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  • Trigeminal Nerve Stimulation as a Novel Therapy for Traumatic Brain Injury

    Final Number:
    742

    Authors:
    Chunyan Li; Eugene Golanov MD, PhD; Neal Mehan MD; Raj K. Narayan MD, FACS

    Study Design:
    Laboratory Investigation

    Subject Category:

    Meeting: Congress of Neurological Surgeons 2015 Annual Meeting

    Introduction: Despite the tremendous efforts to modulate the secondary damage for traumatic brain injury (TBI), pharmacological agents have yielded disappointing results. Recent studies have shown that activation of parasympathetic system through electrical stimulation of the vagus nerve can improve the prognosis of TBI. Trigeminal nerve stimulation (TNS) is conceptually allied with vagus nerve stimulation, but has the advantage of being able to be employed non-invasively. We hypothesized that TNS can modulate parasympathetic, sympathetic and respiratory systems, which will ameliorate TBI induced consequences and can be used as a therapeutic intervention.

    Methods: A controlled cortical impact model was used to create severe TBI in male Sprague-Dawley rats. Electrical stimulation of the trigeminal nerve was performed by introducing two needles (23 ga) subcutaneously bilaterally at imaginary lines connecting ear and eye. Rectangular cathodal pulses (0.5ms, 25Hz, 10V) were delivered by electrical stimulator for 60 minutes. Mean arterial blood pressure (MAP), pulse pressure (PP), and respiration rate were measured by using pressure transducer. Brain edema, blood brain barrier (BBB) permeability, and lesion volume were measured 24 h after TBI. Levles of TNF and IL-6 were determined 4 h after TBI.

    Results: During the stimulation, MAP (81±9 vs. 102±11 mmHg) and PP (11±6 vs. 27±8 mmHg) increased significantly (n=5, p<0.05); while respiration rate (43±5 vs. 29±7 per min) decreased compared to TBI rats (n=4). TBI produced brain lesion accompanied by brain edema and increase of BBB permeability. After TNS treatment, there was a 2.9% decrease in brain edema, 56% decrease in BBB permeability, and 40% decrease in lesion volume (table). TNS also resulted in attenuation of inflammatory responses (TNF 200.1 vs. 147.8 pg/mg; IL-6 234.0 vs. 177.0 pg/ml; n=6, p<0.05 TBI vs. TBI with TNS).

    Conclusions: The data demonstrate that trigeminal nerve activation can offer a novel treatment of TBI by activation of endogenous neuroprotective mechanisms.

    Patient Care: Trigeminal nerve stimulation can modulate parasympathetic, sympathetic and respiratory systems, which will ameliorate traumatic brain injury induced consequences and can be used as a therapeutic intervention.

    Learning Objectives: 1. Factors contributing to pathophysiology of severe traumatic brain injury 2. Effects of trigeminal nerve stimulation 3. Understanding the endogenous neuroprotective mechanisms

    References:

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