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Biomedical subjects

M Benatar

Publications and source records attributed to M Benatar.

10 recordsLinked to original sources
PubMed2006

Medical and surgical treatment for ocular myasthenia.

BACKGROUND: Approximately 50% of people with myasthenia gravis present initially with purely ocular symptoms, so called ocular myasthenia and between 50 to 60% of these people will progress to develop generalized disease. The vast majority will do so within the first one to two years. There is controversy surrounding the appropriate management of patients with ocular myasthenia. OBJECTIVES: To perform a systematic review of the literature relevant to the treatment of ocular myasthenia and to answer three specific questions. Are there any medical or surgical treatments that have an impact on the risk of progression from ocular to generalized myasthenia gravis? Are there any medical or surgical treatments that improve symptoms of diplopia or ptosis in ocular myasthenia? What is the frequency of side effects associated with treatments used in people with ocular myasthenia? SEARCH STRATEGY: We searched the Cochrane Neuromuscular Disease Group Trials Register (searched December 2004), MEDLINE (1996 to 2004) and EMBASE (1980 to 2004) for randomized controlled trials as well as case-control and cohort studies. The titles and abstracts of all articles were read by both authors and the full text of all articles that were of possible relevance was reviewed in full. The references of all manuscripts included in the review were scanned to identify additional articles of relevance and experts in the field were contacted to identify additional published and unpublished data. Where necessary and possible, we contacted authors for further information. SELECTION CRITERIA: To be included in the review, studies had to meet three criteria: (a) randomized (or quasi-randomized) controlled study design; (b) active treatment compared to placebo, no treatment or some other treatment; and (c) results reported separately for patients with ocular myasthenia (grade 1) as defined by the Myasthenia Gravis Foundation of America. DATA COLLECTION AND ANALYSIS: We collected data regarding the risk of progression to generalized myasthenia gravis, improvement in ocular symptoms, and the frequency of treatment-related side effects. MAIN RESULTS: We identified two randomized controlled trials relevant to the treatment of ocular myasthenia, only one of which reported results in terms of the pre-specified outcome measures used in this review. This study included only three participants and was of limited methodological quality. In the absence of data from randomized controlled trials, we present a review of the available observational data. AUTHORS' CONCLUSIONS: There are no data from randomized controlled trials on the impact of any form of treatment on the risk of progression from ocular to generalized myasthenia gravis. The available randomized controlled literature does not permit any meaningful conclusions about the efficacy of any form of treatment for ocular myasthenia. Data from several reasonably good quality observational studies suggest that corticosteroids and azathioprine may be beneficial in reducing the risk of progression to generalized myasthenia gravis.

Adrenocorticotropic Hormone↗
PubMed2001

Presynaptic neuronal antigens expressed by a small cell lung carcinoma cell line.

Small cell lung carcinoma (SCLC) is a tumour of neuroendocrine origin often found in association with autoimmune paraneoplastic neurological disorders. We established a SCLC cell line from a woman with Lambert-Eaton myasthenic syndrome (LEMS) who developed antibodies to both the P/Q-type voltage-gated calcium channels (VGCC) and the muscle acetycholine receptor (AChR). We used a range of techniques to establish which neuronal antigens were expressed in her tumour cell line. The results show that many proteins involved in exocytosis are present in the SCLC cells, and that depolarisation-dependent release of [(3)H]-serotonin is linked to calcium influx through P/Q-type VGCCs. In addition, some of the subunits encoding the AChR and both agrin and ARIA, molecules released from the motor nerve during development, were expressed. These results suggest that many potential antigenic targets are present in SCLC, and indicate a surprising 'motor nerve terminal'-like characteristic of this line.

Autoantibodies↗
PubMed2001

A pain in the fetus: toward ending confusion about fetal pain.

Are fetuses, at any stage of their development, capable of feeling pain? In his paper, "Locating the Beginnings of Pain," Stuart Derbyshire argues that they are not. We argue that he reaches this conclusion by way of conceptual confusion, a misreading of the available scientific data and the inclusion of irrelevant data. Despite his assertion to the contrary, the work of most scientists in the area supports the conclusion that fetuses can feel pain. At the outset we examine the concept of pain and distinguish it from the allied concept of nociception, with which it is sometimes confused. With the relevant conceptual framework in place, we elucidate the problem of determining when, in its development, a human becomes capable of feeling pain. We then examine the available data showing how, on balance, it tends more to support than undermine the claim that fetuses of around 28 to 30 weeks' gestation are capable of feeling pain.

Central Nervous System↗
PubMed2000

Neurological potassium channelopathies.

Potassium channel dysfunction has been implicated in a variety of genetic and acquired neurological disorders that are collectively referred to as the potassium channelopathies. These include acquired neuromyotonia, episodic ataxia type-1, hereditary deafness syndromes, benign familial neonatal convulsions and hypokalaemic periodic paralysis. Insight into potassium channel structure and function is crucial to understanding the pathophysiology of these conditions. This article describes potassium channel structure and function and then outlines what is known about the immunology and genetics of the neurological potassium channelopathies.

Epilepsy, Benign Neonatal↗
PubMed1999

Immune-mediated peripheral neuropathies and voltage-gated sodiums channels.

Antibodies to GM1 ganglioside are found in some patients with the Guillain-Barré syndrome and multifocal motor neuropathy, and may alter neuronal excitability. We measured voltage-gated sodium channel (VGSC) function by 22Na+ influx in a motor neuronal cell line (NSC19) in which we demonstrated GM1 ganglioside and tetrodotoxin-sensitive VGSC function. We were unable to detect any effect of peripheral neuropathy plasmas, with or without complement, on VGSC function in NSC19 cells.

Animals↗
PubMed1991

A critical comparison of three methods for measuring dental models.

A critical comparison of three methods for measuring distances between various fiducial points on orthodontic plaster casts is presented. The first method consisted of using a vernier caliper by which direct measurements (Dv) of the distances were recorded. The second method consisted of measuring the same casts using a reflex metrograph (Dm), where the co-ordinates of the points relative to two axes were recorded and the distances between various points were calculated. In the third method, reflection holograms of the casts were made, and the same distances were measured on the holographic images (Dh) using the reflex metrograph. The Wilcoxon sign rank test indicated no significant differences (p greater than 0.1) between measurements made by the various techniques. The means of the different distances scored varied within less than 0.5 mm (Dv-Dh), 0.5mm (Dv-Dm) and 0.2mm Dm-Dh). This study indicated that holograms can provide sufficiently accurate representations of orthodontic study models. Their retention as case records may solve the problem of the storage of orthodontic plaster casts.

Dental Records↗