Abstract
Traumatic brain injury (TBI) can result in persistent cognitive, behavioral and emotional deficits. However, the vast majority of patients are not chronically hospitalized; rather they have to manage their disabilities once they are discharged to home. Promoting recovery to pre-injury level is important from a patient care as well as a societal perspective. Electrical neuromodulation is one approach that has shown promise in alleviating symptoms associated with neurological disorders such as in Parkinson’s disease (PD) and epilepsy. Consistent with this perspective, both animal and clinical studies have revealed that TBI alters physiological oscillatory rhythms. More recently several studies demonstrated that low frequency stimulation improves cognitive outcome in models of TBI. Specifically, stimulation of the septohippocampal circuit in the theta frequency entrained oscillations and improved spatial learning following TBI. In order to evaluate the potential of electrical deep brain stimulation for clinical translation we review the basic neurophysiology of oscillations, their role in cognition and how they are changed post-TBI. Furthermore, we highlight several factors for future pre-clinical and clinical studies to consider, with the hope that it will promote a hypothesis driven approach to subsequent experimental designs and ultimately successful translation to improve outcome in patients with TBI.
Highlights
There are an estimated 3.8 million new traumatic brain injury (TBI) cases annually, and well over 5.3 million patients report chronic Traumatic brain injury (TBI)-related deficits (Langlois et al, 2006; DeKosky et al, 2010)
While the latest census estimates over 5.3 million patients live with chronic disability, it is clear that that number has grown and continues to grow
Oscillations are known to play a key role in physiological circuit function, whether it is the progression of oscillations through the sleep cycle or theta oscillations in the hippocampus
Summary
There are an estimated 3.8 million new traumatic brain injury (TBI) cases annually, and well over 5.3 million patients report chronic TBI-related deficits (Langlois et al, 2006; DeKosky et al, 2010). The high concentration of K+ and Ca2+ in the extracellular space triggers release of neurotransmitters (e.g., glutamate), which can further exacerbate the ionic disturbance creating a vicious cycle (Faden et al, 1989; Katayama et al, 1990; Nilsson et al, 1990; Lyeth et al, 1993; Reeves et al, 1997; Shin and Dixon, 2015) This wave of depolarization can lead to excitotoxic cell death beyond what is observed in the injury core and surrounding penumbra (Sullivan et al, 1976; Dixon et al, 1987; Lowenstein et al, 1992; Hicks et al, 1993; Yamaguchi et al, 1996; Leonard et al, 1997; Yakovlev et al, 1997; Floyd et al, 2002; Witgen et al, 2005; Fedor et al, 2010). To this end we will first elaborate on what local field oscillations are and how they are generated in the brain
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