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Tissue Barriers in Disease, Injury and Regeneration 1st
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Contents
vii
viii CONTENTS
Introduction 83 III
The Neural Story Net 84
Heuristic Framework for the Neural Story Net in NEUROSENSORY DISORDERS
Symptom Interpretation and Reporting 85 IN CLINICAL PRACTICE
The Informational Elements of Neural Story
Structure 87 10. Vestibular Dysfunction Associated
The Implicit Story Structure of Medical With Mild Traumatic Brain Injury (mTBI)
Diagnosis 90 ABDULAZIZ A. ALKATHIRY, PT, PHD, PATRICK J. SPARTO,
The Application of Story Structural Science to PT, PHD, ANTHONY P. KONTOS, PHD
AND JOSEPH M. FURMAN, MD, PHD
Traumatic Brain Injury Patient-Reported
Symptom Interpretation 92
Overview of the Vestibular System 133
The Inclusion of Story Analysis Into Symptom
Prevalence of Vestibular Disorders After Mild
Inventories: An Example 95
Traumatic Brain Injury 134
Conclusion 96
Vestibular-Related Symptoms and Impairment After
References 97
Mild Traumatic Brain Injury 135
8. Neuropsychological and Psychiatric Assessment of Vestibular Function After Mild
Comorbidities of Mild Traumatic Brain Traumatic Brain Injury 138
Summary 144
Injury
References 144
JEFFREY P. STAAB, MD, MS AND
MATTHEW R. POWELL, PHD, LP 11. Hearing Disorders Associated With
Mild Traumatic Brain Injury (mTBI)
Introduction 99
TANYA SINGH, MS AND MICHAEL D. SEIDMAN, MD, FACS
Acute Neurocognitive Effects of Mild Traumatic
Brain Injury 100
Introduction 149
Postacute Neurocognitive Recovery of Mild
Tinnitus 150
Traumatic Brain Injury 101
Hearing Loss 153
Persisting Neurocognitive and Psychiatric Effects of
Sensorineural Hearing Loss 154
Mild Traumatic Brain Injury 102
Conductive Hearing Loss 155
Psychiatric Disorders Following Mild Traumatic
Hyperacusis 156
Brain Injury 105
Central Auditory Dysfunction 157
Late Neurocognitive of Mild Traumatic Brain
Electrophysiological Studies in Mild Traumatic Brain
Injury 107
Injury 158
Treatment of Neuropsychological and Psychiatric
Mental Health Issues 159
Symptoms Following Mild Traumatic Brain
Future Directions 159
Injury 107
Conclusion 159
References 109
References 160
9. Tauopathies in Traumatic Brain Injury 12. Headache in Mild Traumatic
JONATHAN PACE, MD, BERJE SHAMMASSIAN, MD AND
S. ALAN HOFFER, MD
Brain Injury
TESHAMAE S. MONTEITH, MD AND TAD SEIFERT, MD
Introduction 113
History 113 Introduction 165
Epidemiology 114 Epidemiology 165
CONTENTS ix
Classification 167 Does the Presence of Sleep Disorder
Pathophysiology 168 Symptoms (i.e., Insomnia, Hypersomnia,
Medical Treatment 173 Hyposomnia) Identify Those With
Interventional/Procedural Treatment 175 Concussions Who Are at Increased Risk for
Prognosis 175 Severe/Prolonged Early Impairments, Neurologic
Special Populations 175 Catastrophe, or Chronic Neurobehavioral
Conclusion 177 Impairment? 205
References 178 Do Any Sleep Studies Identify Those at Increased
Risk? 205
13. Cognitive-Emotional-Vestibular Triad Do Any Sleep Interventions Enhance Recovery,
in Mild Traumatic Brain Injury Reduce Recurrent Concussion Risk, or Diminish
NIKHIL BANERJEE, SARAH J. GETZ Long-Term Sequelae? 213
AND BONNIE E. LEVIN References 216
Introduction 183
15. Vision Disorders in Mild
Cognitive, Emotional, and Vestibular Changes in
Traumatic Brain Injury: A Multisystem Traumatic Brain Injury
Model 185 ERIC SINGMAN, MD, PHD AND PATRICK QUAID,
OPTOMETRIST, MCOPTOM, FCOVD, PHD
Effects of Mild Traumatic Brain Injury on
Neuropsychological Function 185
Overview of Concussion and Visual Function 223
Effects of Mild Traumatic Brain Injury on
Specific Oculomotor and Visual Processing
Psychiatric Well-Being 187
Difficulties 225
Effects of Mild Traumatic Brain Injury on
The Generalist’s Approach to Evaluating Visual
Vestibular Function 188
Dysfunction in Patients With Mild Traumatic
Interrelationships Between Vestibular, Cognitive,
Brain Injury 233
and Emotional Function 189
Conclusion 233
Emotion 190
References 235
Neuroanatomical Links Between Cognition,
Emotion and Vestibular Function 190
Changes in Neurological Network Connectivity
and Function in Mild Traumatic Brain
IV
Injury 192 DIAGNOSIS AND
Vestibular Cognitive Emotion Relationships in
Mild Traumatic Brain Injury 194 TREATMENT
References 195 16. Diagnostic Approaches Techniques in
14. Sleep Issues and Mild Traumatic Concussion/Mild Traumatic Brain Injury:
Brain Injury Where are we?
DAVID Y. GOLDRICH, B. TUCKER WOODSON, MD, FACS, REBECCA SMITH, MARIYA CHEPISHEVA,
JASDEEP S. HUNDAL, PSYD, ABPP-CN AND P. ASHLEY THOMAS CRONIN, PHD AND BARRY M. SEEMUNGAL
WACKYM, MD, FACS, FAAP
Introduction 247
Introduction 199 Biomarkers for Concussion and Mild Traumatic
Does Mild Traumatic Brain Injury Contribute to the Brain Injury in Blood and Other Body
Development of Short-Term and/or Long-Term Fluids 253
Sleep Disorders? 200 Neurophysiological Testing and Neuroimaging in
Do Preexisting Sleep Disorders Mild Traumatic Brain Injury 263
Increase/Decrease Concussion and Conclusion 269
Traumatic Brain Injury Risk? 205 References 269
x CONTENTS
Introduction 321
23. Emerging Treatment
Neurological Interventions After TBI 322 Modalities
Conclusion 333 SARA BRESSLER, BS, MIKHAYLO SZCZUPAK, MD
References 334 AND MICHAEL E. HOFFER, MD, FACS
xiii
xiv LIST OF CONTRIBUTORS
xvii
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S E C T I O N I
1
What Is Mild Traumatic Brain Injury?
Translational Definitions
to Guide Translational Research
Michael E. Hoffer, MD1 and Carey D. Balaban, PhD2
1
Department of Otolaryngology and Neurological Surgery, University of Miami, Miller School
of Medicine, Miami, FL, United States 2Departments of Otolaryngology, Neurobiology,
Communication Sciences & Disorders, and Bioengineering, University of Pittsburgh,
Pittsburgh, PA, United States
Mild traumatic brain injury (mTBI) is a common public health concern that has garnered
increased attention in both the lay press and medical literature. mTBI/concussion is
particularly common in the military where up to 20% of individuals deployed to Southwest
Asia have been affected.17 In the US Military, between 2000 and 2016, 361,092 active duty
service members suffered from TBI, ranging from mild (82% of cases) to severe or penetrat-
ing.2 However, the diagnosis is not restricted to the military; recent literature reports that the
incidence and prevalence of TBI in the civilian population is increasing.8 A number of reports
that focused on selected populations, such as high school athletes9 or emergency departments
(EDs) over limited time frames10,11 give estimates of the relative prevalence of mTBI in differ-
ent populations. For example, Marin et al.12 used the Nationwide Emergency Department
Sample to investigate trends of visits to EDs for TBI between 2006 and 2010. The data, pooled
from a sample of 950 hospitals, showed a sharp increase in the weighted rates of ED visits
from 2006 to 2010. In 2006, there were 637 TBI visits per 100,000 ED visits and by 2010 this
figure was up to 822 per 100,000, with a disproportionate increase in the number of reported
mTBI or concussion visits.13 It is noteworthy that there was a commensurate increase in the
number of peer-viewed journal publications in the ISI Web of Science with “mild traumatic
brain” as a term in the title, from 27 in 2006, to 44 in 2010, 49 in 2011, and 158 in 2017
(Fig. 1.1). One may suggest that the increased number of visits reflected an increased recogni-
tion of a common phenomenon rather than a sudden increase in prevalence of mTBI.
Despite the recent focus on the prevalence of this disorder in the media, the question
of the establishment of precise, mechanistically anchored criteria for mTBI remains
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FIGURE 1.1 Peer reviewed research publications by year.
challenging because it requires that the signs and symptoms are linked temporally to a
traumatic event as the proximate cause. The National Institute of Health (NIH) has a
very straightforward definition: “Traumatic brain injury (TBI), a form of acquired brain
injury, occurs when a sudden trauma causes damage to the brain.”14 While this seems
straightforward, the definition of a “sudden trauma” can be the subject of debate as its
causal linkage to acute, subacute, and chronic symptoms can be problematic. For the
purposes of this book we will broadly define the “sudden trauma” as any force (or
“directed energy”) that causes the brain itself or the contents of the brain to be altered
sufficiently to cause physiological dysfunction, biochemical dysfunction, or structural altera-
tions. There is some evidence to suggest that there are significant differences in the mode of
TBI presentation based on etiology, but these differences still produce effects that are within
a spectrum of those that can be seen in TBI irrespective of the etiology.15,16 Despite the
debate, the NIH definition was crafted pragmatically to allow general acceptance.
Initially TBI was broadly divided into mild, moderate, and severe using the well-
established Glasgow Coma Scale (GCS) as an acute metric.15 While this method seems
straightforward given the objective nature of the GCS, this criterion has three main short-
comings. Firstly, most of the individuals with GCS scores less than 13 have some form of
severe TBI, meaning the remaining individuals are compressed into a fairly tight range of
1315 with the vast majority of these being 15. As such the numerical value of the GCS
seems ideally suited to distinguish severe from mild or moderate TBI, but this distinction is
generally clinically apparent. Beyond that, the scale provides little value for individuals with
mild TBI. Secondly, the vast majority of individuals with mTBI do not receive a GCS at the
time of injury. Hence, the value of any subsequent or “retrospective” GCS, especially days
later, is suspect at best. Finally, individuals with mTBI have a range of sequelae and different
outcomes despite having a GCS of 14 or 15; as such, the value does little to distinguish
patients on the basis of signs and symptoms that characterize the functional pathology.
This description incorporates three generally accepted definitions of mTBI that have
been published over time.17 In 1993 the American Congress of Rehabilitation Medicine
(ACRM) described mTBI as an alteration of brain function caused by an external force
with one of more to the following: (1) loss of consciousness (LOC) of 030 minutes; (2)
posttraumatic amnesia (PTA) lasting 024 hours; (3) focal neurologic deficits may or may
not be transient; and (4) alteration of mental state at the time of the accident (confusion,
disorientation, slow-thinking).18 In 2003, the Centers for Disease Control and Prevention
(CDC) offered a slightly less specific classification in which an individual must have any
period of observed or self-reported transient confusion, disorientation, or impaired con-
sciousness around the time of a head injury with LOC lasting 030 minutes.19 In 2009, the
Department of Defense (DoD) established guidelines similar to the ACRM guidelines, but
added that the alteration of consciousness (AOC) lasts less than 24 hours.20 The DoD
updated this definition in 2016 and defined mTBI as: “traumatically induced structural or
physiologic disruption of brain function as a result of an external force with new onset or
worsening of at least one of the following: loss or decreased level of consciousness,
(LOC , 30 minutes, AOC ,24 hours), PTA (,1 day), alteration in mental status (e.g., con-
fusion, disorientation, etc.), Neurological deficit (weakness, loss of balance, sensory losses,
etc.)." They added that the GCS should be 1315 and structural imaging should be nor-
mal.21 To summarize colloquially, mild TBI is diagnosed by a documented directed energy
event that results in the patient reporting symptoms or displaying nonlocalizing signs of
being “not quite right.”
Complicating these definitions of mTBI include the subcategories of “complicated
mTBI” and concussion. Some investigators use the term “complicated mTBI” when the
mTBI symptoms are accompanied by positive findings with radiologic imaging.2224 The
difficulty with this diagnosis is that imaging changes over time. The original definition of
“complicated mTBI” relied on CT scans that showed abnormalities; there is some evidence
that these individuals followed a course more similar to moderate TBI.23,24 Therefore, posi-
tive CT scan findings often shift diagnosis to the moderate TBI group. However, more
modern imaging, including traditional MRI, fMRI, high Tesla MRI, and other scans, do
detect abnormalities in some individuals and it is unclear whether these abnormalities
have any longer term clinical or functional implications that distinguish them from symp-
tomatic, but radiologically negative, patients.
The term concussion is often used synonymously with mTBI. It is likely the case that
concussion is simply a type of mTBI. While it is usually on the milder side of the spec-
trum, the short-term and long-term consequences provide little basis for distinguishing
between these terms. The diagnostic criteria for concussion in athletes has been examined
by a group of experts meeting every other year who have published updated guidelines
after each of these meetings.25,26
While the diagnosis of mTBI and concussion remain difficult to differentiate, postconcus-
sion syndrome has an acceptable definition provide for the International Classification of
Diseases 10th edition (ICD-10).27 This World Health organization-accepted medical definition
requires the following: (1) The syndrome follows a head trauma, and (2) The individual pres-
ent with at least three of the following eight symptoms: headache, dizziness, fatigue, irritabil-
ity, difficulty concentrating, memory impairment, insomnia, and intolerance to stress,
emotion, or alcohol. Because this definition of concussion appears to be synonymous with
mTBI, there seems to be little value in assigning this term only to the “mildest” cases until
there is a more objective and precise way of making this determination.
We must acknowledge that: the diagnosis of mTBI or concussion requires the presump-
tion of a causal link to a documented traumatic event. The dilemma becomes most evident
when a patient appears for a workman’s compensation examination, reporting a plethora
of nonspecific symptoms that could indicate mTBI. The patient attributes the symptoms to
an unwitnessed head-bump several weeks earlier. If one subjects the patient to a large bat-
tery of neurologic tests and advanced imaging, what is the likelihood that incidental
chronic findings might be misattributed to an undocumented traumatic event? These con-
siderations obviously mandate a healthy skepticism prior to asserting post hoc diagnoses
from unknown cranially directed energy exposures. Although we can document signs and
symptoms that appear after documented traumatic events, the observations of a similar
clinical syndrome are insufficient to substantiate a causal claim regarding an unverified
(or assumed) traumatic incident.
The structure of symptom complexes in acute mTBI suggests that integrative, objective
diagnosis should be tractable. For example, principal component analysis of a standard 22-
item symptom scale showed acute mTBI and control subjects differed by a posttraumatic
migraine/headache symptom cluster, a dizziness/mild cognitive impairment symptom clus-
ter, an emotional lability symptom cluster, a cervicogenic (neck painfatiguemalaise)
symptom cluster, and nausea.28 Unfortunately, attempts to devise integrative approaches to
overall objective diagnosis of mTBI signs have been complicated by several issues. Firstly,
the symptom clusters do not unambiguously point to localized injury. Secondly, concerns
have been raised about the accuracy of symptom self-reports, which seem to be inherently
unreliable and unstable in patients with mTBI.29,30 For example, symptom reports may be
exaggerated or understated (denial) for secondary gain, which can produce symptom com-
plex component scores on both tails of the distributions in acute mTBI patients (Hoffer et al.
PLoS One, symptom complex paper) Thirdly, the heterogeneous presentation of mTBI makes
unified objective diagnostic criteria difficult to identify. The presentation can vary with small
changes in the magnitude or direction of the force, by the subjects’ past medical and particu-
larly, past head injury, history, and by a variety of other factors including anatomic and
genetic differences. Fourthly, the manifestations of the mTBI change over time, based on
external environmental and epigenetic influences that are independent of the trauma and,
again, affect every individual differently. Fifthly, mTBI in an individual case may involve a
number of parallel, but very small injuries, in more than one location in the brain or intracra-
nial sensory organs Sixthly, home remedies, spontaneous compensation, and variations in
treatment regimens complicate the subacute and chronic presentations. These factors may
contribute to the conclusion that the trend of attempts to classify the disorder in terms of
common objective features has been fraught with difficulty.15