The mechanism that caffeine increases activity by is via antagonizing adenosine A2 A receptors (the standard mechanism of caffeine). Adenosine normally suppresses the effects of dopamine on locomotion (via working in opposition on neuronal excitation  ) in the striatum where A2 A and dopaminergic neurons co-exist, and preventing this suppression with an antagonist increases the effects of dopamine on D2, of which include spontaneous activity and (in rats) rotational behaviour when unilateral lesions are induced in the striatum.   Non-caffeine adenosine antagonists also share this effect on locomotion, further implicating A2A antagonism and dopamine as the cause rather than a separate, unseen effect of caffeine.  As for why A2 A is mentioned more frequently than A1 in this section, it is since A2 A receptors appear to co-exist with dopamine receptors in many parts of the brain (nuclear accumbens, striatum, tuberculum olfactorium) whereas although A1 are heterogeneously expressed in the brain, there is no pattern with dopamine receptors.  Interactions with motor control appear to be highly relevant to the striatum, where A2 A predominates.
These are unwanted effects that you consider are linked to taking a medicine. Side effects also include any effects from: misuse, abuse, an error in the way the medicine has been given or overdose (taking too much medicine). Reports can be made for any medicine (including specials and unlicensed products), any vaccine, herbal product, and complimentary remedies such as homeopathic remedies, blood factors (. factors I to XIII) and immunuloglobulins (. anti-D (RHO) immunoglobulin). You can even report suspected side effects from a drug you think might be happening as a result of interactions with food and drink.