cases, regardless of the clinical category ( HYPERLINK "http://www.robbinspathology.com/passthru/linktopage.cfm?showtab=toc&xrefID=C00601871" \o "Go here now" \t "body" Chapter 6). The specificities of autoantibodies are quite varied, but those directed against tRNA synthetases seem to be more or less specific for inflammatory myopathies.  The pathogenesis of inclusion body myositis is less clear. As in polymyositis, CD8+ cytotoxic T cells are found in the muscle, but in contrast to the other two forms of myositis, immunosuppressive therapy is not beneficial. Intracellular deposits of -amyloid protein, amyloid -pleated sheet fibrils, and hyperphosphorylated Tau protein are features in common with Alzheimer disease that have drawn attention to a possible relationship to aging. Abnormalities of protein folding have received some attention in inclusion body myopathy, HYPERLINK "http://www.robbinspathology.com/passthru/linktopage.cfm?showtab=toc&xrefID=R027074" \o "Go here now" \t "body" 74 as have similar deposits of amyloid fibrils in Alzheimer disease. HYPERLINK "http://www.robbinspathology.com/passthru/linktopage.cfm?showtab=toc&xrefID=R027075" \o "Go here now" \t "body" 75 The hereditary forms of inclusion body myopathy have a similar morphology but result from genetic mutations. The autosomal-recessive form is caused by mutations in the GNE gene (encoding UDP-N-acetylglucosamine-2 epimerase/N-acetylmannosamine kinase), and the autosomal-dominant form is caused by mutations in the gene encoding myosin heavy chain IIa. HYPERLINK "http://www.robbinspathology.com/passthru/linktopage.cfm?showtab=toc&xrefID=R027074" \o "Go here now" \t "body" 74 The role of these mutations in the pathogenesis of inclusion body myopathy is unclear.  Morphology. The histologic features of the individual forms of myositis are quite distinctive and are described separately. Dermatomyositis. The inflammatory infiltrates in dermatomyositis are located predominantly around small blood vessels and in the perimysial connective tissue. Typically, groups of atrophic fibers are particularly prominent at the periphery of fascicles. This "perifascicular atrophy" is sufficient for diagnosis, even if the inflammation is mild or absent ( HYPERLINK "http://www.robbinspathology.com/content/" \o "View now" Fig. 27-14B). The perifascicular atrophy is most likely related to a relative state of hypoperfusion of the periphery of muscle fascicles. Quantitative analyses reveal a dramatic reduction in the intramuscular capillaries, believed to result from vascular endothelial injury and fibrosis. Necrotic muscle fibers and regeneration may also be seen throughout the fascicle, as in polymyositis. Polymyositis. In this condition, the inflammatory cells are found in the endomysium. CD8+ lymphocytes and other lymphoid cells surround and invade healthy muscle fibers. Both necrotic and regenerating muscle fibers are scattered throughout the fascicle, without the perifascicular atrophy seen in dermatomyositis. There is no evidence of vascular injury in polymyositis. Inclusion Body Myositis. The diagnostic finding in inclusion body myositis is the presence of rimmed vacuoles ( HYPERLINK "http://www.robbinspathology.com/content/" \o "View now" Fig. 27-14C). The vacuoles are present within myocytes, and they are highlighted by basophilic granules at their periphery. In addition, the vacuolated fibers may also contain amyloid deposits that reveal typical staining with Congo Red. Under the electron microscope, tubular and filamentous inclusions are seen in the cytoplasm and the nucleus, and they are composed of -amyloid or hyperphosphorylated tau. HYPERLINK "http://www.robbinspathology.com/passthru/linktopage.cfm?showtab=toc&xrefID=R027076" \o "Go here now" \t "body" 76 The pattern of the inflammatory cell infiltrate is similar to that seen in polymyositis.  INCLUDEPICTURE "http://www.robbinspathology.com/images/pixel.gif" \* MERGEFORMATINET  The diagnosis of myositis is based on clinical symptoms, electromyography (EMG), elevated creatinine kinase in serum, and biopsy. EMG is particularly in formative in in flammatory myopathies, with mixed neurogenic and myopathic findings suggestive of inflammatory myopathy. As might be expected, muscle injury is associated with elevated serum levels of creatine kinase. Biopsy is required for definitive diagnosis. Immunosuppressive therapy is beneficial in adult and juvenile dermatomyositis and in polymyositis.  TOXIC MYOPATHIES  Thyrotoxic Myopathy  page 1343 INCLUDEPICTURE "http://www.robbinspathology.com/images/pixel.gif" \* MERGEFORMATINET page 1344 Thyrotoxic myopathy presents most commonly as an acute or chronic proximal muscle weakness that may precede the onset of other signs of thyroid dysfunction. Exophthalmic ophthalmoplegia is characterized by swelling of the eyelids, edema of the conjunctiva, and diplopia. In hypothyroidism, there may be cramping or aching of muscles, and movements and reflexes are slowed. Findings include fiber atrophy, an increased number of internal nuclei, glycogen aggregates, and, occasionally, deposition of mucopolysaccharides in the connective tissue.  In thyrotoxic myopathy, there is myofiber necrosis, regeneration, and interstitial lymphocytosis. In chronic thyrotoxic myopathy, there may be only slight variability of muscle fiber size, mitochondrial hypertrophy, and focal myofibril degeneration; fatty infiltration of muscle is seen in severe cases. Exophthalmic ophthalmoplegia is limited to the extraocular muscles, which may be edematous and enlarged. Another muscle disease associated with thyroid dysfunction is thyrotoxic periodic paralysis, which is characterized by episodic weakness that is often accompanied by hypokalemia. Males are affected four times more often than are females, with a high incidence in individuals of Japanese descent.  Ethanol Myopathy  Binge drinking of alcohol is known to produce an acute toxic syndrome of rhabdomyolysis with accompanying myoglobinuria, which may lead to renal failure. Clinically, the patient may acutely develop pain that is either generalized or confined to a single muscle group. Some patients have a complicated clinicopathologic syndrome consisting of proximal muscle weakness with electrophysiologic evidence of myopathy superimposed on alcoholic neuropathy. On histologic examination, there is swelling of myocytes, with fiber necrosis, myophagocytosis, and regeneration. There may also be evidence of denervation.  Drug-Induced Myopathies  Proximal muscle weakness and atrophy can occur as a result of the deleterious effects of steroids on muscle, whether in Cushing syndrome or during therapeutic administration of steroids, a condition known as steroid myopathy. The severity of clinical disability is variable and not directly related to the steroid level or the therapeutic regimen. It is characterized by muscle fiber atrophy, predominantly affecting type 2 fibers. HYPERLINK "http://www.robbinspathology.com/passthru/linktopage.cfm?showtab=toc&xrefID=R027076" \o "Go here now" \t "body" 76 When the myopathy is severe, there may be a bimodal distribution of fiber sizes, with type 1 fibers of nearly normal caliber and markedly atrophic type 2 fibers. Electron microscopy has shown dilation of the sarcoplasmic reticulum and thickening of the basal laminae.   HYPERLINK "http://www.robbinspathology.com/content/" \o "View drug information" Chloroquine INCLUDEPICTURE "http://www.robbinspathology.com/images/linkdrug.gif" \* MERGEFORMATINET , originally used in the treatment of malaria but subsequently used in other clinical settings, can produce a proximal myopathy in humans. The most prominent finding in  HYPERLINK "http://www.robbinspathology.com/content/" \o "View drug information" chloroquine INCLUDEPICTURE "http://www.robbinspathology.com/images/linkdrug.gif" \* MERGEFORMATINET  myopathy is the presence of vacuoles within myocytes. Two types of vacuoles have been described: autophagic membrane-bound vacuoles containing membranous debris and curvilinear bodies with short curved membranous structures with alternating light and dark zones. Vacuoles can be seen in as many as 50% of the myocytes, most commonly type 1 fibers, and with progression, myocyte necrosis may develop. A similar vacuolar myopathy occurs in some patients treated with hydrochloroquine. HYPERLINK "http://www.robbinspathology.com/passthru/linktopage.cfm?showtab=toc&xrefID=R027077" \o "Go here now" \t "body" 77  DISEASES OF THE NEUROMUSCULAR JUNCTION  Myasthenia Gravis  Now recognized as one of the best-defined forms of autoimmune disease, myasthenia gravis is a muscle disease caused by immune-mediated loss of acetylcholine receptors and having characteristic temporal and anatomic patterns as well as drug responses. The disease has a prevalence of about 3 in 100,000 persons. HYPERLINK "http://www.robbinspathology.com/passthru/linktopage.cfm?showtab=toc&xrefID=R027078" \o "Go here now" \t "body" 78 When arising before age 40 years, it is most commonly seen in women, but there is equal occurrence between the sexes in older patients. Thymic hyperplasia is found in 65% and thymoma in 15% of patients. Analysis of neuromuscular transmission in myasthenia gravis shows a decrease in the number of muscle acetylcholine receptors (AChRs), and circulating antibodies to the AChR are present in nearly all patients with myasthenia gravis. HYPERLINK "http://www.robbinspathology.com/passthru/linktopage.cfm?showtab=toc&xrefID=R027079" \o "Go here now" \t "body" 79, HYPERLINK "http://www.robbinspathology.com/passthru/linktopage.cfm?showtab=toc&xrefID=R027080" \o "Go here now" \t "body" 80 The disease can be passively transferred to animals with serum from affected patients.  Morphology. By light microscopic examination, muscle biopsy specimens from patients with myasthenia are usually unrevealing. In severe cases, disuse changes with type 2 fiber atrophy may be found. The postsynaptic membrane is simplified, with loss of AChRs from the region of the synapse. Immune complexes as well as the membrane attack complex of the complement cascade (C5-Cq) can be found along the postsynaptic membrane as well.  INCLUDEPICTURE "http://www.robbinspathology.com/images/pixel.gif" \* MERGEFORMATINET  Pathogenesis. In most cases, the autoantibodies against the AChR lead to loss of functional AChRs at the neuromuscular junction by: (1) fixing complement and causing direct injury to the post-synaptic membrane, (2) increasing the internalization and degradation of the receptors, and (3) inhibiting binding and function of ACh. Electrophysiologic studies are notable for decrement in motor responses with repeated stimulation; nerve conduction study findings are normal. 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Interestingly, in light of the immune-mediated etiology of the disease, thymic abnormalities are common in these patients, but the precise link with autoimmunity to AChRs is uncertain. Regardless of the pattern of thymic pathology, most patients show improvement after thymectomy.  Clinical Course. Typically, weakness begins with extraocular muscles; drooping eyelids (ptosis) and double vision (diplopia) cause the patient to seek medical attention. However, the initial symptoms may include generalized weakness. The weakness fluctuates, with alterations occurring during days, hours, or even minutes, and intercurrent medical conditions can lead to exacerbations of the weakness. Patients show improvement in strength in response to administration of anticholinesterase agents. This remains a most useful test on clinical examination.84 Respiratory compromise was a major cause of mortality in the past; 95% of patients now survive more than 5 years after diagnosis because of improved methods of treatment and better ventilatory support. Effective forms of treatment include anticholinesterase drugs,  HYPERLINK "http://www.robbinspathology.com/content/" \o "View drug information" prednisone INCLUDEPICTURE "http://www.robbinspathology.com/images/linkdrug.gif" \* MERGEFORMATINET , plasmapheresis, and resection of thymoma if it is present. HYPERLINK "http://www.robbinspathology.com/passthru/linktopage.cfm?showtab=toc&xrefID=R027081" \o "Go here now" \t "body" 81  Lambert-Eaton Myasthenic Syndrome  page 1344 INCLUDEPICTURE "http://www.robbinspathology.com/images/pixel.gif" \* MERGEFORMATINET page 1345 Lambert-Eaton myasthenic syndrome is a disease of the neuromuscular junction that is distinct from myasthenia gravis. It usually develops as a paraneoplastic process, most commonly with small cell carcinoma of the lung (60% of cases), although it can occur in the absence of underlying malignant disease. Patients develop proximal muscle weakness along with autonomic dysfunction. Unlike in myasthemia gravis, no clinical improvement is found upon administration of anticholinesterase agents, and electrophysiologic studies show evidence of enhanced neurotransmission with repetitive stimulation. These clinical features allow this disorder to be distinguished from myasthenia gravis.  The content of anticholinesterase is normal in neuromuscular junction synaptic vesicles, and the postsynaptic membrane is normally responsive to anticholinesterase, but fewer vesicles are released in response to each presynaptic action potential. Some patients have antibodies that recognize pre synaptic PQ-type voltage-gated calcium channels, and a similar disease can be transferred to animals with these antibodies. 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