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Tadanobu Mizuguchi - One of the best experts on this subject based on the ideXlab platform.

  • OP-1206, a prostaglandin E1 derivative, attenuates the thermal Hyperesthesia induced by constriction injury to the sciatic nerve in the rat.
    Anesthesia and analgesia, 1995
    Co-Authors: Tatsuo Yamamoto, Naohito Shimoyama, Hidefumi Asano, Tadanobu Mizuguchi
    Abstract:

    Nerve ischemia induces wallerian degeneration and peripheral neuropathy, and nerve constriction injury induces thermal Hyperesthesia. Nerve ischemia is one possible mechanism in the development of thermal Hyperesthesia in the nerve constriction injury model. Prostaglandin E 1 increases tissue blood flow. In the present study, the authors examine the role of nerve ischemia in the maintenance of the thermal Hyperesthesia induced by nerve constriction injury by orally administering OP-1206, a prostaglandin E 1 derivative. A nerve constriction injury model was created by making four loose ligations around the rat sciatic nerve, which induces thermal Hyperesthesia in the ligated paw in 2-5 days. OP-1206, was administered six times (Day 7, one time; Day 8, two times; Day 9, two times; Day 10, one time). A single administration of OP-1206 had no effect on the thermal Hyperesthesia. Six hours after the sixth-administration of OP-1206, the level of the thermal Hyperesthesia was attenuated in a dose-dependent manner, and this effect lasted more than 1 day after the last drug administration. These data indicate that nerve ischemia plays an important role in maintaining the thermal Hyperesthesia induced by nerve constriction injury in the rat

  • Time-dependent effect of morphine and time-independent effect of MK-801, an NMDA antagonist, on the thermal Hyperesthesia induced by unilateral constriction injury to the sciatic nerve in the rat.
    Anesthesiology, 1994
    Co-Authors: Tatsuo Yamamoto, Naohito Shimoyama, Hidefumi Asano, Tadanobu Mizuguchi
    Abstract:

    BACKGROUND It is known that peripheral nerve injury induces time-dependent changes in dorsal horn function. The current study investigated the time dependency of the effects of intrathecal morphine and MK-801, an N-methyl-D-aspartate antagonist, on the thermal Hyperesthesia evoked by unilateral constriction injury to the sciatic nerve in the rat. METHODS In rats with a unilateral constriction injury to the sciatic nerve, paw withdrawal latency against thermal stimulation for the injured paw was typically 3 s less than that for the uninjured paw during the first 5 weeks after the injury. Drugs were administered intrathecally 1 or 5 weeks after the nerve injury. RESULTS Intrathecal morphine increased the paw withdrawal latencies of both the injured paw and the uninjured paw in an equally dose dependent manner in the 1-week study. In the 5-week study, morphine increased the paw withdrawal latency of the uninjured paw in a dose-dependent manner, but not that of the injured paw. Intrathecal MK-801 increased the paw withdrawal latency of the injured paw to the level of the uninjured paw in a dose-dependent manner in both the 1- and 5-week studies. CONCLUSIONS These data indicate that (1) an N-methyl-D-aspartate receptor-mediated spinal facilitation may be the common mechanism maintaining the thermal Hyperesthesia evoked by the constriction injury, and (2) the effects of intrathecal morphine on this thermal Hyperesthesia are time-dependent.

  • Role of the injury discharge in the development of thermal Hyperesthesia after sciatic nerve constriction injury in the rat
    Anesthesiology, 1993
    Co-Authors: Tatsuo Yamamoto, Naohito Shimoyama, Tadanobu Mizuguchi
    Abstract:

    Background Usually, a barrage of impulses (“injury discharge”) is evoked following sensory nerve damage. It has been suggested that injury discharge may produce the hyperexcitatory state in the spinal cord, and this hyperexicitability may cause neurogenic pain. In the present study, the authors examined the role of injury discharge in developing the hyperesthetic state following nerve constriction injury. Methods A model of thermal Hyperesthesia caused by a constriction injury created by making four loose ligations around the rat sciatic nerve was examined. To block the injury disharge, 0.5% bupivacaine was applied to the sciati nerve before constriction injury. To block the hyperexcitatory state, (+)-MK-801, an N-methyl-D-aspartate antagonist, was administered intrathecally 15 min before the nerve lesion. Results: Blocking injury discharge significantly delayed the development of Hyperesthesia. Bupivacaine had no effect on the development of hyperesthasia when bupivacaine was applied to the sciatic nerve 15 min after the nerve constriction injury. Systemic bupivacaine had no effect on the development of thermal Hyperesthesia. Intrathecal (+)-MK-801 also delayed the development of Hyperesthesia when (+)-MK-801 was administered intrathecally 15 min before the nerve injury. When (+)-MK-801 was administered 15 min before the nerve injury, (+)-MK-(801) had no effect on the development of Hyperesthesia. Conclusion: These results suggest that injury discharge may induce facilitation of spinal dorsal horn neurons, and this spinal facilition may play an important role in developing thermal Hyperesthesia following sciatic nerve constriction injury.

  • Effects of FK224, a novel cyclopeptide NK1 and NK2 antagonist, and CP-96,345, a nonpeptide NK1 antagonist, on development and maintenance of thermal Hyperesthesia evoked by carrageenan injection in the rat paw.
    Anesthesiology, 1993
    Co-Authors: Tatsuo Yamamoto, Naohito Shimoyama, Tadanobu Mizuguchi
    Abstract:

    BACKGROUND The role of tachykinins, such as substance P and neurokinin A, in the development or maintenance of thermal Hyperesthesia during inflammation is unclear. In the current study, the authors examined the role of NK1 and NK2 receptors on the thermal Hyperesthesia evoked by injection of carrageenan into the rat paw using FK224, a cyclopeptide NK1 and NK2 antagonist, and CP-96,345, a nonpeptide NK1 antagonist. METHODS In rats injected with 2 mg carrageenan, the paw withdrawal latency (PWL) for the injected paw was typically 5-6 s less than that for the untreated paw, at 2 h after the carrageenan injection. In the pretreatment study, drugs were administered intravenously or intrathecally 10 min before the carrageenan injection. In the posttreatment study, drugs were administered intravenously or intrathecally 2 h after the carrageenan injection. RESULTS In the pretreatment study, both intravenous CP-96,345 and intravenous FK224 blocked the development of thermal Hyperesthesia and reduced paw edema in a dose-dependent manner 2 h after the carrageenan injection. The effect of CP-96,345 on thermal Hyperesthesia was stereospecific, but that on paw edema was not. Posttreatment with intravenous CP-96,345 and intravenous FK224 failed to reduce the level of thermal Hyperesthesia or paw edema, and intrathecal injections, either pre- or posttreatment, had no effect on thermal Hyperesthesia or paw edema. CONCLUSIONS These data indicate that: 1) spinal NK1 and NK2 receptors do not play an important role in development and maintenance of thermal Hyperesthesia evoked by paw carrageenan, and 2) the peripheral NK1 receptor may play an important role in the development of thermal Hyperesthesia, but not of paw edema.

  • The effects of morphine, MK-801, an NMDA antagonist, and CP-96,345, an NK1 antagonist, on the Hyperesthesia evoked by carageenan injection in the rat paw.
    Anesthesiology, 1993
    Co-Authors: Tatsuo Yamamoto, Naohito Shimoyama, Tadanobu Mizuguchi
    Abstract:

    BACKGROUND The spinal mechanisms underlying the hyperesthetic state during inflammation are little understood. To gain a better understanding of these mechanisms, this study evaluated the effects of intrathecal morphine; MK-801, an N-methyl-D aspartic (NMDA) antagonist; and CP-96,345, an NK1 antagonist, on the Hyperesthesia observed after carageenan injection of the rat paw. METHODS In rats injected with 2 mg carageenan, the paw withdrawal latency (PWL) for the injected paw was typically 5-6 s less than that for the untreated paw, at 2 h after the carageenan injection. Drugs were administered 2 h after the carageenan injection. The magnitude of Hyperesthesia was evaluated with the difference score (DS), which was calculated by subtracting the PWL of the untreated paw from the PWL of the injected paw. RESULTS Intrathecal morphine increased PWLs of both the injected and the untreated paws equally in a dose-dependent manner, but intrathecal morphine did not affect the level of DS. Intrathecal MK-801 increased PWLs of the injected paw to the level of the untreated paw in a dose-dependent manner and increased the DS levels. Intrathecal CP-96,345 had no effect on PWLs of either the injected or the untreated paw. Coadministration of MK-801 with morphine reduced the DS for each dose of morphine. CONCLUSIONS These data indicate that (1) an NMDA receptor, but not an NK1 receptor, plays an important role in maintaining the Hyperesthesia after carageenan injection; and (2) NMDA antagonism has a simple additive interaction with morphine in the carageenan model of inflammatory Hyperesthesia.

Tatsuo Yamamoto - One of the best experts on this subject based on the ideXlab platform.

  • Clonidine, but Not Morphine, Delays the Development of Thermal Hyperesthesia Induced by Sciatic Nerve Constriction Injury in the Rat
    Anesthesiology, 1996
    Co-Authors: Tatsuo Yamamoto, Natsuko Nozaki-taguchi
    Abstract:

    BackgroundIt has been shown that the spinal facilitation induced by the injury discharge evoked by a nerve constriction injury is crucial in the development of thermal Hyperesthesia. Both opioids and alpha2 agonists have been reported to prevent the development of spinal facilitation evoked by the s

  • OP-1206, a prostaglandin E1 derivative, attenuates the thermal Hyperesthesia induced by constriction injury to the sciatic nerve in the rat.
    Anesthesia and analgesia, 1995
    Co-Authors: Tatsuo Yamamoto, Naohito Shimoyama, Hidefumi Asano, Tadanobu Mizuguchi
    Abstract:

    Nerve ischemia induces wallerian degeneration and peripheral neuropathy, and nerve constriction injury induces thermal Hyperesthesia. Nerve ischemia is one possible mechanism in the development of thermal Hyperesthesia in the nerve constriction injury model. Prostaglandin E 1 increases tissue blood flow. In the present study, the authors examine the role of nerve ischemia in the maintenance of the thermal Hyperesthesia induced by nerve constriction injury by orally administering OP-1206, a prostaglandin E 1 derivative. A nerve constriction injury model was created by making four loose ligations around the rat sciatic nerve, which induces thermal Hyperesthesia in the ligated paw in 2-5 days. OP-1206, was administered six times (Day 7, one time; Day 8, two times; Day 9, two times; Day 10, one time). A single administration of OP-1206 had no effect on the thermal Hyperesthesia. Six hours after the sixth-administration of OP-1206, the level of the thermal Hyperesthesia was attenuated in a dose-dependent manner, and this effect lasted more than 1 day after the last drug administration. These data indicate that nerve ischemia plays an important role in maintaining the thermal Hyperesthesia induced by nerve constriction injury in the rat

  • Time-dependent effect of morphine and time-independent effect of MK-801, an NMDA antagonist, on the thermal Hyperesthesia induced by unilateral constriction injury to the sciatic nerve in the rat.
    Anesthesiology, 1994
    Co-Authors: Tatsuo Yamamoto, Naohito Shimoyama, Hidefumi Asano, Tadanobu Mizuguchi
    Abstract:

    BACKGROUND It is known that peripheral nerve injury induces time-dependent changes in dorsal horn function. The current study investigated the time dependency of the effects of intrathecal morphine and MK-801, an N-methyl-D-aspartate antagonist, on the thermal Hyperesthesia evoked by unilateral constriction injury to the sciatic nerve in the rat. METHODS In rats with a unilateral constriction injury to the sciatic nerve, paw withdrawal latency against thermal stimulation for the injured paw was typically 3 s less than that for the uninjured paw during the first 5 weeks after the injury. Drugs were administered intrathecally 1 or 5 weeks after the nerve injury. RESULTS Intrathecal morphine increased the paw withdrawal latencies of both the injured paw and the uninjured paw in an equally dose dependent manner in the 1-week study. In the 5-week study, morphine increased the paw withdrawal latency of the uninjured paw in a dose-dependent manner, but not that of the injured paw. Intrathecal MK-801 increased the paw withdrawal latency of the injured paw to the level of the uninjured paw in a dose-dependent manner in both the 1- and 5-week studies. CONCLUSIONS These data indicate that (1) an N-methyl-D-aspartate receptor-mediated spinal facilitation may be the common mechanism maintaining the thermal Hyperesthesia evoked by the constriction injury, and (2) the effects of intrathecal morphine on this thermal Hyperesthesia are time-dependent.

  • Role of the injury discharge in the development of thermal Hyperesthesia after sciatic nerve constriction injury in the rat
    Anesthesiology, 1993
    Co-Authors: Tatsuo Yamamoto, Naohito Shimoyama, Tadanobu Mizuguchi
    Abstract:

    Background Usually, a barrage of impulses (“injury discharge”) is evoked following sensory nerve damage. It has been suggested that injury discharge may produce the hyperexcitatory state in the spinal cord, and this hyperexicitability may cause neurogenic pain. In the present study, the authors examined the role of injury discharge in developing the hyperesthetic state following nerve constriction injury. Methods A model of thermal Hyperesthesia caused by a constriction injury created by making four loose ligations around the rat sciatic nerve was examined. To block the injury disharge, 0.5% bupivacaine was applied to the sciati nerve before constriction injury. To block the hyperexcitatory state, (+)-MK-801, an N-methyl-D-aspartate antagonist, was administered intrathecally 15 min before the nerve lesion. Results: Blocking injury discharge significantly delayed the development of Hyperesthesia. Bupivacaine had no effect on the development of hyperesthasia when bupivacaine was applied to the sciatic nerve 15 min after the nerve constriction injury. Systemic bupivacaine had no effect on the development of thermal Hyperesthesia. Intrathecal (+)-MK-801 also delayed the development of Hyperesthesia when (+)-MK-801 was administered intrathecally 15 min before the nerve injury. When (+)-MK-801 was administered 15 min before the nerve injury, (+)-MK-(801) had no effect on the development of Hyperesthesia. Conclusion: These results suggest that injury discharge may induce facilitation of spinal dorsal horn neurons, and this spinal facilition may play an important role in developing thermal Hyperesthesia following sciatic nerve constriction injury.

  • Effects of FK224, a novel cyclopeptide NK1 and NK2 antagonist, and CP-96,345, a nonpeptide NK1 antagonist, on development and maintenance of thermal Hyperesthesia evoked by carrageenan injection in the rat paw.
    Anesthesiology, 1993
    Co-Authors: Tatsuo Yamamoto, Naohito Shimoyama, Tadanobu Mizuguchi
    Abstract:

    BACKGROUND The role of tachykinins, such as substance P and neurokinin A, in the development or maintenance of thermal Hyperesthesia during inflammation is unclear. In the current study, the authors examined the role of NK1 and NK2 receptors on the thermal Hyperesthesia evoked by injection of carrageenan into the rat paw using FK224, a cyclopeptide NK1 and NK2 antagonist, and CP-96,345, a nonpeptide NK1 antagonist. METHODS In rats injected with 2 mg carrageenan, the paw withdrawal latency (PWL) for the injected paw was typically 5-6 s less than that for the untreated paw, at 2 h after the carrageenan injection. In the pretreatment study, drugs were administered intravenously or intrathecally 10 min before the carrageenan injection. In the posttreatment study, drugs were administered intravenously or intrathecally 2 h after the carrageenan injection. RESULTS In the pretreatment study, both intravenous CP-96,345 and intravenous FK224 blocked the development of thermal Hyperesthesia and reduced paw edema in a dose-dependent manner 2 h after the carrageenan injection. The effect of CP-96,345 on thermal Hyperesthesia was stereospecific, but that on paw edema was not. Posttreatment with intravenous CP-96,345 and intravenous FK224 failed to reduce the level of thermal Hyperesthesia or paw edema, and intrathecal injections, either pre- or posttreatment, had no effect on thermal Hyperesthesia or paw edema. CONCLUSIONS These data indicate that: 1) spinal NK1 and NK2 receptors do not play an important role in development and maintenance of thermal Hyperesthesia evoked by paw carrageenan, and 2) the peripheral NK1 receptor may play an important role in the development of thermal Hyperesthesia, but not of paw edema.

Naohito Shimoyama - One of the best experts on this subject based on the ideXlab platform.

  • OP-1206, a prostaglandin E1 derivative, attenuates the thermal Hyperesthesia induced by constriction injury to the sciatic nerve in the rat.
    Anesthesia and analgesia, 1995
    Co-Authors: Tatsuo Yamamoto, Naohito Shimoyama, Hidefumi Asano, Tadanobu Mizuguchi
    Abstract:

    Nerve ischemia induces wallerian degeneration and peripheral neuropathy, and nerve constriction injury induces thermal Hyperesthesia. Nerve ischemia is one possible mechanism in the development of thermal Hyperesthesia in the nerve constriction injury model. Prostaglandin E 1 increases tissue blood flow. In the present study, the authors examine the role of nerve ischemia in the maintenance of the thermal Hyperesthesia induced by nerve constriction injury by orally administering OP-1206, a prostaglandin E 1 derivative. A nerve constriction injury model was created by making four loose ligations around the rat sciatic nerve, which induces thermal Hyperesthesia in the ligated paw in 2-5 days. OP-1206, was administered six times (Day 7, one time; Day 8, two times; Day 9, two times; Day 10, one time). A single administration of OP-1206 had no effect on the thermal Hyperesthesia. Six hours after the sixth-administration of OP-1206, the level of the thermal Hyperesthesia was attenuated in a dose-dependent manner, and this effect lasted more than 1 day after the last drug administration. These data indicate that nerve ischemia plays an important role in maintaining the thermal Hyperesthesia induced by nerve constriction injury in the rat

  • Time-dependent effect of morphine and time-independent effect of MK-801, an NMDA antagonist, on the thermal Hyperesthesia induced by unilateral constriction injury to the sciatic nerve in the rat.
    Anesthesiology, 1994
    Co-Authors: Tatsuo Yamamoto, Naohito Shimoyama, Hidefumi Asano, Tadanobu Mizuguchi
    Abstract:

    BACKGROUND It is known that peripheral nerve injury induces time-dependent changes in dorsal horn function. The current study investigated the time dependency of the effects of intrathecal morphine and MK-801, an N-methyl-D-aspartate antagonist, on the thermal Hyperesthesia evoked by unilateral constriction injury to the sciatic nerve in the rat. METHODS In rats with a unilateral constriction injury to the sciatic nerve, paw withdrawal latency against thermal stimulation for the injured paw was typically 3 s less than that for the uninjured paw during the first 5 weeks after the injury. Drugs were administered intrathecally 1 or 5 weeks after the nerve injury. RESULTS Intrathecal morphine increased the paw withdrawal latencies of both the injured paw and the uninjured paw in an equally dose dependent manner in the 1-week study. In the 5-week study, morphine increased the paw withdrawal latency of the uninjured paw in a dose-dependent manner, but not that of the injured paw. Intrathecal MK-801 increased the paw withdrawal latency of the injured paw to the level of the uninjured paw in a dose-dependent manner in both the 1- and 5-week studies. CONCLUSIONS These data indicate that (1) an N-methyl-D-aspartate receptor-mediated spinal facilitation may be the common mechanism maintaining the thermal Hyperesthesia evoked by the constriction injury, and (2) the effects of intrathecal morphine on this thermal Hyperesthesia are time-dependent.

  • Role of the injury discharge in the development of thermal Hyperesthesia after sciatic nerve constriction injury in the rat
    Anesthesiology, 1993
    Co-Authors: Tatsuo Yamamoto, Naohito Shimoyama, Tadanobu Mizuguchi
    Abstract:

    Background Usually, a barrage of impulses (“injury discharge”) is evoked following sensory nerve damage. It has been suggested that injury discharge may produce the hyperexcitatory state in the spinal cord, and this hyperexicitability may cause neurogenic pain. In the present study, the authors examined the role of injury discharge in developing the hyperesthetic state following nerve constriction injury. Methods A model of thermal Hyperesthesia caused by a constriction injury created by making four loose ligations around the rat sciatic nerve was examined. To block the injury disharge, 0.5% bupivacaine was applied to the sciati nerve before constriction injury. To block the hyperexcitatory state, (+)-MK-801, an N-methyl-D-aspartate antagonist, was administered intrathecally 15 min before the nerve lesion. Results: Blocking injury discharge significantly delayed the development of Hyperesthesia. Bupivacaine had no effect on the development of hyperesthasia when bupivacaine was applied to the sciatic nerve 15 min after the nerve constriction injury. Systemic bupivacaine had no effect on the development of thermal Hyperesthesia. Intrathecal (+)-MK-801 also delayed the development of Hyperesthesia when (+)-MK-801 was administered intrathecally 15 min before the nerve injury. When (+)-MK-801 was administered 15 min before the nerve injury, (+)-MK-(801) had no effect on the development of Hyperesthesia. Conclusion: These results suggest that injury discharge may induce facilitation of spinal dorsal horn neurons, and this spinal facilition may play an important role in developing thermal Hyperesthesia following sciatic nerve constriction injury.

  • Effects of FK224, a novel cyclopeptide NK1 and NK2 antagonist, and CP-96,345, a nonpeptide NK1 antagonist, on development and maintenance of thermal Hyperesthesia evoked by carrageenan injection in the rat paw.
    Anesthesiology, 1993
    Co-Authors: Tatsuo Yamamoto, Naohito Shimoyama, Tadanobu Mizuguchi
    Abstract:

    BACKGROUND The role of tachykinins, such as substance P and neurokinin A, in the development or maintenance of thermal Hyperesthesia during inflammation is unclear. In the current study, the authors examined the role of NK1 and NK2 receptors on the thermal Hyperesthesia evoked by injection of carrageenan into the rat paw using FK224, a cyclopeptide NK1 and NK2 antagonist, and CP-96,345, a nonpeptide NK1 antagonist. METHODS In rats injected with 2 mg carrageenan, the paw withdrawal latency (PWL) for the injected paw was typically 5-6 s less than that for the untreated paw, at 2 h after the carrageenan injection. In the pretreatment study, drugs were administered intravenously or intrathecally 10 min before the carrageenan injection. In the posttreatment study, drugs were administered intravenously or intrathecally 2 h after the carrageenan injection. RESULTS In the pretreatment study, both intravenous CP-96,345 and intravenous FK224 blocked the development of thermal Hyperesthesia and reduced paw edema in a dose-dependent manner 2 h after the carrageenan injection. The effect of CP-96,345 on thermal Hyperesthesia was stereospecific, but that on paw edema was not. Posttreatment with intravenous CP-96,345 and intravenous FK224 failed to reduce the level of thermal Hyperesthesia or paw edema, and intrathecal injections, either pre- or posttreatment, had no effect on thermal Hyperesthesia or paw edema. CONCLUSIONS These data indicate that: 1) spinal NK1 and NK2 receptors do not play an important role in development and maintenance of thermal Hyperesthesia evoked by paw carrageenan, and 2) the peripheral NK1 receptor may play an important role in the development of thermal Hyperesthesia, but not of paw edema.

  • The effects of morphine, MK-801, an NMDA antagonist, and CP-96,345, an NK1 antagonist, on the Hyperesthesia evoked by carageenan injection in the rat paw.
    Anesthesiology, 1993
    Co-Authors: Tatsuo Yamamoto, Naohito Shimoyama, Tadanobu Mizuguchi
    Abstract:

    BACKGROUND The spinal mechanisms underlying the hyperesthetic state during inflammation are little understood. To gain a better understanding of these mechanisms, this study evaluated the effects of intrathecal morphine; MK-801, an N-methyl-D aspartic (NMDA) antagonist; and CP-96,345, an NK1 antagonist, on the Hyperesthesia observed after carageenan injection of the rat paw. METHODS In rats injected with 2 mg carageenan, the paw withdrawal latency (PWL) for the injected paw was typically 5-6 s less than that for the untreated paw, at 2 h after the carageenan injection. Drugs were administered 2 h after the carageenan injection. The magnitude of Hyperesthesia was evaluated with the difference score (DS), which was calculated by subtracting the PWL of the untreated paw from the PWL of the injected paw. RESULTS Intrathecal morphine increased PWLs of both the injected and the untreated paws equally in a dose-dependent manner, but intrathecal morphine did not affect the level of DS. Intrathecal MK-801 increased PWLs of the injected paw to the level of the untreated paw in a dose-dependent manner and increased the DS levels. Intrathecal CP-96,345 had no effect on PWLs of either the injected or the untreated paw. Coadministration of MK-801 with morphine reduced the DS for each dose of morphine. CONCLUSIONS These data indicate that (1) an NMDA receptor, but not an NK1 receptor, plays an important role in maintaining the Hyperesthesia after carageenan injection; and (2) NMDA antagonism has a simple additive interaction with morphine in the carageenan model of inflammatory Hyperesthesia.

Audun Stubhaug - One of the best experts on this subject based on the ideXlab platform.

  • Hyperesthesia one year after breast augmentation surgery increases the odds for persisting pain at four years A prospective four-year follow-up study
    Scandinavian journal of pain, 2010
    Co-Authors: Torill Kaasa, Luis Romundstad, Helge E Roald, Knut Skolleborg, Audun Stubhaug
    Abstract:

    Abstract In this long-term follow-up study of 175 women, we investigated the prevalence of and factors associated with persisting pain and sensory changes four years after augmentation mammoplasty. Previously the women had participated in an acute postoperative pain study, and follow-up investigations at 6 weeks and 1 year after surgery. In the present study, the women were mailed questionnaires about pain, sensory changes, and affection of daily life, quality of life and pain catastrophizing 4 years after surgery. One hundred and sixteen women answered the questionnaire. The fraction of women reporting evoked- and/or spontaneous pain during the last 24h had declined from 20% at 1 year to 14% at 4 years. Hyperesthesia had declined from 46% at 1 year to 32% at 4 years, while the change in hypoesthesia was small, 47% at 1 year to 51% at 4 years. Methylprednisolone and parecoxib given preincisionally reduced acute postoperative pain and reduced the prevalence of Hyperesthesia after 6 weeks/1 year, but after 4 years we found no significant differences between the test drug groups. Those having concomitant pain and Hyperesthesia at 6 weeks and 1 year had high odds for persisting pain at 4 years (OR 7.8, 95% CI 2.1–29.8, P =0.003; OR 13.2, 95% CI 2.5–71.3, P =0.003). In patients without pain but with Hyperesthesia at 1 year, the Hyperesthesia increased the odds for pain at 4 years (OR 2.6 95% CI 1.1–6.1, P =0.03). Hypoesthesia at 6 weeks or at 1 year did not affect the odds for pain at 4 years. A good general health condition (mental and physical) was associated with reduced odds for pain at 4 years (OR=0.56, 95% CI 0.35–0.88, P =0.01). However, using the Short Form health survey, SF-12, the Mental Component Summary Score seemed to affect the odds for chronic pain more than the Physical Component Summary Score. To conclude, the prevalence of pain and Hyperesthesia after breast augmentation declined from 1 to 4 years. Nevertheless, the most striking finding in the current trial was that pain coinciding with Hyperesthesia at 6 weeks and 1 year resulted in highly increased odds for persistent postoperative pain. Even Hyperesthesia alone, without pain, increased the odds for chronic postsurgical pain. Thus, the present study suggests Hyperesthesia as an independent risk factor for chronic postsurgical pain.

  • chronic pain and sensory changes after augmentation mammoplasty long term effects of preincisional administration of methylprednisolone
    Pain, 2006
    Co-Authors: Luis Romundstad, Harald Breivik, Helge E Roald, Knut Skolleborg, Pal Richard Romundstad, Audun Stubhaug
    Abstract:

    We studied the prevalence of chronic pain and long term sensory changes after cosmetic augmentation mammoplasty and the effects of a single i.v. preoperative dose of methylprednisolone 125 mg (n=74), parecoxib 40 mg (n=71), or placebo (n=74). A questionnaire was mailed 6 weeks and 1 year after surgery. Response rate after 1 year was 80%. At 1 year non-evoked pain was present in 13%, and evoked pain was present in 20% with no statistically significant differences between the groups. Methylprednisolone was associated with reduced odds for Hyperesthesia at 1 year (OR 0.3, 95% CI 0.1-0.6), and significantly reduced the prevalence of Hyperesthesia (30%) compared with placebo (56%, P<0.01) and parecoxib (51%, P<0.04). Factors associated with increased odds for pain at 1 year were intensity of pain during the first 6 days after surgery (OR 1.3, 95% CI 1.1-1.6), pain at 6 weeks (OR 18.4, 95% CI 6.9-49.3), Hyperesthesia at 6 weeks (OR 2.3, 95% CI 1.1-5.1) and present Hyperesthesia (OR 3.1, 95% CI 1.4-6.7). We conclude that persistent pain and sensory changes are common after augmentation mammoplasty, and that patients having pain at 6 weeks most likely will have pain also at 1 year. Acute postoperative pain, Hyperesthesia at 6 weeks, and the presence of Hyperesthesia increased the odds for pain at 1 year. Preoperative methylprednisolone resulted in significantly less Hyperesthesia compared with both parecoxib and placebo, but did not significantly reduce the prevalence of persistent spontaneous or evoked pain.

  • Chronic pain and sensory changes after augmentation mammoplasty: Long term effects of preincisional administration of methylprednisolone
    Pain, 2006
    Co-Authors: Luis Romundstad, Harald Breivik, Helge E Roald, Knut Skolleborg, Pal Richard Romundstad, Audun Stubhaug
    Abstract:

    We studied the prevalence of chronic pain and long term sensory changes after cosmetic augmentation mammoplasty and the effects of a single i.v. preoperative dose of methylprednisolone 125 mg (n=74), parecoxib 40 mg (n=71), or placebo (n=74). A questionnaire was mailed 6 weeks and 1 year after surgery. Response rate after 1 year was 80%. At 1 year non-evoked pain was present in 13%, and evoked pain was present in 20% with no statistically significant differences between the groups. Methylprednisolone was associated with reduced odds for Hyperesthesia at 1 year (OR 0.3, 95% CI 0.1-0.6), and significantly reduced the prevalence of Hyperesthesia (30%) compared with placebo (56%, P

Tony L. Yaksh - One of the best experts on this subject based on the ideXlab platform.

  • a novel model of primary and secondary hyperalgesia after mild thermal injury in the rat
    Neuroscience Letters, 1998
    Co-Authors: Natsuko Nozakitaguchi, Tony L. Yaksh
    Abstract:

    Abstract Secondary Hyperesthesia was investigated in a rat thermal injury model. After a mild focal thermal injury (52°C / 45 s) to the rat heel, the response latency for a thermal stimulus directed at the injured site was reduced (10→6 s; e.g. primary thermal hyperalgesia) but no change was seen at the distal site. Conversely, tactile threshold at the distal site was significantly reduced (15→5 g; e.g. secondary tactile allodynia) but much less so at the injured site. Magnitude of the secondary tactile allodynia paralleled the severity of the primary injury. Accordingly, this model has the same characteristics seen in human post-tissue-injury hyperesthetic states and provides a tool for the study of mechanisms underlying primary and secondary Hyperesthesia.

  • the role of focal nerve ischemia and wallerian degeneration in peripheral nerve injury producing Hyperesthesia
    Anesthesiology, 1993
    Co-Authors: Robert R Myers, Tatsuo Yamamoto, Tony L. Yaksh, Henry C Powell
    Abstract:

    BACKGROUND: A new model of pain associated with an experimental peripheral mononeuropathy has stimulated interest in mechanisms of pain and their structural correlates in peripheral nerve, the site of the experimental lesion. METHODS: The pathology of the neuropathy was studied and the results correlated with alterations in nerve blood flow and with the behavioral response to heat applied to the foot. The focal neuropathy was created by loosely tying several ligatures around rat sciatic nerve, which produces Hyperesthesia in the ligated limb in 3-5 days. The neuropathology was striking with epineurial and endoneurial vascular stasis, edema, and extensive nerve fiber injury in the ligated segment noted at 1 week after ligation. RESULTS: Nerve blood flow was reduced significantly in the ligated segment during the development of the Hyperesthesia response, suggesting that changes in nerve blood flow caused by the ligature compression of the epineurial vessels contributes to the nerve fiber injury and pathophysiology of the model. To further test this hypothesis, the epineurial vasculature was removed from 1-cm lengths of rat sciatic nerve, which reduces nerve blood flow by 58%, and by ligation of the ipsilateral femoral artery, which focally reduces nerve blood flow by 70%, and the behavioral response to heating of the paw was evaluated at 1 week. Crush injury was used as a positive control creating Wallerian degeneration without a substantial reduction in nerve blood flow. CONCLUSIONS: The results suggest that ischemia is an important initial pathogenic mechanism in the Hyperesthesia associated with the loose ligature pain model, in so far as it produces Wallerian degeneration and axonal injury. Modest degrees of ischemia producing only demyelination did not produce significant Hyperesthesia.