Chemical weapons including nerve agents pose an ongoing issue in global conflicts, terrorism, and assassination plots. The current treatment protocol against nerve agents include atropine sulfate, HI-6 oxime, and benzodiazepine, which have been successful in prolonging survival after nerve agent exposure. However, the treatments are unable to prevent neurological damage associated with nerve agent-induced seizures. The objective of this thesis is to use imaging modalities to improve our understanding of the physiological and structural changes in the brain following a sub-lethal dose of nerve agent (soman) exposure. First, we investigated changes in oxygenation using chronically implanted oxygen sensors in awake and freely moving rats. We were able to measure oxygenation before, during, and after soman exposure. We found distinct oxygen profiles that oscillated based on seizure onset, which may be due to abnormal hemodynamics. Additionally, hyperoxygenation was detected during status epilepticus and remained elevated at 24 hours. Next, in order to validate the results, we measured cerebral blood flow using continuous arterial spin labelling (CASL) MRI. We found global hypoperfusion at 1 hour and hypoperfusion in the piriform network at 18-24 hours in isoflurane anaesthetized rats. Following this, we combined a way to simultaneously measure cerebral blood flow using CASL MRI and oxygenation using oxygen sensors in isoflurane anaesthetized rats. Here, we found hypoperfusion but normoxia in the cortex, suggesting a decrease in metabolism. Further investigation of whether changes are due to neurological damage was explored by correlating quantitative T2 (qT2) MRI to a histological marker of neurodegeneration. No changes in qT2 or neurodegeneration was found at 1 hour after soman, suggesting hypoperfusion and hypometabolism may be mediated through oxidative stress. At 18-24 hours after soman exposure, changes in qT2 MRI correlated with neurodegenerative markers, with the strongest correlation being in the piriform cortex. This suggests hypoperfusion in the piriform network at 18-24 hours, which may be the result of damage to the neurovascular unit. Overall, this thesis identifies impairment of vasodynamics following soman exposure as a potential therapeutic target and the use of qT2 MRI to guide efficacy of these therapies.