Do antipsychotics have a delayed onset of action similar to (monoamine) antidepressants? I've been trying to understand the position of Steve Hyman (a former NIMH director), who has been amply quoted in an recent article in Quartz, saying among ohter things that


  There’s not “an iota of direct evidence” for the theory that a chemical imbalance causes depression.


I looked into Hyman's papers and I found a fairly cited (~500 in Google Scholar) paper of his some 20 years ago in AJP, co-authored with Eric J. Nestler, in which they propose that


  drug-induced neural plasticity [...] underlies the long-term actions of psychotropic drugs in the brain [...] Biological investigation in psychiatry has often focused too narrowly on synaptic pharmacology,
  especially on neurotransmitter turnover and neurotransmitter receptors. A paradigm is presented to help understand the long-term effects of psychotropic drugs, including
  the latency in onset of their therapeutic actions.


The paper further details that


  Acute dosing of the antidepressants
  produces little in the way of subjective or
  behavioral effects (other than side effects). Initial doses
  of the antipsychotic drugs produce subtle motor effects
  or some degree of sedation, and initial doses of the
  stimulants produce euphoria and locomotor activation.
  However, substantial improvement in depressive or
  psychotic symptoms, or the development of addiction
  to psychostimulant drugs, occurs only if the drugs are
  taken at adequate dosage and with adequate frequency
  and chronicity. For example, depressive symptoms
  would not be expected to improve if an antidepressant
  were taken at too low a dose, only occasionally, or for
  too short a period of time.
  
  We therefore conceptualize antidepressant-induced
  increases in synaptic serotonin or norepinephrine, antipsychotic-
  induced blockade of dopamine neurotransmission,
  and cocaine- and amphetamine-induced increases
  in synaptic dopamine as initiating events for longerterm
  changes in neural function. It is the adaptive response
  of the nervous system to adequate repeated perturbations
  mediated through these initial targets that
  produces the therapeutic responses to antidepressants
  or antipsychotic drugs or, in the case of the psychostimulants,
  addiction [...].


I'm somewhat familiar with the slow, cumulative effect of monoamine antidepressants and with the mechanism of addiction. Hyman and Nestler can be probably be forgiven for not anticipating the ketamine-as-fast-antidepressant fervor 20 years later. But what I want to ask here is: 

What is the evidence that anti-psychotics also work in this delayed manner? Is it uncontroversially so?
There seem to be multiple studies generally pointing to a delay of clinical antipsychotic action of these drugs, typically between a week and two weeks (e.g.., Zedkova et al (2011) and Mousavi et al. (2013)). However, there is evidence that antipsychotics may start working after a day, or even within a few hours after starting the meds. See for an interesting review Agid et al. (2006).

From reading these papers my understanding is that a lot of it depends on where the researcher puts the threshold of clinical effectiveness and which outcome measure is used to define that effectiveness. 

References
- Agid et al., J Psychiatry Neurosci (2006); 31(2): 93–100
- Mousavi et al., J Res Pharm Pract (2013); 2(4): 138–44
- Zedkova et al., Neuro Endocrinol Lett (2011); 32(5): 667-70