Muscle Fiber Splitting Research Articles

LONGITUDINAL FIBRE SPLITTING IN NEUROGENIC MUSCULAR DISORDERS—ITS RELATION TO THE PATHOGENESIS OF ‘MYOPATHIC’ CHANGE

In 15 patients with neurogenic muscular disorders, including cases of motor neuron disease, Wohlfart-Kugelberg-Welander disease, Davidenkow's scapuloperoneal syndrome, peripheral neuropathy and traumatic neuropathies, muscle biopsies were carried out, usually after EMG or single fibre EMG investigation. Enzyme histochemical and electronmicroscopic techniques were used to study longitudinal fibre splitting and its quantitative relation to the general changes in the biopsies. In 9 cases serial sections were used to study the longitudinal extent and character of fibre splitting. Longitudinal fibre splitting was found in 14 cases. It was prominent in Type 1 fibres, and in those biopsies in which hypertrophy was most marked. It was often associated with central migration of sarcolemmal nuclei. Ultrastructurally there was evidence that splitting consisted of mechanical disruption of the myofibrillar pattern, followed by an active process of membrane formation. We suggest that longitudinal splitting of muscle fibres, induced by overload of poorly innervated, hypertrophied fibres, can account for many of the "myopathic" changes found in neurogenic muscular disorders.

Internal structure of cat extraocular muscle

Teasing preparations of cat extraocular muscles (EOM) were used to study the arrangement of muscle fibers and the distribution of the different cholinesterase-positive sites, i.e. (1) large motor endplates, (2) small motor endings of the 'en grappe' type, (3) myotendinous junctions and (4) myomyous junctions. The distribution of these cholinesterase-positive structures gives clear evidence of a complex muscle architecture of cat EOM. In the global layer of cat EOM, only multiply innervated muscle fibers run the whole length of the muscle. The focally innervated muscle fibers are generally shorter; they are usually arranged in series of two to three fibers being interconnected by myomyous junctions. Moreover, muscle fiber splitting is frequently present resulting in a netlike arrangement of muscle fibers. Most of the myomyous junctions occur between focally innervated muscle fibers, but also end-to-side connections of focally to multiply innervated muscle fibers are observed; multiply innervated muscle fi0ers have not been found connected to each other. In this layer, large motor endplates are distributed in several bands between origin and insertion. In the orbital layer all muscle fibers run from tendon to tendon, focally as well as multiply innervated ones. Here, large motor endplates are confined to a band in the middle of the muscle, and myomyous junctions are generally absent. Some functional implications of this complex architecture of cat EOM are discussed.

Abnormal intrafusal muscle fibres in myotonic dystrophy: a study using serial sections

Studies of the extent and complexity of intrafusal muscle fibre splitting in myotonic dystrophy have been carried out in three spindles obtained at muscle biopsy, and in nine spindles found in the lumbrical muscle of a case that came to necropsy. It is suggested that splitting, due to mechanical stresses, leads to a regenerative response in the separated fragments.

Changes in the electron microscopic structure of slow and fast skeletal muscle fibres of the mouse after the local injection of botulinum toxin

A sublethal dose of botulinum toxin was injected into the calf muscles of one leg in mice and caused paralysis of those muscles within 24 hr. Recovery from paralysis took place after several weeks. Electron-microscopic studies were made of muscle fibres of soleus (a “slow” muscle) and of the superficial part of gastrocnemius (composed of “fast” fibres) from animals surviving from 4 days to 33 weeks after the injection of toxin. Muscle fibres from both regions became atrophied during the first 2–3 weeks and folds of redundant basement membrane became dissociated from the plasma membranes of the atrophied fibres. The atrophied fibres contained lysosomes and multivesicular bodies but their glycogen content was much reduced. By the 4th–6th week the fibres of soleus became restored to normal in size and abnormally abundant glycogen was then found. Fibres of gastrocnemius became more severely atrophied and showed many changes which were not seen in soleus fibres. These included focal disintegration of myofilaments, tubular aggregates, “helical complexes” and dilatation of cisternae. Recovery of gastrocnemius fibres began only after the 5th–6th week. In later stages there was splitting of muscle fibres in gastrocnemius and tubular aggregates, disoriented myofibrils forming annulets and centrally-located nuclei were common. Some fibres became considerably larger than normal but others showed extreme atrophy and disorganization of their internal structure many months after the injection of the toxin.