Pain in fibromyalgia syndrome

M. Cazzola, F. Atzeni, Piercarlo Sarzi-Puttini

Research output: Contribution to journalArticle

1 Citation (Scopus)

Abstract

The fibromyalgia syndrome (FM) is identified as widespread pain in combination with tenderness at 11 or more out of 18 specific tender point sites. Premorbid psychiatric condition and poor coping skills seem to predispose patients for development of FM. The origin of the pain symptoms in FM, according to the major of the researchers, stands for an alteration of the mechanisms of transmission, modulation and processing of the nociceptive stimuli in the central nervous system (CNS). The problem of FM pain can therefore be faced following two different conceptual models: a) a biomedical model, which addressed the scientific research, in the last century, toward an anatomo-pathological, neurophysiological and neuroendocrine analysis; b) a biopsychosocial model, which is collecting more and more consensus, in which the importance of emotional, cognitive and behavioural factors on the perception and above-all on the chronicity of pain is underlined. The physio-pathological mechanism for the reduction of the pain threshold should be identified in the central neuronal sensitization, which involves cells localized both at spinal level (posterior horns of the spinal tissue) both at supraspinal level. The central sensitization can be defined as a state Of neuronal hyperexcitability in response to peripheral stimuli; the result is a modification of the sensorial process that can determine: a) increase of pain perception in the site of a nociceptive stimulation (primary hyperalgesia); 2) appearance of in the normal tissues adjacent to the site of the nociceptive stimulation (secondary hyperalgesia); 3) pain in normal tissues distant from the site of the noxious stimuli (referred pain); 4) appearance of pain followed by a non-pain mechanical stimuli (allodynia). According to the biopsychosocial model pain experience in FM patients may be the result of highly interrelated biological, cognitive-behavioural, environmental and socio-cultural variables which explain the different symptoms patterns of each patient and also the different response to the proposed therapeutic approaches. The most sustained theories, actually, is that FM, as many other syndromes classified in the group of the spectrum of affective disorders, represents the consequence of a series of neuroendocrine and autonomic responses to a socio-environmental stress situation; these responses have lost, in this context, their original meaning of maintenance of homeostasis becoming, on the opposite, a cause of maladaptive behaviour.

Original languageEnglish
Pages (from-to)57-68
Number of pages12
JournalJournal of Functional Syndromes
Volume2
Issue number1
Publication statusPublished - Jul 2002

Fingerprint

Fibromyalgia
Pain
Hyperalgesia
Central Nervous System Sensitization
Referred Pain
Pain Perception
Pain Threshold
Psychological Adaptation
Horns
Mood Disorders
Psychiatry
Consensus
Homeostasis
Central Nervous System
Maintenance
Research Personnel
Research

Keywords

  • Fibromyalgia syndrome
  • Nociception
  • Pain
  • Pain threshold

ASJC Scopus subject areas

  • Internal Medicine
  • Psychiatry and Mental health
  • Leadership and Management

Cite this

Cazzola, M., Atzeni, F., & Sarzi-Puttini, P. (2002). Pain in fibromyalgia syndrome. Journal of Functional Syndromes, 2(1), 57-68.

Pain in fibromyalgia syndrome. / Cazzola, M.; Atzeni, F.; Sarzi-Puttini, Piercarlo.

In: Journal of Functional Syndromes, Vol. 2, No. 1, 07.2002, p. 57-68.

Research output: Contribution to journalArticle

Cazzola, M, Atzeni, F & Sarzi-Puttini, P 2002, 'Pain in fibromyalgia syndrome', Journal of Functional Syndromes, vol. 2, no. 1, pp. 57-68.
Cazzola M, Atzeni F, Sarzi-Puttini P. Pain in fibromyalgia syndrome. Journal of Functional Syndromes. 2002 Jul;2(1):57-68.
Cazzola, M. ; Atzeni, F. ; Sarzi-Puttini, Piercarlo. / Pain in fibromyalgia syndrome. In: Journal of Functional Syndromes. 2002 ; Vol. 2, No. 1. pp. 57-68.
@article{0f523aa10ffe4e2e850d7bd59e64e1ef,
title = "Pain in fibromyalgia syndrome",
abstract = "The fibromyalgia syndrome (FM) is identified as widespread pain in combination with tenderness at 11 or more out of 18 specific tender point sites. Premorbid psychiatric condition and poor coping skills seem to predispose patients for development of FM. The origin of the pain symptoms in FM, according to the major of the researchers, stands for an alteration of the mechanisms of transmission, modulation and processing of the nociceptive stimuli in the central nervous system (CNS). The problem of FM pain can therefore be faced following two different conceptual models: a) a biomedical model, which addressed the scientific research, in the last century, toward an anatomo-pathological, neurophysiological and neuroendocrine analysis; b) a biopsychosocial model, which is collecting more and more consensus, in which the importance of emotional, cognitive and behavioural factors on the perception and above-all on the chronicity of pain is underlined. The physio-pathological mechanism for the reduction of the pain threshold should be identified in the central neuronal sensitization, which involves cells localized both at spinal level (posterior horns of the spinal tissue) both at supraspinal level. The central sensitization can be defined as a state Of neuronal hyperexcitability in response to peripheral stimuli; the result is a modification of the sensorial process that can determine: a) increase of pain perception in the site of a nociceptive stimulation (primary hyperalgesia); 2) appearance of in the normal tissues adjacent to the site of the nociceptive stimulation (secondary hyperalgesia); 3) pain in normal tissues distant from the site of the noxious stimuli (referred pain); 4) appearance of pain followed by a non-pain mechanical stimuli (allodynia). According to the biopsychosocial model pain experience in FM patients may be the result of highly interrelated biological, cognitive-behavioural, environmental and socio-cultural variables which explain the different symptoms patterns of each patient and also the different response to the proposed therapeutic approaches. The most sustained theories, actually, is that FM, as many other syndromes classified in the group of the spectrum of affective disorders, represents the consequence of a series of neuroendocrine and autonomic responses to a socio-environmental stress situation; these responses have lost, in this context, their original meaning of maintenance of homeostasis becoming, on the opposite, a cause of maladaptive behaviour.",
keywords = "Fibromyalgia syndrome, Nociception, Pain, Pain threshold",
author = "M. Cazzola and F. Atzeni and Piercarlo Sarzi-Puttini",
year = "2002",
month = "7",
language = "English",
volume = "2",
pages = "57--68",
journal = "Journal of Functional Syndromes",
issn = "1591-0989",
number = "1",

}

TY - JOUR

T1 - Pain in fibromyalgia syndrome

AU - Cazzola, M.

AU - Atzeni, F.

AU - Sarzi-Puttini, Piercarlo

PY - 2002/7

Y1 - 2002/7

N2 - The fibromyalgia syndrome (FM) is identified as widespread pain in combination with tenderness at 11 or more out of 18 specific tender point sites. Premorbid psychiatric condition and poor coping skills seem to predispose patients for development of FM. The origin of the pain symptoms in FM, according to the major of the researchers, stands for an alteration of the mechanisms of transmission, modulation and processing of the nociceptive stimuli in the central nervous system (CNS). The problem of FM pain can therefore be faced following two different conceptual models: a) a biomedical model, which addressed the scientific research, in the last century, toward an anatomo-pathological, neurophysiological and neuroendocrine analysis; b) a biopsychosocial model, which is collecting more and more consensus, in which the importance of emotional, cognitive and behavioural factors on the perception and above-all on the chronicity of pain is underlined. The physio-pathological mechanism for the reduction of the pain threshold should be identified in the central neuronal sensitization, which involves cells localized both at spinal level (posterior horns of the spinal tissue) both at supraspinal level. The central sensitization can be defined as a state Of neuronal hyperexcitability in response to peripheral stimuli; the result is a modification of the sensorial process that can determine: a) increase of pain perception in the site of a nociceptive stimulation (primary hyperalgesia); 2) appearance of in the normal tissues adjacent to the site of the nociceptive stimulation (secondary hyperalgesia); 3) pain in normal tissues distant from the site of the noxious stimuli (referred pain); 4) appearance of pain followed by a non-pain mechanical stimuli (allodynia). According to the biopsychosocial model pain experience in FM patients may be the result of highly interrelated biological, cognitive-behavioural, environmental and socio-cultural variables which explain the different symptoms patterns of each patient and also the different response to the proposed therapeutic approaches. The most sustained theories, actually, is that FM, as many other syndromes classified in the group of the spectrum of affective disorders, represents the consequence of a series of neuroendocrine and autonomic responses to a socio-environmental stress situation; these responses have lost, in this context, their original meaning of maintenance of homeostasis becoming, on the opposite, a cause of maladaptive behaviour.

AB - The fibromyalgia syndrome (FM) is identified as widespread pain in combination with tenderness at 11 or more out of 18 specific tender point sites. Premorbid psychiatric condition and poor coping skills seem to predispose patients for development of FM. The origin of the pain symptoms in FM, according to the major of the researchers, stands for an alteration of the mechanisms of transmission, modulation and processing of the nociceptive stimuli in the central nervous system (CNS). The problem of FM pain can therefore be faced following two different conceptual models: a) a biomedical model, which addressed the scientific research, in the last century, toward an anatomo-pathological, neurophysiological and neuroendocrine analysis; b) a biopsychosocial model, which is collecting more and more consensus, in which the importance of emotional, cognitive and behavioural factors on the perception and above-all on the chronicity of pain is underlined. The physio-pathological mechanism for the reduction of the pain threshold should be identified in the central neuronal sensitization, which involves cells localized both at spinal level (posterior horns of the spinal tissue) both at supraspinal level. The central sensitization can be defined as a state Of neuronal hyperexcitability in response to peripheral stimuli; the result is a modification of the sensorial process that can determine: a) increase of pain perception in the site of a nociceptive stimulation (primary hyperalgesia); 2) appearance of in the normal tissues adjacent to the site of the nociceptive stimulation (secondary hyperalgesia); 3) pain in normal tissues distant from the site of the noxious stimuli (referred pain); 4) appearance of pain followed by a non-pain mechanical stimuli (allodynia). According to the biopsychosocial model pain experience in FM patients may be the result of highly interrelated biological, cognitive-behavioural, environmental and socio-cultural variables which explain the different symptoms patterns of each patient and also the different response to the proposed therapeutic approaches. The most sustained theories, actually, is that FM, as many other syndromes classified in the group of the spectrum of affective disorders, represents the consequence of a series of neuroendocrine and autonomic responses to a socio-environmental stress situation; these responses have lost, in this context, their original meaning of maintenance of homeostasis becoming, on the opposite, a cause of maladaptive behaviour.

KW - Fibromyalgia syndrome

KW - Nociception

KW - Pain

KW - Pain threshold

UR - http://www.scopus.com/inward/record.url?scp=0041852718&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0041852718&partnerID=8YFLogxK

M3 - Article

AN - SCOPUS:0041852718

VL - 2

SP - 57

EP - 68

JO - Journal of Functional Syndromes

JF - Journal of Functional Syndromes

SN - 1591-0989

IS - 1

ER -