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"A Possible Role of Altered Vestibular Function in Symptoms of Vertigo, Dizziness and Disequilibrium among US Veterans with Posttraumatic Stress Disorder"

Yaa Haber
Cell Biology, Neuroscience and Physiology Program
MBS, 2010, University of Medicine and Dentistry of New Jersey, NJ
B.S. 2007, University of Maryland College Park, College Park, MD

Thesis Advisor: Jorge Serrador, PhD
Associate Professor
Department of Pharmacology and Physiology

Thesis Advisor: Helena Chandler, PhD
Deputy Director
War Related Illness Injury Study Center
NJ VA Healthcare System

Thursday, October 19, 2017
Cancer Center, G-1196


Posttraumatic Stress Disorder (PTSD) is an anxiety disorder that is highly prevalent in combat exposed Veterans, and has been classically described by psychological symptoms of hyperarousal, avoidance and intrusive thoughts. However recent evidence suggests that patients with PTSD also experience dizziness, disorientation, vertigo and avoid visually challenging environments such as grocery stores and shopping malls. These symptoms are not unique to PTSD and have also been identified in another population group, namely patients with vestibular disorders. The vestibular system is located within the inner ear and is comprised of sensory organs that detect forces of gravity and rotation. Dysfunction of the vestibular system leads to symptoms of dizziness, disorientation and vertigo and such patients also avoid environments that worsen their symptoms. Although there are similarities between the physical symptoms of PTSD and patients with vestibular disorders, there is a knowledge gap regarding vestibular function in PTSD. The goals of this thesis include the following a) identify if there is evidence for vestibular symptom reports in a sample of veterans who may or may not have PTSD; b) determine if there is evidence for any altered vestibular function in PTSD c) identify if altered cerebellar control of vestibular reflexes may explain altered vestibular function in PTSD.

We used validated clinical tools to assess PTSD and vertigo. We compared the responses between our two groups, namely veterans with and without PTSD. Our second goal was to determine if there was any evidence for altered central or peripheral vestibular function. The peripheral component was primarily measured using the Bilateral roll tilt test and vestibular evoked myogenic potential test. Canal function was assessed both directly using the Video Head Impulse Test and by quantifying the time constant of the slow phase velocity of nystagmus. Lastly we measured the cerebellar control of the vestibular system by assessing the magnitude of the suppression of the vestibular ocular reflex during active head impulses. We compared the extent to which suppression occurred between the two groups.

Our results indicated that veterans with PTSD report worse vestibular symptoms than veterans without PTSD and that the symptoms are a source of handicap. Otolith function in veterans with PTSD was comparable to that of the non PTSD. However with regards to canal function, veterans with PTSD took longer to extinguish canal stimuli. This longer decay may be indicative of a hyper vestibular response in PTSD. Lastly with regard to neural control of vestibular reflexes, veterans with PTSD failed to suppress their eye position using active head turns in comparison to those without PTSD. This may be indicative of reduced vestibular control from the cerebellum.

Overall the findings from this thesis have provided evidence of increased vestibular symptoms in veterans with PTSD which are primarily explained by altered vestibular function due to reduced cerebellar inhibition of adaptive vestibular responses.

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