Primary Sjögren syndrome, which involves lesions in both the brain and spinal cord, is rarely reported. Related symptoms, such as intractable pain due to central nervous system involvement, are very rare. A 73-year-old woman diagnosed with primary Sjögren syndrome manifested with subacute encephalopathy and extensive transverse myelitis. She complained of severe whole body neuropathic pain. Magnetic resonance imaging demonstrated a non-enhancing ill-defined high intensity signal involving the posterior limb of the both internal capsule and right thalamus on a T2 fluid-attenuated inversion recovery image. Additionally, multifocal intramedullary ill-defined contrast-enhancing lesion with cord swelling from the C-spine to L-spine was also visible on the T2-weighted image. Her intractable pain remarkably improved after administration of concomitant oral doses of gabapentin, venlafaxine, and carbamazepine.
Citations
Supernumerary phantom limb (SPL) resulting from spinal cord lesions are very rare, with only sporadic and brief descriptions in the literature. Furthermore, the reported cases of SPL typically occurred in neurologically incomplete spinal cord patients. Here, we report a rare case of SPL with phantom limb pain that occurred after traumatic spinal cord injury in a neurologically complete patient. After a traffic accident, a 43-year-old man suffered a complete spinal cord injury with a C6 neurologic level of injury. SPL and associated phantom limb pain occurred 6 days after trauma onset. The patient felt the presence of an additional pair of legs that originated at the hip joints and extended medially, at equal lengths to the paralyzed legs. The intensity of SPL and associated phantom limb pain subsequently decreased after visual-tactile stimulation treatment, in which the patient visually identified the paralyzed limbs and then gently tapped them with a wooden stick. This improvement continued over the 2 months of inpatient treatment at our hospital and the presence of the SPLs was reduced to 20% of the real paralyzed legs. This is the first comprehensive report on SPLs of the lower extremities after neurologically complete spinal cord injury.
Citations
Patients with spinal cord injury (SCI) may experience several types of chronic pains. Abdominal pain in patients with SCI has gained limited attention and little is yet known about its characteristics and mechanisms. It often has been regarded as visceral pain associated with constipation and distention. Neuropathic pains localized in the abdomen have rarely been reported. We experience a case of intractable abdominal pain in a patient with SCI, neither of visceral pathology nor of musculoskeletal origin. The nature of pain fulfilled the diagnostic criteria for neuropathic pains. The pain was therefore regarded as neuropathic and managed accordingly. The first- and second-line oral drugs available were being performed, unfortunately, adequate pain control was not achieved. We tried an intrathecal lidocaine injection as another treatment option, and the injection had considerable effects.
Citations
Objective: To evaluate effects of gabapentin in post-stroke reflex sympathetic dystrophy (RSD).
Method: To 20 RSD patients after stroke, gabapentin was administrated. We started medication with 300 mg per day and increased dosage by 300 mg per two days up to maximum 900∼1,200 mg. We evaluated RSD symptom severities with hand pain, hand swelling and shoulder pain before gabapentin administration. Severity of each symptoms was graded and scored (0: no pain/swelling, 1: mild, 2: moderate, 3: severe). Severities of RSD symptoms were reevaluated on every dose increasing and on 1 week, 2 weeks and 4 weeks later after administrating maximum dosage. We defined as no effect group didn't have any improvement in symptom severity score in comparison with baseline score. Medications other than gabapentin were administrated in no effect group.
Results: Among 19 subjects whom we could follow-up, 4 subjects were defined as no effect group. 15 (78.9%) subjects showed improvement in symptom severity score. Statistically significant symptom improvements were observed after 4 weeks in comparison with baseline in hand pain and shoulder pain (p=0.000). From gabapentin 300∼600 mg dosage, hand and shoulder pain showed significant pain decrease. Improvement of hand edema was observed after 4 weeks, but it was statistically insignificant.
Conclusion: We conclude the gabapentin is effective for RSD pain, however further control study is required. (Korean Acad Rehab Med 2002; 26: 502-507)
Objective: To evaluate the axonal degeneration after nerve block with phenol and ethanol injection into tibial nerve.
Method: Tibial nerves of thirty Sprague-Dawley rats were exposed. For the developement of neuropathic pain, the method of intraneural injection was performed. Five percent phenol, 90% ethanol or normal saline were injected into the epineurial sheath of tibial nerve at each group. The mechanical and thermal allodynia were evaluated in post- injection 1, 2, 3, and 4 weeks. The mechanical allodynia was evaluated by withdrawal response to 10 stimulations with von Frey hair. Thermal allodynia was tested by withdrawal response to 5 stimulations with acetone. Motor nerve conduction study was performed in post-injection 1, 2, and 4 weeks.
Results: In behavioral test, the experimental group exhibited increased withdrawal response to mechanical and cold stimulation, but there was no significant difference between two groups, phenol and ethanol groups. In motor nerve conduction study, compound motor action potential amplitude loss were observed in experimental group, but there was no significant difference between two groups, phenol and ethanol groups.
Conclusion: These results suggest that axonal degeneration of ethanol is roughly similar to those of phenol block. (J Korean Acad Rehab Med 2002; 26: 470-474)
Objective: To investigate the neuropathic changes induced by nucleus pulposus and possible role of nitric oxide (NO) in the pathogenesis of painful radiculopathy.
Method: Autologous nucleus pulposus was harvested from the rat coccygeal intervertebral disc and grafted to the sciatic nerve. Pain behavior, neurophysiologic and pathologic changes were compared between autografted and sham operated group during 14-day-period. Western immunoblotting and immunohistochemistry with anti-nitrotyrosine mouse monoclonal antibody were used to compare the NO production and nerve damage in autografted and sham operated nerve tissues.
Results: Mechanical allodynia and thermal hyperalgesia were observed 2 days after autograft of nucleus pulposus and persisted during 14-day-period (p＜0.05). Motor nerve conduction latency was delayed and compound muscle action potential amplitude was decreased 5 days after autograft (p＜0.05). Histologically, nucleus pulposus induced severe inflammatory reaction with fibroblast proliferation and foamy macrophage infiltration, which were persisted during 14-day- period. More nitrated proteins were detected consistently in nerve tissues with autograft of nucleus pulposus and immunohistochemical staining of nitrotyrosine was prominent around foamy macrophages.
Conclusion: These data suggest that nucleus pulposus induce mechanical allodynia, thermal hyperalgesia and nerve dysfunction through inflammatory reaction with macrophage infiltration. NO and NO related tissue injury may play an important role in the pathogenesis of painful radiculopathy.
Objective: The purpose of this study was to develop a new neuropathic pain model in rat.
Method: Twenty Sprague-Dawley adult male rats, 10 for control and 10 for experimental, were anesthetized and their sciatic nerves were exposed. In an experimental group, exposed nerve was injured with 10 volts electrical current for 10 seconds. The mechanical and thermal allodynia and pain behavior were evaluated in pre-electrical injury and post-injury 1, 2, 3 days, 1, 2, 3, 4, 6 and 8 weeks. The mechanical allodynia was evaluated by the frequency of response to 5 stimulations of von Frey hairs (4.31 and 4.56) and the thermal allodynia was tested by withdrawal latency to stimulation with radiant heat. Spontaneous pain behavior (paw shaking, paw elevation) was observed for 5 minutes in the cage.
Results: The experimental group exhibited significantly higher withdrawal frequency to mechanical stimulation: from post-injury 3 days to 6 weeks for von Frey hair 4.31 and from 2 days to 4 weeks for von Frey hair 4.56 (p＜0.05). There was no difference between two groups in withdrawal latency to radiant heat stimulation. The experimental group showed spontaneous pain behavior but control group did not. In electron microscopic finding, prominent myelin destruction and axonal sprouting were observed in experimental group.
Conclusion: These results suggest that a new neuropathic pain model can be made by 10 volts electrical injury for 10 seconds to rat sciatic nerve.
Objective: To evaluate the effects of gabapentin and clonidine on neuropathic pain in an experimental pain model.
Method: 24 male adult rats were anesthetized and the sciatic nerve was exposed. Each exposed nerve was electrically injured with 10 volts for 10 seconds by two needle electrodes. Rats were divided into three groups by treating with gabapentin, clonidine and sham. Gabapentin and clonidine were given orally from post operation day 3 to 7 in gabapentin and clonidine groups respectively. To evaluate the presence of mechanical allodynia, withdrawal frequency was tested by Von Frey hair in the same days. After post operation day 7, all the medications were discontinued and mechanical allodynia was evaluated at post operation day 14.
Result: Neuropathic pain was developed after electrical injury in all the rats. Withdrawal frequency is more decreased in gabapentin and clonidine groups than sham group in post operation day 4 to 7. The withdrawal frequency was 2.88⁑0.83, 2.75⁑0.89, 3.13⁑0.99, 3.25⁑1.28 in gabapentin group and 3.38⁑0.92, 4.50⁑2.20, 3.25⁑1.17, 3.50⁑0.93 in clonidine group in post operation day 4, 5, 6, 7, respectively. In post operation day 14, withdrawal frequency was increased and showed no difference compared to the sham group.
Conclusion: Gabapentin and clonidine can suppress the neuropathic pain in an experimental pain model. There was no different effect on the neuropathic pain suppression between gabapentin and clonidine.
Objective: To evaluate usefulness of the current withdrawal threshold (CWT) on evaluation of the neuropathic pain in animal model.
Method: Surgical neuropathy was induced in 40 Sprague-Dawley rats. Fourteen days after the surgery, neuropathic rats were evaluated by von Frey hair. The CWT was determined by various stimulus intensities which induce the tail-withdrawal response or vocalization of rats. The experimental group was compared with the control group by CWT. Then the experimental group was subdevided to two groups. The experimental group 1 was injected with beta-methasone 0.1 mg/kg, intra-peritoneally and experimental group 2 was injected with normal saline with the same amount as steroid. The CWT of two experimental subgroups were measured before and 30 minutes after injections.
Results: The experimental group showed significant decrease of the CWT compared with the control group after the neuropathic pain was induced. The CWT of experimental group 1 was increased after steroid administration (p＜0.01).
Conclusion: This preliminary study suggests that the measurement of CWT would be an useful tool to study the neuropathic pain in experimental animal model.
Objective: The purpose of this study was to evaluate the anti-inflammatory effect of steroid in the neuroma plays a key role in the development of neuropathic pain.
Method: Materials consisted of 21 male Sprague-Dawley rats (8 weeks old, 180∼200 g), which were divided into a steroid (n=9) and control group (n=12). Neuropathic pain was produced by unilateral transection of the superior caudal trunks at the level between the S3 and S4 spinal nerves. We compared two groups of rats, the steroid group injecting 1 ml (40 mg) of Methylprednisolone (Depo-Medrol), and the control group injecting 1 ml of nomal saline on operation site just after operation.
Behavioral reactions to mechanical allodynia were checked using a von Frey hairs of 2.0 g (19.6 mN) bending force at pre-operation, post-operative 1, 4, 7, 10 & 14 day to evaluate the steroid effect on the development of neuropathic pain.
Results: The steroid group exhibited less tail-flick frequencies to mechanical stimulation: 14.8⁑17.0%, 28.1⁑18.3%, 38.1⁑28.3% at post-operative 4, 7, 10 days respectively in control group; 30.3⁑21.2% 43.6⁑21.3%, 47.2⁑20.8% at post-operative 4, 7, 10 days, respectively. But there was no significant difference between both groups at post-operative 14 days. The steriod reduced the pain at early stage of neuropathic pain development, but failed to decrease the pain level in late stage.
Conclusion: These results suggest that the steroid induced anti-inflammatory effect in the injured neuroma is not a key factor in the development of neuropathic pain.
Objective: In a rat model of peripheral neuropathy, to determine whether neuropathic pain is related to the α-2 adrenergic receptor.
Method: The neuropathic pain was produced by unilateral transection of the superior caudal trunk between the S3 and S4 spinal nerves. These animals showed the behavioral signs of neuropathic pain in the tail. Two weeks after the neuropathic surgery, tail withdrawal responses to the mechanical stimuli with von Frey hair (2.0 g) were examined 1, 2 and 24 hrs following the administration of clonidine, α-2 receptor agonist. One week after the clonidine test, the same behavioral test was done after the administration of clonidine along with yohimbine, α-2 receptor antagonist.
Results: Clonidine significantly reduced the frequency of tail response and yohimbine reversed the clonidine-induced anti-allodynic effect.
Conclusion: These results suggest that neuropathic pain is related to the sympathetic nervous system via α-2 adrenergic receptor.
Objective: The purpose of this study is to develop a new neuropathic pain model in the rat.
Method: Each male adult rat was anesthetized and the sciatic nerve was exposed. Each exposed nerve was injected with 0.03 cc of 1% phenol solution. Normal saline 0.03 cc was injected to the placebo group. Rats were tested for the presence of mechanical allodynia by von Frey hair. Spontaneous pain behavior (paw shaking, paw elevation) was examined for 5 minutes in the cage.
Results: Phenol injected group developed allodynia after the second post-injection day for up to 1 month. Allodynia was also observed in the contralateral legs of phenol injected group. The control group did not develop allodynia. Spontaneous pain behavior was not observed in either group.
Conclusion: Neuropathic pain model was developed by 1% phenol solution injection to the rat sciatic nerve. This study suggests an easier method for making the neuropathic pain model. Key_words: 페놀, 신경병증성 통증 모형, 좌골 신경, Phenol, Neuropathic pain model, Sciatic nerve
Objective: To evaluate the effects of high and low frequency transcutaneous electrical stimulation (TENS) on the neuropathic pain and to determine opioid-system involve to analgesia.
Method: Under pentobarbital anesthesia (55 mg/kg i.p.), twenty male Sprague-Dawley (250∼300 g) rats were operated that tibial and sural nerves were ligated and cut unilaterally. Pain sensitivity was assessed using the von Frey filament (8 mN) and acetone through behavioral test. After neuropathic pain developed, the various modes of TENS were applied to the rat with neuropathic pain and pain sensitivity was assessed to evaluate the analgesic effects. Naloxone was injected intraperitoneally to observe reversal of pain sensitivity.
Results: 1) Neuropathic pain was obtained successfully through selective cut of sciatic nerve branches in the rat. 2) Neuropathic pain were reduced by more than 10 minutes stimulation of TENS. 3) The analgesic effects of TENS on mechanical and cold stimulation were sustained for 60 minutes and 30 minutes, respectively. 4) Both high and low frequency TENS showed analgesic effects. 5) Analgesic effects of TENS were reversed by the intraperitoneal administration of naloxone.
Conclusion: The results suggest that low and high frequency TENS have an analgesic effects to neuropathic pain and opioid-system was involved to reduce of neuropathic pain.
Objective: The present study was conducted to investigate the effects of transcutaneous electrical nerve stimulation (TENS) and microcurrent electrical neuromuscular stimulation (MENS) on pain-like behaviors developed in rats with an experimental neuropathy.
Method: Neuropathic surgery was done by a unilateral ligation of L5 and L6 spinal nerves of the rat. Allodynic behavior was examined by measuring foot withdrawal frequency in response to 10 applications of a von Frey filament (2.5 g) to the plantar surface of the foot. Ongoing pain behavior was examined by measuring cumulative time in 3 min that the rat lifted its foot off a plate held at cold temperature (5oC). TENS (square pulses; 3 Hz, 30 mA) or MENS (bipolar pulses; 10 Hz, 300 μA) was applied for 15 min or 5 min, respectively, to the skin of the affected foot.
Results: Behavioral signs of mechanical allodynia and cold-induced ongoing pain had developed after nerve injury. Either TENS or MENS, when applied once, alleviated allodynic behavior, lasting up to 2 hrs. Such an alleviation lasted much longer when TENS or MENS was applied repeatedly (once a day for 6 days); 3 days by TENS and 1 day by MENS. Cold-induced ongoing pain behavior, however, was not affected by the repeated application of either TENS or MENS.
Conclusion: The results suggest that both TENS and MENS are useful tools for the treatment of mechanical allodynia. Repeated application of TENS or MENS is more effective in alleviating mechanical allodynia than its single application. Either TENS or MENS, however, seems not effective in alleviating cold-induced ongoing pain.
Objective: The purpose of this study was to evaluate the short- and long-term effects of exercise on neuropathic pain.
Method: Pain responses between rats in the exercise and control groups were compared to evaluate the effects of exercise in neuropathic pain. Materials consisted of 30 male Sprague-Dawley rats (8 weeks old, 180∼200 g), which were divided into an exercise group (n=15) and a control group (n=15). Neuropathic pain was produced by partially injuring the nerve innervating the tail. Running exercise was given on a Rota-rod treadmill exercise machine for 3 weeks (3.1 Km/day, 6 cycle of 9 minutes exercise and 1 minute rest). Behavioral reactions to mechanical allodynia were checked using a von Frey hairs of 2.0 g (19.6 mN) bending force at 10 minutes, 1 hour and 24 hours post-exercise to evaluate the short term effects of exercise. Behavioral reactions to mechanical and thermal allodynia with 4oC or 40oC were evaluated 7, 14, 21 and 28 days following exercise.
Result: The exercise group exhibited less tail-flick frequencies to mechanical stimulation from 58.8⁑6.8% to 41.1⁑5.4%, 37.6⁑13.2% at 1 and 24 hours post-exercise compared to the control group, but there was no significant difference between the groups at weeks 1 through 4. In the exercise group, the decrease of tail-flick frequencies were blocked by naloxone (2 mg/kg i.p.). It is suggested that long-lasting muscle exercise (e.g. running) which influences central endorphin mechanisms giving analgetic effects.
Conclusion: The results of this study support the hypothesis that the exercise can reduce neuropathic pain in the acute stage.
Objective: To evaluate the effect of clonidine on the experimental neuropathic pain model and to observe whether neuropathic pain is related to the sympathetic nervous system in this model by reversal of allodynia with administration of epinephrine.
Method: The neuropathic pain was produced by unilateral transection of the superior caudal trunk innervating the rat's tail. Tail withdrawal responses based on mechanical (withdrawal frequency to bending force of von Frey hair 2.0 g) and the thermal (withdrawal latency to tail immersion in a 4oC or 40oC water with a cut-off time of 15 seconds) stimuli were used. Experiments were performed two weeks after surgery when neuropathic pain had fully been developed. Experimental group by administration of clonidine was examined by tail withdrawal responses at Day 1, Day 3 and Day 5. After one week of wash-out period, reversal of allodynia by administration of epinephrine was examined by the same test.
Results: Clonidine significantly decreased the frequency of withdrawal with the mechanical stimuli compared with control (P＜0.01), but did not significantly decrease with the cold or warm stimuli. Epinephrine tended to aggravate the mechanical allodynia, but it was not significant compared with the control.
Conclusion: Clonidine may relieve mechanical allodynia in neuropathic pain, but the mechanism of neuropathic pain that is related to the sympathetic nervous system in this experimental model may be unreliable.
Thermography shows skin temperature changes in various conditions of body. Skin temperature changes according to the subcutaneous blood flow which is regulated by the autonomic nervous system. Peripheral neuropathic pain can be influenced by the sympathetic activities which also can change the skin temperature of affected sites.
To evaluate the usefulness of thermography in the detection of peripheral neuropathic pain, authors analyzed thermographic images of 47 cases with peripheral nerve injuries of upper extremities.
The peripheral nerve injuries were confirmed by Electromyographic studies in all of the cases. The peripheral neuropathic pain was present in twenty three cases.
The results show that 97.5% of nerve injury patients with pain and 45.8% of nerve injury patients without pain had abnormal thermograms with a mean temperature changes of △ T=0.99oC △T=0.13oC respectively. Authors conclude that thermography can be an usefal tool for the detection of peripheral neuropathic pain.
First
Prev
