Rosenthal, Dreskin and Rosenthal (1953) described a familial haemorrhagic disorder due to plasma thromboplastin antecedent (PTA) deficiency. Further studies have established the properties of this factor and its action in the early phase of thromboplastin generation (Rosenthal, 1954; Rosenthal, Dreskin and Rosenthal, 1955; Ramot, Angelopoulos and Singer, 1955; Campbell, Mednikoff and Dameshek, 1957; Cavins and Wall, 1960). The mode of hereditary transmission of this deficiency has been discussed by various authors (Cavins and Wall, 1960; Campbell et al., 1957; Rosenthal et al., 1955). Recently Rapaport, Proctor, Patch and Yettra (1961), using a quantitative assay of PTA, suggested that this deficiency is transmitted by an intermediate gene, which produces major PTA deficiency in the homozygote and minor PTA deficiency in the heterozygote. In the present communication, 10 families with PTA deficiency will be described and the mode of its inheritance will be discussed.

The course of cystoid macular oedema (CMO) following extracapsular cataract extraction with posterior chamber intraocular lens implantation was prospectively studied in 44 eyes of 44 consecutive diabetic patients without preoperative CMO. In 50% of eyes CMO was observed 6 weeks after surgery and in 25% was still present at 1 year. The preoperative presence of diabetic retinopathy significantly affected the postoperative onset and persistence ofCMO. CMO occurred postoperatively in only 32% of eyes without pre-existing diabetic retinopathy and in 81% of eyes with pre-existing diabetic retinopathy (p<005). CMO persisted at 1 year after surgery in only 7% of eyes without pre-existing diabetic retinopathy and in 56% of eyes in which diabetic retinopathy persisted (p<001). Angiographic CMO (that is, detectable only on fluorescein angiography) was more common than clinical CMO (detectable on ophthalmoscopic examination as well) in eyes with no pre-existing diabetic retinopathy, whereas clinical CMO was seen more often than angiographic CMO when diabetic retinopathy was present preoperatively (p<001). The course and final visual outcome of angiographic CMO were more favourable than in clinical CMO. Final visual acuity of at least 6/12 was achieved in 86% of eyes with angiographic CMO and in only 33% of eyes with clinical CMO. On the basis of the above findings we believe that cataract extraction should not be recommended for eyes with pre-existing diabetic retinopathy until the vision has deteriorated to at least 6/30-6/60.

The role of early visual experience in the establishment of human high-order visual areas is poorly understood. Here we investigated this issue using human amblyopia--a developmental visual disorder, which manifests a central vision (acuity) deficit. Previous fMRI studies of amblyopes have described abnormal functional activations in early retinotopic areas. Here we report the surprising finding of a selective object-related abnormality in high-order occipitotemporal cortex. Specifically, we found that face-related cortical areas show a severe disconnection from the amblyopic eye, while building-related regions remain essentially normal. The selectivity of the deficit highlights the differential computations performed in the different object-related areas and is compatible with the suggested association of face regions with analysis of fine detail.

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