eMedicine Specialties > Physical Medicine and Rehabilitation > Muscular Dystrophy

Limb-Girdle Muscular Dystrophy: Differential Diagnoses & Workup

Author: Vinod Sahgal, MD, MS, Chairman, Department of Physical Medicine and Rehabilitation Services, The Cleveland Clinic Foundation; Professor, Department of Physical Medicine and Rehabilitation, Ohio State University
Coauthor(s): Steven Reger, PhD, CP, Professor, Department of Industrial and Manufacturing Engineering, Cleveland State University; Director of Rehabilitation Technology, Department of Physical Medicine and Rehabilitation, Cleveland State University
Contributor Information and Disclosures

Updated: Apr 30, 2009

Differential Diagnoses

Becker Muscular Dystrophy

Other Problems to Be Considered

Acute polio
Chronic inflammatory myopathies
Malignancy
Metabolic and congential myopathies
Mixed connective-tissue disease
Polyarteritis
Primary lateral sclerosis
Rheumatoid arthritis
Steroid-induced myopathy

Duchenne muscular dystrophy: Duchenne or Becker dystrophies tend to manifest in childhood with a male predominance, calf hypertrophy, scoliosis, and marked elevation of CK levels. Sex-linked recessive inheritance and the demonstration of absence or alteration of dystrophin confirm the diagnosis of these disorders. Approximately 60% of cases are sporadic; thus, muscle biopsy is an important diagnostic tool.

Scleroderma, polymyositis, and dermatomyositis: Differentiation from scleroderma, polymyositis, and dermatomyositis may be made by their clinical courses, which are often characterized by more rapid progression, involvement of skin and neck muscles, and dysphagia.

Polymyositis: Electromyography (EMG) in patients with polymyositis reveals polyphasic and fibrillation potentials, as well as myopathic potentials and positive sharp waves. A clinical response to steroids solidifies the diagnosis of polymyositis.

Chronic spinal muscular atrophy: This is another entity that can have proximal weakness and elevated CK levels; however, neurogenic changes seen during EMG may include fibrillation and fasciculation potentials and a reduced recruitment pattern, as well as giant action potentials. Muscle biopsy results showing target fibers and group atrophy with angular fibers also help confirm this diagnosis.

Metabolic and congenital myopathies (eg, central core disease, nemaline centronuclear myopathy, congenital fiber-type disproportion): These may appear clinically similar to limb-girdle muscular dystrophy (LGMD) syndrome, but all of these conditions have typical diagnostic muscle biopsy findings that show central cores, nemaline rods, centronuclear fibers of congenital fiber-type disproportions, and sarcoplasmic body myopathy. Onset is also generally at an early age, and a more diffuse distribution of weakness occurs.

In summary, evaluation of a patient with LGMD syndrome must take into consideration an accurate clinical history with special emphasis on family history; a detailed physical examination; laboratory investigation, including CK; EMG; and possibly, muscle biopsy, molecular genetic studies, and an evaluation of the absence or alteration of dystrophin.

Workup

Laboratory Studies

  • The single biochemical abnormality in limb-girdle muscular dystrophy (LGMD) syndrome is the elevation of the CK level. The CK elevation in the recessively inherited varieties is significantly higher than in the rest of the spectrum of LGMDs (eg, dominantly inherited, Erb dystrophy, pelvifemoral variety). However, the CK level is usually significantly lower than in patients with Duchenne or Becker dystrophy. Individuals with Duchenne or Becker dystrophy may have elevated creatine in the urine, but they do not have myoglobinuria.42

Other Tests

  • Electromyographic abnormalities are atypical in limb-girdle muscular dystrophy (LGMD), and EMG is more useful to exclude other disorders in the differential. Nerve conduction velocities do not show abnormalities in cases of LGMD. Repetitive stimulation produces good posttetanic potentiation and no myasthenic response. Rarely, EMG of a single fiber may reveal a mild decrease in fiber density and increased jitter, but the most consistent finding is normal fiber density.

Procedures

  • Muscle biopsy findings in limb-girdle muscular dystrophy are characterized by necrotic fibers with endomysial perivascular or perimysial mononuclear infiltration. (See image below and Image 9.)
Trichrome stain. Note variation in fiber size. Ne...

Trichrome stain. Note variation in fiber size. Necrotic fiber giant fibers and cytoplasmic inclusions.

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Trichrome stain. Note variation in fiber size. Ne...

Trichrome stain. Note variation in fiber size. Necrotic fiber giant fibers and cytoplasmic inclusions.


Histologic Findings

In limb-girdle muscular dystrophy, hematoxylin and eosin stain and trichrome stain show a most striking predilection toward large fiber size (see first image below and Image 1). These large fibers show splitting (see second image below and Image 2) and can be 3-4 times the size of a normal fiber. The splitting of fibers produces the false appearance of grouping and angulation without a large group of atrophic fibers. Frequently, ring fibers and cytoplasmic masses are also observed (see third image below and Image 3). Some fibers are characterized by profuse internal nuclei (see fourth image below and Image 4). The myoarchitecture shows evidence of necrosis and basophilia (see fifth image below and Image 5). Increases in endomysial fibrous tissue are noted, without significant evidence of cellular response.

The histochemistry of the muscle biopsy specimens generally shows a predominance of type I fibers and a reduction of type IIB fibers. Because splitting is a common feature of this disease, the split fibers are shown to belong to the same fiber type and give an appearance of fiber-type grouping (see sixth image below and Image 6). Ultrastructure examination shows nonspecific changes consisting of Z-band spreading, mitochondrial abnormalities with inclusions as central nuclei, and disruption of the A and I bands (see seventh image below and Image 7).

Hematoxylin and eosin stain. Note the variation i...

Hematoxylin and eosin stain. Note the variation in fiber size. Necrotic fiber is shown with many nuclei (magnification 250X).

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Hematoxylin and eosin stain. Note the variation i...

Hematoxylin and eosin stain. Note the variation in fiber size. Necrotic fiber is shown with many nuclei (magnification 250X).


Marked endomysial fibrosis with atrophic and hype...

Marked endomysial fibrosis with atrophic and hypertrophic fibers.

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Marked endomysial fibrosis with atrophic and hype...

Marked endomysial fibrosis with atrophic and hypertrophic fibers.


Hematoxylin and eosin stain. Note the splitting o...

Hematoxylin and eosin stain. Note the splitting of the fiber.

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Hematoxylin and eosin stain. Note the splitting o...

Hematoxylin and eosin stain. Note the splitting of the fiber.


Gomori trichrome stain. Note the variation in fib...

Gomori trichrome stain. Note the variation in fiber size and subsarcolemmal vacuoles, central nuclei, and subsarcolemmal collection of trichrome-positive material.

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Gomori trichrome stain. Note the variation in fib...

Gomori trichrome stain. Note the variation in fiber size and subsarcolemmal vacuoles, central nuclei, and subsarcolemmal collection of trichrome-positive material.


Light type I and dark type IIA fibers.

Light type I and dark type IIA fibers.

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Light type I and dark type IIA fibers.

Light type I and dark type IIA fibers.


Electron micrograph showing abnormal mitochondria...

Electron micrograph showing abnormal mitochondria, a large lysosomal body, and a central nucleus.

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Electron micrograph showing abnormal mitochondria...

Electron micrograph showing abnormal mitochondria, a large lysosomal body, and a central nucleus.


Electron micrograph showing mitochondria with par...

Electron micrograph showing mitochondria with paracrystalline inclusions and lamellar bodies

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Electron micrograph showing mitochondria with par...

Electron micrograph showing mitochondria with paracrystalline inclusions and lamellar bodies


More on Limb-Girdle Muscular Dystrophy

Overview: Limb-Girdle Muscular Dystrophy
Differential Diagnoses & Workup: Limb-Girdle Muscular Dystrophy
Treatment & Medication: Limb-Girdle Muscular Dystrophy
Follow-up: Limb-Girdle Muscular Dystrophy
Multimedia: Limb-Girdle Muscular Dystrophy
References
Further Reading
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Keywords

limb-girdle muscular dystrophy, muscular dystrophy, dystrophy, muscle disease, muscular disease, polymyositis, spinal muscular atrophy, muscular atrophy, muscular dystrophy symptoms, neuromuscular disease, muscle diseases, limb girdle muscular dystrophy, limb girdle dystrophy, muscular dystrophy causes, neuromuscular diseases, Leyden-Mobius muscular dystrophy, pelvofemoral muscular dystrophy, scapulohumeral muscular dystrophy, LGMD, limb-girdle dystrophy, dystrophia muscularis progressiva, sarcoglycanopathy, sarcoglycanopathies

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Contributor Information and Disclosures

Author

Vinod Sahgal, MD, MS, Chairman, Department of Physical Medicine and Rehabilitation Services, The Cleveland Clinic Foundation; Professor, Department of Physical Medicine and Rehabilitation, Ohio State University
Vinod Sahgal, MD, MS is a member of the following medical societies: American Academy of Neurology, American Academy of Physical Medicine and Rehabilitation, American Congress of Rehabilitation Medicine, American Medical Association, and American Spinal Injury Association
Disclosure: Nothing to disclose.

Coauthor(s)

Steven Reger, PhD, CP, Professor, Department of Industrial and Manufacturing Engineering, Cleveland State University; Director of Rehabilitation Technology, Department of Physical Medicine and Rehabilitation, Cleveland State University
Steven Reger, PhD, CP is a member of the following medical societies: Association for Academic Psychiatry and New York Academy of Sciences
Disclosure: Nothing to disclose.

Medical Editor

Elizabeth A Moberg-Wolff, MD, Associate Professor and Pediatric PM&R Fellowship Director, Department of Physical Medicine and Rehabilitation, Medical College of Wisconsin; Program Director, Tone Management and Mobility, Department of Physical Medicine and Rehabilitation, Children's Hospital of Wisconsin
Elizabeth A Moberg-Wolff, MD is a member of the following medical societies: American Academy for Cerebral Palsy and Developmental Medicine and American Academy of Physical Medicine and Rehabilitation
Disclosure: Medtronic Neurological Grant/research funds Speaking and teaching

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Kat Kolaski, MD, Assistant Professor, Departments of Orthopedic Surgery and Pediatrics, Wake Forest University School of Medicine
Kat Kolaski, MD is a member of the following medical societies: American Academy for Cerebral Palsy and Developmental Medicine and American Academy of Physical Medicine and Rehabilitation
Disclosure: Nothing to disclose.

CME Editor

Kelly L Allen, MD, Regional Medical Director, IMX-Medical Management Services
Disclosure: Nothing to disclose.

Chief Editor

Denise I Campagnolo, MD, MS, Director of Multiple Sclerosis Clinical Research and Staff Physiatrist, Barrow Neurology Clinics, St Joseph's Hospital and Medical Center; Investigator for Barrow Neurology Clinics; Director, NARCOMS Project for Consortium of MS Centers
Denise I Campagnolo, MD, MS is a member of the following medical societies: Alpha Omega Alpha, American Association of Neuromuscular and Electrodiagnostic Medicine, American Paraplegia Society, Association of Academic Physiatrists, and Consortium of Multiple Sclerosis Centers
Disclosure: Teva Neuroscience Honoraria Speaking and teaching; Serono-Pfizer Honoraria Speaking and teaching

 
 
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