Neurochemical and pharmacological findings
The primary pharmacological treatments for ADHD are methylphenidate (Ritalin) and amphetamine. Both methylphenidate and amphetamines block re-uptake of dopamine and norepinephrine into the pre-synaptic neuron, acting to increase post-synaptic levels of dopamine and norepinephrine. Of these two monoamines, increased availability of dopamine is considered the primary cause for the ameliorative effects of ADHD medications, whereas increased levels of norepinephrine may be efficacious only to the extent that it has downstream, indirect effects on dopamine. The effectiveness of dopamine re-uptake inhibitors in treating the symptoms of ADHD has led to the hypothesis that ADHD may arise from low tonic levels of dopamine (particularly in the fronto-limbic circuitry), but evidence in support of this theory is mixed. Genetics
There are several difficulties when it comes to trying to identify a gene for complex traits such as impulsivity, such as genetic heterogeneity. Another difficulty is that the genes in question might sometimes show incomplete penetrance, "where a given gene variant does not always cause the phenotype". Much of the research on the genetics of impulsivity-related disorders, such as ADHD, is based on family or linkage studies. There are several genes of interest that have been studied in an attempt to find the major genetic contributors to impulsivity. Some of these genes are:

DAT1  is the dopamine transporter gene which is responsible for the active reuptake of dopamine from the neural synapse. DAT1 polymorphisms have been shown to be linked to hyperactivity and ADHD.
After recovery long term stiffness or limited range of motion may occur in some patients. Visible or limited scarring may also occur for patients. References
External links

Textbook of Hallux Valgus and Forefoot Surgery, links to complete text in PDF files