No abstract available.
Hyperalgesia

No abstract available.
Electroacupuncture ; Hyperalgesia

Background & Objective: It is reported that acute forced swimming stress induces analgesia immediately, and chronic stress induces hyperalgesia. Whereas in response to nociceptive stimulation, small-diameter C-fibers of the excitatory system in the dorsal horn of the spinal cord are activated, therefore, in the present study, the effects of C-fiber lesion in stress and dexamethasone-induced analgesia and hyperalgesia in acute and chronic forms were investigated using Tail-Flick test. Methods: Adults Wistar male rats (180-200 g) were assigned into three groups (n=7): C-normal (intact C-fibers), sham (received capsaicin vehicle at neonate stage) and C-lesion (received capsaicin at neonate stage). Forced swim stress (10 min/day) in water (18±1 ºC) was considered as acute stress and repeated daily forced swim stress as chronic stress, also single-dose of dexamethasone (2 mg/kg, i.p.) was considered as acute dexamethasone and repeated for three days as chronic dexamethasone. Neonatal capsaicin treatment was used for C-fibers depletion. The nociceptive thermal threshold was assessed using Tail-Flick test. Results: In C-lesion group, thermal pain sensitivity was reduced (P<0.001). Acute stress in C-normal group, reduced pain (P<0.001) and in C-lesion group, it caused deeper antinociception in Tail-Flick (P<0.001). Chronic stress and acute-chronic dexamethasone in C-normal group, created hyperalgesia (P<0.001) and induced analgesia in C-lesion groups (P<0.01). Conclusion: It seems that presence of C-fiber is so important in thermal pain transmission in Tail-Flick test; therefore, C-fiber lesion, reduces pain sensitivity (analgesia), increases antinociception effects of acute stress, decreases hyperalgesia of chronic-stress and acute-chronic dexamethasone
Analgesia ; Hyperalgesia

Neuropathic pain has been described following an electrical injury, whether as an immediate response or a late-onset sequela. There is much information on high-voltage injuries in literature due to its dramatic presentation, but limited studies on low-voltage injuries. However, low-voltage injuries can be as diverse and may have symptoms varying from minimal cutaneous involvement to full-thickness injury. Significant injuries may result from multiple factors, including prolonged duration of exposure and a higher amount of current transmitted. We illustrate an atypical presentation of a low-voltage injury in a 17-year-old female. The patient had a low voltage electrical injury with no cutaneous burn noted on the affected extremity. She initially presented with allodynia, which seemed disproportionate to the clinical findings expected in a low-voltage injury. The patient underwent an electrodiagnostic study, which showed cervical polyradiculopathy (C5, C6, C7 polyradiculopathy) and neuromusculoskeletal ultrasonology, which showed enlarged right C5 nerve root. Medical management, daily physical and occupational therapies, and psychological management, were instituted, which resulted in significant improvement of the patient’s pain level and functional status. We describe the importance of the multimodal approach (medical and rehabilitation) in managing this atypical case.
Hyperalgesia ; Pain Management

BACKGROUND: This experimental, comparative, controlled study was conducted to assess whether morphine given locally could block the development of hyperalgesia and allodynia in a guinea pig bone damage model METHODS: Withdrawal responses to mechanical and thermal stimuli applied to the plantar surface of the hind paw were measured before and after bone damage. In separate groups of rats, the effects of administering morphine 150 mcg into the marrow cavity, and on the development of hyperalgesia and allodynia after bone damage were assessed. In another group of rats, naloxone 40 mcg (a mu-opioid anatagonist) was injected into the marrow cavity followed by morphine. RESULTS: In animals that received no treatment, hyperalgesia and allodynia peaked 2 hours after bone injury. Injection of morphine into the marrow cavity immediately after bone injury prevented the development of hyperalgesia and allodynia. Naloxone given into the marrow cavity before giving morphine blocked the antihyperalgesic effect of morphine. CONCLUSION: These findings provide further evidence that local application of morphine at the time of orthopedic surgery, bone graft or marrow harvesting may reduce the amount of postoperative pain. (Author)
Animal ; HYPERALGESIA ; MORPHINE ; GUINEA PIGS

BACKGROUND: Clonidine is an alpha2-adrenergic drug used for analgesic effect, reducing sympathetic stimulation and anesthetic requirement. We examined the analgesic effect of clonidine on incisional pain after its intrathecal administration using a rat postincisional model. METHODS: After an intrathecal (IT) catheter insertion in 20 Spraw Dawley rats, they were divided into two groups; one group (Group S, n = 10) received a saline 20microl injection through an IT catheter, and another (Group C, n = 10) received clonidine 20microgram in 10microl volume followed by another 10microl of saline for washing the catheter. The measurements of the threshold of tactile allodynia (TTA) were performed at 20, 40, 60, 80, 120, 180 and 240 mins after the IT injection. Additionally, 1, 2 and 3 days after the first IT injection, IT injection and the measurements of TTA of pre- and post-injection were repeated. The measurements of TTA were performed in both areas, 5 mm (N-area) and 10 mm (R-area) away from incision by using von Frey hair and up-down method. RESULTS: TTA (N-area) and TTA (R-area) during 4 hours after IT injection in Group C were greater than those in Group S (P< 0.05). TTA (N-area) of post-injection 2 and 3 days after the first IT injection were greater than those of pre-injection in Group C (P< 0.05), and TTA (R-area) after the IT injection 1, 2 and 3 days after the first IT injection were greater than those of pre-injection in Group C (P< 0.05). CONCLUSIONS: A single IT injection of clonidine 20microgram had analgesic effects lasting more than 4 hours in the rat postincisional model. Additional IT clonidine could show antiallodynic effects during three days after the first IT clonidine.
Animals ; Catheters ; Clonidine* ; Hair ; Hyperalgesia ; Rats*

No abstract available.
Animals ; Curcumin* ; Hyperalgesia* ; Ligation* ; Rats* ; Spinal Nerves*

BACKGROUND: The lidocaine patch has been effectively used as a first-line therapy to treat neuropathic pain such as postherpetic neuralgia (PHN). OBJECTIVE: To evaluate the safety and efficacy of the topical piroxicam patch as a treatment option for the treatment of PHN. METHODS: Eighteen patients completed a 3-session study, applying three different patches (lidocaine, piroxicam and control) in random order. A maximum of three patches were applied to the most painful area for three consecutive days (12 hours on followed by 12 hours off). Each session was conducted at least seven days apart. The changes in visual analog scale (VAS) scores based pain intensity, quality of sleep and adverse effects were recorded. RESULTS: When compared to the control, both the lidocaine and piroxicam patches significantly reduced the mean VAS scores of pain intensity of all different types. However, the lidocaine patch was better at reducing allodynia, whereas the piroxicam patch was more effective for dull pain. The lidocaine patch worked faster than the piroxicam patch for the response to overall pain relief. CONCLUSION: The results of this study suggest the use of the piroxicam patch for dull pain and in patients where the lidocaine patch is contraindicated.
Humans ; Hyperalgesia ; Lidocaine ; Neuralgia ; Neuralgia, Postherpetic ; Piroxicam

BACKGROUND: Neuropathic pain resulting from diverse causes is a chronic condition for which effective treatment is lacking. The goal of this study was to test whether dexamethasone exerts a preemptive analgesic effect with bupivacaine when injected perineurally in the spared nerve injury model. METHODS: Fifty rats were randomly divided into five groups. Group 1 (control) was ligated but received no drugs. Group 2 was perineurally infiltrated (tibial and common peroneal nerves) with 0.4% bupivacaine (0.2 ml) and dexamethasone (0.8 mg) 10 minutes before surgery. Group 3 was infiltrated with 0.4% bupivacaine (0.2 ml) and dexamethasone (0.8 mg) after surgery. Group 4 was infiltrated with normal saline (0.2 ml) and dexamethasone (0.8 mg) 10 minutes before surgery. Group 5 was infiltrated with only 0.4% bupivacaine (0.2 ml) before surgery. Rat paw withdrawal thresholds were measured using the von Frey hair test before surgery as a baseline measurement and on postoperative days 3, 6, 9, 12, 15, 18 and 21. RESULTS: In the group injected preoperatively with dexamethasone and bupivacaine, mechanical allodynia did not develop and mechanical threshold forces were significantly different compared with other groups, especially between postoperative days 3 and 9 (P < 0.05). CONCLUSIONS: In conclusion, preoperative infiltration of both dexamethasone and bupivacaine showed a significantly better analgesic effect than did infiltration of bupivacaine or dexamethasone alone in the spared nerve injury model, especially early on after surgery.
Animals ; Bupivacaine ; Dexamethasone ; Hair ; Hyperalgesia ; Neuralgia ; Rats

BACKGROUND AND OBJECTIVES: Although pain resulting from thalamic stroke was described by D jerine & Roussy in 1906, its pathomechanism & anatomical substrate have not been defined yet. Several clinical & experimental studies suggest that laterality of lesion for generation of central pain is as important as location of lesion. We performed this study to evaluate clinical features of thalamic pain syndrome, including incidence, onset interval from stroke, nature, distribution, accompaniments, and to assess the relationships between laterality & location of lesion and occurrence of pain. METHODS: We reviewed the medical records and brain imaging of all patients with thalamic stroke from 1990 to 1997. Patients with thalamic pain syndrome due to a single well-demarcated thalamic stroke were included, and excluded tumoral, non-vascular etilogy, and patients with sensory deficit without pain and excluded patients who had multiple cerebral lesions even they have thalamic pain syndrome. RESULTS: One-hundred one cases were selected under the inclusion criteria, and twenty-four patients(24%) with thalamic pain syndrome were identified from 101 thalamic stroke. Pain onset within the first week poststroke was 17(71%). The patients with allodynia were 8(33%), increased by movement, stress, and thermal contact. The painful area distributed mainly limbs(50%), especially arm(35%), face plus hemibody(34%), and hemibody below face(8%). Thalamic pain syndrome accompanied with the pain and temperature loss was 17(71%). Thirteen patients had a right-sided lesion, 11 left-sided lesion. The lesion causing thalamic pain syndrome mainly located in the posterolateral areas(75%). CONCLUSIONS: We conclude that the thalamic pain syndrome resulting from mainly posterolateral thalamic lesion cause the spontaneous pain on the contralateral body, especially upper extrimity, and accompanied with pain & tempterature loss. The laterality of lesion is not represent for generation of thalamic pain syndrome. Key word : thalamic stroke, central pain.
Humans ; Hyperalgesia ; Incidence ; Medical Records ; Neuroimaging ; Stroke*