text: rodent models.24,50,53,56 Some 
  nerve injury in experimental 
  studies have suggested that neuron loss occurs in certain patient 
  cohorts,48,66 but this is yet to be definitively demonstrated in 
  humans. In rodents, most studies support a preferential loss of 
  small cells that give rise to unmyelinated fibers53 but some 
  contrasting studies describe the preferential loss of large cells6 or 
  loss of cells of all sizes.46 Variation is evident across studies in 
  terms of experimental species, age, 
  injury, and 
  quantification methods.56 Shi et al.50 used stereological counting 
  methods to identify a 54% loss of DRG neuron number 4 weeks 
  after “mid-thigh” sciatic nerve transection in C57BL/6 mice. 
  Estimates for the degree of loss following commonly used nerve 
  injury paradigms (eg, spared nerve injury [SNI] and sciatic nerve 
  crush) are not available and because of the neurochemical 
  changes following injury and the loss of subpopulation marker 
  gene expression,5,44,50 the vulnerability of molecularly defined 
  subpopulations has not been characterized. Moreover, more 
  recent studies have cast doubt on the extent or even presence of 
  DRG neuron death following nerve injury. One study which 
  developed a deep learning approach to assess rat DRG cellular 
  plasticity found no loss of neurons up to 2 weeks post-SNI,49 
  while another observed no loss of genetically labelled damaged 
  DRG neurons 2 months after sciatic nerve crush.44 
  
  type of 