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About the Authors:
Michael E. Hoffer
Contributed equally to this work with: Michael E. Hoffer, Carey Balaban
* E-mail: [email protected]
Affiliation: Spatial Orientation Center, Department of Otolaryngology, Naval Medical Center San Diego, San Diego, California, United States of America
Carey Balaban
Contributed equally to this work with: Michael E. Hoffer, Carey Balaban
Affiliation: Departments of Otolaryngology, Neurobiology, Communication Sciences and Disorders, and Bioengineering, University of Pittsburgh, Pittsburgh, Pennsylvania, United States of America
Martin D. Slade
Affiliation: Department of Internal Medicine, Yale University, New Haven, Connecticut, United States of America
Jack W. Tsao
Affiliation: Wounded, Ill and Injured Directorate (M9), US Navy Bureau of Medicine and Surgery, Washington, D.C., United States of America
Barry Hoffer
Affiliation: Department of Neurosurgery, Case Western University, Cleveland, Ohio, United States of America
Introduction
Mild traumatic brain injury (mTBI) is the most common injury seen in the current conflicts in Iraq and Afghanistan and an increasingly common injury in modern society. An estimated 19.5–22.8% of all returning deployed troops suffer from mTBI [1]. The most common cause of mTBI is blast exposure from improvised explosive devices (IEDs) or other explosive ordinances. Over the last three decades the mechanisms, characteristics, diagnostic schemes, and treatment strategies for blunt head trauma have been studied extensively. Unfortunately, many of the lessons learned from blunt head trauma cannot be applied automatically to blast injured subjects [2].
Disentangling the neurological features of mTBI from PTSD is important for improving diagnosis and treatment of low-level blast injuries [3]. Many previous studies were conducted well after the actual blast injury and focused on the role of mTBI as a precursor of PTSD [1], [4]. Diagnosis of mTBI requires a documented traumatic event, with a transient loss or alteration of consciousness, accompanied by at least one of a list of neurologic, neurotologic, or cognitive symptoms [5]. One highly prevalent symptom is dizziness, a subjective marker of balance dysfunction.
N-acetylcysteine (NAC) is a logical choice for a field-based clinical trial. NAC is the active agent in Mucomyst, an FDA approved medication with a forty-year safety history. NAC is an effective neuroprotective agent in animal ischemia-reperfusion cerebral stroke models [6], [7], [8], a rodent closed head trauma model [9], a sensory nerve axotomy model [10] and inner ear neuronal death after noise...