Muscle hypertonia following upper motor neurone lesions (referred to here as 'spasticity') is a common problem in patients with neurological disease, and its management is one of the major challenges in clinical practice. Understanding the pathogenesis and clinical course of spasticity is essential for the effective management of this condition. The hypertonia initially results from increased excitability of the alpha motor neurones due to an imbalance between the excitatory and inhibitory influences of the vestibulospinal and reticulospinal tracts. This is the 'neural component' of muscle hypertonia. However, usually within 3-4 weeks, changes in the structure and mechanical properties of the paralysed muscles and the effect of thixotropy also contribute to the hypertonia. The selection of the optimal treatment option is often influenced by whether the neural or the non-neural component is more pronounced. Muscle spasticity often interferes with motor function or causes distressing symptoms, such as painful muscle spasms. If untreated, spasticity may also lead to soft tissue shortening (fixed contractures). However, spasticity can also be beneficial to patients. For example, despite severe leg muscle weakness, most hemiplegic patients are able to walk because the spasticity of the extensor muscles braces the lower limb in a rigid pillar. Other reported benefits of spasticity include the maintenance of muscle bulk and bone mineral density and possibly a reduced risk of lower limb deep vein thrombosis. Several factors, such as skin pressure sores, faecal impaction, urinary tract infections and stones in the urinary bladder, can aggravate muscle spasticity. These factors should always be looked for as their adequate treatment is often sufficient to reduce muscle tone without the need for specific antispasticity medication. Therefore, a careful evaluation of the patient's symptoms and their impact on function, and the setting of clear and realistic therapy goals are important prerequisites to treatment. The best treatment outcomes are usually achieved when pharmacological and non-pharmacological treatment modalities are used in tandem. Different drugs are available for the management of spasticity, including oral muscle relaxants, anticonvulsant drugs, intrathecal baclofen, cannabis extract, phenol and alcohol (for peripheral nerve blocks) and botulinum toxin injections. Similarly, there is a range of non-pharmacological methods of treatment, e.g. regular muscle stretching, the use of splints and orthoses, electrical stimulation, etc. Although these are not discussed here, this should not detract from the importance of combining them with antispasticity drugs in order to maximize the clinical benefit of treatment.