Amyloid neuropathy: (A) scattered Congo Red positive material in endoneurium displays apple green birefringence under polarized light.

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2 Cơ vân

3 Cơ vân

4 Cơ vân (cắt dọc)

5 Amyloid neuropathy: (A) scattered Congo Red positive material in endoneurium displays apple green birefringence under polarized light. (A, Congo Red).

6 Amyloid neuropathy: (B) scattered Congo Red positive material in endoneurium displays apple green birefringence under polarized light. (B, Congo Red and polarized light).

7 Neurogenic atrophy with reinnervation. Fiber type grouping and targets in most type I fibers are shown (Cryosection, SDH).

8 Chronic neurogenic atrophy with reinnervation. The checkerboard staining pattern is lost and fiber type grouping is seen. (Cryosection, routine ATPase).

9 Two necrotic myofibers with pale sarcoplasm. (H&E).

10 Duchenne s muscular dystrophy. Regenerating myofibers characterized by vesicular nuclei with prominent nucleoli and sarcoplasmic basophilia. (H&E).

11 Infarct-like areas of necrosis are characteristic of dermatomyositis. (A) Transverse section.

12 Infarct-like areas of necrosis are characteristic of dermatomyositis.(b) Longitudinal section. (H&E).

13 Perifascicular fiber atrophy is typical of dermatomyositis. (Cryosection, H&E).

14 Inclusion body myositis. Sarcoplasmic vacuoles are decorated by hematoxyphilic granules. (A) Cryosection, transverse. (H&E).

15 Inclusion body myositis. Sarcoplasmic vacuoles are decorated by hematoxyphilic granules. (B) Plastic resin, longitudinal. (Toluidine Blue).

16 Inclusion body myositis. Amyloid deposition within sarcoplasm shows apple-green birefringence. (Congo Red).

17 Inclusion body myositis. Three intranuclear Congo Red positive inclusions (A) which all show apple-green birefringence (B).

18 Inclusion body myositis. Three intranuclear Congo Red positive inclusions (A) which all show apple-green birefringence (B).

19 Sarcoidosis. Epithelioid granuloma in endomysium. (H&E).

20 Trichinosis. (A) In compression test, the viable worm can be visualized by compressing a piece of fresh muscle between glass slide and coverslip. (Bright field optics).

21 Trichinosis. (B) Encysted organisms in skeletal muscle. (H&E).

22 Trichinosis: organisms in skeletal muscle. (H&E).

23 Trichinosis: organisms in skeletal muscle. (H&E).

24 Duchenne s dystrophy. Hypercontracted fibers are due to a plasma membrane defect that allows the influx of calcium ions. (Masson trichrome).

25 Duchenne s dystrophy carrier. A small number of non-necrotic fibers show attenuation or no reaction for dystrophin. (Immunostaining on cryosection).

26 Becker s dystrophy. The myopathic changes overlap with those of Duchenne s dystrophy. (Cryosection, routine ATPase).

27 Ring fibers. Circumferentially oriented myofibers are seen at the periphery of two transversally sectioned fibers. (Cryosection, modified Gomori trichrome).

28 Congenital fiber type disproportion. Hypertrophy of type II fibers and atrophy of type I fibers are shown. (Routine ATPase).

29 Centronuclear myopathy. Most fibers display central nucleus. Note a perinuclear halo of abnormality of myofibrils. (Cryosection, H&E).

30 Central core disease. Central areas of reduced activity are seen in all fibers. All fibers react as type I. (Cryosection, Succinic acid dehydrogenase).

31 Multicore disease. Spherical zones of reduced enzyme activity are present in type I fibers. Larger type II fibers are unaffected. (Cryosection, Phoshphotungstic acid

32 Nemaline myopathy. Thread-like subsarcolemmal aggregates are shown on longitudinal sections. (Phoshphotungstic acid hematoxylin).

33 Cytoplasmic bodies in desmin-related myopathy. (Plastic resin).

34 Hypokalemic periodic paralysis. Many fibers display large, optically empty vacuoles. (Plastic resin).

35 Acid maltase deficiency. (A) Sarcoplasmic vacuoles in a patient with acid maltase deficiency. (Cryosection, H&E).

36 Acid maltase deficiency. (B) Vacuoles filled with glycogen. (Cryosection, PAS).

37 Acid maltase deficiency. In adult onset the type I fibers are predominantly affected. Cryosection with SDH demonstrates type I fiber involvement (A) and PASdiastase shows no staining of vacuoles (B).

38 Acid maltase deficiency. In adult onset the type I fibers are predominantly affected. Cryosection with SDH demonstrates type I fiber involvement (A) and PASdiastase shows no staining of vacuoles (B).

39 McArdle s disease. Loss of myophosphorylase activity in patient with McArdle s disease ((A) compared to control (B) cryosection, myophosphorylase).

40 McArdle s disease. Loss of myophosphorylase activity in patient with McArdle s disease ((A) compared to control (B) cryosection, myophosphorylase).

41 Lovastatin toxicity. About 40% of the myofibers are undergoing necrosis. (Plastic resin).

42 Chloroquine myopathy. Severe vacuolization of myofibers with most of the affected fibers are type I in (A) with SDH and in (B) with modified Gomori trichrome. (Cryosection).

43 Chloroquine myopathy. Severe vacuolization of myofibers with most of the affected fibers are type I in (A) with SDH and in (B) with modified Gomori trichrome. (Cryosection).

44 Type II atrophy. This is a consistent finding in steroid-induced myopathy. (Cryosection, routine ATPase).