This is a progressive neurodegenerative disease of complex causation though there is a clear genetic basis to a proportion of early onset cases and it is implausible that environmental factors are not relevant. The principal clinical features consist of bradykinesia (slowed movement), rigidity (muscle stiffness), tremor and loss of postural reflexes though other manifestations commonly complicate the course. It is more common with advancing age, usually begins unilaterally, and the main structural pathological change is loss of neurones in the substantia nigra pars compacta with accompanying gliosis and Lewy Body formation. The main neurotransmitter deficit is loss of dopamine in the striatum, which causes increased striatal activity and ultimately the clinical features, via changes in function of both the indirect and direct pathways. Therefore, the treatment of the motor disorder is based on increasing dopamine levels in the brain through the use of L Dopa (which is turned into dopamine in neurones by decarboxylation), eg as the proprietary Sinemet or Madopar, dopamine agonists (which activate dopamine receptors thus mimicking dopamine, eg pramipexole, bromocriptine, ropinirole), or blocking the breakdown of dopamine by the enzyme Catechol-O-Methyltransferase (eg Tasmar).