Ketamine does not increase intracranial pressure in neurologically impaired patients when used with controlled ventilation, a GABA receptor agonist, and without nitrous oxide (level II evidence). Its hemodynamic stimulation may improve cerebral perfusion, making it a preferred sedative after brain injury. In laboratory studies, ketamine shows neuroprotective effects, and S(+)-ketamine may have neuroregenerative effects, even when given after a cerebral insult, though improved outcomes were only seen in studies with brief recovery periods. Large-dose ketamine caused neurotoxic effects in developing animals and certain brain areas of adult rats without injury, but these were prevented by coadministering GABA receptor agonists.
Ketamine can help manage chronic neuropathic pain, which is often undertreated. Intravenous racemic ketamine at 0.5–1.5 mg/kg/day for 4–5 days is recommended as an initial hospital-based approach, providing pain relief lasting 1–3 months. Non-IV administration with de-escalating doses can then be tailored to individual patients, and infusions may be repeated quarterly if necessary. Neurocognitive side effects can cause discomfort or treatment discontinuation, but psychological guidance and GABA-ergic agents can reduce adverse effects. Despite some challenges, the potential benefits often outweigh the risks. Further high-quality trials are urgently needed to refine ketamine use for neuropathic pain.