Injury can lead to devastating and often untreatable chronic pain. While acute pain perception (nociception) evolved over 500 million years ago, virtually nothing is known about the molecular origin of chronic pain. Here we provide the first evidence that nerve injury leads to chronic neuropathic sensitisation (allodynia) in insects. Mechanistically, peripheral nerve injury triggers an excitotoxic loss of central inhibition that drives escape circuit plasticity and neuropathic allodynia. At the molecular level, excitotoxic signalling within GABAergic neurons required the acetylcholine receptor nAChRα1 and lead to caspase-dependent death of GABAergic neurons. Conversely, disruption of GABA signaling on primary nociceptive sensory neurons was sufficient to trigger allodynia without injury. Finally, we screened for neuronal excitotoxicity death genes and identified the conserved basic helix-loop-helix transcription factor twist as a critical downstream regulator driving caspase activation, GABAergic cell death, escape circuit plasticity, and neuropathic allodynia. Together, we define how injury leads to allodynia in insects, and suggest that a primordial precursor to neuropathic pain may have been advantageous, protecting animals after serious injury.