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PubMed2000

Rheumatologists and neck pain.

Many authors have suggested that chronic pain syndromes are psychosocial in origin; maladaptive behaviours favoured by psychosocial and political factors. Sometimes this may be true, but neither the individual patients nor the accumulated scientific evidence deserve such a routine dismissal. In this editorial I will review issues of responsibility, the nature of referred pain and referred tenderness, evidence for the value of tender point examination as an objective measure, techniques of assessment of the cervical spine, techniques of assessment of pain behaviour, and the determinants of the specific symptom patterns associated with cervical injury.

Humans↗

PubMed1986

Tender points: evolution of concepts of the fibrositis/fibromyalgia syndrome.

The association of chronic pain, exhaustion, and multiple somatic complaints with apparent physical good health and long survival has a long history. The syndrome was called by many names including neuresthenia, rheumatism, and invalidism. When skeletal pain and stiffness were prominent, many observers recorded the existence of sites of tenderness and sometimes of areas of induration. The work of Lewis and Kellgren provided an experimentally reproducible method of study of the phenomena of referred pain and referred tenderness, which led to hypotheses about the nature of many of these syndromes, which were unfortunately too numerous and often contradictory. More recently, it has been learned that the sites of tenderness are precisely predictable in location and, under some circumstances, experimentally inducible. They are unknown to the patient and, therefore, due to mechanisms other than distortions of interpretation. The association with a variety of forms of sleep disturbance was discovered. These events have permitted the rapid evolution of controlled, numerical studies of these associations, which are reviewed briefly in this article.

Fibromyalgia↗

PubMed1996

Respiratory dysfunction related to diaphragmatic shoulder pain after abdominal and pelvic laparoscopy.

Many recent studies registered respiratory dysfunction after laparoscopic surgery; it is well known that the stimulation of the diaphragmatic tendon centre produces a typical shoulder pain. We hypothesize that diaphragmatic tendon centre stress causes postlaparoscopic ventilatory alterations; the aim of this study was to verify whether clinically respiratory dysfunction and shoulder pain relationship exists, after laparascopy with or without contemporaneous stimulation of gallbladder area. So we evaluated, preoperatively and 24 hours after the operation, 20 patients undergoing laparoscopic cholecystectomy (CP), 20 gynaecological patients undergoing laparoscopic ovarian surgery (GP) and 20 control patients undergoing orthopaedic limbs operations (OP) by pulmonary function tests, using computerized spirometry. Diaphragm referred pain was assessed for location and intensity. No orthopaedic patient showed postoperatively pain or pulmonary dysfunction demonstrating that the typical postlaparoscopic restrictive pattern is independent of general anaesthesia. In the CP and GP groups postoperative pulmonary functions were significantly reduced if compared with the orthopaedic control group but not significantly different between them. Moreover, 8 patients from the CP group and 13 from the GP group referred diaphragmatic pain: they showed significantly greater reduction of pulmonary function in comparison with the patients without pain in the respective groups. We conclude that diaphragmatic dysfunction after pneumoperitoneum, and not gallbladder area stimulation, seems to play the most important role in the pathogenesis of both shoulder pain and respiratory restrictive abnormalities after laparoscopy.

Abdomen↗

PubMed1998

Treatment with either high or low frequency TENS reduces the secondary hyperalgesia observed after injection of kaolin and carrageenan into the knee joint.

For years, physical therapists have been utilizing a variety of modalities, including transcutaneous electrical nerve stimulation (TENS), in an attempt to manage pain associated with inflammation. However, the data on clinical effectiveness is conflicting and the neurophysiological mechanism of action is not known. The purpose of this study was to investigate the effects of high and low frequency TENS on the secondary hyperalgesia that occurs after joint inflammation. Secondary hyperalgesia is thought to reflect changes in central neurons and is thus a measure of activity of central neurons. This study utilized the kaolin and carrageenan model of knee joint inflammation and measured the effects of TENS treatment on paw withdrawal latency to radiant heat (secondary hyperalgesia), spontaneous pain behaviors and joint circumference. Either high (100 Hz) or low (4 Hz) frequency TENS was applied to the knee joint for 20 min after the development of hyperalgesia. Both high and low frequency TENS resulted in a reversal of the hyperalgesia immediately following treatment. The effects of high frequency TENS lasted through at least 24 h while those of low frequency TENS lasted through 12 h. There was no effect of TENS on spontaneous pain behaviors or joint swelling when compared to controls. Thus, TENS appears to be more effective in reducing referred pain (or secondary hyperalgesia) without affecting guarding or splinting of the affected limb. Thus, clinically, the choice to use TENS may depend on patient symptoms; specifically TENS should be effective in reducing referred or radiating pain.

Animals↗

PubMed1996

Assessment of cancer pain: a prospective evaluation in 2266 cancer patients referred to a pain service.

Although pain assessment is a vital preliminary step towards the satisfactory control of cancer pain, data on the prevalence of different pain syndromes are rare. In a prospective study of 2266 cancer patients, we assessed localisations, aetiologies and pathophysiological mechanisms of the pain syndromes. Thirty percent of the patients presented with 1, 39% with 2 and 31% with 3 or more distinct pain syndromes. The majority of patients had pain caused by cancer (85%) or antineoplastic treatment (17%); 9% had pain related to cancer disease and 9% due to aetiologies unrelated to cancer. Pain could be classified as originating from nociceptors in bone (35%), soft tissue (45%) or visceral structures (33%) or otherwise as of an neuropathic origin (34%). In most patients, pain syndromes were located in the lower back (36%), abdominal region (27%), thoracic region (23%), lower limbs (21%), head (17%) and pelvic region (15%). The main pain syndrome was also coded according to the IASP Classification of Chronic Pain. Regions and systems affected by the main pain syndrome showed large variation depending on the site of cancer origin, whereas temporal characteristics, intensity and aetiology were not markedly influenced by the cancer site. The variety of pain syndromes evaluated in our patients confirms the importance of comprehensive pain assessment prior to treatment.

Adult↗

PubMed2002

The diagnosis of referred orofacial dental pain.

Every patient's description of the location of pain must be treated with caution. In order to arrive at a diagnosis of pain a logical method should be employed. This consists of the history and clinical examination including pulp tests and radiographs. Where the patient complains of pain on hot or cold, an attempt should be made to reproduce the patient's pain to check on the accuracy of its description and to aid in localisation. Patients frequently refer pain to previously endodontically-treated teeth. These may not be the cause of the problem. In order to facilitate the process of diagnosis the following hypothesis has been advanced. A tooth can only be the source of pain if there are objective signs associated with that tooth. Lack of response to pulp tests constitutes such a sign, provided the tooth has not previously been endodontically treated. If, however, such treatment has taken place, (regardless of whether this was well or poorly executed), a further objective sign other than lack of vitality is required before such a tooth can be implicated as the source of pain. The guidelines suggested are illustrated by means of clinical examples.

Adult↗

PubMed1994

Chronic obscure groin pain is commonly caused by enthesopathy: 'tennis elbow' of the groin.

Forty-nine patients with chronic obscure groin pain, bilateral in four, presented to one general surgeon in a 12-month period. Inflammation ('enthesopathy') at the pubic insertion of the inguinal ligament was the cause in 30 patients (32 groins). This has not previously been recognized as a cause of chronic groin pain, possibly because the exact site of tenderness can be obscured by the pubic pad of fat. Enthesopathy also occurred in five rectus and one adductor longus tendons (one patient had inflammation in both). Infiltration with long-acting steroid (1 per cent triamcinolone) and local anaesthetic (2 per cent lignocaine) was offered to all patients with localized tenderness of tendon or ligament. A questionnaire survey 3-15 months after injection showed a better outcome after treatment than when injection was declined. Other causes of pain included nerve entrapment (five cases), spinal referred pain (five in four patients) and ureteric stones (two). Inguinal hernia is sometimes coincidental rather than causative of the pain. In three patients the pain had subsided and no diagnosis was made. Simple diagnostic and therapeutic measures may relieve chronic groin pain and spare patients elaborate investigation or unnecessary operation.

Adult↗

PubMed2007

Protein kinases as potential targets for the treatment of pathological pain.

Pathological pain or clinical pain refers to tissue injury-induced inflammatory pain and nerve injury-induced neuropathic pain and is often chronic. Pathological pain is an expression of neural plasticity that occurs both in the peripheral nervous system (e.g., primary sensory nociceptors), termed peripheral sensitization, and in the central nervous system (e.g., dorsal horn and brain neurons), termed central sensitization. Our insufficient understanding of mechanisms underlying the induction and maintenance of injury-induced neuronal plasticity hinders successful treatment for pathological pain. The human genome encodes 518 protein kinases, representing one of the largest protein families. There is growing interest in developing protein kinase inhibitors for the treatment of a number of diseases. Although protein kinases were not favored as targets for analgesics, studies in the last decade have demonstrated important roles of these kinases in regulating neuronal plasticity and pain sensitization. Multiple protein kinases have been implicated in peripheral and central sensitization following intense noxious stimuli and injuries. In particular, mitogen-activated protein kinases (MAPKs), consisting of extracellular signal-regulated kinase (ERK), p38, and c-Jun N-terminal kinase (JNK), are downstream to many kinases and are activated in primary sensory and dorsal horn neurons by nociceptive activity, growth factors and inflammatory mediators, contributing to the induction and maintenance of pain sensitization via posttranslational, translational, and transcriptional regulation. MAPKs are also activated in spinal glial cells (microglia and astrocytes) after injuries, leading to the synthesis of inflammatory mediators/neuroactive substances that act on nociceptive neurons, enhancing and prolonging pain sensitization. Inhibition of multiple kinases has been shown to attenuate inflammatory and neuropathic pain in different animal models. Development of specific inhibitors for protein kinases to target neurons and glial cells will shed light on the development of new therapies for debilitating chronic pain.

Animals↗

PubMed1977

Trigger points and acupuncture points for pain: correlations and implications.

Trigger points associated with myofascial and visceral pains often lie within the areas of referred pain but many are located at a distance from them. Furthermore, brief, intense stimulation of trigger points frequently produces prolonged relief of pain. These properties of trigger points--their widespread distribution and the pain relief produced by stimulating them--resemble those of acupuncture points for the relief of pain. The purpose of this study was to determine the correlation between trigger points and acupuncture points for pain on the basis of two criteria: spatial distribution and the associated pain pattern. A remarkably high degree (71%) of correspondence was found. This close correlation suggests that trigger points and acupuncture points for pain, though discovered independently and labeled differently, represent the same phenomenon and can be explained in terms of the same underlying neural mechanisms. The mechanisms that play a role in the genesis of trigger points and possible underlying neural processes are discussed.

Acupuncture Therapy↗

PubMed1993

Ipsilateral referral of pain following cordotomy.

We report a patient who developed ipsilateral referred pain following unilateral percutaneous cervical cordotomy (PCC). A right-sided PCC was performed on a 44-year-old woman who had been suffering from left groin and thigh pain caused by a fibrosarcoma. PCC produced analgesia below T7 on the left side, and the pain disappeared. A novel spontaneous pain with prominent allodynia occurred postoperatively in the right infraclavicular region (C3-C4). Strong pressure on the left groin where severe spontaneous pain and tenderness had been before PCC increased the new pain, and an epidural block which produced analgesia below T10 relieved the new pain. These facts indicate that the new pain was induced by afferent inputs from the originally painful region.

Adult↗

PubMed1997

Peripheral and central hyperexcitability: differential signs and symptoms in persistent pain.

This target article examines the clinical and experimental evidence for a role of peripheral and central hyperexcitability in persistent pain in four key areas: cutaneous hyperalgesia, referred pain, neuropathic pain, and postoperative pain. Each suggests that persistent pain depends not only on central sensitization, but also on inputs from damaged peripheral tissue. It is instructive to think of central sensitization as comprised of both an initial central sensitization and an ongoing central sensitization driven by inputs from peripheral sources. Each of these factors, initial sensitization, ongoing central sensitization, and inputs from peripheral sources, contributes to the net activity in dorsal horn neurons and thus influences the expression of persistent pain or hyperalgesia. Since each factor, peripheral inputs and central sensitization (initial or ongoing), can contribute to both the initiation and maintenance of persistent pain, therapies should target both peripheral and central sources of pathology.

Anesthetics, Local↗

PubMed1989

Hemicranial attacks or permanent hemicrania--a sequel of upper cervical root compression.

After many years of unsuccessful conservative treatment 16 patients suffering from hemicrania are relieved of their pain or are improved by operative treatment. Hemicranial attacks or permanent hemicrania is found to be caused by upper cervical nerve root compression. Vascular compression of C2 (n = 9) or scar tissue surrounding C2 (n = 1) or C3 (n = 1) is the pathology identified in cases of cervicogenic headache or "cluster headache-like" headache. Compression attributable to tumor, prolapsed disc, or spondylotic changes is found to be a cause of permanent headache. Only in those patients with permanent headache are radiological or electrophysiological findings helpful for diagnosis. In patients with hemicranial attacks and compression of nerve root C2 (n = 10) or C3 (n = 1), only vasoactive tests (provoking or relieving pain) or local anaesthesia prove to be helpful in diagnosing and localizing the origin of pain. The operation involves freeing the nerve roots from vascular compression. In two patients the C2 ganglion is resected. Thirteen patients subsequently become pain free. In three patients, hemicrania improves. Four of the 16 patients experience a recurrence of pain after the decompressive operation. After additional thermorhizotomy two patients have no further complaints and one patient has improved. One patient can tolerate his pain with occasional analgesics. The problem of referred pain into the fronto-ocular region is discussed.

Adult↗

PubMed2000

[Diagnosis and treatment of orofacial pain].

Management of orofacial pain should address factors that contribute to the continuation of the pain complaint. This requires elimination of etiologic factors, modification of nociceptive mechanisms, and support of adaptive mechanisms. In addition, methods that help the patient to cope with (remaining) complaints should be applied. A specific diagnosis of the pain problem is the basis for successful management. From the history and clinical examination it should become clear whether the pain problem is acute or chronic, whether its characteristics suggest a somatic or neuropathic basis, and whether the experienced pain is primary or secondary (i.e., hyperalgesia, referred pain). It is important to regard pain as a multidimensional phenomenon, in which psychosocial factors are involved. It is the responsibility of the dentist to judge as early as possible whether he/she is capable of managing the pain problem, or further consultation or referral is necessary for diagnosis and/or management.

Acute Disease↗

PubMed2006

[Patients with orofacial pain: treatment or referral (and to whom)?].

The anatomical complexity of the head and neck region may cause difficulties in the diagnostic process and management of orofacial pain. The general dentist is expected to thoroughly use his specific areas of competence in the diagnosis and treatment of odontogenic, joint and muscle pain. The need to interact with and refer patients to dental or medical colleagues and specialists will especially occur in cases of diagnostic doubt, referred pain, neuropathic or neurogenic/neurovascular pain, and complex chronic pain in the orofacial region.

Clinical Competence↗

PubMed1978

Oral--facial pain: old puzzles, new postulates.

Dental examples are given (e.g. referred pain, V neuralgia) which exemplify the multifactorial and puzzling nature of pain. Pain results from a noxious stimulus activating some of the small-diameter myelinated and unmyelinated afferent nerve fibres that innervate skin, mucosa, teeth etc. It is complex experience including the sensation experienced as well as the emotional, cognitive and motivational reactions evoked by the stimulus. Pain is not a simple function of the magnitude of damage caused by the stimulus, but also depends on factors such as the person's emotions, past experience of pain, and other concomitant sensory experiences (e.g. with acupuncture). Early postulates of pain failed to take all these factors into account. In the V system (Fig. 1), the specificity theory would maintain that there exists a 'private pain path' from oral-facial tissues to the cerebral cortex, with nerve fibres and brain cells in this path responsive only to stimulu of a noxious character (Fig. 2). But anatomical, physiological and psychological observations have failed to give full support to this theory and other postulates of pain. Although some details of the more recently proposed gate control theory have not been sustantiated, this theory has provided a good general framework for viewing pain and has stimulated much recent research. It emphasizes sensory interaction between large and small-diameter afferent nerve fibres in the gate control system, and regulation over central pain transmission through the gate by descending central controls (Fig. 3). In the V system, brain cells involved in central pain transmission have now been found (Fig. 4), and sensory interactions and descending controls on these brain cells noted (Fig. 5). Neural mechanisms such as these have been implicated in pain, and in its control by procedures such as acupuncture, suggestion, distraction and narcotic analgesia.

Brain↗

PubMedDate not supplied

[Clinical and coronary angiographic characteristics of hypertensive angina].

The sample studied consisted of 46 patients with systemic hypertension. Of these, 21 had angor pectoris and constituted group I; 12 showed left ventricular hypertrophy, constituting group II; the other 13 subjects did not have complications and they formed group III. All patients, aside from the usual clinical evaluation, were submitted to exercise electrocardiography, coronary angiography and cineventriculography. The average age of patients in group III was lower than in the others (38.6 +/- 8.4 years), and so was the percentage of smokers (15.3%), and of patients with diabetes (23.0%). The number of smokers in group II represented 41.3% and in group I, 38%. The percentage of patients with diabetes was 33.3% in group II and 52.3% in group I. Pain in the patients of group I had the following characteristics: retrosternal pain was present in all cases, while referred pain to the neck and left arm appeared in 61% of the subjects. In 66.3% of the individuals the pain lasted between 5 and 15 minutes. In 52.3% of the group, pain was not always related to effort, but appeared also at rest. Temporal periodicity was present in 52.7% of the patients. Also in group I, 95.2% of the cases had a depression of the S-T segment in the leads corresponding to the anterior aspect of the left ventricle. In 86.6% of the subjects, there was a positive exercise test. The Sokoloff's index was 26.4 +/- 7.9 mm. In 75% of the subjects in group II, a depression of the S-T segment was present, and a positive exercise test was found in 50% of them. Their sokoloff's index was 26.7 +/- 6.4. None of the patients in group III had depressions of the S-T segment and 20% resulted with a positive exercise test. Their sokoloff's index was 13.3 +/- 2.9. The coronary angiography results showed stenosis in 28% of the subjects in group I and tortuosity of the vessels was apparent in 94.8% of them. None of the patients of group II and III had stenosis of the coronaries, but tortuosity was observed in 74.9% of the individuals in group II and in 69.1% of the cases in group III. Based in these data we conclude that there is a type of angor pectoris in hypertensive subjects which is related to hypertrophy of the left ventricle, but not to coronary stenosis. The management of this type of patient should be different to the regular one.

Adult↗

PubMed1981

Myofascial trigger point syndromes in the practice of rheumatology.

Pain referred from a muscle can mimic both pain from a joint and radicular pain associated with disease of spinal joints, leading to mistakes in diagnosis and in treatment. When articular disease is present, it predisposes to myofascial trigger point (TP) syndromes. With arthritis, TPs in muscles may result from decreased mobility with prolonged shortening of muscles, from abnormal mechanical stress on muscles and from stimuli arising in diseased joints. During examination for signs of myofascial disorders, the numbers of tender points and of local twitch responses in women with rheumatoid arthritis were twice those found in women free of any rheumatic illness. It is important to consider this high frequency of myofascial syndromes in persons with arthritis, when treating pain or weakness which could be due to the muscles rather than the joints. Conversely, it has been proposed, on theoretical and clinical grounds, that muscular TPs can cause joint disease. This hypothesis has important implications for the treatment of arthritis.

Arthritis↗

PubMed2006

N-methyl-D-aspartate (NMDA) and non-NMDA receptor antagonists suppress the superior sagittal sinus-evoked activity of C1 spinal neurons responding to tooth pulp electrical stimulation in rats.

The aim of the present study was to determine whether there is a convergence of inputs from tooth pulp (TP) and the superior sagittal sinus (SSS) on rat C1 spinal neurons, and to examine the effects of iontophoretically applied N-methyl-D: -aspartate (NMDA) and non-NMDA receptor antagonists on the SSS-evoked activity of C1 neurons. Extracellular single unit-recordings were made from 20 C1 units responding to TP electrical stimulation with a constant temporal relationship to a digastric electromyogram signal, using a multibarrel electrode in pentobarbital-anesthetized rats. Ninety percent of C1 neurons (18/20) responding to TP stimulation also responded to the SSS stimulation. These neurons were considered to be SSS-afferent inputs from Adelta-fibers (5.8 +/- 0.6 m/s; n = 18), based on the calculation of nerve conduction velocity. After the iontophoretic application (30, 50, and 70 nA) of an NMDA receptor blocker (5R-10S)-(+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d] cycloheptene-5,10-imine hydrogen maleate (MK801) or a non-NMDA receptor blocker (6-cyano-7-nitroquinoxaline-2,3-dione) (CNQX), the mean number of spikes responding to the SSS stimulation significantly decreased (30, 50, and 70 nA; P < 0.05). These results suggest that there is a convergence of inputs from SSS and TP afferents on C1 neurons; it is possible that both NMDA and non-NMDA receptors located on C1 neurons may be targets for the treatment of the trigeminal referred pain associated with migraine.

6-Cyano-7-nitroquinoxaline-2,3-dione↗