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Referred shoulder pain is an important yet potentially distracting sign of serious intra-abdominal illness. A case is presented wherein shoulder pain preceded by several hours the onset of abdominal pain in a teenage girl with gastric perforation. The range of causes of gastric perforation and the pathophysiology of referred shoulder pain are discussed.
The purpose of this study is to describe an out-patient Pain Center population on the basis of IASP Classification of Chronic Pain. Furthermore, the study investigates the relationship between diagnostic subgroups of chronic non-malignant pain patients and psychosocial parameters. The average age of the patients was 42 and the mean age at the onset of pain was 34.2. In the present study about x of all the patients had severe pain with a duration of 48 months (median value), patients with dysfunctional pain, one of three diagnostic subgroups, had a significantly longer pain duration (80 months). Nearly (1/3) of all patients are not able to work regularly and 85 % felt impaired in their daily work activities. Nearly (1/3) of the patients without any somatic pathological findings had at least one invasive intervention, just like the patients in the other diagnostic subgroups, and the need-controlled pain medication reached its highest level in this group (45 %). Only 19 % of the 323 patients investigated had nociceptive-neuropathic pain complaint, whereas 53 % were suffering from dysfunctional, and 28 % had a somatoform pain disorder. So, in patients suffering from chronic pain, simultaneous somatic and psychic or psychosomatic diagnostics are indispensable due to the relevance of psychic and psychosocial factors to pain genesis, modulation and persistence. For patients in each of the described subgroups additional psychological factors such as attitudes, beliefs, self-efficacy, fear-avoidance beliefs and motivational factors always have a significant influence on the persistence of chronic pain syndromes. So, as a rule, to make a reliable diagnosis and to give a profound prognosis for the course of treatment, a close interdisciplinary cooperation is required.
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We report a case of a latissimus dorsi muscle strain that presented as a recurrence of chronic abdominal pain. One explanation of the referral of acute pain to a site of chronic pain is the convergence-projection theory, which hypothesizes that pain signals of visceral and somatic origin converge at some point in the sensory pathway. Upon reaching the cortex, these signals are interpreted as coming from the afferents which have previously excited this pathway. In this case an extensive gastrointestinal diagnostic evaluation was pursued unsuccessfully before the latissimus dorsi muscle strain was diagnosed. Outpatient therapy of spray and stretch combined with a home stretching program produced a prompt and persistent resolution of the symptoms.
In a study of 44 patients with different types of chronic pain, mostly associated with deafferentation, chronic percutaneous epidural spinal stimulation has proved useful treatment achieving an initial 52% incidence of pain amelioration overall. Long-term result showed at six months in 86%, at 1 year in 90%, although technical problems, which included electrode displacement and required minor operative readjustment, affected 48% of those permanently implanted. No other complications were seen. Success bore no relationship to quality of pain reported by the patients or to duration of pain. The patients with denervation caused by nerve or root lesions responded better than those with cord lesions even though electrical paresthesia were delivered to the area of pain in each case. A decline in effectiveness with time was noted in small numbers of our cases despite persistence of paresthesia in the area of pain. It is suggested that late failure reflects plasticity of the nervous system in adapting to new inputs. Morphine study was carried out in some of these patients. Morphine did not help to ameliorate the pain in many cases with deafferentation pain. And also Naloxone was administered during successful pain-relieving stimulation. This did not result in recurrence of pain. The Somato Sensory Responses were recorded in 25 patients before and during neurostimulation. When stimulation was applied the late component was suppressed in most of those who enjoyed a good result. The early component was not changed in those patients even during stimulation. These results suggest that spinal cord stimulation would suppress the denervative hypersensitivity of dorsal horn in the patients with deafferentation pain.(ABSTRACT TRUNCATED AT 250 WORDS)
1. Referred pain of visceral origin has three major characteristics: visceral pain is referred to somatic areas that are innervated from the same spinal segments as the diseased organ; visceral pain is referred to proximal body regions and not to distal body areas; and visceral pain is felt as deep pain and not as cutaneous pain. The neurophysiological basis for these phenomena is poorly understood. The purpose of this study was to examine the organization of viscerosomatic response characteristics of spinothalamic tract (STT) neurons in the rostral spinal cord. Interactions were determined among the following: 1) segmental location, 2) effects of input by cardiopulmonary sympathetic, greater splanchnic, lumbar sympathetic, and urinary bladder afferent fibers, 3) location of excitatory somatic field, e.g., hand, forearm, proximal arm, or chest, 4) magnitude of response to hair, skin, and deep mechanoreceptor afferent input, and 5) regional specificity of thalamic projection sites. 2. A total of 89 STT neurons in segments C3-T6 were characterized for responses to visceral and somatic stimuli. Neurons were activated antidromically from the contralateral ventroposterolateral oralis or caudalis nuclei of the thalamus. Cell responses to visceral and somatic stimuli were not different on the basis of the thalamic site of antidromic activation. Recording sites for 61 neurons were located histologically; 87% of lesion sites were located in laminae IV-VII or X. There was no relationship between response properties of the neurons and spinal laminar location. 3. Different responses to visceral stimuli were observed in three zones of the rostral spinal cord: C3-C6, C7-C8, and T1-T6. In C3-C6, urinary bladder distension (UBD) and electrical stimulation of greater splanchnic and lumbar sympathetic afferent fibers inhibited STT cells. Electrical stimulation of cardiopulmonary sympathetic afferents increased cell activity in C5 and C6 and either excited or inhibited STT cells in C3 and C4. In the cervical enlargement (C7-C8), STT cells generally were either inhibited or showed little response to stimulation of visceral afferent fibers. In T1-T6, input from greater splanchnic and cardiopulmonary sympathetic afferent nerves increased activity of STT cells. Lumbar sympathetic afferent input inhibited cells in T1-T2 and had little effect on cells in T3-T6, whereas UBD decreased cell activity in all segments studied. 4. In general, stimulation of somatic structures increased activity of STT neurons in segments that received primary afferent innervation from the excitatory somatic receptive field or in the segments immediately adjacent to these segments. Only input from the forelimb, especially the hand, markedly excited cells in C7 and C8.+
The mechanisms leading to the frequent occurrence of referred muscle pain (RP) are largely unknown. It is possible that RP is caused by the increased sensitivity of local muscle nociceptors and/or by a central sensitisation. When deep pressure by palpation is used on a subject with smooth fibrotic lesions (myofibrosis) in a muscle, RP can originate as a hyperalgesic cutaneous area, adjacent to, or totally apart from the pressure pain locus. It is currently postulated that a chain reaction is activated implicating triggering of an ever-increasing number of afferent neurons and facilitation of the synaptic connection at the level of the spinal cord, causing more distally a distributed RP via convergent efferent pathways. The human interpretation of this phenomenon can be misleading when the tested person positions, after a few seconds, his RP distally from the site of pressure to the distally located RP area. As a result of what we have found in our experimentally induced RP probes, we hypothesize that deep pressure on a myofibrosis will, in the first place, within a few seconds, increase the nociceptive excitability of the afferent sensitive nerves from the RP area to the local spot of pressure on the muscle, which in return will, in the second place, excite the whole dependent RP area. The mechanism for referred muscle pain proposed in this article is linked to the "pre-local hyper-excitability theory" or "barrier-dam theory". The afferent sensitive peripheral nerves might be entrapped in local muscle hardenings (barrier-dam) with the consequence of the hyper-excitation of pre-local nerves between the distally referred pain area and the local muscular zone of tenderness. The primary pathogenesis of referred muscle pain is likely to be a peripheral sensitization with additionally a central modulation and not vice versa. Clinical and fundamental studies with experimentally induced RP are nevertheless needed to examine the hypothesis.
Dorsal root ganglion neurones with dichotomising axons are present in several species and are considered to play a role in referred pain. Clinically, patients with lesions in the lower lumbar discs occasionally complain of pain in the groin. We investigated the existence of dichotomising afferent neurones projecting axons both to the lumbar disc and to the groin skin, using the double fluorescent-labelling technique in rats. We observed neurones labelled with a tracer applied at the ventral portion of the LS-L6 disc and another tracer placed on the groin skin in L1 and L2 dorsal root ganglia. Our results showed that the double-labelled neurones had peripheral axons which dichotomised into both the LS-L6 disc and the groin skin, indicating the convergence of afferent sensory information from the disc and groin skin. Our findings provide a possible neuroanatomical mechanism for referred groin pain in patients with disc lesions.
Several clinical characteristics of angina pectoris are reflected in the nature of the cardiac nervous system. The extent of silent ischemia, the slow onset of angina during the ischemic cascade, the diffuse character of the visceral component of the pain and the referred pain. Of putative myocardial pain messengers so far only adenosine fulfills Lewis criteria for a cardiac pain messenger. Dependent on the pattern of ischemic release, adenosine appears to stabilize or sensitize afferent cardiac nerves with silent or painful ischemia as a result. Through spatio-temporal summation sensitization may result in an alarm whereby the myocardium signals centrally its precarious state. The activity of adenosine-sensitized afferent nerves may become enhanced by additional stimuli such as potassium, protons, substance P and bradykinin. Primary and secondary afferents from the intrinsic and extrinsic intrathoracic cardiac nervous systems project towards the central nervous system via sympathetic and vagal elements. The main part of primary afferents have their cell bodies in extrinsic cardiac ganglia and only a minority in the dorsal root ganglia. No cardiotopical representation exists in the intrathoracic ganglia. The majority of neurons in intrinsic and extrinsic cardiac ganglia are interneurons integrating cardiac inotropic and vasomotor functions on a beat to beat basis. Multisynaptic transmission over secondary afferents may not only delay the anginal pain message; as somatic afferents also connect to the intrathoracic ganglia, these multisynaptic transmissions may also be a basis for referred pain or pain inhibition. Dorsal root afferents appear to convey only excitatory impulses. Probably due to interneurons, cardiac nodose ganglia activities can become either excitatory or inhibitory. Cardiocardiac reflexes occur from the axonal level up to the brain stem cerebral levels. The brain defense system including the basal ganglia and limbic system and the prefrontal but not the sensory cortex are activated during myocardial ischemia indicating its traumatic nature. The reflexogenic nature of angina pectoris is evident as in silent ischemia similar central nervous system activation occurs as in angina pectoris but with less intense prefrontal activation while in Syndrome X more intense activation occurs. Therapeutic interference of the reflex mechanism by sympathectomy, electrical stimulation or pharmacological interventions can counteract angina pectoris and relax the reflexogenic stress and vasomotor drive on the heart.
Hyperthermia in conjunction with radiation therapy is a promising method for the treatment of superficially or eccentrically located recurrent or advanced primary malignant tumours. The external hyperthermia applicators most commonly used are radiative electromagnetic (including microwave) or ultrasound devices. Each type of device has its own limitations. The aim was to evaluate the temperature distributions obtained as well as the acute and subacute toxicities in patients that were treated with both radiative radiative electromagnetic and ultrasound applicators to the same tumours. Thirty-nine patients treated to 41 hyperthermia fields for a total of 197 hyperthermia treatments were analysed. Thermal parameter include mean, Tmax, mean Tave, mean Tmin, T50, T90, %T > 43.5 degrees C and %T < 41 degrees C. Acute toxicities including pain in field, referred pain, blister/ulceration, positional discomfort and subacute toxicities (occurring with 24 h of treatment) were determined for each type of hyperthermia applicator. Although there were increased acute toxicities (in-field or referred pain) associated with the ultrasound treatments no significant differences between the two methods of heating were observed in temperature distributions or subacute toxicities. We conclude that there is no generally preferred method of heating superficially or eccentrically located tumours and the type of applicator should be selected on a tumour-size and site-specific basis.
The whiplash syndrome has immense socio-economic impact. Despite extensive studies over the past years, the mechanisms involved in maintaining the pain in chronic whiplash patients are poorly understood. The aim of the present experimental study was to examine the muscular sensibility in areas within and outside the region involved in the whiplash trauma. Eleven chronic whiplash patients and 11 sex and age matched control subjects were included in the study. Before the experiment, the whiplash patients had pain in the neck and shoulder region with radiating pain to the arm. Five patients reported pain that was more widespread. The somatosensory sensibility in the areas over the infraspinatus, brachioradial, and anterior tibial muscles was assessed by pressure stimulation, pin-prick stimulation, and cotton swap stimulation. Infusion of hypertonic saline (5.85%, 0.5 ml) into the infraspinatus and anterior tibial muscles was performed to assess the muscular sensibility and referred pain pattern. The saline-induced muscle pain intensity was assessed on a continuous visual analogue scale (VAS). The distribution of pain was drawn on an anatomical map. The pressure pain thresholds were significantly lower in patients (P<0. 01) compared with controls: infraspinatus (mean 152.2 vs. 172.7 kPa), brachioradial (mean 70.0 vs. 363.8 kPa), and anterior tibial muscle (mean 172.7 vs. 497.8 kPa). The skin sensibility to pin-prick stimulation and cotton swap stimulation was not different between patients and controls. Infusion of hypertonic saline caused significantly higher VAS scores with longer duration in patients compared to control subjects (P<0.01). The area under the VAS-time curve was significantly (P<0.01) increased in patients compared to control subjects after injection into the infraspinatus muscle (mean 4138.1 vs. 780.0 cm s) and anterior tibial muscle (mean 4370.8 vs. 978.7 cm s). The saline infusion caused local pain defined as pain located around the injection site and referred pain areas not included in the local pain area. The area of local and referred pain were significantly larger in patients compared to control subjects (P<0.01). In the control group, the referred pain areas to infusion of hypertonic saline into the anterior tibial muscle were found at the dorsal aspect of the ankle. In contrast, the areas of referred pain were quite widespread in the patient group with both distal and proximal referred pain areas. In the present study, muscular hyperalgesia and large referred pain areas were found in patients with chronic whiplash syndrome compared to control subjects both within and outside the traumatised area. The findings suggest a generalised central hyperexcitability in patients suffering from chronic whiplash syndrome. This indicates that the pain might be considered as a neurogenic type of pain, and new pharmacological treatments should be investigated accordingly.
We have tested the hypothesis that referred pain of pelvic viscera is elicited by dichotomizing branches of unmyelinated primary afferents projecting via the pelvic nerve to the viscera and through the pudendal nerve to the perineum where pelvic pain is commonly referred to. Using neurophysiological techniques 588 unmyelinated single units projecting into either nerve were recorded in the ventral (n = 228) and dorsal (n = 360) root S2. In each sample only one neurone sent an axon into both nerves. Thus, dichotomizing afferents account for less than 0.5% of the afferent neurones and appear to be an unlikely explanation for referred pain in this body area.
The ability of muscle pain to generate somatosensory sensibility changes is controversial. Thus, in the present study, tonic infusion of hypertonic saline (5%, 7.1 ml administered over 15 min) into the tibialis anterior (TA) muscle was used as an experimental model to induce local and referred pain. The sensibility to high-intensity pressure stimuli applied to the local pain area, referred pain area and an arm was assessed in 14 healthy volunteers. Infusion of isotonic (0.9%) saline into the other leg served as control. The subject continuously scored the pain intensity on an electronic visual analogue scale (VAS). Pressure pain threshold (PPT) was determined on the TA muscle (2 cm and 10 cm from the infusion site), at the frontal aspect of the ankle (area of referred pain) and on the arm. To minimise the skin component of the PPT, the skin covering the assessment sites was anaesthetised with an anaesthetic creme. The PPTs were obtained before and after cutaneous analgesia, 1 min and 10 min after infusion start and 10 min after the pain had disappeared. Infusion of hypertonic saline caused significantly (P<0. 05) higher VAS scores than infusion of isotonic saline. A significant (P<0.04) increase of the PPT (i.e., decreased sensibility) was found at the ankle and on the arm during muscle pain compared to the control condition. No significant differences in PPTs on the TA muscle were found during saline-induced muscle pain compared to the infusion of isotonic saline. The decrease in deep sensibility at the heterotopic sites (referred pain area and arm), but not at homotopic sites (TA muscle), probably reflected the phenomenon of diffuse noxious inhibitory control (DNIC). The inhibitory mechanism during muscle pain was shown to be effective for the deep tissue sensibility in healthy subjects. Thus, a pathologically disturbed inhibitory mechanism may result in widespread deep hyperalgesia in muscle pain patients.
The generation of transgenic mice that lack or overexpress genes relevant to pain is becoming increasing common. However, only one visceral pain model, the writhing test, is widely used in mice. Here we describe a novel model, chemical stimulation of the colon, which we have developed in mice. Mice of either sex were injected i.v. with 30 mg/kg Evan's Blue for subsequent determination of plasma extravasation. For behavioural testing, they were placed on a raised grid and 50 microl of saline, mustard oil (0.25-2.5%) or capsaicin (0.03-0.3%) was administered by inserting a fine cannula into the colon via the anus. Visceral pain-related behaviours (licking abdomen, stretching, contractions of abdomen etc) were counted for 20 min. Before intracolonic administration, and 20 min after, the frequency of withdrawal responses to the application of von Frey probes to the abdomen was tested. The colon was removed post-mortem and the Evan's Blue content measured. Mustard oil and capsaicin administration evoked dose-dependent visceral pain behaviours, referred hyperalgesia (significant increase in responses to von Frey hairs) and colon plasma extravasation. The peak behavioural responses were evoked by 0.1% capsaicin and by 1% mustard oil respectively. The nociceptive behavioural responses were dose-dependently reversed by morphine (ED50 = 1.9 +/- 1 mg/kg s.c.). We conclude that this model represents a useful tool both for phenotyping mutant mice and for classical pharmacology since information on visceral pain, referred hyperalgesia and colon inflammation can all obtained from the same animal.
Musculoskeletal pains are often characterised by referred pain and hyperalgesia. The aim of the present study was to examine the sensitivity to pressure and pinprick at sites ipsi- and contralateral to capsaicin-induced pain in the tibialis anterior (TA) muscle. Visual analogue scale (VAS) scores of the sensation to sub- and supra-pain threshold stimuli by pressure and pinprick were recorded before, during and after experimental muscle pain. It was found that pressure stimulation (120% of baseline pain threshold) delivered over the ipsilateral deep peroneal nerve between the 1st and 2nd metatarsal bones showed a significant increase in VAS scores during muscle pain. The referred pain did not overlap this hyperalgesic site. Ipsilateral test sites at the TA muscle, great toe and between the 3rd and 4th metatarsal bones did not show any changes in response to pressure stimulation during pain. In contrast, test sites at the ipsilateral ankle showed hypoalgesia to pressure during muscle pain. In the contralateral leg hypoalgesia to pressure was found at all sites during pain. The decreased sensitivity to pressure was confirmed with both sub- and supra-pressure pain-threshold stimuli. VAS scores to pinprick were either decreased or unchanged during pain compared to before pain. Naloxone administrated in a placebo-controlled manner had no effect on hypoalgesia to pressure or pinprick during muscle pain. Thus, the generalised decreased sensitivity may reflect activation of non-opioid endogenous pain inhibitory systems. The lack of change in sensitivity at some sites could indicate a competitive balance between excitatory and inhibitory mechanisms. The deep peroneal nerve specifically innervates both the TA muscle and the only site of hyperalgesia indicating spatial summation of afferent activity from these structures.
Gluteal, pelvic, and lower extremity muscles are common sites of origin of myofascial low back pain. Trigger points (TPs) in the gluteus maximus and medius muscles refer pain locally to the gluteal and sacral regions, while those in the gluteus minimus are likely to refer pain down the lower extremity as far as the ankle on the same side. TPs in intrapelvic muscles refer pain chiefly to the pelvic region. Besides producing referred myofascial pain, TPs in the piriformis muscle can cause symptoms of entrapment of the peroneal portion or all of the sciatic nerve. TPs in the soleus muscle may refer pain to the sacroiliac joint.
OBJECT: This is the first observational study to compare perioperative pain character and intensity in patients undergoing different types of elective neurosurgical procedures. METHODS: A structured questionnaire was used to inquire about pain intensity, character, and management during the perioperative course, and the anticipated visual analogue scale (VAS) score in 649 patients during a 1-year period. The anticipated maximal postoperative VAS score was lower than the actual postoperative maximal VAS score and was independent of operation type and preoperative VAS score. Patients undergoing craniotomy experienced less pain than those undergoing spinal surgery. A majority of patients did not receive analgesic medication after surgery. Patients undergoing spinal surgery experienced higher preoperative VAS scores than those undergoing other neurosurgical treatments, with a shift from preoperative referred pain to postoperative local pain. After lumbar flavectomy, referred pain was greater than local pain. Patients with preoperative pain suffered significantly more postoperative pain than those without preoperative pain. In patients with postoperative surgery-related complications, VAS scores were higher than in those without complications. CONCLUSIONS: Neurosurgical procedures cause more pain than anticipated. Anticipated pain intensity is independent of the operation type and preoperative pain intensity. Postcraniotomy on-demand analgesic medication is appropriate, if the nurses on the ward react quickly. Otherwise, patient-controlled analgesia might be an option. Other neurosurgical procedures require scheduled analgesic therapies. Spinal surgery requires intensive preoperative pain treatment; a shift in pain character from preoperative referred pain to postoperative local pain is expected. Patients with referred pain after lumbar flavectomy are prone to the most intense pain. Patients with preoperative pain experience more postoperative pain than those without preoperative pain and require more intensive pain management. Increased postoperative VAS scores are associated with surgery-related complications.
BACKGROUND AND AIMS: Experimental pain models based on single stimuli have to some degree limited visceral pain studies in humans. Hence, the aim of this study was to investigate the effect of multi-modal visceral pain stimuli of the oesophagus in healthy subjects before and after induction of visceral hyperalgesia. We used a multi-modal psychophysical assessment regime and a neurophysiological method (nociceptive reflex) for the characterisation of the experimentally induced hyperalgesia. METHODS: A probe for multi-modal (cold, warm, electrical, and mechanical) visceral stimulation was positioned in the lower part of the oesophagus in eleven healthy subjects. Mechanical stimuli were applied as distensions with a bag, which also had electrodes mounted for electrical stimulation. Thermal stimulation with temperatures from 0 to 60 degrees C was applied with re-circulating water in the bag. To assess the interaction between visceral and somatic pathways, the nociceptive withdrawal reflex to electrical stimuli at the ankle was measured with and without simultaneous mechanical oesophageal distension to painful levels. Finally, the oesophageal sensitisation was induced by perfusion with hydrochloric acid. Multimodal responses (pain threshold, stimulus response function, size of nociceptive reflex, and referred pain areas) were assessed before and after the induced hyperalgesia. RESULTS: The multi-modal psychophysical responses and reflex sizes were assessed twice before sensitisation, and the parameters were reproducible. Sensitisation of the oesophagus resulted in hyperalgesia to electrical and mechanical stimuli (29 and 35% decrease in pain threshold) and allodynia to cold and warmth stimuli (11% increase in sensory rating). After sensitisation, the referred pain area to mechanical stimuli increased more than 300% with a change in the localisation of the referred pain to all stimuli, and the amplitude of nociceptive reflex increased 100%, all indicating the presence of central hyperexcitability. CONCLUSIONS: Visceral hyperalgesia/allodynia can be induced experimentally and assessed quantitatively by the newly introduced multi-modal psychophysical assessment approach. The significant changes of the experimentally evoked referred pain patterns and of the nociceptive reflex evoked from a distant somatic structure indicate that even short-lasting visceral hyperalgesia can generate generalised sensitisation.