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
65 - Pathophysiology of nerve and root disorders
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
The peripheral nervous system (PNS) represents the final common anatomical pathway linking the brain with the outside world. This chapter deals with the pathological basis of disorders of the PNS, including symptoms and signs related to abnormalities of peripheral nerves, spinal roots, and sensory and autonomic ganglia. Specific neurological disorders are discussed here only in the context of their representative value in understanding PNS dysfunction. Readers are directed to other chapters within this section and the section on Degenerative Disorders for more complete discussions of PNS diseases.
Anatomical organization
The neuronal cell bodies for the PNS are located within the dorsal root ganglia (primary sensory neurons), the cranial and spinal sympathetic and parasympathetic ganglia, and the anterior horn of the spinal cord (motor neurons). The perikaryal organization reflects the enormous synthetic requirements for maintaining the axonal and dendritic processes that may represent many times the volume of the perikaryon itself. Prominent within the perikaryal cytoplasm are mitochondria which are responsible for the production of ATP, and the Nissl substance which is made up of free and membrane-bound ribosomes (rough endoplasmic reticulum). The pattern of Nissl staining seems to reflect the metabolic state of the neuron, and changes in the staining pattern are associated with injury to the neuron. The classic example of these changes is chromatolysis (Fig. 65.1), where axonal injury leads to swelling of the cell body, eccentric displacement of the nucleus, and margination of the Nissl substance (for review see Peters et al., 1991). These changes are not necessarily associated with the death of the neuron; to the contrary they frequently reflect a reparative and regenerative stage after neuronal injury (Bodian & Mellors, 1945). Chromatolytic changes are stimulated by a variety of injuries including root avulsion, axonal transection, and even peripheral neuropathy.
Neurons communicate with one another and with their effector organs by transmitting chemical and electrical signals via dendrites and axons. Dendrites and axons may be distinguished by a variety of structural and functional characteristics (Table 65.1), however a practical distinction is that dendrites are responsible for input to and axons are responsible for output from the cell body.
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- Diseases of the Nervous SystemClinical Neuroscience and Therapeutic Principles, pp. 1075 - 1091Publisher: Cambridge University PressPrint publication year: 2002
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