text: The question of whether DRG neurons die following traumatic 
  injury has been addressed by several groups over the last few 
  decades. Despite contrasting findings on the extent, timing, and 
  form that loss takes, most studies have observed frank loss of 
  DRG neurons.6,38,46,53 However, more recent studies using 
  recombinase driver lines and novel machine-learning approaches 
  have cast doubt on this consensus.44,49 Our data strongly 
  support the loss hypothesis and suggest that approximately 60% 
  of axotomized afferents die within 2 weeks of SNI. The 
  discrepancy between our findings and other recent studies may 
  be partly explained by the sampling method used to estimate 
  neuronal numbers. For example, Schulte et al.49 developed 
  a novel machine-learning approach and found no reduction in 
  neuron density across serial sections of rat DRG following SNI, 
  and they inferred from this that frank loss did not occur. Our 
  results are congruous, in that we also observed no reduction in 
  neuron density. However, we found a substantial loss in the total 
  neuron-containing volume of injured DRG, which underlies our 
  contrasting conclusion of 
  frank loss. Of note, morphological 
  volumetric analysis and MRI have also previously demonstrated 
  volume loss in both rodent and human DRG following nerve 
  injury.35,65,66 These findings occur despite a major increase of 
  nonneuronal cells in the injured DRG30 and support the notion 
  that the total DRG neuron number is decreased. 