Book contents
- Frontmatter
- Dedication
- Contents
- List of contributors
- Editor's preface
- PART I INTRODUCTION AND GENERAL PRINCIPLES
- PART II DISORDERS OF HIGHER FUNCTION
- PART III DISORDERS OF MOTOR CONTROL
- PART IV DISORDERS OF THE SPECIAL SENSES
- PART V DISORDERS OF SPINE AND SPINAL CORD
- PART VI DISORDERS OF BODY FUNCTION
- PART VII HEADACHE AND PAIN
- PART VIII NEUROMUSCULAR DISORDERS
- 65 Pathophysiology of nerve and root disorders
- 66 Toxic and metabolic neuropathies
- 67 Guillain–Barré syndrome
- 68 Hereditary neuropathies
- 69 Disorders of neuromuscular junction transmission
- 70 Disorders of striated muscle
- 71 Pathophysiology of myotonia and periodic paralysis
- 72 Pathophysiology of metabolic myopathies
- PART IX EPILEPSY
- PART X CEREBROVASCULAR DISORDERS
- PART XI NEOPLASTIC DISORDERS
- PART XII AUTOIMMUNE DISORDERS
- PART XIII DISORDERS OF MYELIN
- PART XIV INFECTIONS
- PART XV TRAUMA AND TOXIC DISORDERS
- PART XVI DEGENERATIVE DISORDERS
- PART XVII NEUROLOGICAL MANIFESTATIONS OF SYSTEMIC CONDITIONS
- Complete two-volume index
- Plate Section
70 - Disorders of striated muscle
from PART VIII - NEUROMUSCULAR DISORDERS
Published online by Cambridge University Press: 05 August 2016
- Frontmatter
- Dedication
- Contents
- List of contributors
- Editor's preface
- PART I INTRODUCTION AND GENERAL PRINCIPLES
- PART II DISORDERS OF HIGHER FUNCTION
- PART III DISORDERS OF MOTOR CONTROL
- PART IV DISORDERS OF THE SPECIAL SENSES
- PART V DISORDERS OF SPINE AND SPINAL CORD
- PART VI DISORDERS OF BODY FUNCTION
- PART VII HEADACHE AND PAIN
- PART VIII NEUROMUSCULAR DISORDERS
- 65 Pathophysiology of nerve and root disorders
- 66 Toxic and metabolic neuropathies
- 67 Guillain–Barré syndrome
- 68 Hereditary neuropathies
- 69 Disorders of neuromuscular junction transmission
- 70 Disorders of striated muscle
- 71 Pathophysiology of myotonia and periodic paralysis
- 72 Pathophysiology of metabolic myopathies
- PART IX EPILEPSY
- PART X CEREBROVASCULAR DISORDERS
- PART XI NEOPLASTIC DISORDERS
- PART XII AUTOIMMUNE DISORDERS
- PART XIII DISORDERS OF MYELIN
- PART XIV INFECTIONS
- PART XV TRAUMA AND TOXIC DISORDERS
- PART XVI DEGENERATIVE DISORDERS
- PART XVII NEUROLOGICAL MANIFESTATIONS OF SYSTEMIC CONDITIONS
- Complete two-volume index
- Plate Section
Summary
Muscle cells develop from mesenchymal cells in the embryo. They differentiate into two distinct morphologies, striated and non-striated. Striated muscle has an organized structure, and is able to contract rapidly. This is most commonly found as skeletal muscle, but also as cardiac muscle. Non-striated muscle, or smooth muscle, is generally not under voluntary control, maintains slow contraction, and is found in organs such as blood vessel walls, gastrointestinal tract, and urinary tract. In this chapter we deal with the skeletal form of striated muscle.
The basic unit of skeletal muscle is the muscle fibre. This is a single cell, with many nuclei. The muscle fibres are arranged in fascicles. Connective tissue within the fascicle is termed endomysium, the fascicle is surrounded by perimysium, and the whole muscle is surrounded by epimysium. Individual muscle fibres are 10–60 μ diameter, but are elongated, and may extend the full length of the muscle, up to 30 cm. The cytoplasm of the muscle fibre, or sarcoplasm, is composed of longitudinal threads of myofibrils, 1 μ diameter. In longitudinal section the myofibrils are transected by striations, or Z bands, which divide the myofibril into sarcomeres, 2.5 μ long at rest, and lead to the classification as striated muscle (Williams et al., 1989).
Within the sarcomere, two types of myofilament are present. Actin (5 nm diameter) attached to the Z band, and interdigitating myosin (12 nm diameter). In contracting muscle the actin filaments slide in relation to myosin. It is the making and breaking of connections between lateral projections on the myosin, and the actin, filaments, which causes the mechanical muscle contraction.
Within the muscle fibre are organelles and enzymes to provide the high level of energy necessary for muscle contraction. These include mitochondria, lipid vacuoles, and glycogen granules. Two main physiological groups of muscle fibres are recognized: slow (Type I) and fast (Type II). Slow muscles are more red than fast, and are rich in mitochondria and oxidative enzymes, but poor in phosphorylation. Slow fibres perform aerobic metabolism, in addition to the glycolytic metabolism which predominates in fast fibres. Slow muscles are particularly suited to sustained contraction, as in postural muscles, and fast muscle to more rapid movements. Most muscles contain a mixture of the two types of fibre.
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- Diseases of the Nervous SystemClinical Neuroscience and Therapeutic Principles, pp. 1163 - 1182Publisher: Cambridge University PressPrint publication year: 2002