A theory of CP must be able to explain:

1. its idiosyncratic character, i.e., why it arises only in some individuals and not in others with apparently identical lesions;

2. its immediate or delayed (even for years) onset;

3. why both a small lesion of the dorsal horn of the spinal cord or a huge infarct of the parietal cortex can equally trigger CP;

4. its continuous, spontaneous nature in the vast majority of patients, but also its evoked components (allodynia, hyperalgesia) – which, in some instances, can be the only or opening symptom, plus radiation and prolonged aftersensations;

5. its many different qualities, even simultaneously (including dysesthesias and pruritus);

6. referral to superficial and/or deep structures;

7. pain intensity fluctuations, from day to day or month to month, for no obvious reason and increases by both somatic stimuli and emotion;

8. constant somatotopical referral of pain to areas of sensory loss;

9. differential response of patients with apparently identical lesions, i.e., of the same size, site and nature, to some treatments but not others.

In the end, the winning theory is the one that leads to a cure. In this sense, all past and present theories fail.