from the moment of damaging impact on the brain until stabilization of functions or death of the patient
Rehabilitation after traumatic brain injury (TBI):
the role of Mexidol® in restoring cognitive functions
Traumatic brain injury (TBI) is characterized by high mortality and disability rates. According to the WHO, the incidence of TBI is 1.8–5.4 cases per 10,000 population and is growing at an average annual rate of 2%. In Russia, over 600,000 TBIs are observed annually. Most TBI cases occur in individuals of working age [1].
TBI (ICD-10 code S06) is damage to the skull and intracranial contents, including brain matter, brain vessels, cranial nerves and meninges, which is accompanied by clinical symptoms and often morphological changes [2].
Types of TBI 2
Easy
Moderately heavy
Heavy
By severity
Easy -
concussions
Moderate -
mild to moderate brain contusion, epidural-subperiosteal hematomas without brain compression
Heavy -
severe brain contusion, intracranial hematomas with compression, diffuse axonal injury
By the nature of the damage (Glasgow Coma Scale)
Easy -
13–15 points (mild concussion and brain contusion)
Moderate -
9–12 points (moderate brain contusion)
Heavy -
3–8 points (severe brain contusion)
Periods of the course of TBI 2
Acute (2 to 10 weeks)
Intermediate
(2 to 6 months)
(2 to 6 months)
from stabilization of functions to complete or partial recovery.
Remote (up to 2 years)
clinical recovery, rehabilitation of impaired functions, or the emergence and/or progression of new pathological conditions is taking place
The impact of TBI on cognitive function
In the context of severe TBI, mechanical damage to brain cells and blood vessels immediately develops, which triggers a cascade of events including neuroinflammation, neurodegeneration, increased permeability of the blood-brain barrier, microvascular damage to the brain, and severe oxidative stress[1][6].
In the pathogenesis of brain tissue damage in the acute and intermediate periods of TBI, a significant role is played by excessive activation of lipid peroxidation (LPO) processes in cell membranes and, as a consequence, disruption of the structural and functional properties of membranes[5].
After a traumatic brain injury, general weakness, headache, dizziness, slow mental activity, sleep disturbances, anxiety, depression, affective lability, apathy, and autonomic dysfunction are possible[7].
Post-traumatic stress disorder (PTSD) is diagnosed in 20–40% of patients with mild TBI, which can lead to cognitive impairment[1]. More serious consequences are also possible, including impaired comprehension of oral and written language, speech impairment, and memory loss[1].
In children and adolescents, even mild TBI (concussion) cannot be considered a completely reversible phenomenon; it should be considered as a predictor of psychopathological disorders (anxiety, depression, and impaired control of emotions and behavior) [1].
According to MRI/CT data, neurodegenerative changes were detected in the chronic stage of individuals who suffered from severe TBI, mainly in the white matter of the brain[1].
Treatment for TBI
The treatment strategy and prognosis for TBI depend on the severity of the condition and strict adherence to the doctor's recommendations. Early rehabilitation (within the first 3-6 months after the injury) is essential to ensure the fastest possible recovery of lost functions. With mild TBI, full recovery occurs within 3-12 months; with severe TBI, it may take longer due to the development of permanent impairments.
Non-drug rehabilitation methods for TBI include emotional-cognitive rehabilitation (analgosedation, prevention of disturbances and restoration of circadian rhythm, overcoming cognitive-afferent dissonance) and physiotherapy (kinesiotherapy, verticalization, electrical therapy, massage, etc.) [2].
Since there is a direct relationship between the degree of lipid peroxidation activation and the severity of the pathological process, therapy aimed at reducing oxidative stress should be as early and proactive as possible.[3] Antioxidant medications play a significant role in combating cerebral hypoxia.
One of the well-known drugs in this group is Mexidol® (the original ethylmethylhydroxypyridine succinate). Mexidol® exhibits antioxidant, antihypoxic, and membrane-stabilizing pharmacological effects, which constitute its multimodal mechanism of action[3][10].
- It exhibits antioxidant, membrane-protective, antihypoxic and antistress activity, as well as vaso- and rheoprotective effects.
- Reduces oxidative stress and normalizes metabolic processes in the brain.
- Promotes restoration of oxygen and glucose consumption by the brain.
The drug is effective in conservative treatment of TBI. Patients experience faster restoration of the brain's integrative capacity during treatment.
For patients with mild to moderate TBI, sequential therapy with the drug is indicated: initially intramuscularly or intravenously, 5 ml (250 mg) - 10 ml (500 mg) for 15 days, followed by a transition to tablets of 250 mg 3 times a day for 2 months [6]. In severe TBI, the high efficacy and favorable safety profile of Mexidol® in higher doses (up to 1200 mg (24 ml) intravenously by drip for 7-10 days) have been proven [12].
According to MRI/CT data, neurodegenerative changes were detected in the chronic stage of individuals who suffered from severe TBI, mainly in the white matter of the brain [1].
Clinical studies of the drug Mexidol®
- It helps stabilize lipid peroxidation and antioxidant protection of the body, relieve headaches, improve sleep, and normalize blood pressure in patients with TBI [9][14].
- Improves cognitive functions and reduces manifestations of anxiety, which allows for increased adherence to therapy in patients with PTSD after traumatic brain injury [1].
- Helps reduce the severity of endogenous intoxication syndrome in patients with severe TBI [4][6].
- It helps eliminate and prevent cerebral edema, stabilize vital functions and reduce mortality in complex therapy in patients with severe TBI [4].
- It has no side effects, does not cause sleep disturbances or increased seizure readiness [4].
The use of Mexidol® in severe TBI at the pre-hospital stage leads to an improvement in neurological status - an improvement in general cerebral symptoms, restoration of nervous system functions, a decrease in increased intracranial pressure, relief of seizures and neurological symptoms, earlier resolution of post-traumatic encephalopathy and restoration of consciousness are observed.
Against the background of treatment with the drug Mexidol®, a more favorable course of the early post-traumatic period and a reduction in complications were noted [8][11][12][13].
The stated pharmacological properties, high efficiency, rapid onset of therapeutic effect, and favorable safety profile allow the use of Mexidol® in clinical practice in the complex treatment of TBI.
How to take Mexidol® for traumatic brain injury?
Block of articles on this topic
List of literature
- Chuklovina M.L., Chuklovin A.A. Peculiarities of managing patients with traumatic brain injury. S.S. Korsakov Journal of Neurology and Psychiatry. 2021;121(9):119–125.
- Clinical guidelines. Focal brain injury. 2022.
- Shokin M.N., Vlasov A.P., Khovryakov A.V. Clinical and laboratory effect of Mexidol in traumatic brain injury // Bulletin of new medical technologies. 2011. No. 1. Electronic publication.
- Radushkevich V.L. Clinical evaluation of the drug Mexidol in the treatment of severe traumatic brain injury at the stages of medical care. Review // Medical alphabet. Emergency medicine. 2012. No. 1. P. 29–32.
- Savitskaya I.B., Nikonov V.V., Chernov A.V. et al. Efficiency of the drug "Mexidol" in patients with combined traumatic brain injury // Bulletin of Intensive Care. Neuroreanimatology. 2012. No. 3. P. 23–31.
- Chukhlovina M.L. Features of diagnosis and treatment of post-traumatic stress disorder in individuals who suffered mild traumatic brain injury // Neurosurgery. 2011. Vol. III. No. 1. P. 53–56.
- Radushkevich V.L., Tkachenko N.V. Pharmacological and non-pharmacological neuroprotection in severe traumatic brain injury at the prehospital stage // Bulletin of Experimental Biology and Medicine. 2012. Supplement 1. P. 122–127.
- Smirnov V.O., Smirnova O.B. Corrective effect of Mexidol on the dynamics of polypeptide and antioxidant enzymes in post-traumatic syndrome // Bulletin of Experimental Biology and Medicine. 2012. Appendix 1. P. 213–214.
- Instructions for medical use of the medicinal product Mexidol. 2024.
- Trukhanova I.G., Tsybin A.V. Experience of using Mexidol in providing prehospital care to patients with acute cerebrovascular accident and traumatic brain injury // Bulletin of Experimental Biology and Medicine. 2012. Appendix 1. P. 118–121.
- Govorova N.V. Oxidative stress and its drug correction with Mexidol in traumatic brain injury // Emergency medical care. 2013. No. 2. P. 36–40.
- Radushkevich V.L., Okunevsky A.I. Neuroprotection in cerebral accidents at the stage of emergency medical care // Medical alphabet. Emergency medicine. 2017. Vol. 1. No. 19. P. 11–15.
- Abramova E.A., Voennov O.V., Boyarinov G.A., Trofimov A.O. Cerebral circulation and metabolism in victims with traumatic brain injury // General reanimatology. 2018. Vol. 14. No. 1. P. 4–11.
THE INFORMATION IS INTENDED FOR HEALTHCARE AND PHARMACEUTICAL PROFESSIONALS. THIS INFORMATION IS NOT INTENDED AS A SUBSTITUTE FOR MEDICAL ADVICE.
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