Lidocaine apparently blocks voltage-gated sodium channels in sensory neurons and thus prevents action potentials, but photoreceptors like rod cells require hyperpolarization (through blockage of its sodium channels) for the neurotransmitter to be released / generator potential set up, so would adding lidocaine to the retinal cells stimulate them? Would it hypothetically make us think there's light even when it's dark?
See Wikipedia for an overview of the signal transduction that occurs in photoreceptor cells.
Briefly, light results in increases in cGMP; cGMP binds a cGMP-gated sodium channel (not a voltage-gated sodium channel) causing the channel to close. Therefore, light -> less sodium entry.
Lidocaine blocks a different type of sodium channel: the fast voltage-gated sodium channels involved in neurotransmission. It's possible there is some cross-reactivity, but it would be entirely coincidental as it's from a completely different family of channels.
In any event, the retina has all sorts of other neuron types: bipolar cells, retinal ganglion cells, and various interneuron types, that all communicate with each other through action potentials mediated by voltage-gated sodium channels. If you were to apply lidocaine to the retina, you'd lose all this neurotransmission.