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
- 58 Peripheral nociception and the genesis of persistent clinical pain
- 59 Central nervous system mechanisms of pain
- 60 Management of chronic pain
- 61 Migraine
- 62 Cluster headache, other trigeminal autonomic syndromes and the short-lived headaches
- 63 Orofacial pain
- 64 Chronic daily headache
- Complete two-volume index
- PART VIII NEUROMUSCULAR DISORDERS
- 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
58 - Peripheral nociception and the genesis of persistent clinical pain
from PART VII - HEADACHE AND PAIN
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
- 58 Peripheral nociception and the genesis of persistent clinical pain
- 59 Central nervous system mechanisms of pain
- 60 Management of chronic pain
- 61 Migraine
- 62 Cluster headache, other trigeminal autonomic syndromes and the short-lived headaches
- 63 Orofacial pain
- 64 Chronic daily headache
- Complete two-volume index
- PART VIII NEUROMUSCULAR DISORDERS
- 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
Pain can be divided into two distinct categories, nociceptive and clinical. The detection of, or reaction to damaging or noxious stimuli, the phenomenon of nociception, is mediated in the periphery by highly specialized primary sensory neurons, the nociceptors. These have peripheral terminals that are activated only by high intensity mechanical, thermal and chemical stimuli. Nociceptive pain, the ‘ouch’ pain typically experienced on touching a hot object or stubbing a toe, is the readout from a protective system fundamental to maintaining bodily integrity in a potentially lethal environment. The key physiological role of this system is well illustrated by the tissue destruction produced both in the denervated (Charcot) joints and neuropathic ulcers in diabetic patients, or in the mutilating injuries seen in patients with congenital insensitivity to pain due to a loss of nociceptor sensory neurons during development, as a result of a mutation of the TrkA receptor (Indo et al., 1996).Nociceptive pain contributes to the pain associated with the onset of acute trauma and is amenable to a variety of therapies that directly target the nociceptor neuron. These include blocking input to the spinal cord with local anesthetic nerve blockade, epidural or spinal anesthesia or reducing transmission from the nociceptor to the CNS with high dose opioids.
Clinical pain has two general manifestations, that associated with tissue injury and inflammation, inflammatory pain, and that generated as a result of damage to the nervous system, neuropathic pain. Multiple distinct, but commonly coexisting pathophysiological mechanisms are responsible for the generation of clinical pain and these typically involve the recruitment of pain in response to sensory inputs other than just nociceptors (the pain is no longer purely nociceptive). Clinical pain, is moreover, the manifestation of profound alterations in sensory processing within the peripheral and central nervous systems, neuroplasticity. Two key features of clinical pain are that the pain may present in the absence of any obvious peripheral stimulus (spontaneous pain) and that there is typically an abnormal hypersensitivity to applied innocuous and noxious stimuli. Clinical pain can arise from insults to, or changes induced anywhere along, the somatosensory neuraxis from the peripheral innervation targets (as with osteo- or rheumatoid arthritis), in inflammatory pain, along peripheral nerves (postherpetic neuralgia and diabetic neuropathy), in the spinal cord (spinal cord injury) or the brain (stroke), for neuropathic pain.
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- Diseases of the Nervous SystemClinical Neuroscience and Therapeutic Principles, pp. 873 - 887Publisher: Cambridge University PressPrint publication year: 2002