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Photodynamic therapy (PDT) is a new and promising treatment modality for the treatment of malignant disease. This paper reports the preliminary experience of our group in the use of this therapy for the treatment of tumours arising in the head and neck. The majority of treatments in these cases have used a second generation systemic photosensitizer, weto-tetrahydroxyphenylchlorin (ra-THPC). Two other cases were treated with either Photofrin 2 (a first generation systemic sensitizer) or with the topical photosensitizer, delta-aminolaevulinic acid (8-ALA).The initial results have been encouraging with good clinical responses evident in patients presenting with a variety of differing tumour types. We feel there is now sufficient evidence of the efficacy of this treatment to warrant a multicentre prospective study into the treatment of early head and neck cancer with PDT.

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709pressure produced as a result of rupture of the aneurysm into the tight fascia1 compartment of the psoas and iliacus muscles. The cause of the sciatic palsy was attributed to direct pressure of a common iliac artery aneurysm impinging on the nerve trunks arising from L.V.4, L.V.5, S.V.1, and S.V.2.It is interesting to speculate on the mechanism of the lateral popliteal palsy recorded in our second case. It seems unlikely that direct pressure on the nerve trunks in the pelvis can be held responsible since the medial popliteal component of the sciatic nerve was not involved. Ischaemic neuropathy is rare since nerves receive a blood-supply from several anastomosing vessels. However, the sciatic nerve is supplied by a named vessel, the arteria comitans nervi ischiadici. It is conceivable that sudden occlusion of this vessel by embolism or thrombosis might result in ischaemic damage of vulnerable nerve-fibres, particularly in a limb already the site of extensive peripheral vascular disease. Although it is possible that the lateral popliteal palsy in our second case arose from some other cause, its development in a limb with extensive peripheral vascular disease shortly before the rupture of an abdominal aortic aneurysm makes it very likely that the neurological signs were related to the arterial disease. It is tempting to suggest that the aneurysm produced the peripheral nerve lesion either via ischaemia or pressure and that the consequent foot-drop caused the fall which precipitated aneurysmal rupture.

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