680 thickened. Paraffin sections with conventional stains showed no abnormality of the mucosa, submucosa, and muscle coats; the myenteric plexus was identified, containing scanty neurones and showing some fibrosis but no inflammatory infiltrate. Detailed study of the myenteric plexus was carried out using the specific technique advocated by Smith.6 Thick sections from formalin-fixed material were cut parallel to the bowel lumen and stained with Bielchowsky’s silver stain. Sections from a control of normal small bowel were prepared in a similar way. Severe damage to the myenteric plexus was demonstrated. The neurones were reduced in numbers and displayed degenerative changes such as retraction and vacuolisation of the cytoplasm as well as misshapen and fragmented dendrites. There was considerable increase in Schwann cells. Detailed neuropathological study in c.i.i.p. is not of merely academic interest. If myenteric plexus damage can be demonstrated at the time of their first operation, patients with recurrent episodes of C.L.P. may be treated conservatively and repeated laparotomies may be avoided. If clinicians and pathologists specifically look for damage to the myenteric plexus in cases of c.i.i.p., this might provide some insight into the pathogenesis of the C.I.I.P. syndrome. Institut Jean Godinot, 51100 Reims, France

W. V. BOGOMOLETZ

Centre Hospitalier Regional, Reims

P. BIREMBAUT D. GAILLARD D. DUPOUY

Hopital Broussais,

J. P. CAMILLERI

chemical markers of Reye’s syndrome appeared (blood-sugar 0-4 mmol/1, plasma-ammonia 500 umol/l; alanine aminotransferase 259 i.u./l, aspartate aminotransferase 303 t.u./1 [reference ranges