This occurs when a mutation at the target-site of the insecticide results in occlusion, due to steric or electronic hindrance.
As an example we can look at the mutation that occurs in the peach-potato aphid, Myzus persicae, where a single mutation results in resistance to pirimicarb.

In the native protein (above), pirimicarb would bind to Serine 204 fitting in to the gap between this and the Serine 333 residue; a space of around 11 angstroms.

In the mutated protein, Serine 333 is replaced by a phenylalanine. The aromatic ring of this residue projects into the space to be occupied by pirimicarb, reducing the distance from 11 to around 7 angstroms. This reduction in the available space prevents the insecticide binding to the active site of the protein, resulting in a loss of inhibition.

This mutation only results in resistance to pirimicarb, and generally target-site resistance is fairly specific. For this reason it is suggested that insecticides are rotated i.e. different chemical classes of insecticide are used against pests through the year.