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PubMedDate not supplied

Difficult pain syndromes: bone pain, visceral pain, and neuropathic pain.

Cancer pain is prevalent in approximately two thirds of all cancer patients and can undermine the quality of life in this patient population. Uncontrolled pain can cause physical as well as psychological distress in cancer patients. As the disease progresses in cancer, pain and suffering increase. Knowledge about pain management is paramount in the comprehensive treatment of cancer patients. Difficult cancer pain syndromes may arise from interruption of bone, viscera, and neural structures by malignant spread of the disease. Familiarity with opioids, adjuvants, and procedures that can abate pain in cancer patients is discussed in a practical manner for clinical application in this text.

Bone Neoplasms↗
PubMed2004

Visceral pain.

Visceral pain, which originates from organ tissues of the thorax, abdomen or pelvis, is generally perceived as a deep, dull and vague sensation; in most cases it cannot even be clearly described, being a sense of discomfort, malaise or oppression rather than real pain. Crushing, cutting and burning generally have no algogenic effect in the viscera whereas mechanical stimulation, ischemia and chemical stimulation, separately or in combinations, may cause pain. With these characteristics, visceral pain differs from somatic pain. The characteristics of visceral pain, perception and transmission of painful visceral stimuli are explained, some common visceral pain syndromes are presented and sympathetic neurodestructive approaches as a treatment option are described in this review.

Abdominal Pain↗
PubMed1999

Visceral pain.

Visceral pain is the most common form of pain produced by disease and one of the most frequent reasons why patients seek medical attention. Yet much of what we know about the mechanisms of pain derives from experimental studies of somatic not visceral nociception. The conventional view is that visceral pain is simply a variant of somatic pain, a view based on the belief that a single neurological mechanism is responsible for all pain. However, the more we learn about the mechanisms of somatic and visceral pain, the more we realise that although these two processes have much in common, they also have important differences. Although visceral pain is an important part of the normal sensory repertoire of all human beings and a prominent symptom of many clinical conditions, not much clinical research has been done in this field and there are few clinical scientists with expertise in the management of visceral pain. Instead, visceral pain is usually treated by a range of specialists who take quite different approaches to the management of this type of pain. Thus, the management of visceral pain is frequently unsatisfactory. In this review, we consider visceral pain as a separate form of pain and examine its distinct sensory properties from a clinical perspective. We describe recent research findings that may change the way we think about visceral pain and, more importantly, may help develop new procedures for its management.

Humans↗
PubMed2000

Visceral pain.

Visceral pain, although different from somatic pain in several important features, is not as widely researched and consequently our knowledge of neurophysiologic mechanisms as well as clinical management of visceral pain states remains unsatisfactory. Several recent studies have employed different visceral pain animal models to provide insight into the peripheral and central nervous system mechanisms underlying pain originating from the urinary bladder, ureter, and gastrointestinal tract. The effects of opioid and nonopioid drugs in these models have also been evaluated and are reviewed in this article. The importance of anatomic pathways relaying pain sensation in the central nervous system, particularly the newly described dorsal column pathway, is also discussed. In human subjects, new techniques like positron emission tomography are now being used to better understand visceral pain perception. Such findings deriving from basic animal research and human studies summarized in the present overview lead to a better understanding of visceral pain states and may be helpful in developing better treatment strategies to combat visceral pain states in the clinical setting.

Afferent Pathways↗
PubMed2002

[Epidemiology and clinical phenomenology of visceral pain].

Visceral pain is characterized by a subjectively painful perception located in the abdominal area. Distinct structural lesions or biochemical abnormalities which could serve as explanation for these painful sensations can be only detected in a proportion of patients. In the absence of precise causes for visceral pain, the symptoms are attributed to functional disorders. The two major single entities among functional disorders of the gut are functional dyspepsia and irritable bowel syndrome. Patients with functional dyspepsia characteristically localize the symptoms in the upper abdomen. Functional gastrointestinal disturbances which are localized in the lower abdomen are summarized as irritable bowel syndrome. Interestingly,both functional dyspepsia and irritable bowel syndrome may overlap.

Dyspepsia↗
PubMed2002

[Physiology and pathophysiology of visceral pain].

Visceral pain is diffusely localized, referred to deep somatic tissues, skin and viscera, frequently not correlated with an actual trauma, commonly correlated with strong negative affective reactions and accompanied by strong protective autonomic and motor reactions. It is correlated with the excitation of spinal (thoraco-lumbar, sacral) visceral afferents and (with a few exceptions) not with the excitation of vagal afferents. Spinal visceral afferents are polymodal and can be excited by physical and chemical stimuli. All groups of visceral afferents can be sensitized (e.g.by inflammation). Normally silent (mechanically insensitive) visceral afferents are recruited by inflammation. Individual visceral afferent neurons project in laminae I and V of the dorsal horn over several segments, medio-lateral over the entire width of the dorsal horn and to the contralateral side. Their activity is synaptically transmitted, in these and deeper laminae, to viscero-somatic convergent neurons which receive additional afferent synaptic input from skin and deep somatic tissues of the corresponding dermatomes,myotomes and sclerotomes. The mechanism of sensitization of viscerosomatic convergent neurons (central sensitization) during sensitization of spinal visceral afferents is unclear.Viscero-somatic tract neurons project to lower and upper brain stem,hypothalamus and via the thalamus to various cortex areas. Visceral nociception and pain is presumably (together with other visceral sensations and homeostatic regulations of autonomic body functions) primarily represented in the insula in the context of interoception. The insula obtains its main peripheral afferent input from lamina I neurons via the Nucleus ventromedialis posterior of the thalamus. The transmission of visceral impulses in the spinal cord is modulated by the endogenous control systems in the brain stem which are in turn under the control of cortex and limbic system.

Afferent Pathways↗
PubMed2001

Gastrointestinal afferents as targets of novel drugs for the treatment of functional bowel disorders and visceral pain.

An intricate surveillance network consisting of enteroendocrine cells, immune cells and sensory nerve fibres monitors the luminal and interstitial environment in the alimentary canal. Functional bowel disorders are characterized by persistent alterations in digestive regulation and gastrointestinal discomfort and pain. Visceral hyperalgesia may arise from an exaggerated sensitivity of peripheral afferent nerve fibres and/or a distorted processing and representation of gut signals in the brain. Novel strategies to treat these sensory bowel disorders are therefore targeted at primary afferent nerve fibres. These neurons express a number of molecular traits including transmitters, receptors and ion channels that are specific to them and whose number and/or behaviour may be altered in chronic visceral pain. The targets under consideration comprise vanilloid receptor ion channels, acid-sensing ion channels, sensory neuron-specific Na(+) channels, P2X(3) purinoceptors, 5-hydroxytryptamine (5-HT), 5-HT(3) and 5-HT(4) receptors, cholecystokinin CCK(1) receptors, bradykinin and prostaglandin receptors, glutamate receptors, tachykinin and calcitonin gene-related peptide receptors as well as peripheral opioid and cannabinoid receptors. The utility of sensory neuron-targeting drugs in functional bowel disorders will critically depend on the compounds' selectivity of action for afferent versus enteric or central neurons.

Animals↗
PubMed2006

Visceral pain and public speaking stress: neuroendocrine and immune cell responses in healthy subjects.

Whereas responses to psychological stressors are well-characterized, little is known regarding responses to painful visceral stimuli. We analyzed the emotional, cardiovascular, neuroendocrine, and cellular immune responses to painful rectal stimulation and psychological stress in healthy individuals. Eleven healthy subjects were studied in three conditions on separate days: painful rectal distension, public speaking stress, and rest. Blood was drawn for endocrinological and immunological analyses; heart rate and blood pressure were measured continuously; state anxiety was assessed with a questionnaire (STAI-S). Anxiety scores were highest in the rectal distension condition. This was evident following rectal distension (mean STAI-S scores: 44.2+/-3.5 post-distension vs. 36.6+/-3.8 post-speech, p<.05), but anxiety was also elevated at baseline (41.6+/-3.9 vs. 32+/-3.2 recovery, p<.01). This anticipatory effect was reflected by elevated baseline cortisol (p<.05) and baseline ACTH (p<.01) levels, as well as circulating lymphocytes and lymphocyte subsets, including decreased basal CD3+CD4+ cells (p<.05) and increased CD16+CD56+ cells (p=.06) compared to rest. Both public speech and rectal distension induced cardiovascular activation, but the effect was more pronounced following rectal distension (+63.8+/-9.4 mmHg in response to distension vs. +36.4+/-6.2 mmHg in response to speech for systolic BP, p<.05). Different response patterns were also observed in the distribution of circulating leukocytes and lymphocyte subsets, including CD16+CD56+ cells (p<.05). An acute visceral pain stimulus causes profound emotional, neuroendocrine, and immune cell responses, which are markedly affected by anticipatory anxiety. These findings may have implications for conditions associated with visceral hyperalgesia.

Adult↗
PubMed2001

Pelvic pain: a chronic visceral pain syndrome.

Patients with chronic pelvic pain are usually evaluated and treated by gynecologists, gastroenterologists, urologists, and internists. In many patients with chronic pelvic pain the examination and work-up remain unrevealing and no specific cause of the pain can be identified. In these cases it is important to recognize that pain is not only a symptom of pelvic disease, but that the patient is suffering from a chronic pelvic pain syndrome. Once the diagnosis of chronic pelvic pain is made, treatment should be directed to symptomatic pain management. This article outlines treatment options currently available. Despite the challenge inherent in the management of chronic pelvic pain, many patients can be treated successfully using a multidisciplinary pain management approach. The first important step is to recognize that patients with chronic pelvic pain might suffer from a chronic visceral pain syndrome.

Acupuncture Analgesia↗
PubMed2000

Pathobiology of visceral pain: molecular mechanisms and therapeutic implications IV. Visceral afferent contributions to the pathobiology of visceral pain.

Functional bowel and other visceral disorders exhibit multiple characteristics that suggest the presence of visceral hyperalgesia. The discomfort, pain, and altered sensations (e.g., to intraluminal contents) that define the hyperalgesia typically arise in the absence of tissue insult or inflammation. Visceral hyperalgesia thus differs from somatic hyperalgesia, which is commonly associated with tissue injury and inflammation. Hyperalgesia could develop and be maintained by either peripheral or central mechanisms; the altered sensations associated with functional visceral disorders are contributed to by both peripheral and central mechanisms. The relative contributions of peripheral and central mechanisms are not well understood, and the focus in this Themes article is on potential peripheral contributions: sensitization of visceral receptors, nerve injury, and ion channels.

Afferent Pathways↗
PubMed1991

Mechanisms of acute visceral pain.

Acute visceral pain is dull, aching, ill-defined, badly localized and often referred to remote areas of the body. These properties indicate that the representation of internal organs within the CNS is very imprecise. There is evidence for the existence of specific visceral nociceptors in some viscera and for the existence of non-specific receptors in other internal organs. Some visceral receptors are 'silent' in normal viscera but become active following acute injury or inflammation of the internal organ that they innervate. The number of nociceptive afferent fibres in viscera is very small but these few nociceptive afferents can excite many second order neurones in the spinal cord which in turn generate extensive divergence within the CNS, sometimes involving supraspinal loops. Such a divergent input activates several systems--sensory, motor and autonomic--and thus triggers the general reactions that are characteristic of visceral nociception: a diffuse and referred pain, and prolonged autonomic and motor activity.

Acute Disease↗
PubMed2000

Pathobiology of visceral pain: molecular mechanisms and therapeutic implications. III. Visceral afferent pathways: a source of new therapeutic targets for abdominal pain.

Visceral pain is the major cause of consulting in gastroenterology and the principal symptom of functional bowel disorders. This symptom is often associated with gut hypersensitivity to distension. The use of animal models has recently permitted the identification of some mediators supposed to play a pivotal role in the genesis of visceral hypersensitivity. Serotonin, through different receptor subtypes, as well as kinins and calcitonin gene-related peptide, are known to be involved, but other putative transmitters arise and are new potential targets for the development of efficacious treatments. This themes article addresses both physiological and preclinical issues of interest for the selection of active new drugs in regard to the clinical pharmacology of visceral pain.

Analgesics↗
PubMed2002

[Psychophysiology of visceral pain syndromes].

Psychosomatics of visceral pain syndromes. From a psychosomatic point of view visceral pain syndromes can be classified into nociceptive (somatic and visceral) pain syndromes without and with maladaptive pain coping resp.psychic comorbidity, functional pain syndromes (typical symptom clusters without biochemical or structural abnormalities in clinical routine diagnostics) and psychic disorders with pain as main symptom. With regard to the etiology and the course of chronic inflammatory bowel diseases (IBD) as representatives of somatic pain syndromes and of irritable bowel syndrome/chronic pelvic pain as representatives of functional pain syndromes empirically validated psychosocial aspects are summarized: Personality traits, illness behavior, daily hassles, life events and psychic comorbidity and effects of psychotherapy. Psychosocial factors are decisive in the etiology and the course of functional pain syndromes as determinants of their severity (psychosomatic disease in a narrow sense). Psychosocial factors are not decisive for the etiology, but for the course of IBD (psychosomatic disease in a broader sense). Within general pain therapy of visceral pain syndromes a biopsychosocial approach should be applied right from the beginning (psychosomatic basic care). Within special pain therapy of visceral pain syndromes a qualified psychiatric - psychotherapeutic diagnostics and co-therapy should be mandatory.

Female↗
PubMed1991

Central mechanisms of visceral pain.

Deep pain arising from muscle, joints, connective tissue, and the viscera is different in character and quality from pain arising from cutaneous structures. Deep pains, particularly visceral pain, are poorly localized, typically referred or transferred to a cutaneous site, and generally produce strong emotional and autonomic responses and tonic muscle contractions. Despite the prevalence and clinical importance of deep pains, it is only relatively recently that investigative efforts have begun to focus on the mechanisms of deep pain. The present report briefly reviews the development and use of a model of visceral pain that employs constant pressure distension of the colon and rectum as a noxious stimulus. Converging behavioral, pharmacological, and physiological evidence that colorectal distension is a valid, reliable, noxious, visceral stimulus is presented.

Animals↗
PubMed2006

Nonsteroidal antiinflammatory drugs suppress pain-related behaviors, but not referred hyperalgesia of visceral pain in mice.

Visceral pain is characterized by spontaneous pain and referred hyperalgesia. After inducing visceral pain in mice using intracolonic mustard oil administration, we examined the effects of various nonsteroidal antiinflammatory drugs (NSAIDs) on pain-related behavior and on Evans blue dye extravasation. Animals were given one of the following: saline, ethanol, dimethylsulfoxide (DMSO), morphine, ketoprofen, ketorolac, or DFU (a cyclooxygenase-2 inhibitor). After drug treatment, mice underwent intracolonic administration of 50 microL 1.5% mustard oil. Spontaneous pain-related responses were assessed for the next 20 min. The frequency of withdrawal responses to the application of von Frey hairs to the abdomen, foot, and tail was determined. After completion of the behavioral tests, Evans blue was injected into the animals via the tail vein. Two hours later, the colon was removed postmortem and Evans blue content was measured. Spontaneous pain behaviors were significantly less in animals administered 3 and 10 mg/kg morphine, 50 mg/kg ketorolac, 100 mg/kg ketoprofen, and 20 mg/kg DFU (P < 0.05). Response frequencies to the application of von Frey hairs were lower in mice administered 3 and 10 mg/kg morphine (P < 0.05) but were not affected by ketorolac, ketoprofen, or DFU treatment. Colonic Evans blue content was smaller in mice given 100 mg/kg ketoprofen and 20 mg/kg DFU (P < 0.05). We concluded that NSAIDs reduced pain behavior and inflammation but had little effect on referred hyperalgesia.

Animals↗