The path to care in autism: Is it better now?

Parents of children with autism often report problems associated with obtaining a diagnosis of their child's condition, family support, information, and appropriate services. To evaluate any changes in the situation over the last two decades, the families of all members of the West Midlands Autistic Society, age 19 years and below, were asked to fill in a questionnaire that covered aspects of detection, diagnosis, help and information received, and educational provision. Responses were obtained from 127 families, the children of whom formed an older group ages 10 years and above (n=67) and a younger group ages 9 years and below (n=61). Findings show that there have been improvements for the younger group in some areas, such as earlier referral, diagnosis, and statementing. However, the situation with respect to advice given by professionals and the support and provision available after referral is still much the same as that experienced by families of the older group of children. Many difficulties and hurdles remain which hinder parents and children on the path to care in autism.     

Mechanisms of connective tissue damage by crystals containing calcium

From available clinical, radiographic, and synovial fluid findings, coupled with in vivo radiolabelled crystal turnover data and in vitro experimental data, a hypothesis has been formulated relative to the pathogenesis of BCP crystal deposition diseases (Fig. 2). Synovial lining cells phagocytose BCP crystals and particulate collagens in the joint fluid. During and/or after internalization these cells are stimulated in a variety of ways: 1) protease synthesis and secretion is relentlessly stimulated, which may damage joint tissues producing clinically evident loss of collagenous tissues including cartilage, bone, and tendon, and which may release additional amounts of crystals and particulate collagens into the synovial fluid, completing a vicious cycle; 2) PGE2 production is greatly augmented; 3) DNA synthesis is stimulated as a result of increased inositol phospholipid turnover and intracellular crystal dissolution. The increased number of synovial cells also augments the total local generation of proteases and prostenoids. Mechanical factors such as trauma or joint overuse also contribute to the pathogenesis of joint destruction as discussed in the article on the clinical aspects of BCP crystal deposition.     

Comparing diffusion-weighted and T2-weighted MR imaging for the quantification of infarct size in a neonatal rat hypoxic–ischemic model at 24 h post-injury

PURPOSE: In a neonatal rat model of hypoxic-ischemic (HI) brain injury, using T2-weighted imaging (T2WI) and diffusion-weighted imaging (DWI), we aim to determine the best MRI method of lesion quantification that reflects infarct size. MATERIALS AND METHODS: Twenty 7-day-old rats underwent MRI 24h after HI brain injury was induced. Lesion size relative to whole brain was measured using T2WI and apparent diffusion coefficient (ADC) maps, applying thresholds of 60%, 70% and 80% contralateral control hemisphere mean ADC, and at day 10 post-HI on pathology with TTC staining. Multiple linear regression analysis was used to study the relationships between lesion size at MRI and pathology. RESULTS: Lesion size measurement using all MRI methods significantly correlated with infarct size at pathology; using T2WI, r=0.808 (p<0.001), using 80% ADC, 70% ADC and 60% ADC thresholds, r=0.888 (p<0.001), 0.761, (p<0.001) and 0.569 (p=0.014), respectively. Eighty percent ADC threshold was found to be the only significant independent predictor of final infarct volume (adjusted R(2)=0.775). CONCLUSION: At 24h post-HI, lesion size on DWI, using 80% ADC threshold is the best predictor of final infarct volume. Although T2WI performed less well, it has the advantage of superior spatial resolution and is technically less demanding. These are important considerations for experiments which utilize MRI as a surrogate method for lesion quantification in the neonatal rat HI model.     

Practice of orthokeratology by a group of contact lens practitioners in Hong Kong

Purpose: The aim of the study was to provide information about the characteristics of three main types of orthokeratology (ortho‐k) lenses used in Hong Kong and to report on their performance based on the clinical impressions of a group of ortho‐k practitioners. Method: Twelve ortho‐k practitioners were interviewed between 1 March and 30 June 2001. Results: Most ortho‐k lenses were ordered from three manufacturers: DreimLens, Fargo and Contex. The median maximum myopia reduction reported for DreimLens, Contex and Fargo lenses were 6.25 D, 6.00 D and 4.50 D respectively. The time to reduce myopia by up to 4.00 D could be up to three weeks for Contex and DreimLens and up to four weeks for Fargo. For reduction of myopia by up to 4.00 D, the treatment usually required only one or two lenses per eye for all three types of lenses. The incidence of lens binding and lens tightening after achieving the optimal reduction was reported to be higher with the DreimLens design. Good centration, less lens binding, relatively lower incidence of complications and lens tightening after achieving the optimal reduction were reported with the Fargo lenses. Conclusions: DreimLens tended to be more effective for myopia reduction. However, some practitioners were concerned with the aggressiveness of myopia reduction using this lens design and the higher potential for ocular complications. Selection of the lens design is dependent on various factors, in particular, practitioners need to be comfortable with the design they choose and to consider the needs of their patients and the final goal of the treatment.     

Defining the Role of Surgery for Primary Gastrointestinal Tract Melanoma

Objective The objective of the study was to determine the outcomes for primary gastrointestinal melanomas (PGIM). Material and methods The Surveillance, Epidemiology, and End Results database (1973–2004) was queried. Results Overall, 659 cases of PGIM were identified. The annual incidence of PGIM was approximately 0.47 cases per million in 2000. Overall median survival time was 17 months. Tumors were identified in the oral–nasopharynx (32.8%), anal canal (31.4%), rectum (22.2%), esophagus (5.9%), stomach (2.7%), small bowel (2.3%), gallbladder (1.4%), and large bowel (0.9%). Univariate analysis demonstrated age, tumor location, stage, surgery, and lymph node status were significant predictors of improved survival. MST has not been reached for tumors located in the large bowel, while tumors located in the stomach demonstrated the shortest median survival (5 months). Improvement in MST was observed for those patients undergoing surgical resection. The presence of lymph node involvement conferred a poorer prognosis. Multivariate analysis of the cohort identified that location, advanced tumor stage, failure to undertake surgical resection, positive lymph node status, and age were all independent predictors of poorer outcome. Conclusion PGIM occurs most often in the oral–nasopharynx and anal canal. Surgical extirpation is the only identifiable treatment modality that significantly improves survival.     

Characterization of acetylcholine-induced membrane hyperpolarization in endothelial cells.

The characteristics of the hyperpolarization response to acetylcholine (ACh) in endothelial cells from the guinea pig coronary artery were studied by microelectrode recording technique. ACh (30 nM to 3 microM) induced membrane hyperpolarization in a dose-dependent manner. The sustenance of the response required the presence of external calcium. The hyperpolarization was not affected by nifedipine (1 microM) but was inhibited by the potassium channel blockers charybdotoxin (10 nM), tetraethylammonium (1 mM), and 4-aminopyridine (0.5 mM). Glibenclamide (10 microM) and apamin (1 microM) were not effective. The inhibitors of endothelium-derived relaxing factor/nitric oxide synthesis N omega-nitro L-arginine (50 microM) and NG-monomethyl L-arginine (30 microM) had no effect on the resting membrane potential or the ACh-induced responses. No hyperpolarization was observed with application of sodium nitroprusside (10 microM) or 8-bromo-cGMP (0.1 microM). Ouabain (10 microM) depolarized the membrane significantly by 5 mV, but the ACh hyperpolarization was not affected. Indomethacin (10 microM) was without effect on the resting membrane potential or the hyperpolarization to ACh. These results show that ACh-induced hyperpolarization is dependent on external calcium and can be inhibited by certain potassium channel blockers. The hyperpolarization response is not mediated by endothelium-derived relaxing factor/nitric oxide, cGMP, a cyclooxygenase product, or stimulation of the Na-K pump.     

Osgood-Schlatter lesion: fracture or tendinitis? Scintigraphic, CT, and MR imaging features.

To determine whether the Osgood-Schlatter lesion (OS) is produced by avulsion fracture or injury to the patellar tendon, all images obtained in 28 cases of OS in 20 patients (16 scintigrams, 34 computed tomographic [CT] scans, and 27 magnetic resonance [MR] images) were retrospectively analyzed. In 21 cases, imaging was performed before and after treatment; in 20 cases, relief from pain was complete at the time of repeat examination. In all patients (100%), abnormal size of the tendon, decreased attenuation, and increase in signal intensity were compatible with the CT and MR imaging appearance of tendinitis. Distended deep infrapatellar bursa was a frequent finding, particularly on MR studies. These abnormalities had partially disappeared at follow-up examination. An ossicle was seen in only nine of 28 cases (32%); in three of seven cases with follow-up, the ossicle remained nonunited to the tibial tuberosity on follow-up studies despite relief from symptoms. This implies that healing of fracture is not essential for relief from symptoms. These results strengthen the argument that in most cases of OS, insult to the tendon and associated soft tissues, rather than avulsion fracture, causes OS.