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Updated: Jul 26, 2026
Controlled Cortical Impact Model for Traumatic Brain Injury
Published on: August 5, 2014
Modulated Neuroprotection in Unresponsive Wakefulness Syndrome after Severe Traumatic Brain Injury
Cristina Daia1,2, Cristian Scheau3, Aura Spinu1,2
1Department of Medical Rehabilitation, "Carol Davila" University of Medicine and Pharmacy, 041914 Bucharest, Romania.
Background:
We aimed to assess the effects of modulated neuroprotection with intermittent administration in patients with unresponsive wakefulness syndrome (UWS) after severe traumatic brain injury (TBI).
Methods:
Retrospective analysis of 60 patients divided into two groups, with and without neuroprotective treatment with Actovegin, Cerebrolysin, pyritinol, L-phosphothreonine, L-glutamine, hydroxocobalamin, alpha-lipoic acid, carotene, DL-α-tocopherol, ascorbic acid, thiamine, pyridoxine, cyanocobalamin, Q 10 coenzyme, and L-carnitine alongside standard treatment.
Main Outcome Measures:
Glasgow Coma Scale (GCS) after TBI, Extended Glasgow Coma Scale (GOS E), Disability Rankin Scale (DRS), Functional Independence Measurement (FIM), and Montreal Cognitive Assessment (MOCA), all assessed at 1, 3, 6, 12, and 24 months after TBI.
Results:
Patients receiving neuroprotective treatment recovered more rapidly from UWS than controls (p = 0.007) passing through a state of minimal consciousness and gradually progressing until the final evaluation (p = 0.000), towards a high cognitive level MOCA = 22 ± 6 points, upper moderate disability GOS-E = 6 ± 1, DRS = 6 ± 4, and an assisted gait, FIM =101 ± 25. The improvement in cognitive and physical functioning was strongly correlated with lower UWS duration (-0.8532) and higher GCS score (0.9803).
Conclusion:
Modulated long-term neuroprotection may be the therapeutic key for patients to overcome UWS after severe TBI.
