Denervated muscle fibres in hereditary mouse dystrophy.

McComas, Alan J.; Mrozek, K

doi:10.1136/jnnp.30.6.526

Cited by 95 publications

(16 citation statements)

References 8 publications

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“…However, reductions in both discharge frequency (Conrad and Glaser, 1964) and amplitude (McComas and Mossawy, 1965) of miniature end plate potentials have been reported in dystrophic muscle, and McComas and Mrozek (1967) showed that many dystrophic muscle fibres were capable of responding to direct stimulation, but not to indirect stimulation. These findings suggest strongly that the 'myasthenic-like' response is presynaptic in origin, although it is not possible to comment on the precise nature of the defect.…”

Section: Each Increment In Tension Is Due To Thementioning

confidence: 99%

“…For three reasons, the validity of the results so obtained may be questioned. Isolated mammalian skeletal muscle rapidly becomes hypoxic, gains sodium ions and loses potassium ions (Kmjevic and Miledi, 1958;Creese, 1960;Creese and Northover, 1961) low temperatures have a marked effect on the mechanical properties of mammalian skeletal muscles, and may lead to misleading figures of, for example, twitch/tetanus ratio (Buller, Ranatunga, and Smith, 1968;Close and Hoh, 1968); direct stimulation of isolated, curarized muscle bears little relationship to the disease process, especially since it is now known that neuromuscular transmission may be impaired (McComas and Mrozek, 1967). This paper describes some mechanical properties of the tibialis anterior muscle of normal and dystrophic mice measured by an in vivo technique.…”

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confidence: 99%

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Mechanical properties of dystrophic mouse muscle

Harris¹,

Wilson²

1971

Journal of Neurology, Neurosurgery & Psychiatry

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Section: Each Increment In Tension Is Due To Thementioning

confidence: 99%

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confidence: 99%

Mechanical properties of dystrophic mouse muscle

Harris¹,

Wilson²

1971

Journal of Neurology, Neurosurgery & Psychiatry

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“…More recently Bradley & Jenkinson (1973) described abnormalities of myelination of the dorsal and ventral nerve roots in dystrophic mice, while Bradley & Jaros (1973) showed reduction in axoplasmic flow. McComas & Mrozek (1967) also indicated a reduction in membrane conductance and demonstrated denervation in gastrocnemius and tibialis anterior muscles of dystrophic mice with micro-electrode techniques and intracellular recording of muscle fibres. Harris & Wilson (1971) were not HALYNA MARUSYK AND G. MONCKTON able to demonstrate any frankly denervated fibres.…”

Section: Introductionmentioning

confidence: 99%

The study of (Methyl‐3H)decamethonium dichloride incorporation into normal and dystrophic mouse muscle.

Marusyk¹,

Monckton²

1976

The Journal of Physiology

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SUMMARY1. decamethonium dichloride was injected intravenously into the tail vein of dystrophic and normal mice of the Bar Harbour strain 129 ReJ/dy in paralysing doses.2. Scintillation counts were made of 1 mm sections of diaphragm and tibialis anterior which showed a normal distribution of tritiated decamethonium in the dystrophic animals.3. Intraperitoneal injections of L-[y-3H]leucine were made into dystrophic and normal mice. Examination of diaphragm and tibialis anterior by scintillation counting showed the abnormal uptake typical of dystrophic involvement of murine muscle.4. The normal distribution of [methyl-3H]decamethonium dichloride uptake by the dystrophic muscle does not support the concept of active denervation in this disease.

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“…There is experimental evidence that blockage of trophic flow will lead to development of fibrillations in the absence of Wallerian degeneration (1 6 ) . Second, single fiber electromyography in myositis has shown that if part of a muscle cell is separated from the neuromuscular junction by degeneration of a short segment of the cell, then fibrillation potentials will develop in the distal part of the cell; and because degeneration and regeneration of muscles is a feature of myositis, this may be a relatively common cause of fibrillation potentials (17). On recovery, reinnervation potentials would not be expected to develop.…”

Section: Discussionmentioning

confidence: 99%

Regional migratory osteoporosis. a denervation disease

McCord

Nies

Campion

et al. 1978

Arthritis & Rheumatism

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Regional migratory osteoporosis is an uncommon entity characterized by sudden attacks of migrating lower extremity paraarticular pain, local edema, and muscle atrophy; the disease is verified by radiologic demineralization and bone scan uptake. The etiology and pathogenesis are unknown. We describe a case of regional migratory osteoporosis followed over nine years by serial electromyographic studies documenting denervation patterns coincident in time and location of each acute attack. The substantiation of denervation in regional migratory osteoporosis is of both diagnostic and pathogenetic significance. clinical picture emerged of severe lower extremity paraarticular pain, muscle atrophy, and localized edema associated with radiologic osteoporosis, with the symptoms lasting 4 t o 12 months (2-13). T h e diagnosis was usually made by exclusion. Multiple biopsies were needed to exclude infectious, granulomatous, and neoplastic diseases.A patient with multiple attacks who was followed over a 9 year period is described. Electromyogram ( E M G ) abnormalities of denervation coincided both anatomically and chronologically to the clinically involved areas. CASE REPORTA SS-year-old white female presented to Harbor General Hospital in June 1966 after 6 months of unprovoked left knee pain followed by 3 months of pain and swelling of the left foot and ankle. She was taking no medication. Physical examination revealed weakness and muscle atrophy confined to the left thigh and calf with grade 4/5 muscle strength in the left quadriceps and anterior tibia1 muscles (strength judged on a 0 to 5 scale with 5/5 normal, 4/5 and 3/5 moderate, 2/5 minimal resistance against gravity, and 1/5 flicker movements). A livido skin pattern overlaid brawny edema of the left foot and ankle. Motion was limited by tenderness and pain. Neurologic examination was normal.Laboratory values that were normal included urinalysis, CBC, calcium, phosphorus, alkaline phosphatase, BUN, creatinine, uric acid, and 24 hour urine calcium. The Wintrobe ESR was 40-50 mm/hr, cholesterol value was 283 mg/dl, and a first strength PPD was positive. Serum electrophoresis, immunoglobulin levels, cryoglobulin, urinary Bence Jones protein, latex fixation, and anti-nuclear antibody studies were also

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Denervated muscle fibres in hereditary mouse dystrophy.

Cited by 95 publications

References 8 publications

Mechanical properties of dystrophic mouse muscle

Mechanical properties of dystrophic mouse muscle

The study of (Methyl‐3H)decamethonium dichloride incorporation into normal and dystrophic mouse muscle.

Regional migratory osteoporosis. a denervation disease

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