Of the listed answers, single photon emission computed tomography (SPECT) is the most sensitive imaging modality to diagnose spondylolysis when AP and lateral radiographs are normal. Initial imaging studies should first include AP and lateral radiographs, which demonstrate 80% of defects, and oblique radiographs which demonstrate an additional 15% of defects. If no lesion is seen on plain radiogaphs, SPECT can be considered as a diagnostic study. Conventional lumbar spine MRI techniques are valuable for demonstrating normality of the pars, but may be associated with a high false positive rate for the diagnosis of pars defects.
The cited reference by Gregory et al. showed that single photon emission computerized tomography can be an effective tool to diagnosis spondylolysis in young patients with back pain.
Illustration A, B, and C demonstrate single photon emission computed tomography images in a patient with spondylolysis.
The mechanism responsible for sensitization of the central nervous system at the level of the spinal cord is different from the one in the thalamus. Tumor necrosis factor-alpha (TNF-alpha) and its receptor are the molecules that seem to be responsible for the sensitization of neurons in the dorsal horns of the spinal cord. Macrophages and lymphocytes infiltrate the spinal cord, for example, because of injury, and release TNF-alpha and other pro-inflammatory molecules.  TNF-alpha then binds to the TNF receptors expressed on nociceptors, activating the MAPK / NF-kappa B pathways. This leads to the production of more TNF-alpha, its release, and binding to the receptors on the cells that released it ( autocrine signalling ).  This mechanism also explains the perpetuation of sensitization and thus allodynia. TNF-alpha might also increase the number of AMPA receptors , and decrease the numbers of GABA receptors on the membrane of nociceptors, both of which could change the nociceptors in a way that allows for their easier activation.  Another outcome of the increased TNF-alpha is the release of PGE 2 , with a mechanism and effect similar to the ones in the thalamus. 
In addition, the 2010 JSAP research suggested that there may be a "failure of communication" between the paraxial mesoderm * and the cranial somites ** with the closing neural tube *** in the embryo, resulting in loss of coordination between the growth of the skull and the hindbrain. When functioning properly, the growth of the mesoderm supports and helps to facilitate the closure process of the neural tube. They concluded that overgrowth of the cerebellum in the embryo may cause the mis-match, because cavaliers have proportionately more hindbrain volume than other small breed dogs. They stated: "Early growth plate closure may result in CM because despite the dynamic nature of osseous tissue, it would be unable to accommodate the developing brain."