Pain management in functional gastrointestinal...

Pain management infunctional gastrointestinal

disordersANTONIO VIGANO MD, EDUARDO BRUERA MD

AN INTERNATIONAL WORKING

panel recently defined functionalgastrointestinal disorders (FGID) as a“variable combination of chronic or re-current gastrointestinal symptoms notexplained by structural or biochemicalabnormalities. FGID include symptomsattributed to the pharynx, esophagus,stomach, biliary tree, small and largeintestine or anorectum” (1). The com-mon symptom among FGID is pain,while other specific symptoms charac-terize the different functional symptomcomplexes.

Irritable bowel syndrome (IBS) is theprototype of FGID in terms of preva-lence, physiopathology, clinical find-ings and therapeutic opportunities (2).The description of IBS is beyond thispaper’s purposes. However, IBS will beconsidered a model to describe the cur-rent understanding of the physiopa-thology and treatment of pain in FGID.

PHYSIOPATHOLOGYIn an attempt to understand the

causes and the mechanism of pain inIBS, the features of visceral sensationand clinical evidences for altered painperception in the gastrointestinal tracthave been extensively reviewed. Vis-ceral sensation can be subdivided intotwo functional categories: nonpainfulconscious sensation which informs theindividual about the state of the gastro-intestinal tract with sensations of full-

REVIEW

A VIGANO, E BRUERA. Pain management in functional gastrointestinal dis-orders. Can J Gastroenterol 1995;9(2):85-90. Pain is a common feature infunctional gastrointestinal disorders (FGID). An abnormally low visceral sensorythreshold, as well as a number of central, spinal and peripheral pain-modulatingabnormalities, have been proposed for this syndrome. Clinical aspects of pain as-sociated with irritable esophagus, functional dyspepsia, biliary dysmotility, in-flammatory bowel syndrome and proctalgia fugax are reviewed. Because of itsunclear pathophysiology, pain expression is the main target for the successful as-sessment and management of symptomatic FGID. The sensory, cognitive and af-fective components of pain intensity expression need to be addressed in thecontext of a good physician-patient rapport. A multidisciplinary team approachis ideal for the smaller subset of patients with severe and disabling symptoms. Al-though pharmacotherapy may target specific functional disorders, the role of be-havioural techniques and psychotherapy appears much more important for painmanagement in FGID. Functional performance and quality of life improvement,rather than pain intensity, are the main therapeutic goals in these patients.

Key Words: Functional gastrointestinal disorders, Pain assessment and management,Quality of life

Traitement de la douleur dans la maladie gastro-intestinalefonctionnelle

RÉSUMÉ : La douleur est une caractéristique fréquente des troubles gastro-intestinaux fonctionnels (TGIF). Un seuil sensoriel viscéral anormalement bas,de même qu’un nombre d’anomalies sensorielles au niveau central, spinal et pé-riphérique ont été avancées pour expliquer ce syndrome. Les aspects cliniques dela douleur associés à l’oesophage irritable, à la dyspepsie fonctionnelle, à la dys-motilité biliaire, au syndrome inflammatoire intestinal et à la proctalgie fugacesont passés en revue. À cause de sa physiopathologie imprécise, l’expression de ladouleur est la principale cible d’une évaluation et d’un traitement réussis des

Palliative Care Program, Edmonton General Hospital, University of Alberta, Edmonton,Alberta

Correspondence: Dr Antonio Vigano, Fellow in Clinical Research, Palliative Care Program,Edmonton General Hospital, 11111 Jasper Avenue, Edmonton, Alberta T5K 0L4. Telephone(403) 482-8531

Received for publication July 14, 1994. Accepted August 15, 1994

voir page suivante

CAN J GASTROENTEROL VOL 9 NO 2 MARCH/APRIL 1995 85

ness, hunger, satiety and nausea; andpainful visceral sensation which in-forms the individual about potentiallynoxious events such as irritation of themucosa or serosa, gross distension ofthe viscus, torsion or traction on themesentery, forceful contractions andischemia. Nociceptors have not beenidentified in viscera; noxious and non-noxious stimuli are identified withinthe central nervous system (CNS) bytheir intensity of discharge. Further-more, there is no specific pathway forvisceral afferents in the spinal cord.Visceral and somatic inputs convergein the same second-order neurons of so-matic sensory. Subsequently, visceralpain is poorly localized and is accompa-nied by autonomic and somatic reflexesas frequently seen in FGID.

Pain modulation is accomplished bycentral, spinal and peripheral mecha-nisms. The central structures play animportant role in the processing of thesensory experience of pain. Descendinginhibitory pathways can be activatedby endorphins from the periaqueductalgrey area of the brain. The conver-gence of various sensory inputs into thesame second-order neuron within thespinal cord can facilitate or inhibit thepain transmission as suggested in thegate-control theory by Melzak andWall. Finally, inflammatory mediators,neuropeptides released from afferentterminals (antidromic nerve stimula-tion) and smooth muscle tone maymodulate the sensory function of vis-ceral receptors (3).

It has become apparent that pain inFGID is related to an abnormally lowvisceral sensory threshold (4). How-ever, it is still unclear where in the pain

modulating mechanisms the deregula-tion may take place.

An increased visceral sensitivity hasbeen shown by intraluminal balloondistension of the stomach in functionaldyspepsia. Similar findings have beenextensively reported in the colon andin the esophagus for IBS patients. Thedistension-induced pain was never re-lated to an abnormal visceral compli-ance (5). In IBS patients, stressfulstimuli seem to influence intestinalmotility and pain perception to agreater extent than in normal individu-als. Conversely, those gut disturbancesmay influence the central nervous sys-tem. IBS patients with balloon disten-sion in the colon experienced pain atmany extracolonic sites such as theshoulder, back and thigh. These find-ings may suggest an alteration in vis-ceral pain discrimination and afacilitation of referred pain mecha-nisms (3).

Pain in FGID may be partly caused bya hypoactive CNS antinociceptive sys-tem. A decreased level of cerebrospinalfluid beta-endorphins has been foundin patients with long-lasting functionallower abdominal pain (6). However,the pain sensitivity for ischemia in thispopulation was not found to be signifi-cantly increased as previously shownfor upper abdominal pain in functionaldyspepsia. The possible effect of a lowlevel of beta-endorphins on painthreshold may be enhanced or counter-balanced by neuropsychologicalmechanisms such as level of attention,anxiety, depression and mood.

Even though the role of psychologi-cal factors in the etiology of FGID is stillunclear, a common feature of these

conditions is the frequent associationwith psychiatric illness, especiallymood changes, anxiety or somatizationdisorders (7). Life threatening events,loss of a job or loved one, long-standingstress and severe emotional upset ap-pear to precede the development offunctional abdominal pain more fre-quently than the onset of organic gas-trointestinal disease (8). Furthermore,a history of sexual and physical abusewas particularly common in womensuffering from FGID (9). Those eventsalso seem to enhance symptom report-ing and health care utilization espe-cially for pain management. A psycho-logical similarity has been foundbetween persons having IBS who do notconsult a physician and normal indi-viduals (10). So far, psychosocial dis-turbances appear to influence, ratherthan directly cause, the greater sympto-matic and physiological response tostressor in FGID patients compared withnormal individuals (1).

CLINICAL ASPECTS OF THEPAIN SYNDROMES

A description of all the symptomscharacterizing FGID with the related di-agnostic approaches is beyond thescope of this paper. Only pain manifes-tations in the major FGID, such as irrita-ble esophagus, functional dyspepsia,biliary dysmotility, IBS and proctalgiafugax, will be reviewed.

Chest pain resulting from irritableesophagus may fall into three clinicalmanifestations: pyrrhosis or heart burn;odynophagia or pain on swallowing;and spontaneous pain. While pyrrhosisor odynophagia may easily be attrib-uted to an esophageal disorder, sponta-neous chest pain of esophageal origin ismore difficult to diagnose. In the ab-sence of other specific symptoms, be-sides the irritable esophagus syndrome,one should consider gastrointestinal(eg, peptic ulcer disease), cardiac (eg,angina pectoris) or musculoskeletal(eg, costochondritis) organic disease(11).

Burning or gnawing pain at the epi-gastrium is present in the majority ofpatients suffering from functional dys-pepsia. Because of the frequent over-lapping of functional dyspepsia

TGIF symptomatiques. Les composantes sensorielles, cognitives et affectives quicaractérisent l’expression de la douleur dans son intensité doivent être abordéesdans le contexte d’un bon rapport médecin-patient. Une approche pluridiscipli-naire est idéale chez un sous-groupe de patients plus restreint atteints desymptômes graves et invalidants. Bien que la pharmacothérapie puisse s’attaquerà certains troubles fonctionnels spécifiques, le rôle de techniques comportemen-tales et de la psychothérapie semble beaucoup plus important pour le traitementde la douleur associée aux TGIF. L’amélioration du rendement fonctionnel et de laqualité de vie plutôt que le soulagement de la douleur sont donc les principauxobjectifs thérapeutiques chez ces patients.

86 CAN J GASTROENTEROL VOL 9 NO 2 MARCH/APRIL 1995

VIGANO AND BRUERA

symptoms with those of classic pepticulcers, ulcer and nonulcer dyspepticshave been identified. In nonulcer dys-pepsia, eating-related pain is frequent,while nocturnal pain, male preponder-ance and family history appear to beless important than in peptic ulcer dis-ease (12).

Epigastric or right hypogastric painsimulating the biliary colic of gall-stones, but without identifiable disease,may be caused by disordered motility ofthe sphincter of Oddi. Pain in biliarydysmotility may be precipitated by fattyfoods or codeine but is often spontane-ous and sometimes nocturnal.

Abdominal pain in IBS is generallycolicky and dull. Its location may beover the anatomical location of the co-lon or extracolonic. The spasmodic at-tacks may start during or right after ameal, but the acute phase is mostly re-ported 1 to 1.5 h after eating. The se-verity of abdominal discomfort may berelated to different kinds of foods, eventhough exacerbation and relief of IBS

pain are variable in different individu-als. Passage of flatus and bowel move-ments generally decrease the sympto-matology (2).

Finally, severe pain occurringaround the anus during defecation, af-ter coitus or spontaneously in the ab-sence of organic diseases is thehallmark of proctalgia fugax. This painrecurs in paroxysms during the day andnight, ceasing without residue in lessthan 10 to 20 mins. During these at-tacks syncope, priapism and a tight,tender band across the lower rectummay be observed (13).

ASSESSMENTPain production in FGID may be re-

lated to three stages: nociception (con-cerning the genesis of the noxiousstimulus); perception (related to thecentral, spinal and peripheral modula-tions of the nociceptive input); and ex-pression (representing the final proc-essing of the sensory experience ofpain). Because the first and secondstages cannot be assessed or monitoredclinically, treatment will be aimed todecrease the pain expression.

It has been shown in both acute andchronic syndromes that the intensity of

pain can be easily measured by subjec-tive assessments. Numerical, verbaland visual scales provide an idea of the‘quantity’ of the patient’s pain expres-sion. Those tools may be assimilated toa sphygmomanometer or to a glucome-ter that measures blood pressure or gly-cemia, respectively, by unidimensionaland standardized criteria.

The intensity of pain, however, can-not be considered a simple entity. Aunidimensional approach considerspain expression a direct manifestationof nociception (similar to a blood pres-sure reading in hypertension or bloodglucose determination in diabetes mel-litus). Such simplified assessment as-sumes that pain is always what the pa-tient defines as pain, and that theintensity the patient reports is 100%nociception. This approach may leadto lack of a disciplined assessment ofthe different dimensions of painexpression, to misuse/overuse ofantinociceptive interventions and to un-deruse of nonpharmacological inter-ventions (Table 1).

Pain is “a multidimensional experi-ence with sensory as well as cognitive

and affective components modulatedby environmental contingencies...”(14). Functional disorders from illness,level of cognitive function, positivehistory of addiction/alcoholism, drugtolerance and toxicity, environmentalstressors, psychiatric illness, impair-ment in daily and social function, un-conscious secondary gain, somatizationand other illness coping behavioursmay contribute to the final ‘construct’,which is the pain intensity expression.

The multidimensional evaluation ofphysical, social, psychological andspiritual components of pain is neces-sary for the management of bothchronic benign and malignant syn-dromes. Table 2 reports some of thosedimensions. Therefore, a multidisci-plinary team approach is useful, par-ticularly for patients with severe anddisabling symptoms.

MANAGEMENTOnce diagnosis and a good rapport

between the physician and the patienthave been established, an accurate set-ting of goals and instruments for paincontrol in FGID is possible. As shown in

TABLE 2Multidimensional pain assessment

Pain

syndrome

Neuropathic/Incidental

Social Family/Financial/Cultural

Drug Dose/Rapid tolerance?/

Toxicity

Patient Renal function/Psychological

distress, coping history/

Addiction/Cognition

(hypoalert/hyperalert?)/

Spiritual

Classic model

Cancer pain syndrome Chronic benign pain syndrome

Pain relief Functional improvement

Emerging model

Cancer pain syndrome Chronic benign pain syndrome

Pain relief

Functional improvement

Figure 1) The classic and emerging model of the cancer pain syndrome and the chronic benign painsyndrome

TABLE 1Unidimensional pain assessment

Problems:

Lack of disciplined assessment

Misuse of pharmacological and

nonpharmacological interventions

Over-use of antinociceptive interventions

and underuse of other interventions

Increased drug-related toxicity


Pain management in GI disorders

Figure 1, pain relief and functional im-provement have been proposed as themain outcome measurements of the pa-tient with the cancer pain syndromeand the chronic benign pain syndrome,

respectively (14). The cancer paradigmproposed mostly pharmacological ap-proaches based on a need to decreasepain expression, while chronic benignpain management emphasized non-

pharmacological treatments to in-crease patient autonomy and function.These paradigms were based on a seriesof identified differences between thetwo syndromes (Table 3). However, inrecent years it has become apparentthat many of those differences are notso clear-cut. The result has been anemerging model based on a multidisci-plinary and multimodal managementof both patient populations. Therefore,pharmacological, physical, psychologi-cal or behavioural treatments are all in-dicated as part of comprehensive painmanagement in FGID.

PHARMACOLOGICALAPPROACH

Pharmacotherapy may play an im-portant role for targeting specific func-tional disorders. ‘Antispasmodic’ drugsare most frequently used to treat painsymptoms in FGID, even though a clearrelationship between pain and gut mo-tility has not been firmly established.However, in view of the cholinergi-cally mediated gastrocolonic response,the patient with recurrent abdominalpain after meals may benefit from ananticholinergic agent before meals (ie,10 to 20 mg dicycloverine 30 mins be-fore meals). Other antispasmodicdrugs, such as calcium channel block-ers, peppermint oil, naloxone and se-lective serotonin and cholecystokininantagonist, have been proposed but re-quire more clinical trials before accep-tance (15).

Small doses of acetominophen maybe useful in the short term while nar-cotics are not particularly encouraged(14). Whenever opioids are indicatedfor the pharmacological treatment ofpain in FGID, the guidelines issued bythe College of Physicians and Surgeonsin the Province of Alberta are recom-mended (Table 4) (16).

Presently, neither the medical lit-erature nor clinical experience supportlong term opioid use for patients withchronic nonmalignant pain. There areno adequate controlled trials of thesedrugs. The data appear to support theuse of empirical therapeutic trials in se-lected patients, followed by carefullymonitored long term therapy in thosewho benefit (17). Specifically, patients

TABLE 3Comparison of cancer pain with chronic benign pain

Cancer pain patients Chronic benign pain patients

Short survival Long survival

Multiple severe symptoms (cachexia,

dyspnea, nausea)

Pain-only symptom

Multiple drugs Few drugs

Frequent cognitive failure Somatization, addiction, affective problems

Mechanism: somatic, visceral,

neuropathic

Frequent neuropathic mechanism

Palliative care Seen by chronic pain clinics

Cancer pain Chronic benign pain

Mechanism of pain evident Mechanism less evident and predictable

Assessment of pain intensity

(ill patients)

Assessment of functional status (pain as illness)

Focus on pain intensity and aggravating

factors

Discourage pain behaviour (maladaptive),

reinforce rehabilitation

Opioids main treatment Discontinue all possible drugs (antidepressants,

NSAIDs, opioids)

Nonpharmacological treatments

rare

Emphasis on increased control (TENS, relaxation,

etc)

NSAIDs Nonsteroidal anti-inflammatory drugs; TENS Transdermal electrical stimulation

TABLE 4Guidelines for the opioid use in chronic nonmalignant pain

Establish the medical diagnosis underlying the pain

Consider a recent/remote history of substance abuse

Exclude any benefit from first line nonopioid analgesic and adjuvant drugs

Identify only one physician to prescribe opioids

Employ the World Health Organization ‘analgesic ladder’ principles for cancer pain

management

Avoid short-acting (eg, meperidine) and agonist-antagonist (eg, pentazocine) opioids

Identify the dose associated with meaningful partial analgesia and no opioid toxicity

compromising comfort or function

Advance to a higher step on the analgesic ladder whenever the previous has been

unsatisfactory

Whenever a strong opioid is indicated, the oral morphine is convenient for titration. The

starting dose should be 10 mg by mouth every 4 h. This dose should be increased once

or twice weekly by 25 to 50% until the desired effect is achieved

Include with ‘around the clock’ administration, the prescription of extra opioid doses as

required to treat breakthrough pain

If there are no contraindications (eg, features suggesting abuse) the patient on a stable

and effective dose of short-acting morphine preparation should be switched to a

long-acting one (every 8 to 12 h)

Parenteral administration of opioids is strongly discouraged

Define a clear ‘contract’ between the prescribing physician and the patient regarding

opioid management

Reassess frequently the patient on opioids to evaluate analgesic efficacy and toxicity,

physical and psychological function and the occurrence of drug abuse-related

behaviours


VIGANO AND BRUERA

with a history of alcoholism or drug ad-diction, psychiatric disorders or somati-zation are particulary poor candidatesfor opioid trials.

Psychopharmacological agents suchas antidepressants and anxiolytics seemto be effective in some patients. Cen-tral analgesia, anticholinergic actionon the gut and relief of depression oranxiety may provide symptom remis-sion in FGID (1). Tricyclic antidepres-sants and fluoxetine are often indicatedin chronic pain management becauseof their brain serotoninergic action.They should be started in small doses(eg, 50 to 75 mg amitriptyline at bed-time, 20 mg fluoxetine in a single, day-time dose) with a gradual increase to ef-fective and tolerated therapeuticlevels. However, recent trials suggestthat tricyclic antidepressants are moreeffective analgesics than specificserotonin-reuptake inhibitors (18).Benzodiazepine-type anxiolytics areoccasionally helpful to relieve epi-sodes of stress-related symptom flares.Their long term use and combinationwith anticholinergic drugs are not rec-ommended (15).

NONPHARMACOLOGICALAPPROACHES

Physical therapy may play an impor-tant role for pain management in FGID.Modalities such as heat, cold,soft-tissue massage and transdermalelectrical stimulation (TENS) can aid indecreasing or controlling pain. Exerciseprograms are implemented to correctsecondary dysfunctions. Patient educa-tion in this context may enhance thepatients’ coping strategies with chronicdisease, improve functional status andprevent excessive stress on both the in-volved and noninvolved body struc-tures (19).

Among physical therapies, acu-puncture has been used in chronic be-nign pain. Although its mechanism ofaction is still unclear, acupunctureplays a neuromodulating role in thementioned stages of pain production(20).

Whenever psychosocial stressors arepredominant, psychotherapy may beuseful in diminishing their role in thepathogenesis of FGID symptomatology.

Although beneficial in some cases, psy-choanalytic psychotherapy can betime-consuming and costly (21). Thetechniques proposed by behaviouralpsychologists appear efficacious man-agement tools in dealing with chronicand intractable pain syndromes. Be-havioural treatments are mainly in-tended to modify an abnormal illnessbehaviour. This behaviour is defined as“the persistence of a maladaptive modeof experiencing, perceiving, evaluatingand responding to one’s own healthstatus, despite the fact that a doctor hasprovided a lucid and accurate appraisalof the situation and management to befollowed (if any), with opportunitiesfor discussion, negotiation and clarifi-cation based on adequate assessment ofall relevant biological, psychologicaland cultural factors” (21).

Behavioural techniques include re-laxation response training, autogenictraining, hypnosis and biofeedback,with the contribution of some of thepharmacological (eg, antidepressants)and physical (eg, massage, TENS) treat-ments previously mentioned. Relaxa-tion response and autogenic traininglower sympathetic nervous system ac-tivity and produce skeletal muscle re-

laxation. Because of their simplicity,they are the primary treatment in thebehavioural approach (1).

Hypnosis may reduce pain percep-tion in the gut, particularly in patientswithout associated psychopathologicalabnormalities.

In biofeedback, skeletal muscle ac-tivity and other physiological functionsare monitored by audio or visual in-struments. The patients use this infor-mation to achieve a general state of re-laxation or to gain control over usuallyunconscious physiological functions.

All those noninvasive methodsmay be performed by psychologists,behaviourally trained nurses, techni-cians and physicians. The choice oftreatment depends on cost and avail-ability (1).

The behavioural approach may helpmotivated patients to reduce anxietyand maladaptive illness behaviours.Productive behaviours can be restoredby those treatments, which finally en-hance pain tolerance (21).

Whenever pain and disability ap-pear refractory to simple pharmacologi-cal interventions and basic counsellingby the treating physician, FGID patientsmay be re-evaluated and managed by a

TABLE 5Multidisciplinary pain centre

Clarify the diagnosis. Review medical records and the need for further diagnostic studies or

invasive procedures

Improve pain control (eliminate pain if possible) through physical therapies:

Help the patient to be more comfortably active

Promote the use of alternative modalities other than potent medications

With individually structured exercise programs, reduce the patient’s fear of reinjury

Teach proper body mechanics and postural awareness

Evaluate limitations and restrictions

Improve psychological functioning:

Define and address psychosocial issues influencing the chronic pain syndrome

Relieve drug dependency

Treat depression and its frequently associated insomnia

Address primary and secondary gains from pain

Assess family system

Strengthen support network (eg, personal, family and community)

Provide access to occupational and vocational rehabilitation and any other significant

health care personnel, and resolve disability when possible

Communicate with the patient’s referring physician via discharge summary, telephone or

personal meetings to obtain any information that will assist in the continued

management of the patient

Reduce inappropriate use of the health care system

Decrease the cost of medical care associated with chronic pain syndrome

Reproduced with permission from reference 22


Pain management in GI disorders

multidisciplinary pain centre. Theunderlined goals are reported in Table5 (22).

SUMMARYPain is a common feature in FGID.

An abnormally low visceral sensorythreshold, as well as a number of cen-tral, spinal and peripheral pain-modulating abnormalities, have beenproposed for this syndrome. Clinical

aspects of pain associated with irritableesophagus, functional dyspepsia, biliarydysmotility, IBS and proctalgia fugaxhave been reviewed. Because of itsunclear pathophysiology, pain ex-pression is the main target for the suc-cessful assessment and management ofsymptomatic FGID.

The sensory, cognitive and affectivecomponents of pain intensity expres-sion need to be addressed in the con-text of a good physician-patient

rapport. A multidisciplinary team ap-proach is ideal for the smaller subset ofpatients with severe and disablingsymptoms. Although pharmacotherapymay target specific functional disor-ders, the role of behavioural techniquesand psychotherapy appears much moreimportant for pain management inFGID. Functional performance andquality of life improvement, ratherthan pain intensity, are the main thera-peutic goals in these patients.

ACKNOWLEDGEMENTS: We ac-knowledge the Italian Association for Can-cer Research, Milano, Italy, for funding DrVigano’s Research Fellowship with the Pal-liative Care Program at Edmonton GeneralHospital, Edmonton, Alberta.

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