There is a family of diabetic neuropathies that mimic the entire spectrum of peripheral neuropathies. Distal sensory neuropathy is the most common. In small-fibre neuropathy, autonomic failure and loss of sense of pain and temperature are prominent. Painfulness is seen in a number of diabetic neuropathies. The asymmetric neuropathies are distinctive and are probably caused by a combination of microvascular and immune-mediated mechanisms. The pathogenesis of diabetic neuropathy is probably multifactorial. Hyperglycaemia is central to any pathogenic scheme whereby nerve blood flow is reduced by an effect on microvessels mediated by perturbations such as oxidative stress, reduction of nitric oxide, prostaglandins and an increase in endothelin. It may also affect nerve fibres directly. Recent clinical trials have clearly demonstrated the importance of strict glycaemic control. There is also support for essential fatty acids, antioxidants and aldose reductase inhibitors. Treatment of diabetic neuropathy is focused on improving glycaemic control and treatment of symptoms. The precise role of other modalities of treatment of diabetic neuropathy remain to be firmly established.