What determines whether sensitization or desensitization occurs? I am familiar with desensitization. For example, if you are afraid of driving, driving every day will eventually reduce your fear, desensitizing you.

But today I came across another concept, that of sensitization.  I looked up the wiki article on Sensitization, which says at the end,


  Sensitization may also contribute to psychological disorders such as post-traumatic stress disorder, panic anxiety and mood disorders.


So which is it then? What determines whether repeated exposure to something sensitizes someone or desensitizes them? With the example of PTSD, for instance, should not repeated exposure to war actually desensitize people?

I searched google scholar but could not find a paper that discusses both sensitization and desensitization.  Mostly discuss the latter, in terms of reducing fears.  

Appreciate any references or books that might help me understand this.  

Thanks you.
The terminology in this area can be a source of confusion because sensitization is not usually meant as the opposite of desensitization but of habituation. E.g., Blumstein (2016)


  People have written about habituation, a process that leads to decreased responsiveness to a stimulus, as
  well as its counterpart, sensitization, or an increased responsiveness to a stimulus, for over 2000 years.


So what's desensitization then? Well...

Systematic desensitization is basically an extinction procedure for (assumed) previously conditioned stimuli:


  Behavior therapy employs interventions based on classical and operant conditioning. An early example is Wolpe’s (1954) systematic desensitization in which patients are taught progressive relaxation techniques and then are systematically exposed to stimuli that elicit fear while in a relaxed state. Because the relaxation response is incompatible with anxiety, it weakens the learned association between a stimulus and an anxiety response. 


And desensitization is often taken to mean the roughly the same as the systematic one, e.g. Clay (2007):


  Desensitization is generally described as a process by which the active pairing of a positive reinforcer with a negative event causes the negative event to slowly lose its ability to adversely influence behavior (Chance, P., 2003). This active process is also called counter-conditioning. Systematic desensitization has been used successfully to treat human phobias, such as fear of flying, fear of public speaking, and fear of spiders, and has also been used to reduce the intensity of Post-Traumatic Stress Disorder in veterans of the Vietnam War (Chance, P., 2003). For animals, a similarly competing response could be eating. Using competing responses to interfere with a fearful response is an integral part of the systematic desensitization process as defined by Wolpe (1958, as cited by Callen, E.J., &amp; Boyd, T.L., 1990).


To add to this confusion, some mean by sensitization only the conditioned version, e.g.


  Sensitization occurs when a reaction to a stimulus causes an increased reaction to a second stimulus. It is essentially an exaggerated startle response and is often seen in trauma survivors.


But this is actually not that wrong, because unlike for habituation, it's hard to come up with many examples of unconditioned sensitization, e.g. what does Blumstein give (for both)?


  Habituation is a process that leads to decreased responsiveness
  to a stimulus with repeated presentation and is often adaptive in
  that it makes it less likely that individuals will respond to harmless
  stimuli. Found throughout the animal kingdom, some plants have
  also been shown to habituate (Jensen, Dill, &amp; Cahill, 2011). However,
  habituation may also have consequences. Aesop recognized
  the consequences of habitation 2500 years ago when he noted that
  the boy who cried wolf would ultimately be ignored when he
  needed help to fend off a real wolf.    
  
  Habituation's counterpart is sensitization--the increased
  responsiveness to a stimulus with repeated presentation. Sensitization
  may be adaptive if it helps animals avoid potentially risky or
  costly situations. Being sensitized to the sound of bees may help
  elephants avoid getting their sensitive trunks stung (sensu King,
  Douglas-Hamilton, &amp; Vollrath, 2007), and may help allergic
  humans avoid an anaphylactic reaction. But it too may be costly. For
  instance, while drug addiction is usually thought to involve some
  degree of tolerance to drugs, indeed, it also involves sensitized
  responses that can be used diagnostically because greater salience
  is attached to the drugs and drug-associated cues (Steketee &amp;
  Kalivas, 2011). Living without risk is impossible (Sagarin et al.,
  2010), and the public may become sensitized to real or manufactured
  threats repeated by the press (e.g. consider the U.S. government
  assertions that Iraq had weapons of mass destruction, or the
  American response to Ebola cases being treated in the United States
  in September--November 2014). Over-reacting to risk can lead to
  costly foreign policy mis-steps and costly public health responses.


Somewhat more interesting examples are given by Çevik (2014)


  The signal value of a stimulus is correlated with its potential to support responsiveness, which for a given set of physical parameters depends largely on the history of non-associative learning, i.e., habituation and sensitization for the stimulus. Habituation refers to the reduction in the probability or amplitude of responding that is observed upon inconsequential stimulus repetition. For example, repeated delivery of an odor at constant inter-stimulus-intervals (ISI) would eventually lead to the habituation of the response that is initially triggered by the odor. I say eventually, because depending on the parameters of the stimulation protocol (e.g., odor concentration, frequency of odor presentation), a temporary increment in responsiveness might initially be observed. If, however, an appetitive gustatory stimulus (e.g., sugar) is repeated with the same ISI, depending again on the concentration of sugar, frequency of stimulation, and the physiological state of the organism, this protocol is likely to result in an increment in the probability of responding, i.e., sensitization. Finally if odor and sugar are paired instead of being presented separately, the standard paradigm for Pavlovian conditioning would ensue, where the two stimuli would now be termed conditioned (CS) and unconditioned stimuli (US), respectively. Hence, associative learning can be suggested to entail an evasion from habituation for the CS as it signals the arrival of a sensitizing event, the US, and a conditioned response (CR) would then be triggered during the CS in anticipation of the US.


And he actually proposes some general rules:


  habituation might be the default fate for most stimuli in the absence of top-down modulation (although see Horn and Hinde, 1970 for examples of non-habituating reflexes). [...]
  
  the likelihood of habituation, i.e., the inability of a perceivable stimulus to control behavior is higher for distal stimuli, whereas the likelihood of sensitization is higher for stimuli that come into direct contact with the body to activate gustatory and/or mechanoreceptors. 


Although his rules are derived from research on flies.



The wiki sensitization page you mention doesn't talk of PTSD as far as I can tell.

From what I know of PTSD research in this area, it involves conditioned stimuli, e.g. a fairly cited paper in this line, Orr et al.:


  Differential conditioning was assessed in 15 medication-free individuals meeting Diagnostic and Statistical Manual of Mental Disorders (4th ed.; American Psychiatric Association, 1994) criteria for chronic posttraumatic stress disorder (PTSD) and 18 trauma-exposed individuals who never developed PTSD (non-PTSD). Conditioned stimuli (CSs) were colored circles, and the unconditioned stimulus was a "highly annoying" electrical stimulus. Individuals with PTSD had higher resting heart rate (HR) and skin conductance (SC) levels and produced larger SC orienting responses. During conditioning, the PTSD group showed larger differential SC, HR, and electromyogram responses to the reinforced vs. nonreinforced stimuli (CS+ vs. CS-) compared with the non-PTSD group. Only PTSD participants continued to show differential SC responses to CS+ vs. CS- during extinction trials. Results suggest that individuals with PTSD have higher sympathetic nervous system arousal at the time of conditioning and are more conditionable than trauma-exposed individuals without PTSD.


In that paper, PTSD patients were harder to de-condition or "desensitize" to use your terminology (see the sentence about extinction in the abstract I quoted above); PTSD patients also showed increased responses (compared to controls) to conditioned stimuli after conditioning took place, although as far as I can tell they were not easier to "sensitize"/condition, at least in that experiment.

The interaction between conditioned and unconditioned exposures to a stressful stimulus is fairly complex (even in animal [models]) and assumed to be of importance in PTSD. It's been known for a long time (Rescorla, 1974) that giving stronger unconditioned footshocks to rats increases their conditioned response to moderate footshock. So this is a kind of sensitization when conditional and unconditional effects interact. A more recent line of work on this interaction:


  Rats presented with a single session of repeated
  painful footshocks normally express a robust and persistent
  associative fear of the training context (Gale et al., 2004; Poulos
  et al., 2009), whereas subsequent new fear learning to a single
  footshock of the same intensity becomes sensitized to a newly
  trained context or a tone (Rau et al., 2005). We call this phenomenon
  stress-enhanced fear learning (SEFL). Pharmacologically
  induced (NMDA antagonism) and naturally occurring (preweaned
  pups) amnesia of the repeated footshock context fail to disrupt this
  sensitized fear learning (Rau et al., 2005; Long &amp; Fanselow, 2012;
  Poulos et al., 2013). These results suggest that prior exposure to a
  repeated footshock stress, independent of a contextual fear memory,
  enhances subsequent fear learning when footshock intensity is
  held constant. Further evidence that stress influences future learning
  and does not produce its effect by generalization between the
  stress and conditioning contexts is that SEFL only occurs when the
  stress occurs prior to the one-trial fear conditioning (Rau et al.,
  2005). [...]
  
  SEFL would be a particularly problematic component of posttrauma behavior if intense
  stress results in substantial fear conditioning under conditions that would not normally support conditioning.
  Therefore, we determined if SEFL occurred when the conditioning shock was substantially
  milder than the SEFL-inducing shock. The results indicate that exposure to a sensitizing regimen of shock
  can convert a mild footshock that normally does not support measurable levels of fear conditioning into
  one that causes substantial learned fear. Moreover, as the intensity of single footshock increases, so does
  the capacity of the prior stressor to contribute to the sensitization of fear responses.