An unusually rapid spontaneous recovery in a patient with spinal epidural hematoma.

BACKGROUND: Spontaneous epidural hematoma is a rare condition, which usually requires urgent surgical treatment. OBJECTIVES: To report two cases of spontaneous epidural hematoma, one of which was treated conservatively, and the other surgically, and discuss the possibility of unusual spontaneous recovery and treatment decision-making. CASE REPORT: We encountered 2 patients with spontaneous spinal epidural hematoma, both of whom were taking an anti-platelet agent, producing severe paraplegia. One patient with a hematoma at C2-T3 experienced a rapid neurological recovery while a magnetic resonance imaging scan was being performed. A complete resolution of the hematoma and complete neurological recovery ensued without surgical intervention. A second patient with a hematoma at T10-12 showed no neurological recovery up to the time emergency surgery started and was treated surgically by T10-12 laminectomy and excision of the hematoma. Neurological function returned to normal in both patients. CONCLUSION: The occurrence of spontaneous recovery in some patients makes the decision for surgery difficult. Emergency physicians need to be aware of the possibility of spontaneous rapid neurological recovery in patients with spinal epidural hematoma. To avoid unnecessary surgery in patients who will spontaneously have neurological recovery, neurological evaluations need to be repeatedly performed up to the time the emergency surgery begins. However, unfortunately, there is no diagnostic tool at present to identify the patients who recover spontaneously, and the interval between onset and surgery is correlated with clinical results, therefore, conservative treatment should be prescribed only for those patients who exhibit improving neurological signs early in the clinical course.

The role of the AMPA receptor and 5-HT(3) receptor on aggressive behavior and depressive-like symptoms in chronic social isolation-reared mice.

Chronic social isolation (SI)-reared mice exhibit aggressive and depressive-like behaviors. However, the pathophysiological changes caused by chronic SI remain unclear. The hypothalamus and amygdala have been suggested to be associated with the stress of SI. In addition to serotonin 3 (5-HT3) receptors, AMPA receptors have also been suggested to be involved in aggressive behavior and depressive-like symptoms in animals. Therefore, we examined whether chronic SI affects AMPA and 5-HT3 receptor expression levels in these regions. A Western blot analysis revealed that after four weeks of SI, mice exhibited up-regulated AMPA receptor subunit (GluR1, GluR2) protein levels in the amygdala and down-regulated hypothalamic 5-HT3 receptor protein levels. The AMPA/kainate receptor antagonist NBQX (10 mg/kg; i.p.) attenuated SI-induced depressive-like symptoms but not aggressive behavior. Intra-amygdalar infusions of the selective AMPA receptor agonist (S)-AMPA (10 µM) induced despair-like behavior, but not sucrose preference or aggressive behavior, in mice not reared in SI (naïve mice). Alternatively, treatment with the 5-HT3 receptor agonist SR57227A (3.0 mg/kg; i.p.) decreased aggression levels. In addition, intra-hypothalamic infusions of the 5-HT3 receptor antagonist ondansetron (3 µM) did not trigger aggressive behavior in naïve mice; however, the administration of ondansetron (0.3 mg/kg; i.p.) increased aggression levels in two-week SI mice, which rarely exhibited the aggressive behavior. Moreover, ondansetron did not affect the depressive-like symptoms of the SI mice. These results suggest that SI-induced up-regulation of GluR1 and GluR2 subunits protein levels in the amygdalar region and down-regulation of 5-HT3 receptor proteins level in the hypothalamic region are associated with the effect of AMPA receptor agonist and 5-HT3 receptor antagonist -induced aggressive behavior and depressive-like symptoms.

The development of depression-like behavior is consolidated by IL-6-induced activation of locus coeruleus neurons and IL-1ß-induced elevated leptin levels in mice.

RATIONALE: Many studies have supported the cytokine hypothesis as the underlying pathophysiology of depressive disorder. OBJECTIVES: We previously reported that lipopolysaccharide (LPS)-induced depression-like behavior is abrogated by the α1-adrenoceptor antagonist prazosin. Since cytokines are involved in LPS effects on the brain, we investigated the effects of cytokines on noradrenergic neurons in the locus coeruleus (LC) and whether central α1-adrenoceptors can cause the development of depression-like behavior. METHODS: Adult male CD1 mice were treated with LPS (1 mg/kg, i.p.) or saline and sacrificed 2 h later for immunofluorescence studies of c-fos and tyrosine hydroxylase (TH) expression in LC neurons. Serum cytokines were measured using enzyme-linked immunosorbent assay (ELISA). Another group of mice were implanted with intracerebroventricular (i.c.v.) cannulae and given artificial cerebrospinal fluid (CSF) (control), interleukin (IL)-1ß (0.5 µg), IL-6 (1 µg), or tumor necrosis factor (TNF)-α (1 µg), and sacrificed 2 h later for c-fos and TH immunofluorescence analysis. Serum samples were analyzed for leptin levels. In addition, tail suspension test (TST), forced swimming test (FST), and sucrose preference (SP) test were conducted in a separate group of mice treated i.c.v. with cytokines, recombinant mouse leptin (5 µg) or phenylephrine (40 µg). These effects were countered by i.c.v. administration of prazosin and a leptin antagonist. RESULTS: LPS increased c-fos expression in TH-positive neurons. Central administration of IL-6 and IL-1ß increased c-fos immunoreactivity and serum leptin levels. Phenylephrine, an α1-adrenoceptor agonist, given i.c.v., increased the immobility time during FST and decreased SP, but had no effect on TST. Central leptin administration increased immobility time during FST but did not affect TST or SP. The combination of phenylephrine and leptin increased immobility time during FST and TST, and decreased SP. Induction of depression-like behavior by co-administration of IL-1ß and IL-6 was prevented by pretreatment with prazosin alone. CONCLUSION: These results suggest that IL-6-dependent LC neuronal activation induced depression-like behavior and IL-1ß-induced increase in leptin levels enhanced α1-adrenoceptor-mediated depression-like behavior.

[Anesthetic management of a patient with severe hyponatremia].

A 62-year-old woman was scheduled for an operation for ileus. Before the operation, we noticed severe hyponatremia (Na 117 mEq x l(-1)) probably due to dehydration. We corrected her hyponatremia slowly to avoid central pontine myelinolysis. Serum Na level increased to 131 mEq x l(-1) after surgery. She recovered from anesthesia without any neurologic problems.

[Diagnosis and differential diagnoses of osteoarthritis by radiography, CT, MRI, and RI].

Osteoarthritis is a disease of high occurrence; moreover, with increase of the elderly population, proper diagnosis and suitable treatment are vital. Proper diagnosis necessitates not only detailed patient history and clinical examination, but, most importantly, proper knowledge of radiological findings. This article presents the radiological examinations necessary for diagnosis of osteoarthritis, including X-ray, CT, contrast X-ray, MRI and RI. Important differential diagnoses are also presented.

Examining risk factors for posterior migration of fusion cages following transforaminal lumbar interbody fusion: a possible limitation of unilateral pedicle screw fixation.

OBJECT: Because the authors encountered 4 cases of hardware migration following transforaminal lumbar interbody fusion, a retrospective study was conducted to identify factors influencing the posterior migration of fusion cages. METHODS: Patients with lumbar degenerative disc disease (125 individuals; 144 disc levels) were treated using transforaminal lumbar interbody fusion and followed for 12-33 months. Medical records and pre- and postoperative radiographs were reviewed, and factors influencing the incidence of cage migration were analyzed. RESULTS: Postoperative cage migration was found in 4 patients at or before 3 months. Because all the cages that migrated postoperatively were bullet-shaped (Capstone), only these cages were analyzed. The analysis of preoperative radiographs revealed that higher posterior disc height ([PDH] > or = 6 mm) significantly increased the incidence of postoperative cage migration, but percent slippage, translation, range of motion, and Cobb angle did not. The incidence of cage migration in patients with unilateral fixation (3 [8.3%] of 36) was not significantly different from that in patients with bilateral fixation (1 [2.1%] of 48). Patients who had scoliotic curvature with a Cobb angle > 10 degrees when treated with unilateral fixation demonstrated a tendency to have more frequent postoperative cage migration than patients treated with bilateral fixation. To examine the influence of the height of fusion cages, a value obtained by subtracting preoperative anterior disc height (ADH) or PDH from cage height was defined as "Cage height - ADH" (or "Cage height -PDH"). The analysis revealed that the value for "Cage height -ADH" as well as "Cage height -PDH" was significantly lower in migrated levels than in nonmigrated levels, suggesting that the choice of undersized cages may increase the incidence of cage migration. CONCLUSIONS: The results suggest that the use of a bullet-shaped cage, higher PDH, the presence of scoliotic curvature, and undersized fusion cages are possible risk factors for cage migration. One patient with postoperative cage migration following bilateral screw fixation underwent revision surgery, and the pedicle screw fixation was found to be disrupted. Other than in this patient, cage migration occurred only in those treated by unilateral fixation. The potential for postoperative cage migration and limitations of unilateral fixation should be considered by spine surgeons.

Relationship between low-back pain, muscle spasm and pressure pain thresholds in patients with lumbar disc herniation.

It is not known whether or not muscle spasm of the back muscles presented in patients with sciatic scoliosis caused by lumbar disc herniation produces muscle pain and/or tenderness. Pressure pain thresholds (PPTs) of the lower back and low-back pain were examined in 52 patients (13 of 52 presenting sciatic scoliosis) with lumbar disc herniation who complained of radicular pain and in 15 normal subjects. PPTs were measured at five points bilaterally using an electronic pressure algometer. Low-back pain was evaluated using visual analogue scale (VAS) ratings. All patients complained of radicular leg pain and were divided into the following three groups according to the presence of and the region of low-back pain: no low-back pain group, low-back pain with no laterality group, and low-back pain dominantly on the herniation side group; the VAS rating on the side ipsilateral to the herniation side was higher than that on the contralateral side. In the normal subjects, there were no statistically significant differences between sides in mean PPTs at all sites examined. PPTs were not lower in the spasmodic side (concave side) than the convex side in patients with sciatic scoliosis. PPTs on the herniation side were significantly lower than those on the contralateral side in patients with low-back pain dominantly on the herniation side. Furthermore, the areas of low PPTs were beyond the innervation area of dorsal ramus of L5 and S1 nerve root. It was considered that not only the peripheral mechanisms but also the hyper excitability of the central nervous system might contribute in lowering PPTs of the lower back on the herniation side.