Review of an 11-year Experience in Retrosigmoid Approach for Treatment of Acoustic Neuromas.

This study reviews surgery on acoustic neuromas by the second author using retrosigmoid approach from January 2000 to June 2010 in the state of Sarawak. There was a total of 32 patients in this study. The commonest presenting symptom was hearing loss (81.3%), followed by headache and tinnitus (each 37.5%), ataxia (34.4%) and facial numbness (21.9%). Twenty-seven patients (84.4%) had large tumor (≥ 3cm) while 5 patients (15.6%) had medium size tumor (1.5-2.9cm). The mean tumor size was 3.6 cm. Facial nerve outcome was good to moderate in 93.7% (House and Brackmann Grade I-IV). The most common complications were CSF leak with 3 patients(9.4%) and facial numbness with 2 patients(6.3%). All either resolved with treatment or improved. There was no mortality. Excision of acoustic neuromas using retrosigmoid approach could achieve acceptable facial nerve outcome with a low incidence of morbidity without mortality.

CD45 fraction bone marrow cells as potential delivery vehicles for genetically corrected dystrophin loci.

Targeted correction of mutations in muscle can be delivered by direct i.m. injection of corrective DNA to the dystrophic muscle or by autologous injection of cells that have been genetically corrected after isolation from the individual with the dystrophic muscle. The successful application of chimeraplasty and short fragment homologous replacement to correct the exon 23 nonsense mdx transition at the mouse dys locus has opened up the possibility that with further development, targeted gene correction may have some future application for the treatment of muscular dystrophies. In vitro, application of targeted gene correction at the mdx dys locus results in better correction efficiencies than when applied directly to dystrophic muscle. This suggests that at least for the time being, a strategy involving ex vivo correction may be advantageous over a direct approach for delivery of gene correction to dystrophic muscle. This, particularly in view of recent developments indicating that bone-marrow-derived cells are able to systemically remodel dystrophic muscle, whilst penetration of DNA introduced to muscle is limited to individually injected muscles. Application of targeted gene correction to Duchenne dystrophy needs to account for the fact that about 65% of Duchenne muscular dystrophy cases involve large frame-shift deletion of gene sequence at the dys locus. Traditionally, whilst targeted gene correction is able to restore point mutations entirely, it remains to be seen as to whether a strategy for the 'correction' of frame shift deletions may be engineered successfully. This communication discusses the possibility of applying targeted gene correction to dystrophic muscle in Duchenne dystrophy.