Bruns in 1890 was the first to recognize the main clinical features of 'diabetic amyotrophy'. The term itself was coined by Hugh Garland in 1955 when he reported 12 elderly patients with type 2 diabetes. The aetiology is controversial, and both ischaemic and metabolic hypotheses have been proposed. The current evidence, however, points to a vasculitic aetiology of ischaemia followed by axonal degeneration and demyelination. The main features of diabetic amyotrophy are weakness, wasting and pain, most commonly in the quadriceps muscle. Though the weakness starts on one side, it almost always spreads to the other side in an asymmetrical manner. Patients also complain of sensory symptoms in the thigh such as severe pain, dysaesthesiae and paraesthesiae. On examination, there is weakness in the involved muscles. Tendon jerks, especially the patellar, are absent. Extensor plantar responses may be elicited in some patients. The course of the disease is variable but good functional improvement can be expected in most patients though weakness, sensory symptoms and absent tendon jerks may persist. Some patients experience multiple episodes of the condition commencing mostly on the opposite side. Conservative treatment constitutes optimizing diabetic control along with active physiotherapy and analgesia. Recently, intravenous immunoglobulins have been found to produce dramatic improvement in both clinical and electrophysiological parameters in patients with diabetic polyradiculopathy.