Many clinicians identify EPS with parkinsonian tremor and rigidity, and they will often include (tardive dyskinesia) TD as part of EPS. This definition omits akathisia, which PL believes is the most important type of EPS, as it is associated with suicidality, easily confused with other conditions, and is most highly associated with noncompliance.
A common idea is that there is a relation between acute EPS and future risk of TD, but this appears to be a false assumption. High potency typical neuroleptics do not appear to be more likely to cause TD than low-potency agents. TD is discussed in detail here.
EPS are usually immediate (not delayed, like TD): acute parkinsonian tremor or rigidity, acute dystonia, acute dyskinesias (usually reversible and not progressive to TD), and akathisia.
Of these, parkinsonian tremor and rigidity often elicit the most clinical attention because they are objective and relatively easily observable. Such parkinsonian side effects are responsive to anticholinergic effects. Hence, low potency traditional neuroleptics demonstrate a lower amount of parkinsonian symptoms than high potency agents. Alternatively, anticholinergic drugs, like benztropine (Cogentin), can reduce these parkinsonian effects. On the other hand, those anticholinergic effects cause their own side effects (including dry mouth, constipation, cognitive impairment).
In contrast to parkinsonian side effects, akathisia is more difficult to detect and treat. It is discussed in detail here.