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Turner syndrome is a chromosomal disorder in which of all or part one of the X chromosomes is absent, and this syndrome affects females. The syndrome leads to a constellation of physical findings that often includes congenital lymphedema, a short stature and gonadal dysgenesis. The prevalence of inflammatory bowel diseases in the general population is estimated to be 150∼250 per 100,000 population. A 2-fold increase in the risk of developing inflammatory bowel diseases has been reported in women with Turner syndrome. We describe here a case of Turner syndrome with Crohn's disease. 32세의 터너증후군 환자가 10대 말부터 시작된 반복되는 하복부 통증과 설사가 1달 전부터 악화되어 내원하였다. 대장내시경 소견에서 항문연 상방 50 cm까지 직장과 상행결장에 종주 궤양과 지도상 혹은 둥근 모양의 아프타 궤양이 관찰되었고, 구불결장에서는 조약돌 점막 소견과 협착 소견을 보였다. 대장조영술에서 전 대장에 걸쳐서 다발성 미세 과립상과 원형의 충만결손 소견을 보였고, 하행결장과 근접 구불결장에 전반적인 협착소견을 보였으며, 대장내시경 조직검사 결과 궤양과 만성 염증소견을 보였다. 조직소견으로 궤양성 대장염과 크론병을 감별하기 어려웠지만, 임상증상, 내시경 소견, 대장조영술 소견을 바탕으로 크론병으로 진단하였다. 터너증후군 환자는 염증성 장질환의 발생 위험도가 일반인보다 증가하는 것으로 보고 된 적 있으나, 국내에서는 아직 터너증후군 환자에서 크론병이 동반된 증례 보고가 없었다. 저자들은 32세 터너증후군 환자에서 크론병을 진단하고 치료한 예를 경험하여 문헌고찰과 함께 보고 한다.
Fourty-seven patients with non-aneurysmal spontaneous subarachnoid hemorrhage were reviewed retrospectively. Attention was directed to the distribution and amount of subarachnoid hemorrhage on computerized tomography scans. Though the hemorrage could be distributed in all cisterns, the frequency and amount of hemorrhage were higher in infratentorial cisterns than in supratentorial cisterns. Among infratentorial cisterns, the hemorrhage was distributed to cisterns around the brainstem mainly and it had a predilection for interpeduncular cistern. Also the telangiectasia of thalamoperforating artery might be one of the causes of non-aneurysmal spontaneous subarachnoid hemorrhage.
Spinal cord injury causes immediate neuronal dysfunction and remained paralysis in life without clinical improvement. The spinal cord injury is caused by initial mechanical damage and secondary neuronal damage. The exact mechanisms of secondary neuronal damage are still unknown and their treatment is obscure even though many studies about them. The vascular change after injury is supported widely as a mechanism of secondary neuronal damage which causes decreased microcirculation and cord ischemia. There is considerable evidence that Ca ^(++) ions play a key role in the pathogenesis of posttraumatic ischemia and Ca^(++) ion influx promotes cellular dysfuction and cell death. So calcium antagonist is considered that it can improve spinal cord blood flow and restore impaired neuronal function. In this report, the effects of calcium channel blocker, nimodipine on spinal cord blood flow and spinal somatosensory evoked potential were measured and it was compared with vehicle group in 400 g-cm cord injured cat. And the effects of nimodipine were compared between nimodipine and adrenaline treated group of which mean systolic blood pressure was maintained above 100㎜Hg and nimodipine only treated group. Spinal cord blood flow was measured at T_(6)(injury level). T_(4), T_(12) by the hydrogen clearance technique and spinal somatosensory evoked potential was recorded at T_(4), T_(12) after injury at T6 level. The results of this study are summarized as follows: 1) The spinal cord blood flow was decreased abruptly just after spinal cord injury and it deceased progressively. 2) In nimodipine treated group, there was a improvement of spinal cord blood flow inspite of decreased mean systemic arterial pressure. It might be thought that the vasodilatory effect of nimodipine was more potent in spinal vasculature than in systemic peripheral vessels. 3) The increased spinal cord blood flow was more prominant and prolonged in nimodipine and adrenaline treated group than nimodipine only treated group. It was thought that increased heart beat and cardiac contratility by adrenaline counteracted systemic hypotension which resulted from vasodilatory effect of nimodipine. It suggests that maintenance of mean systemic arterial pressure is inportant during nimodipine theraphy in spinal cord injury. 4) The improvements of spinal somatosensory evoked potential were more evident in nimodipine and adenaline treated group. It might be caused by spinal cord blood flow improvement. From the above result it is speculated that the calcium channel blocker, nimodipine can improve spinal blood flow and impaird neuronal function in spinal cord injury.
Since developmental lumber atenosis was described by Verbiest in 1954, there have been many reports on lumbar stenosis. But there have been many limitations in diagnosis and treatment of lumbar stenosis. Recently, the development of water-soluble contrast media and high resolution spine CT scan have not only brought about significant progress in diagnosis of the etiology and levels of lumbar stenosis, but also better surgical therapetic results could be expected. The author has reviewed 433 patients with lumber stenosis operated at the department of Neurosurgery YUMC Yongdong Severance hospital from March 1983 to September 1987 and analized the measurements of various parts of the spinal canal by high resolution spine CT scan, and evaluated the clinical courses and their surgical outcomes. The results were summarized as following : 1) Male to female ratio was 1 : 1.3. The peak age incidence were 40's in male and 50's in female. 2) By the causes of lumbar stenosis, degenerative stenosis was most common as 78%, and followed by degenerative spondylolisthesis 17.2%, spondylolytic spondylolisthesis(1.6%), iatrogenic stenosis(1.6%), developmental stenosis(0.7%) and posttraumatic stenosis(0.7%). 3) Single level stenosis was most common(47.1%), two levels 32.8% and three levels or more 20.1%. In the single level stenosis L4/5 was most common as 85.8% and L5/S1 10.3. In the two levels stenosis, L4/5 and L4/S1 were most common as 72.5% and L3/4 26.1%. 4) The characteristic clinical symptoms were chronic back pain and neurogenic intermittent claudication(65.6%). Few patient showed abnormal neurological findings. Common abnormal sign was loss or decrease of ankle jerk(73%). The straight leg raising test was not significant, and it was positive only in 10.3% 5) In diagnosis of lumbar stenosis, it was most important to identify the causes of lumbar stenosis and degree of compression on cauda equina, or lateral recess stenosis by the spine CT or spine CT myelograms. 6) On myelogram, the findings of complete or incomplete block were present in 44.1%, and indentations of contrast dye column at the levels of stenosis was noted in 55.9%. 7) The common findings on spine CT scan were hypertrophy of posterior articular facet joints(65.8%), osteophyte formation(37.1%), thicking of yellow ligament(21.7%), ossification of posterior longitudinal ligament(23.8%), ossification of yellow ligament(4.9%). 8) In the diagnosis of degenerative lumbar stenosis with high resolution of spine CT scan, anteroposterior diameter of spinal canal was not so significant, but the cross sectional areas of dural sac and spinal canal were sensitive indexes. The anteroposterior diameter of dural sac and interfacetal distance provided the clue of lumbar stenosis. If the anteroposterior diameter of the lateral recess was less than 3㎜ it could be diagnosed as the lateral recess stenosis. And if the angle between both yellow ligaments(yellow ligament angle, Y-angle) was less than 60° it must be suspected as the central stenosis. 9) In the examination of degenerative spondylolisthesis with spinal CT scan, anterior-posterior diameter and cross sectional area of spinal canal and dural sac at the disc level were smaller than those of upper and lower vertebral levels. The angle of yellow ligament was almost normal. 10) For the definite treatment wide decompressive laminectomy, medial facetectomy and foraminotomy should be carride out. 11) Our results of surgery were good to excellent in 90.3% and fair to poor 9.7%.