Pain is one of the cardinal manifestations of rheumatic disorders, which are quite prevalent and an important cause of morbidity and mortality in the population. In inflammatory rheumatic disorders, synovial inflammation causes peripheral and central sensitization by the nociceptive stimuli. This process is affected by the interaction of cognitive, sociocultural and enviromental factors of the individual, which affect the perception and interpretation of pain. Treatment of the underlying cause is the most important goal of the pain management. Treatment strategies only focusing on pain management can not prevent joint damage and disability. Therefore, we have been experiencing very promising results with the new disease-modifying antirheumatic drugs and biological agents, which control the inflammatory process efficiently. Since there is an interaction of the somatic components (nociception and its central transmission) with the cognitive components (belief, mood and behavior), a combination of pharmacologic and cognitive-behavioral (including physical) therapies, appropriate to the individual patient, is recommended.

Duration and recalling of pain, occuring by stimulated unmyelinated C and A-delta fibers, can be described as memory of pain. The memory of pain is a procces that executes in from dorsal horn sensory neurons to cingulate cortex in brain. This description includes hyperalgesia and synaptic plasticity.

Pain is an important problem for patients with cancer, occuring in half of all cancer patients and more than 90 % of patients with advanced disease. Pain related to cancer is a complex, multidimensional phenomenon composed of sensory, affective, cognitive, and behavioural components. The World Health Organization (WHO) has idendified cancer pain as a major international problem and pain control has become a critical element in the comprehensive care of many cancer patients. Pain and quality of life are phenomena that share several fundamental characteristics. Pain control plays a key role in determining health-related quality of life (HRQOL). Pain, when it is ongoing and uncontrolled, has a detrimental, deteriorative effect on virtually every aspect of a patient's life. It produces anxiety and emotional distress; undermines well-being; interferes with functional capacity; and hinders the ability to fulfill familial, social, and vocational roles. With such broad-based effects, it is apparent that pain would have the effect of diminishing quality of life. In patients with moderate or severe pain, interference with sleep, daily life activities, enjoyment of life, work ability, and social interactions have been reported.

Cervicogenic headache is a relatively common and still controversial form of headache arising from structures in the neck. Cervicogenic headache is a unilateral fixed headache characterised by pain that starts in the neck and spreads to the ipsilateral oculo-fronto-temporal area. The pathophysiology of cervicogenic headache probably depends on the effects of various local pain-producing or eliciting factors, such as intervertebral dysfunction, cytokines and nitric oxide. A reliable diagnosis of cervicogenic headache can be made based on the criteria established in 1998 by the Cervicogenic Headache International Study Group or the International Headache Society’s most recent International Classification of Headache Disorders (2004). Various therapies have been used in the management of cervicogenic headache. These range from lowly invasive, drug-based therapies to highly invasive, surgical-based therapies. Unfortunately, the paucity of experimental models for cervicogenic headache and the relative lack of biomolecular markers for the condition mean much is still unclear about cervicogenic headache and the disorder remains inadequately treated.

The aim of this investigation was to assess the role that NO plays in the antinociceptive activity of tramadol using a rat model of neuropathic pain. Thirty male Wistar rats weighing 200-250 g were randomly divided into five equal groups. The neuropathic pain model used for the study was chronic constrictive injury (CCI) model. Three weeks after the surgical procedure, each rat was tested to assess mechanical threshold in grams using an electronic algometer. After CCI was induced, tramadol hydrochloride was administered by intraperitoneal (i.p.) injection in all groups, and N(omega) - nitro - L - arginine (L-NA) and L-arginine were administered i.p. or intrathecally (i.t.) depending on the group. Tramadol was administered in 10 mg/kg doses i.p., L-NA was given in 10 mg/kg doses i.p. and in 30 μg/kg doses i.t.. L-arginine was given in 10 mg/kg doses i. p. and in 50 μg/kg doses i.t.. The multiple agents were given 30 minutes apart from cach administration. Intraperitoneal administration of tramadol (Group 1) only increased mechanical threshold in the rats' left hind paw, whereas in i.p. L-NA group (10 mg/kg) (Group 2) produced a significant reduction of the mean mechanical antinociceptive threshold (p<0.05). Like this, in i.t. L-NA group (30 μg/kg) (Group 4) a significant reduction of the mean mechanical antinociceptive threshold (p <0.05) was also observed. The mean threshold values in Group 2 (i.p. tramadol + i.p. L-NA) and Group 4 (i.p. tramadol + i.t. L-NA) were not significantly different. The mean threshold values in Groups 3 (i.p. tramadol + i.p. L-NA + i.p. L-arginine) and 5 (i.p. tramadol + i.t. L-NA + i.t. L-arginine) were also similar. The mean mechanical antinociceptive threshold was significantly increased in Group 3 (i.p. L-NA + L-arginine) and Group 5 (i.t. L-NA + L-arginine) when compared to Group 1 (i.p. tramadol only) (p<0.05 for both). The results of this study support the involvement of the L-arginine/nitric oxide pathway in the antinociceptive effect of tramadol in a rat model of neuropathic pain.

The aim of this study was to test antinociceptive properties of venlafaxine in rats with carrageenan-induced pain and inflammation. Pain was provoked with carrageenan (1%) injection into the plantar surface of the rat paw-pad. The effect of venlafaxine on carrageenan-induced mechanical hypersensitivity, mechanical stimulation response (the von Frey monofilament test) as well as the size of carrageenan-induced paw edema were tested at 2 to 24 hours following the toxin injection into the rat paw-pad. Pretreatment with venlafaxine significantly reduced or completely abolished the enhanced sensitivity to mechanical stimuli provoked by peripheral carrageenan injection. The study demonstrated the efficacy of peripherally applied venlafaxine pretreatment on the pain component of inflammatory process.

Transdermal nitroglycerine can improve analgesic effects when used with other analgesics. The aim of the study was to investigate the additive effects of nitroglycerine combined with lornoxicam for acute pain in rats. Thirty-nine Wistar male rats were divided into five groups; Group SF (n=8, saline), Group L-1 (n=8, lornoxicam 1.3 mg/kg), Group L-2 (n=8, lornoxicam 2.6 mg/kg), Group LNO (n=8, nitroglycerine and lornoxicam, 1 mg/kg + 1.3 mg/kg), and Group LNO-2 (n=8, nitroglycerine and lornoxicam, 1 mg/ kg + 2.6 mg/kg). Tail flick and hot plate tests were measured in all groups before the intraperitoneal injections of drug and 30, 60 and 90 minutes after the injections. Cut-off time was 20 s and 60 s in tail-flick and hot-plate tests. Although there were significant differences between the groups according to hot-plate test at the 30th, 60th and 90th minutes (p<0.05), there was no difference between the groups with tail flick test. The most increasing of latency response in hot-plate assays was seen in Group LNO-1 compared to other groups at the 30th minute (p<0.05). The latency response increased significantly in Group L-1, L-2, LNO-1 and LNO-2 compared with saline group at the 60th and 90th minutes (p <0.05). There were significant differences in latency responses in Group L-1 and Group LNO-1 compared to Group L-2 and Group LNO-2 at the 60th and 90th minutes. In conclusion, 1.3 mg/kg dose of lornoksicam with the use of nitrogliserine provided early and efficient analgesia, but the increasing dose of lornoksicam did not maintain better analgesia.

Postoperative abdominal and shoulder pain are common complications after laparoscopy. The aim of this study is to compare the effects of intraperitoneal local anesthetics on postoperative abdominal and shoulder pain after laparoscopy. 55 women, physical status ASA I, who were undergoing diagnostic or minor gynecologic surgery, was enrolled to the study. In Group 1 (Bupivacaine, n: 17) and Group 2 (Ropivacaine, n: 18), 80 ml solution which contains one of the local anesthetics (60 ml saline and 20 ml % 0.5 bupivacaine in Group 1, 60 ml saline and 20 ml % 0.75 ropivacaine in Group 2), was injected into the right subdiaphragmatic (30 ml) and abdominopelvic space (50 ml) at the beginning of the surgical procedure. Patients in Group 3 (Control, n: 20) didn't received any solution intraperitoneally. Shoulder and abdominal pain was assessed with a visual analogue scale, and any other complications were noted during the first 24 hours after surgery. Shoulder and abdominal pain intensity and frequency were significantly less in the local anesthetic groups than control group, similar between ropivacaine and bupivacaine groups.