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SUMMARY Benign laryngeal polyps and normal larynxes have been studied by histochemical and other staining methods. These show that the polyps contain much free hyaluronic acid and 6-chondroitin sulphate. Their mode of production may be the mechanical separation of these compounds from collagen fibres by vibration. An alcian-elastic stain may be a helpful diagnostic method. Received for publication 3 January 1980 who presented with hoarseness of voice was also available.All the polyps had been diagnosed independently as showing characteristic histological features of the lesion, including vascular proliferation, fibrosis, or a myxoid appearance of the underlying stroma.The specimens were all fixed for 24 hours in Lillie's buffered formalin, post-fixed for 16 hours in formol-corrosive, dehydrated in alcohol, cleared in toluene, and embedded in paraffin wax. Sections were cut at 6 /im. Sections were stained by the following methods:9 alcian blue at pH 0-2, 10, and 2-5; alcian blue at pH 2-5 after treatment with hyaluronidase; alcian blue/aldehyde fuchsin and alcian blue/PAS at pH 2-5, and Weigert's elastic stain. Additionally, some sections were stained with Congo red for amyloid and by the martius scarlet blue (MSB) technique for fibrin.

proportion (55/932) of all cases of cerebral palsy in that period. The aetiology of cerebral palsy in low birthweight infants in multiple births is probably similar to that in singletons.In a few cases a cotwin died antenatally, with resulting brain damage in the surviving twin. This is seen in our data and has been known for many years.2 As rates of multiple births are rising it is important to keep monitoring the rates of cerebral palsy in these births.We agree with Judith Glynn and David Leon's comments. It is impossible from our epidemiological data to ascertain when brain damage occurred. We agree that in infants of 1500 g who develop cerebral palsy the sequence could have started antenatally, perinatally, or postnatally and the epidemiological picture would be similar. We recently reviewed this.3In normal birthweight infants it is also likely that there has been a shift from deaths to survivors with cerebral palsy, and possibly from survivors with cerebral palsy to non-handicapped survivors. We still believe that our data, in conjunction with other data to which we referred in our paper, can be interpreted as suggesting that birth asphyxia is not the main cause of cerebral palsy.