BACKGROUND: Phantom limb sensation is an unusual position sense of the extremity during nerve block that the position of extremity is misinterpreted as being flexed, or elevated, when actually they are in neutral position. Whether it is from the fixation of proprioceptive input at the time of motor blockade or from unmasking of the pattern which has been already present in the CNS is still controversial. We perfomed this study under the assumption that phantom limb sensation can still be reproduced without the influence of position at the time of nerve blockade. METHODS: Thirty-six patients scheduled for elective orthopedic surgery were randomly assigned. For 26 patients, spinal anesthesia was performed with hyperbaric 0.5% tetracaine or bupivacaine at lateral decubitus position and the position was changed to supine immediately. Existence of phantom limb sensation and the level of anesthesia was recorded at 10 and 20 minutes after injection of local anesthetics. For 10 patients, same local anesthetics were injected after patient's legs were straightened in lateral decubitus position. RESULTS: Forteen out of 26 patients whose position were changed to supine immediately after the injection of local anesthetics experienced phantom limb sensations. Five out of 10 patients whose legs were kept straight before the injection of local anesthetics experienced phantom limb sensations. Previous history of trauma was positively related to the expression of phantom limb sensation. CONCLUSION: Our data showed that the expression of phantom limb sensation is reproducible. And this was not related to the position at the time of spinal anesthesia. Trauma seems to be an important factor related to the expression of phantom limb sensation.
Anesthesia ; Anesthesia, Spinal* ; Anesthetics, Local ; Bupivacaine ; Extremities ; Humans ; Leg ; Nerve Block ; Orthopedics ; Phantom Limb* ; Proprioception ; Sensation* ; Tetracaine

BACKGROUND: Upregulation of one type of the pro-inflammatory chemokine (CCL2) and its receptor (CCR2) following peripheral nerve injury contributes to the induction of neuropathic pain. Here, we examined whether another type of chemokine (CCL3) is involved in neuropathic pain. METHODS: We measured changes in mechanical and thermal sensitivity in the hind paws of naive rats or rats with an L5 spinal nerve ligation (SNL) after intra-plantar injection of CCL3 or met-RANTES, an antagonist of the CCL3 receptor, CCR1. We also measured CCL3 levels in the sciatic nerve and the hind paw skin as well as CCR1 expression in dorsal root ganglion (DRG) cells from the lumbar spinal segments. RESULTS: Intra-plantar injection of CCL3 into the hind paw of naive rats mimicked L5 SNL-produced hyperalgesia. Intra-plantar injection of met-RANTES into the hind paw of rats with L5 SNL attenuated hyperalgesia. L5 SNL increased CCL3 levels in the sciatic nerve and the hind paw skin on the affected side. The number of CCR1-positive DRG cells in the lumbar segments was not changed following L5 SNL. CONCLUSIONS: Partial peripheral nerve injury increases local CCL3 levels along the degenerating axons during Wallerian degeneration. This CCL3 binds to its receptor, CCR1, located on adjacent uninjured afferents, presumably nociceptors, to induce hyperalgesia in the neuropathic pain state.
Animals ; Axons ; Chemokine CCL3 ; Chemokine CCL5 ; Diagnosis-Related Groups ; Ganglia, Spinal ; Hyperalgesia ; Ligation ; Neuralgia ; Nociceptors ; Peripheral Nerve Injuries ; Peripheral Nerves ; Rats ; Receptors, CCR1 ; Sciatic Nerve ; Skin ; Spinal Nerves ; Up-Regulation ; Wallerian Degeneration

The therapeutic goal for the spinal injury has been focused on preventing the secondary ischemic changes because of the poor regeneration of human spinal cord. Naloxone, an antagonist of endogenous opiates, has been clinically used for the purpose of preventing ischemic change and improving the recovery of neurological function after spinal injury. Recently, thyrotropin releasing hormone(TRH), a hypothalamic hormone inducing the thyrotropin secretion in anterior pituitary gland, has been known as a potent stimulator of cardiovascular functions in shock and the neurologic recovery in injuries of central nervous system, however, its underlying mechanism is still obscure. The present study was designed to determine whether TRH was also effective to improve the experimentally induced spinal injury as naloxone did, Somatosensory evoked potentials(SEPs) have used as an index for recovery of neurological function after the spinal injury which was induced by the 400gm.cm contusion of the T-7 spinal level in cats. The results are summarized as follows : 1. SEPs abolished soon after spinal contusion were reappeared 3 hours after injury when either of naloxone(10mg/kg) or TRH(4mg/kg) was administrated intravenously. Its recovery was completed after 24 hours. 2. The recovery rates of SEPs after treatments of naloxone and TRH were 62.5% and 64.7% of experimental animals, respectively. In conclusion, the present studies confirm the therapeutic benefit of TRH in experimental spinal injury and demonstrate that it is superior to treatment with naloxone. Further studies would be needed to explain the underlying mechanism of TRH effects.
Animals ; Cats* ; Central Nervous System ; Contusions ; Evoked Potentials, Somatosensory* ; Humans ; Naloxone ; Opioid Peptides ; Pituitary Gland, Anterior ; Regeneration ; Shock ; Spinal Cord Injuries* ; Spinal Cord* ; Spinal Injuries ; Thyrotropin* ; Thyrotropin-Releasing Hormone*

BACKGROUND: Dextromethorphan (DEX) is an NMDA receptor antagonist which has recently been introduced for the treatment of chronic pain mainly to reduce the central sensitization component of pain. It is also reported to reduce the pain from acute ischemia of an extremity in a rat model which has a similar mechanism as tourniquet pain. The purpose of this experiment was to see if dextromethorphan could reduce tourniquet pain in normal volunteers. METHODS: A double blind randomized cross-over test was done on ten healthy male volunteers. Each subject was orally administered with three different doses of DEX (placebo, 30, 60 mg) 1 h before the study according to a preallocated randomized table. The subject was not reallocated for the test within two weeks of the previous test. After a 10 minute acclimation period before each test, the degree of tourniquet pain measured by VAS, arterial blood pressure, heart rate, respiration rate, and pressure-evoked pain were measured before and every 5 minutes after inflation of the tourniquet until the subject felt unbearable pain. A mixed model for repeated measurement of data was used for statistical analysis (P < 0.05). RESULTS: There was no statistical difference between different doses of DEX including the placebo. Rather, there was a tendency that DEX increases the pain. And there also was a tendency that average time to reach unbearable pain was decreased by DEX (P > 0.05). CONCLUSIONS: DEX is not effective in controlling tourniquet pain in normal awake subjects.
Acclimatization ; Arterial Pressure ; Central Nervous System Sensitization ; Chronic Pain ; Dextromethorphan* ; Extremities ; Healthy Volunteers* ; Heart Rate ; Humans ; Inflation, Economic ; Ischemia ; Male ; Models, Animal ; N-Methylaspartate ; Respiratory Rate ; Tourniquets* ; Volunteers

BACKGROUND: Venous regurgitation into the infusion line and subsequent occlusion frequently occurs during blood pressure (BP) measurement. The purpose of this study was to obtain the pattern and the actual range of peripheral venous pressure (PVP) change during NIBP measurement before and during enflurane anesthesia. METHODS: Adult size NIBP cuff was placed on the same arm on which IV infusion set was placed. PVP waveforms during BP measurement were recorded from 6 subjects. PVPs were measured before induction and at 30 min after induction of enflurane anesthesia (n=19). As the PVP waveform during NIBP measurement was biphasic in shape, values of baseline PVP (BEFORE), first peak (PEAK1), notch between two peaks (NOTCH), second peak (PEAK2) were measured. Timed control data were obtained from six volunteers. RESULTS: PEAK2 was always higher than PEAK1. Range of peak PVP was 12-130 mmHg (57.6 2.5 mmHg, mean S.E.) and PVP change was augmented during enflurane anesthesia (p<0.05). Enflurane anesthesia accentuated correlationship between mean arterial pressure and PVP. CONCLUSION: Our observation showed that peak PVP occurred during deflation phase and its range of variation was substantial. Changes in the pattern and the autoregulation of PVP by enflurane needs further investigation.
Adult ; Anesthesia* ; Arm ; Arterial Pressure ; Blood Pressure* ; Enflurane* ; Homeostasis ; Humans ; Venous Pressure* ; Volunteers