Nonobstructive Dysphagia in Reflux Esophagitis

Dysphagia in the absence of organic esophageal stricture may occur in patients with reflux esophagitis. Although the exact mechanism of this "nonobstructive dysphagia" (NOD) is not known, it is believed to be related to transient segmental esophageal motor disorder. The goals of this study were to determine the frequency of NOD in patients with reflux esophagitis and correlate it with esophageal pH and motility changes. Sixty-three consecutive patients with symptoms of esophageal dysfunction were studied with endoscopy, infusion esophageal manometry, and 24-h ambulatory esophageal pH monitoring. Forty-seven had severe erosive esophagitis unresponsive to medical therapy; 16 with esophageal motility disorders were used as symptomatic controls. Twenty-eight of 63 patients studied experienced NOD during the 24-h pH study; 22 had esophagitis and six had esophageal dysmotility without esophagitis. NOD was noted with similar frequency in the two groups; 22/47 (46.8%) of patients with esophagitis and 6/16 (37.5%) with esophageal dysmotility experienced NOD during the period of study. NOD correlated with pH less than 4.0 in 88.6% of patients with esophagitis but in only 7% of patients with esophageal dysmotility (p less than 0.001). There was no difference in acid reflux patterns in esophagitis patients who experienced NOD (22/47), and in those who did not (25/47). There was no correlation between NOD and baseline esophageal motility abnormalities. In summary, 1) NOD is a common, intermittent symptom that occurred in up to 46.8% of esophagitis patients and 37.5% of symptomatic controls during the 24-h period of this study; 2) NOD correlates with esophageal pH less than 4.0 in patients with esophagitis and not in patients with esophageal dysmotility. These data strongly suggest that acid in the distal esophagus frequently triggers the sensation of dysphagia in esophagitis patients, but not in patients with esophageal motility disorders. Combined ambulatory intraesophageal motility and pH monitoring may further elucidate the mechanism of dysphagia in these patients.     

Exercise testing in pulmonary sarcoidosis

The change in transfer coefficient (Kco) with increasing heart rate during exercise was studied in 25 normal subjects and in 21 patients with pulmonary sarcoidosis. The slope of the Kco response against heart rate was found to be 0·0053 mmol min⁻¹ kPa⁻¹ l⁻¹ per beat in the normal group but in many of the patients was two standard deviations or more below this normal slope, even when their routine function tests were normal. This response of Kco to exercise is a more sensitive index of changed function than more routine function tests in pulmonary sarcoidosis.     

Magnetic resonance imaging of cervical ligamentous anatomy and traumatic ligamentous injuries

Cervical spine trauma accounts for majority of spinal injuries, and approximately one‐third involve the craniocervical junction (CCJ). Due to its high sensitivity, magnetic resonance imaging (MRI) has become the standard tool for imaging suspected ligamentous injuries in an unstable spine and in patients with neurological deficits having a normal CT. The ligamentous anatomy of the CCJ is complex, and thorough knowledge is a prerequisite for accurate interpretation of the MRI findings. This pictorial essay aims to familiarise radiologists with the ligamentous anatomy, mechanisms of injury and MRI appearances of injuries in the cervical spine, with emphasis on the CCJ.     

内镜下扩大经鼻蝶入路至斜坡区的解剖学研究

目的探索内镜下经扩大鼻蝶入路显露斜坡区的可行性,为切除斜坡区病变提供解剖学参考。方法在10例成人头部固定标本上,内镜下模拟扩大经鼻蝶手术入路显露斜坡区,观察有关显微解剖标志。结果扩大经鼻蝶内镜入路可磨除从鞍后到斜坡、枕骨大孔前缘的骨性结构;可显露斜坡区腹侧硬膜下的椎基底动脉及其分支、后交通动脉及其与大脑后动脉汇合处、动眼神经、脑干腹侧等结构。此入路的手术标志主要包括:蝶筛隐窝、蝶窦开口、视神经隆突、颈内动脉隆突与颈内动脉视神经隐窝、咽结节、枕骨大孔前缘。结论内镜下扩大经鼻蝶手术入路可充分显露鞍后-斜坡区的腹侧硬膜下结构,适用于此区病变的手术治疗。     

NON-CONVULSIVE STATUS EPILEPTICUS AS A COMPLICATION OF Mycoplasma pneumoniae INFECTION

SUMMARY Described is a confirmed case of non-convulsive status epilepticus, an unusual presentation of M. pneumoniae infection. The postulated pathological mechanisms in this infection are reviewed.     

Infections and Wegener's granulomatosis--a cause and effect relationship?

The association of infections and autoimmune disease has been noted by various authors. Several mechanisms have been proposed to explain this, with no current consensus. Wegener's granulomatosis (WG) is an autoimmune disease involving predominantly the pulmonary and renal systems, and is associated with a distinct autoantibody-the anti neutrophil cytoplasmic antibody (ANCA). Although no solid evidence implicates infections in the emergence of WG, direct and circumstantial data suggest this relation. We review this evidence and discuss possible underlying mechanisms. We emphasize the relationship between infections and ANCA, and their role in the maintenance of the 'on- going' inflammatory response.      

Abnormal glucose transport and GLUT1 cell-surface content in fibroblasts and skeletal muscle from NIDDM and obese subjects

Summary Glucose transport and GLUT1 expression were studied in fibroblasts from 7 lean and 5 obese non-insulin-dependent diabetic (NIDDM) subjects with at least 2 NIDDM first-degree relatives and from 12 lean and 5 obese non-diabetic subjects with no family history of diabetes. The obese individuals also had a strong family history of obesity. Fibroblasts from all of the subjects exhibited no difference in insulin receptor binding, autophosphorylation, and kinase and hexokinase activity. At variance, basal 2-deoxyglucose (2-DG) uptake and ³H-cytochalasin B binding were 50 % increased in cells from individuals with NIDDM (p < 0.001) and/or obesity (p < 0.01) as compared to the lean non-diabetic subjects. Insulin-dependent (maximally stimulated – basal) 2-DG uptake and cytochalasin B binding were decreased three-fold in cells from the diabetic and/or obese subjects (p < 0.01). GLUT1 mRNA and total protein levels were comparable in fibroblasts from all the groups. However, basal GLUT1 cell-surface content was 50 % greater in fibroblasts from the NIDDM and/or obese subjects as compared to the lean non- diabetic individuals while insulin-dependent GLUT1 recruitment at the cell surface was diminished threefold. Increased basal GLUT1 content in the plasma membrane was also observed in skeletal muscle of 4 NIDDM and 3 non-diabetic obese individuals (p < 0.05 vs the lean non diabetic subjects). Basal 2-DG uptake in fibroblasts from diabetic/obese individuals and lean control subjects strongly correlated with the in vivo fasting plasma insulin concentration of the donor. A negative correlation was demonstrated between the magnitude of insulin-dependent glucose uptake by the fibroblasts and plasma insulin levels in vivo. We conclude that a primary abnormality in glucose transport and GLUT1 cell-surface content is present in fibroblasts from NIDDM and obese individuals. The abnormal GLUT1 content is also present in skeletal muscle plasma membranes from NIDDM and obese individuals. [Diabetologia (1997) 40: 421–429] Received: 9 August 1996 and in final revised form: 11 December 1996