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Background Cognitive dysfunction adversely effects multiple functional outcomes and social roles after TBI. We hypothesize that chronic systemic inflammation exacerbates cognitive deficits post-injury and diminishes functional cognition and quality of life (QOL). Yet few studies have examined relationships between inflammation and cognition after TBI. Associations between early chronic serum inflammatory biomarker levels, cognitive outcomes, and QOL 6-months and 12-months after moderate-to-severe TBI were identified using unweighted (uILS) and weighted (wILS) inflammatory load score (ILS) formation. Methods Adults with moderate-to-severe TBI (n ​= ​157) completed neuropsychological testing, the Functional Impairment Measure Cognitive Subscale (FIM-Cog) and self-reported Percent Back to Normal scale 6 months (n ​= ​139) and 12 months (n ​= ​136) post-injury. Serial serum samples were collected 1–3 months post-TBI. Cognitive composite scores were created as equally weighted means of T-scores derived from a multidimensional neuropsychological test battery. Median inflammatory marker levels associated with 6-month and 12-month cognitive composite T-scores (p ​, Highlights • Chronic inflammation influences cognitive dysfunction after traumatic brain injury. • Ridge regression generated stable β-values for novel weighted inflammatory scoring. • Weighted inflammatory scores explain more cognitive variance than unweighted scores. • Systemic inflammatory burden also impacts functional cognition and quality of life.

A previously independent 75-yr-old man developed postoperative intracranial hypotension-associated venous congestion after an elective T10-pelvis fusion, which was complicated by durotomy. Postoperative day 0 magnetic resonance imaging noted symmetric edema of the basal ganglia, thalami, and cerebellar cortex as well as smooth diffuse pachymeningeal enhancement and dural thickening, consistent with postoperative intracranial hypotension-associated venous congestion. On postoperative day 0, patient developed tonic clonic seizures, and on postoperative day 2, patient was unable to follow commands or blink to visual threat, able to track eyes to sound only, and spontaneously moved all limbs. Patient was started on zolpidem 2.5 mg on postoperative day 2, and 12 hrs later, he had significantly improved motor function, arousal, verbalization, and followed simple commands. After three doses, patient was fully alert and oriented with improved mobility and comprehension. Six zolpidem doses were administered in total, and repeat magnetic resonance imaging on postoperative day 16 showed markedly improved regional edema. The patient was admitted to a brain injury inpatient rehabilitation unit and was discharged to home 9 days later with Functional Independence Measure gain of 17. Intracranial hypotension can adversely affect primary mesocircuit structures supporting arousal. Zolpidem, a selective α-1-subunit GABA-A agonist, supports GABAergic tone in these regions. This patient's clinical presentation and recovery paralleled selective basal ganglial-thalamic edema development and resolution.