Effects of sensory stimulation on level of consciousness in comatose patients after traumatic brain injury: A systematic review

2021 ◽  
Vol 41 (2) ◽  
pp. 143-153
Author(s):  
Anas R. Alashram ◽  
Giuseppe Annino ◽  
Salameh Aldajah ◽  
Sakher Bani Hamad ◽  
Besan Aliswed ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Brain Plasticity ◽  
Experimental Studies ◽  
Sensory Stimulation ◽  
Controlled Trials ◽  
Sample Sizes ◽  
Pilot Studies ◽  
Level Of Consciousness ◽  
Treatment Dosage

BACKGROUND: A coma is a prolonged unconscious state in which there is no response to various stimuli. In response, sensory stimulation was designed to stimulate brain plasticity and to promote brain regeneration. The effects of sensory stimulation intervention on comatose patients following traumatic brain injury (TBI) remain unclear. OBJECTIVES: This study aimed to examine the effects of sensory stimulation on the level of consciousness (LOC) after TBI and to identify the effective treatment dosage. METHODS: We searched PubMed, REHABDATA, EMBASE, CINAHL, MEDLINE, PEDro, SCOPUS, and Web of Science from inception to February 2020. Experimental studies investigating the influence of sensory stimulation on the LOC in the comatose patients (Glasgow coma scale < 8) following TBI were selected. The Physiotherapy Evidence Database scale (PEDro) was used to evaluate the methodological quality. RESULTS: Eleven studies met the inclusion criteria. Six were randomized controlled trials (RCTs), clinical controlled trials (CCTs) (n = 2), and pilot studies (n = 3). A total of 356 comatose patients (<8 on GCS) post-TBI were included in this study with sample sizes ranging from 5–90 patients. The sample sizes for the selected studies ranged from 5 to 90 patients. The scores on the PEDro scale ranged from three to eight, with a median score of seven. The multimodal sensory stimulation showed beneficial effects on the LOC in the comatose patients following TBI. The evidence for the effects of unimodal stimulation was limited, while the optimal treatment dosage remains unclear. CONCLUSIONS: The multimodal sensory stimulation intervention improves the LOC in patients with coma after TBI compared with unimodal stimulation. Further high-quality studies are needed to verify these findings.

Autonomic reactivity to sensory stimulation is related to consciousness level after severe traumatic brain injury

2006 ◽  
Vol 117 (8) ◽  
pp. 1794-1807 ◽  
Author(s):  
Viona J.M. Wijnen ◽  
Matagne Heutink ◽  
Geert J.M. van Boxtel ◽  
Henk J. Eilander ◽  
Beatrice de Gelder
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Severe Traumatic Brain Injury ◽  
Sensory Stimulation ◽  
Autonomic Reactivity ◽  
Consciousness Level

scholarly journals Steroids for delayed cerebral edema after traumatic brain injury

2021 ◽  
Vol 12 ◽  
pp. 46
Author(s):  
G. Lakshmi Prasad
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Brain Edema ◽  
Cerebral Edema ◽  
Head Injuries ◽  
Experimental Studies ◽  
Symptomatic Improvement ◽  
High Dose ◽  
The Mean ◽  
Key Aspects

Background: Brain edema is a common phenomenon after traumatic brain injury (TBI) resulting in increased intracranial pressure and subsequent neurological deterioration. Experimental studies have proven that brain edema is biphasic (cytotoxic followed by vasogenic). Till date, all studies, including the corticosteroid randomization after significant head injury (HI) trial, have used high-dose steroids in the acute period during which the edema is essentially cytotoxic in nature. No clinical data exist pertaining to delayed cerebral edema (vasogenic) and steroids. Methods: Patients who had received steroids for delayed cerebral edema after TBI were retrospectively analyzed over a 2-year period. Steroid dose, timing of steroid prescription, time to improvement of symptoms, and complications were noted. Results: There were six males and three females. Mean age was 41.1 years. There were no severe HI cases. All subjects had cerebral contusions on imaging. Dexamethasone was the preferred steroid starting with 12 mg/day and tapered in 5–7 days. The mean interval to steroid administration after trauma was 7 days. The mean duration of steroid prescription was 6.3 days. All patients had complete symptomatic improvement. The mean time to symptom resolution was 3.8 days. No patients experienced any complications pertinent to steroid usage. Conclusion: This is the first study to document efficacy of steroids for delayed cerebral edema after TBI, at least in mild/moderate head injuries. The timing of steroid usage and dose of steroids is key aspects that might determine its efficacy in TBI which was the drawbacks of the previous studies. Future prospective trials with the above factors in consideration may confirm/refute above findings.

Role of Decompressive Craniectomy in Traumatic Brain Injury – A Meta-analysis of Randomized Controlled Trials

2019 ◽  
Vol 67 (5) ◽  
pp. 1225 ◽  
Author(s):  
Kanwaljeet Garg ◽  
PreetM Singh ◽  
Raghav Singla ◽  
Ankita Aggarwal ◽  
Anuradha Borle ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Randomized Controlled Trials ◽  
Decompressive Craniectomy ◽  
Meta Analysis ◽  
Controlled Trials ◽  
Randomized Controlled

scholarly journals Reduction of Traumatic Brain Damage by Tspo Ligand Etifoxine

2019 ◽  
Vol 20 (11) ◽  
pp. 2639 ◽  
Author(s):  
Mona Shehadeh ◽  
Eilam Palzur ◽  
Liat Apel ◽  
Jean Francois Soustiel
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Neuronal Damage ◽  
Neuroprotective Effect ◽  
Experimental Studies ◽  
Potential Effect ◽  
Translocator Protein ◽  
Male Rats ◽  
Lesion Volume ◽  
Sprague Dawley

Experimental studies have shown that ligands of the 18 kDa translocator protein can reduce neuronal damage induced by traumatic brain injury by protecting mitochondria and preventing metabolic crisis. Etifoxine, an anxiolytic drug and 18 kDa translocator protein ligand, has shown beneficial effects in the models of peripheral nerve neuropathy. The present study investigates the potential effect of etifoxine as a neuroprotective agent in traumatic brain injury (TBI). For this purpose, the effect of etifoxine on lesion volume and modified neurological severity score at 4 weeks was tested in Sprague–Dawley adult male rats submitted to cortical impact contusion. Effects of etifoxine treatment on neuronal survival and apoptosis were also assessed by immune stains in the perilesional area. Etifoxine induced a significant reduction in the lesion volume compared to nontreated animals in a dose-dependent fashion with a similar effect on neurological outcome at four weeks that correlated with enhanced neuron survival and reduced apoptotic activity. These results are consistent with the neuroprotective effect of etifoxine in TBI that may justify further translational research.

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