No abstract available.
Joints* ; Range of Motion, Articular* ; Spine*

No abstract available.
Follow-Up Studies* ; Humans ; Peptic Ulcer*

The distal tibial physes begins its closure about 18 months prior to complete cessation of the tibial growth, closing first in its midportion, then medially, and finally, laterally. So the patterns of the ankle fracture during this period would be different from those of the adult or the children before this period. During the six year period from 1983 to 1988 at the department of orthopedic surgery, college of medi-cine, Hallym University, we found and analysed 54 adolescent patients with the ankle fracture which developed before the closure of the distal tibial growth plate, which were followed up more than 1 year. The results were as follows 1. During the 6 year period of this study, the adolescent ankle fracture comprise 4.4% (54 cases) of all the ankle fractures(1158 cases). Injury occurred more often in male than in female(44 versus 10). The mean age was 13.7 years. 2. The most common cause of injury was traffic accident being in 26 cases(48.1%), the next was slip down accident in 11 cases, and the third was sports activity in 10 cases. 3. The incidence of the adoescent ankle fractures using the Salter-Harris classification revealed 20 (37%) type II, 7 (13%) type III, 5 (9.3%) type IV, and 4 (7.4%) type I and that using the Dias and Tachdjian classification revealed 14 (25.9%) Supination-Inversion, 10 (18.5%) Supination-External rotation, 7 (12.7%) Pronation-Eversion-External rotation, and 1 (1.9%) no adjustable fracture. There were 9 (16.7%) Tillaux and 9 (16.7%) triplane fractures, which were belonged to both classifications 4. The treatments performed were closed reduction and cast immobilization for 28 cases (51.9 %), open reduction and internal fixation for 20 cases (37%), and closed reduction and percutaneous pinning for 6 cases. 5. There were complications experienced in 9 cases, which were 3 premature epiphyseal closure, 3 joint surface incongruity, 2 angular deformity, and 1 leg shortening. 6. For the prevention of the complication, the treatment of the adolecsent ankle fracture should be treated like as adult fracture.
Accidents, Traffic ; Adolescent ; Adult ; Ankle Fractures ; Ankle ; Child ; Classification ; Clinical Study ; Congenital Abnormalities ; Growth Plate ; Humans ; Immobilization ; Incidence ; Joints ; Leg ; Male ; Orthopedics ; Sports

BACKGROUND: Nitric oxide (NO) is known to play causative role in the development of neuropathic pain following peripheral nerve injury. However, it is yet to be investigated whether the role of NO differs in pain modalities, such as mechanical and thermal stimuli. Also, it has not been investigated whether NO has different roles in the stages of neuropathic pain - its development and maintenance. METHODS: Neuropathic pain was induced by a resection of the lumbar dorsal root 5, 6 (L 5, 6). After N-nitro-L-arginine methyl ester (L-NAME), an NO synthase inhibitor was injected intrathecally or locally around the dorsal root, we observed the behavioral response to the mechanical and thermal stimuli. RESULTS: Mechanical and thermal allodynia was inhibited by the application of L-NAME before the dorsal root injury. However, L-NAME did not affect the mechanical and thermal allodynia during the maintenance of neuropathic pain. CONCLUSIONS: We suggest that NO in the spinal cord or injured perineural site may play an important role in the induction of neuropathic pain, and may be associated with mechanical and thermal allodynia.
Animals ; Hyperalgesia* ; Neuralgia* ; NG-Nitroarginine Methyl Ester ; Nitric Oxide Synthase ; Nitric Oxide* ; Peripheral Nerve Injuries ; Rats* ; Spinal Cord ; Spinal Nerve Roots

No abstract available.
Child* ; Hip* ; Humans ; Osteoma, Osteoid*

No abstract available.
Alcoholics* ; Humans

The authors reviewed the clinical findings and treatment results of 12 cases of spinal meningeal cysts which were detected in MRI of low back patients. In these lesions, large cysts without CSF communication can compressed the nerve roots within spinal canal and it is difficult to confirm the cause of symptom whether it is originated from cysts or from associated spinal disorders. The terms and classifications of spinal meningeal cysts were very confusing. Among 12 cases, we excised 3 cases of large cysts with gluteal and perianal pains that were caused by compressed sacral nerve roots. All three cases were type 2 cyst (classified by Nabors) and located in sacral canal. In one case associated with isthmic spondylolisthesis, posterolateral fusion and pedicle screw fixations were combined with cyst excision. In other two cases, there were not any spinal pathologic findings that compressed sacral nerve roots except mild degenerative changes and intervertebral disc herniation in lower lumbar and sacral levels All 3 excised cases showed good prognosis in more than one year follow up. The other cases were treated conservatively for the associated spinal disorders.
Classification ; Follow-Up Studies ; Humans ; Intervertebral Disc ; Magnetic Resonance Imaging ; Prognosis ; Radiculopathy ; Spinal Canal ; Spondylolisthesis

No abstract available.
Cicatrix, Hypertrophic* ; Skin*

Pain is a sensation induced by activation of the peripheral nociceptors when tissue is damaged by direct stimuli or has a possibility of damage. There exist nociceptors for detecting the noxious stimuli in periphery, and the nociceptive informations were transmitted via A delta- or C-fibers. Acute pain is caused by direct noxious stimuli, and chronic pains are produced by inflammation or nerve damage. The mechanisms of chronic pains are associated with the changes of cen-tral nervous system (CNS) as well as those in peripheral nocicpetors. Immune cells and neurotrophins are also involved in the mechanisms of chronic pain. Recently, there has been a tendency among pain researchers that chronic pain might be explained the plastic changes in the nociceptive synaptic transmission through the spinal cord. These are associated with changes in intracellular Ca(2+)concentration, subsequent intracellular signal transduction pathways, which result in changes in AMPA receptor dynamics. This sequential changes may induce allodynia and hyperalgesia observed in chronic pain patients. This review suggests new interpretation for pain mechanism and new approach for chronic pain.
Acute Pain ; Chronic Pain ; Humans ; Hyperalgesia ; Inflammation ; Nerve Growth Factors ; Nervous System ; Nociceptors ; Plastics ; Receptors, AMPA ; Sensation ; Signal Transduction ; Spinal Cord ; Synaptic Transmission

BACKGROUND: The motor neuronal death in amyotrophic lateral sclerosis (ALS) arise from several mechanisms including excitotoxicity, oxidative stress, immunologic or calcium dysregulation. Though the immunoglobulin mediated neuronal death has been implicated through changes of calcium influx, the direct evidence showing the increase of intracellular calcium level is rare. The purpose of our study is to directly measure the calcium in cultured neurons treated with immunoglobulins from ALS patients to further understand the role of calcium in motor neuron degeneration. METHODS: Immunoglobins purified from serum in patients with ALS (n=8) and in control (n=8) were incubated for 24 hours in PC12 cell line. The intracellular calcium level was measured by fluorometry using calcium chelating dye, fura-2. High concentration of potassium chloride were used to evoke calcium influx, and L-type calcium channel current were measured using nicardipine, the L-type specific calcium channel blocker. RESULTS: Basal level of intracellular calcium was higher in the cells treated with immunoglobulins from ALS. However, the calcium increase evoked by 30 mM or 140 mM potassium chloride were lower in ALS than in control. The calcium increase through L-type calcium channel in ALS group was not significantly different from control. Conclusions ; Considering the proposed role of the calcium in neuronal degeneration, present data suggest increased intracellular calcium is important in neurodegenerative mechanism caused by ALS immunoglobulins.
Amyotrophic Lateral Sclerosis* ; Animals ; Calcium Channels ; Calcium Channels, L-Type ; Calcium* ; Fluorometry ; Fura-2 ; Humans ; Immunoglobulins* ; Motor Neurons ; Neurons ; Nicardipine ; Oxidative Stress ; PC12 Cells* ; Potassium Chloride