Current Perspectives on Traumatic Brain Injury
Traumatic brain injury (TBI) is a common problem, and
awareness of TBI has increased recently because of military
combat operations in Iraq and Afghanistan. Hearing, balance,
tinnitus, and auditory manifestations are particularly prevalent
in TBI. While the Departments of Defense (DoD) and Veterans
Affairs (VA) are recognized leaders in TBI care, the majority of
veterans will seek care in private sector health care facilities.
Therefore, all audiologists should be familiar with the
- Typical TBI symptoms and manifestations
- Pathophysiology and natural history of mild TBI
- Clinical practice guidelines for evaluation and management
of mild TBI
The purpose of this article is to describe some of the
controversies and inadequacies in the diagnosis and coding of
TBI, and to describe some of the more common auditory and
vestibular problems that arise with TBI.
TBI as a Health Problem
An approximate 1.5 million Americans survive TBI each year,
and approximately 230,000 are hospitalized for the condition.
About 50,000 Americans die each year following TBI, representing
one third of all injury-related deaths. Leading causes of TBI are
falls (28%), motor vehicle accidents (20%), struck by/against
events (19%), and assaults (11%). More than 1.1 million patients
with mild TBI are treated and released from emergency departments
each year. The vast majority (75%-90%) of cases involve mild TBI;
these individuals experience few if any ongoing symptoms, and the
cases follow a predictable course without requiring special
medical treatment. Only a small subset of TBI patients (about
10%) experience any persistent postinjury symptoms.
TBI is widely regarded as the signature injury of combat
operations in Iraq and Afghanistan. These conflicts have
dramatically changed the nature of combat-related injuries
because of several factors: new enemy tactics such as improvised
explosive devices (IED), advancements in body armor that protect
vital organs but leave extremities vulnerable, improvements in
battlefield medicine that increase survival of severely wounded
soldiers, and numerous deployments and long periods in conflict
that increase the risk for sustaining multiple mild TBI in a
While individual injuries often produce devastating and
life-changing consequences for service members and veterans, it
is important to keep the magnitude of combat injuries in
perspective. Only a small percentage (less than 2%) of the
overall force has been seriously injured or wounded in action in
current military conflicts. At the peak of conflict (2005-2007),
68% of service members wounded in action had blast-related
injuries, and 28% to 31% of troops evacuated to Walter Reed Army
Medical Center, Washington DC had brain injuries.
VA screens every veteran who served in Operation Enduring
Freedom (OEF) and Operation Iraqi Freedom (OIF) for common
symptoms associated with TBI. Through February 2009, VA screened
281,607 OEF/OIF veterans. Of these, 56,231 screened positive for
TBI symptoms and were referred for comprehensive
neuropsychological evaluation. Of the 35,231 veterans who
completed comprehensive evaluations, 16,508 veterans were
confirmed with a diagnosis of mild TBI, 13,323 were determined
not to have mild TBI, and 5,293 are pending further evaluation.
The estimated prevalence of TBI is approximately 11.4% based on
screening data through February 28, 2009.
Widely reported prevalence statistics should be viewed with
- Not all deployed service members experienced the same level
of exposure. DoD and VA developed a screening methodology to
identify veterans and service members who were exposed to
situations that might have resulted in TBI and who are
currently experiencing symptoms;
- A positive screen does not mean TBI exists; it means only
that the veteran was exposed to an event likely to cause TBI
(e.g., blast exposure) and is currently experiencing symptoms
consistent with TBI;
- These symptoms can be associated with other conditions,
including stress disorders, musculoskeletal problems,
headaches, and sleep disturbances.
Controversies in TBI
There is an ongoing debate over the nature of mild TBI, its
diagnosis (or rather its overdiagnosis), its pathophysiology, its
natural history, and even the terminology to describe the
condition. Some authors have argued that
is inappropriately used to describe unresolved brain injury and
is a more apt description. The terms
are used interchangeably in the clinical and research literature.
Concussion is a form of TBI, although it is clinically and
diagnostically distinct from more severe forms of TBI. Concussion
is a colloquial term, akin to using the term
to refer to myocardial infarction.
There are situations when the use of the term concussion may
be preferred, such as when communicating with the patient to
indicate the mild, transient nature of the condition and to
emphasize the expectation of recovery. Practitioners should avoid
telling a patient that she or he has "brain damage"
because it may induce misconceptions or fear of permanent damage
or long-term perceptions of disability. In this article, I will
use the term mild TBI.
A recent article in the
New England Journal of Medicine
(Hoge, Goldberg, & Castro, 2009) claimed that screening
programs in the DoD and VA overdiagnosed mild TBI because they
attributed TBI symptoms such as alteration of consciousness to
normal reactions to injury, acute stress, sleep deprivation, and
the "confusion of war" as symptoms of TBI. Hoge et al.
argued that screening methods cannot attribute persistent
postconcussive symptoms (e.g., dizziness, imbalance, or problems
with concentration or memory) to TBI without a firm clinical
definition and a time course linking the conditions to an injury
event. These authors concluded that postdeployment screening also
contributed to negative expectations of recovery and perceptions
of permanent disability.
If anything, mild TBI is underdiagnosed. The purpose of
screening is not to establish a diagnosis but rather to identify
service members and veterans who (a) report an injury event
(blast or explosion, vehicular accident, fragment or bullet
wound, or fall); (b) report one or more symptoms immediately
after the event (losing consciousness or being dazed, confused,
or "seeing stars," or not remembering the event,
concussion, or head injury); (c) report one or more problems that
began at the time of injury or got worse (e.g., memory problems,
balance problems or dizziness, sensitivity to bright light,
irritability, headaches, or sleep problems); and (d) have
experienced one or more of the same symptoms in the past
There is no single symptom or collection of symptoms that is
unique to or diagnostic of TBI. Symptoms of mild TBI are often
difficult to recognize and are easily confused with other
conditions. Treatment of these symptoms may be very different for
TBI patients. Other diagnoses such as posttraumatic stress
disorder (PTSD), cervico-cranial injury with headache, or
peripheral vestibular disorders can account for symptoms. It is
also important to recognize that not all patients with a positive
screen will have TBI. A positive screen signals the need for a
comprehensive neuropsychological evaluation with consultation to
specialists who will confirm the TBI or other diagnoses.
TBI is an insult to the brain caused by an external physical
force such as the following:
- Head being struck by an object
- Head striking an object
- Acceleration/deceleration movements without direct external
trauma to head
- Foreign body penetrating the brain
- Forces generated from blast or explosion
Not all individuals exposed to an external force will sustain
TBI. Severity of TBI may range from "mild" (a brief
change in mental status or consciousness) to "severe"
(an extended period of unconsciousness or amnesia after the
injury). About 80% of TBI cases are classified as mild, 10% are
moderate, and 10% are severe.
At a minimum, TBI produces a diminished or altered state
of consciousness. TBI results in a diverse, idiosyncratic
constellation of cognitive, neurological, physical, sensory,
and psychosocial symptoms.
DoD/VA Common Definition
TBI is a traumatically induced structural injury and/or
physiological disruption of brain function as a result of an
external force that is indicated by the onset or worsening of at
least one of the following clinical signs,
- Any period of a loss of or decreased level of
- Any loss of memory for events immediately before or after
- Any alteration in mental state at the time of the injury
(feeling dazed, confused, disoriented, thinking slowly,
- Neurological deficits (weakness, loss of balance, change in
vision, praxis, paresis/plegia, sensory loss, aphasia, etc.)
that may or may not be transient
- Intracranial lesion
While no standard definition or diagnostic criteria for mild
TBI currently exist, there are well-established diagnostic
criteria for stratifying the level of brain injury at the time of
the injury. DoD and VA jointly developed a definition based on
existing TBI definitions and current clinical experience with
Mild TBI is defined as a traumatically induced structural or
physiological disruption of brain function as the result of an
external force that is indicated by the onset or worsening of at
least one of the following clinical signs immediately following
- Loss of consciousness lasting less than 30 minutes
- Alteration of consciousness or mental state lasting up to
- Posttraumatic amnesia up to 24 hours
- Glasgow Coma Scale (best available score during the first
24 hours) of 13-15
This definition has been widely used by the Congress of
Rehabilitation Medicine, American Academy of Neurology, Centers
for Disease Control and Prevention, and the World Health
Organization for more than 10 years and is widely accepted as the
"gold standard" for defining mild TBI. It is important
to understand that meeting these diagnostic criteria does not
predict functional or rehabilitative outcome. The level of injury
is based on the status of the patient at the time of injury based
on observable signs such as level of consciousness, posttraumatic
amnesia, imaging, and coma scaling (see Table 1).
Table 1-Severity of Brain Injury
Normal structural imaging
Normal or abnormal structural
Normal or abnormal structural
LOC > 30 minutes and < 24
LOC > 24 hours
AOC=a moment up to 24 hours
AOC > 24 hours. Severity based on
PTA > 1 and < 7 days
PTA > 7 days
Note: AOC=alteration of
consciousness/mental state; LOC=loss of consciousness;
PTA=posttraumatic amnesia; GCS=Glasgow Coma Scale. For purposes
of injury stratification, the Glasgow Coma Scale is measured at
or after 24 hours. This stratification does not apply to
penetrating brain injuries where the dura mater is
Mild TBI or concussion generally involves loss of
consciousness that lasts 30 minutes or less, posttraumatic
amnesia less than 24 hours, and Glasgow Coma Scale of 13-15.
Concussion can be further graded according to loss of
consciousness and posttraumatic amnesia (see Table 2).
Table 2-Classification of Mild TBI
No LOC; PTA < 5 minutes
No LOC; confusion without amnesia
Transient confusion; no LOC;
Concussive symptoms resolve < 15 minutes
LOC < 5 minutes;
PTA > 30 minutes
No LOC; confusion with amnesia
Transient confusion; no LOC;
Concussive symptoms last > 15 minutes
LOC > 5 minutes;
PTA > 24 hours
Any LOC either brief (seconds) or
Note: Colorado=Workers Compensation
Board, State of Colorado; AAN=American Academy of Neurology;
see "Practice Parameter" (1997).
Acute injury severity is determined
at the time of injury. Assignment of severity level has some prognostic value, but it
does not necessarily reflect the patient's eventual level of
functioning or rehabilitative outcome.
Pathophysiology, natural history, and prognosis for mild TBI
are different than for moderate and severe TBI. Mild TBI is
typically not associated with objective evidence of brain injury
using commonly available imaging technology. Mild TBI is much
less related to severity of injury, and other factors unrelated
to injury may influence symptom persistence (e.g., coexisting
Diagnosis and Treatment
Diagnosis of mild TBI can be difficult because of the
subjective nature of complaints and significant overlap with
other conditions. Focal neurological signs for mild TBI are
frequently mild or transient. Imaging is usually negative. The
natural history of mild TBI is less predictable than for more
severe TBI, but the majority of patients follow a predictable
course, experience few, if any, ongoing symptoms, and do not
require special medical treatment. Specificity of injury sequelae
is less predictable than for more severe forms of TBI, and
sequelae often overlap with other noninjury conditions, such as
Most of what we know about mild TBI is based on sports
injuries and acceleration/deceleration injuries (e.g., motor
vehicle accidents). Research is lacking on blast-induced
brain injuries. The symptom persistence and long-term
implications of blast-related mild TBI and multiple mild TBI
are unknown. However, there is no reason to conclude a priori
that high-energy blast-related mild TBI has the same
pathophysiology and natural history as sports injuries.
Because of the uncertainties regarding mild TBI, the focus
be on diagnosis. Diagnosis, or rather misdiagnosis, can lead to
inappropriate treatment. Furthermore, the diagnosis may carry
unintended stigma. For example, under current coding rules, a
cognitive deficit (e.g., memory problem) resulting from TBI would
be coded as a nonpsychiatric mental disorder due to organic brain
damage. Many service members and veterans and their families
object to this diagnosis because they feel the symptoms are due
to a neurological brain injury. For these reasons, the focus
should be on recovery and treatment of
symptoms using an interdisciplinary approach to care. Mild TBI
can be transient in nature, but it can also cause significant
disruption in employment, education, and relationships, and it
should not be minimized. Audiologists should also note that
auditory manifestations of TBI can significantly affect treatment
and rehabilitation outcomes and are the reason that audiologists
should be part of an interdisciplinary approach to TBI care.
The above criteria define the injury. There is no single TBI
symptom or pattern of symptoms that characterize mild TBI.
Symptoms may resolve quickly, within minutes to hours after the
injury event, or they may persist longer. Some TBI sequelae may
be permanent. Most signs and symptoms will manifest immediately
following the event. However, other signs and symptoms may be
delayed from days to months. These delayed symptoms are
particularly difficult because there may have been significant
untreated impact on the patient's physical, emotional,
behavioral, social, or family status. Attributing these delayed
symptoms to the injury event can be problematic. Signs and
symptoms may occur alone or in varying combinations and may
result in a functional impairment.
The key factor in attributing these signs and symptoms to
TBI is that they are not better explained by preexisting
conditions or other medical, neurological, or psychological
causes, except in cases of an exacerbation of a preexisting
In the case of hearing loss, for example, peripheral hearing
loss due to noise exposure needs to be ruled out, and central
auditory manifestations of TBI may be due to preexisting
TBI symptoms generally fall into one or more of the three
- Physical: headache, nausea, vomiting, dizziness, blurred
vision, sleep disturbance, weakness, paresis/plegia, sensory
loss, spasticity, aphasia, dysphagia, dysarthria, apraxia,
balance disorders, disorders of coordination, or seizure
- Cognitive: problems with attention, concentration, memory,
speed of processing, new learning, planning, reasoning,
judgment, executive control, self-awareness, language, or
- Behavioral/emotional: depression, anxiety, agitation,
irritability, impulsivity, or aggression.
(Note that these signs and symptoms are typical of each
category but are not an exhaustive list of all possible signs and
The following are typical symptoms seen in TBI:
- Loss of Balance
- Poor coordination
- Visual disturbance
- Poor concentration
- Difficulty making decisions
- Slowed thinking
- Light sensitivity
- Hearing difficulty
- Noise sensitivity
- Body/extremity numbness
- Altered taste or smell
- Appetite change
- Feeling anxious
- Feeling depressed
- Easily irritated
- Poor frustration tolerance
The symptoms listed above are frequently interdependent and
often exhibit complex, subtle and overlapping manifestations.
Some symptoms are obvious (e.g., amputations, burns, or scars),
but some TBI symptoms are "invisible" injuries, as
- Mild TBI (concussion)
- Auditory manifestations (peripheral and central auditory
- Cognitive and memory impairments and executive function
- Visual manifestations (vision loss and visual
- Emotional/behavioral disturbances
- Memory impairments
- Musculoskeletal disorders
- Small embedded fragments
Audiologists should note that auditory and vestibular
complaints (hearing loss, tinnitus, balance disorders, and
central auditory manifestations of TBI) are particularly common.
Tinnitus and hearing loss (auditory complaints) are the most
common service-related injuries in OEF/OIF veterans.
There are also many emotional/behavioral problems associated
with TBI, including depression, apathy, anxiety, irritability,
anger, paranoia, confusion, frustration, agitation, sleep
problems, and mood swings. Problem behaviors may include
aggression and violence, impulsivity, acting out, noncompliance,
social inappropriateness, emotional outbursts, childish behavior,
impaired self-control, impaired self-awareness, inability to take
responsibility or accept criticism, and alcohol or drug
abuse/addiction. Some patients' personality problems may be
so severe that they are diagnosed with personality disorders.
Symptoms associated with PTSD may overlap with symptoms of mild
TBI. Differential diagnosis of brain injury and PTSD is required
for accurate diagnosis and treatment.
Cognitive deficits are also particularly prevalent in TBI and
include problems in thinking, reasoning, problem solving,
information processing, and memory. The most common cognitive
impairment among severely head-injured patients is memory loss.
Higher level, executive function deficits include problems in
planning, organizing, abstract reasoning, problem solving, and
making judgments, and can have a significant impact on quality of
life and return to preinjury work activities. Patients with
moderate to severe TBI tend to have more problems with cognitive
deficits than patients with mild TBI. Many service members and
veterans have been exposed to multiple injury events (e.g.,
repeated blast exposures). These multiple mild TBI events may
have an additive effect, causing cognitive deficits equal to more
severe degrees of injury.
The important message to audiologists is that persistent
symptoms such as emotional/behavioral disturbances, attention
problems, memory loss, and executive function deficits can
have a significant impact on auditory and vestibular
Auditory and Vestibular Symptoms
Audiologists may see a wide variety of symptoms related to
- Ear aches
- Aural fullness
- Tinnitus and hyperacusis
- Dizziness and vertigo
- Loudness sensitivity
- Distorted hearing
- Hearing impairment
- Central auditory manifestations TBI
The ear is the organ most affected by blast. Injuries may
include rupture of tympanic membrane (most frequent),
dislocations/fractures of the ossicles, or damage to the cochlea.
Blast overpressure is too rapid to be compensated by air escape
through the eustachian tube.
Because the ear is particularly susceptible to blast, damage
may be a sign of blast exposure. The extent of ear damage from
the blast depends on factors such as size of the blast, distance
from the blast, orientation of ear canal to the blast, and the
environment (e.g., reflective surfaces or enclosed spaces).
Tympanic membrane perforation is the most common otologic injury.
The tympanic membrane ruptures during positive phase of the blast
and occurs in about 50% of adults at about 175-185 dB peak
pressure level (5 PSI) depending on the blast
Primary blast waves can send small fragments of the squamous
epithelium into the middle ear cavity. Therefore, audiologists
should be on guard for cholesteatomas. Careful surgical
debridement is necessary for removal and
close follow-up, as 10%-20% of cholesteatomas recur. If there is a history of
eardrum perforation, follow-up is important.
Ossicular damage ranges from 4% to 33% of eardrum
perforations. The most common ossicular injury is disruption of
the incudomalleal joint. Disruption of the ossicles may absorb
some of the incoming energy of the blast wave, sparing the
structures of the inner ear.
Immediately following blast injury, patients may experience
hearing loss and tinnitus. Hearing loss may be transient, lasting
for minutes to hours, or permanent, with symptoms of tinnitus and
hyperacusis. Inner ear damage caused by explosions results from a
combination of the blast wave and the following impulse
Balance disorders are common symptoms of TBI. These symptoms
can be transient or persistent, and should be evaluated in
consultation with an otolaryngologist. Head trauma is the most
frequent cause of benign paroxysmal positional vertigo (BPPV),
and there are also cases of traumatically induced MÃ©niÃ¨re's
disease. Dizziness from TBI can be caused by injury to the ear,
peripheral neuropathies, whiplash, musculoskeletal injuries,
vascular disorders, oculomotor disturbances, and diffuse
multimodal central nervous system injuries. Eardrum injury
secondary to blast exposure can also be accompanied by perilymph
fistula, labyrinthine damage, and otolith damage.
Perspectives on Central Auditory Manifestations of TBI
TBI patients frequently have auditory complaints of difficulty
hearing or listening that cannot otherwise be explained by basic
audiometric findings. Problems may include difficulties in sound
localization and lateralization; auditory discrimination;
auditory pattern recognition; temporal aspects of sound (e.g.,
integration, discrimination, ordering, and masking); auditory
performance in competing acoustic signals (including dichotic
listening); and auditory performance with degraded acoustic
signals (American Speech-Language-Hearing Association [ASHA],
2005b). These TBI-related auditory manifestations may coexist
with other disorders such as depression, anxiety, insomnia,
hypervigilance, and stress disorders.
There is ongoing debate as to the nature of these auditory
manifestations, which are sometimes diagnosed as central auditory
processing disorders ([C]APD). Broadly defined, (C)APD refers to
the efficiency and effectiveness by which the central nervous
system utilizes auditory information (ASHA, 2005a). Narrowly
defined, (C)APD is a deficit in the processing of information
specific to the auditory modality
(Cacace, 2009; Cacace & McFarland, 1998; Jerger & Musiek,
2000; McFarland & Cacace, 1995).
Central auditory manifestations of TBI have significant
overlap with other auditory, cognitive, and emotional/behavioral
- Peripheral hearing loss
- Noise-induced hearing loss
- Hearing loss secondary to otologic trauma
- Cognitive and memory deficits
- Executive function disorders
- Language impairment
- Attention deficits
- Emotional disorders
- Motivational concerns
Audiologists should exercise caution in making a diagnosis of
(C)APD in TBI cases, especially blast-induced TBI. Most of what
we know about (C)APD is based on developmental data, sports
injuries, motor vehicle accidents, and discrete lesions. We
should not expect a priori that high-energy blast-induced brain
injuries or any traumatic injury to the brain will result in
lesions. These auditory manifestations could be due to true
modality-specific (C)APD, multisensory central processing
disorders, or supramodal (attentional) disorders.
According to ASHA (2005b, p. 2), "any definition of
(C)APD that would require complete modality-specificity as a
diagnostic criterion is neurophysiologically untenable; however,
one should expect the sensory processing perceptual deficit in
(C)APD to be more pronounced, in at least some individuals, when
processing acoustic information." The ASHA working group
concluded that (C)APD "is best viewed as a deficit in neural
processing of auditory stimuli that may coexist with, but is not
the result of, dysfunction in other modalities" (p. 2).
Unless we know otherwise, central auditory manifestations of TBI
should be not be labeled as (C)APD. However, uncertainty about
the diagnosis should NOT delay or prevent evaluation using
available auditory, multisensory, and neuropsychological
Kyle C. Dennis, PhD
Audiology and Speech Pathology Service
Department of Veterans Affairs, Washington, DC
The opinions expressed herein are those of the author and
do not necessarily reflect the opinions or official positions
of the Department of Veterans Affairs or the U.S.
References and Resources
American Speech-Language-Hearing Association.
(Central) auditory processing disorders
[Technical report]. Available from
American Speech-Language-Hearing Association.
(Central) auditory processing disorders-the role of the
[Position statement]. Available from
Repercussions of blast-related traumatic injury on peripheral
and central auditory function. Paper presented at Joint Defense/Veterans Audiology Conference,
Cacace, A.T., & McFarland, D.J.
(1998). Central auditory processing disorder in school-aged
children: A critical review.
Journal of Speech, Language, and Hearing Research, 41, 355-373.
(1992). Cerebral concussion in sport: Management and prevention.
Sports Medicine, 14, 64-74.
Department of Veterans Affairs Office of Quality and
Performance and Department of Defense Quality Management
Directorate, U.S. Army Medical Command.
VA/DoD clinical practice guidelines for management of
concussion/mild traumatic brain injury. Retrieved on June 8, 2009, from
TBI and auditory processing disorder (APD). Paper presented at Effective Practice of Audiology and
Speech-Language Pathology for Traumatic Brain Injury (TBI)
Conference, Washington, DC.
Hart, A.C., Stegman, M.S., & Ford, B.
ICD-9-CM 2009 expert for hospitals, volumes 1, 2, & 3:
International Classification of Diseases, 9th Revision, Clinical
(6th ed.). Salt Lake City, UT: Ingenix.
Hoge, C.W., Goldberg, H.M., & Castro, C.A.
(2009). Care of war veterans with mild traumatic brain
New England Journal of Medicine, 360, 1588-1591.
Jerger, J., & Musiek, F.
(2000). Report of the consensus conference on the diagnosis of
auditory processing disorders in school-aged children.
Journal of the American Academy of Audiology, 11, 467-474.
McFarland, D.J., & Cacace, A.T.
(1995). Modality specificity as a criterion for diagnosing
central auditory processing disorders.
American Journal of Audiology, 4,
National Center for Health Statistics.
ICD-9-CM official guidelines for coding and reporting. Retrieved June 8, 2009, from
Practice parameter: The management of concussion in
sports (summary statement).
Report of the Quality Standards Subcommittee. (1997).
Neurology, 48, 581-585.
Why Is Coding Important?
Audiologists never code injuries, but they do need to
understand the meaning of injury codes because of their
importance in the identification, evaluation, and management of
TBI symptoms. Proper coding leads to proper reimbursement of
TBI-related services, proper tracking and reporting of the
incidence and prevalence of TBI and its manifestations, and
identification of unusual symptom patterns, symptom clusters, and
previously unidentified long-term sequelae.
Basic TBI Coding Principles
International Classification of Diseases, Ninth Revision,
Clinical Modification (ICD-9-CM)
is the current system of disease classification. TBI is
classified into two broad categories: those injuries associated
with skull fracture and those injuries not associated with skull
fracture (intracranial injuries).
Intracranial injuries without skull fracture are further
classified as: concussion (850 series); injuries due to specific
causes, such as laceration, contusion, or hemorrhage (851-853
series); or other or unspecified injuries (854 series). Injuries
are coded only once, at the initial visit, and coding is not
intended to be used every time a patient is seen, to avoid
TBI injury severity is assigned during the acute stage of
injury, usually very early in the care process. At some point,
the condition either resolves or becomes persistent. If the
condition resolves, it is no longer coded. If the symptoms become
persistent, they are coded differently than they are during the
There is no accepted standard for when TBI symptoms cease to
be acute and become persistent. A good rule of thumb (from the
Department of Veterans Affairs, 2009) is:
-symptoms observed for up to 7 days
-symptoms observed for 8-90 days
-symptoms observed for >90 days
(The Chronic and Subacute terms are not defined by
This lack of definition introduces a source of variation in
coding. Currently, there is no mechanism for associating acute
symptoms to TBI, making it difficult to track and report TBI
symptoms, project costs, and identify unusual symptom clusters.
It is important to understand that the presence of a TBI injury
code and a TBI symptom code in the health record (e.g., in the
same year) does not establish causality. Symptoms must be linked
to the TBI.
There are several problems with the way TBI is coded in
ICD-9-CM. First, no actual TBI codes exist in the diagnostic
classification. Brain injuries are described as:
- Intracranial injuries due to skull fracture (800-801,
- Intracranial injuries due to specified nonfracture causes
(851-853) or unspecified nonfracture causes (854)
- Concussion (850)
Second, TBI symptom codes lack specificity. For example,
cognitive and memory symptoms are coded as mental disorders
rather than neurological disorders or symptoms of brain injury.
Emotional and behavioral symptoms are coded as mental disorders
even when no mental health diagnosis has been made. The reason
for this seemingly strange diagnostic classification is that
cognitive, emotional, and behavioral problems can result from
many disorders affecting the same areas of brain involved with
specific mental disorders.
and the American Psychiatric Association's
Diagnostic and Statistical Manual of Mental Disorders
refer to such conditions as "organic" mental disorders.
Such diagnoses can misrepresent TBI, cause undue stigma, and
potentially misdirect appropriate treatment. Memory impairments
may also be coded as 780.93. Mild cognitive deficits cannot be
coded as 331.83.
Finally, there is an imperfect organization and terminology of
intracranial injuries. All intracranial injuries (with or without
skull fracture) are properly called TBI, but the term
"TBI" is never used.
uses the terms "intracranial injury" or
"concussion." Concussion is currently defined and
differentiated by loss of consciousness, but more severe forms of
TBI are inappropriately labeled as concussion. Moderate and
severe TBI are not classifiable either as concussion or as
postconcussion syndrome (310.2). Severity stratification on the
basis of loss of consciousness is different for concussion (850
series) than for other intracranial injuries (800-801, 803-804,
Initial Coding of Injury
TBI classification is typically done at the time of the injury
and reflects the patient's neurological status at that time
or within 24 hours of the injury. Injury is coded only once,
using a code from the 800-804 or 850-854 series. The mechanism of
injury is coded with an E-code.
Stratification of injury is vital to reporting the incidence
prevalence of TBI. However, there are cases where patients
present for an
with symptoms or complaints related to TBI weeks or months after
the injury, but the diagnosis is delayed. If the injury severity
and mechanism of injury have not been previously coded, they need
to be evaluated and coded by a physician or
Associating Symptoms to TBI
As noted above, it is essential to associate symptoms to TBI.
In most cases, symptoms can be due to nontraumatic as well as
traumatic causes. Therefore, the symptom code itself, with some
exceptions, does not link the condition to trauma. For example,
dizziness or tinnitus could be due to many causes. The only way
to associate TBI symptoms to TBI is by using a TBI "late
is a misnomer. Injury late effects are residuals that persist
after the acute stage of the injury and include sequelae that may
at any time
after the injury. All treatment and follow-up for TBI symptoms
are coded as late effects
regardless of when they first appear.
There are two late effect codes:
905.0-Late effect of intracranial injury with skull or facial
907.0-Late effect of intracranial injury without skull
The benefit of coding TBI symptoms in this way is that there
is no need to determine whether the condition is acute or
persistent from the acute stage. Coding eliminates variation in
practice or coding resulting from uncertainty about when a
condition is acute or persistent. In other words, late effect
codes should be interpreted as sequela codes.
Coding of late effects requires two codes sequenced in the
following order: The condition or nature of the late effect is
sequenced first, followed by the late effect code. Late effects
of intracranial injury are coded according to the presence of
skull fracture. Intracranial injury with mention of skull
fracture is coded as 905.0. Intracranial injury without skull
fracture is coded as 907.0.
The first entered or principal diagnosis is the symptom that
best represents the patient's chief complaint or symptom
(e.g., tinnitus, hearing loss, or vertigo). For patients who have
more than one symptom, audiologists must code all symptoms that
are present, that may influence health status, or that are
relevant to clinical decisions. There is an exception. For
patients who are seen for rehabilitation, the appropriate V-code
(see V57.x) is the first entered or principal diagnosis, followed
by the condition(s) treated. In audiology, rehabilitation would
be coded as V57.89 (other specified rehabilitation
Veteran reports a history of IED blast exposure with
persistent bilateral hearing loss and tinnitus and no previous
history; intermittent dizziness and blurred vision for 10 days
after the accident (all resolved); self-report of confusion for
10-15 minutes, poor recall of events for 1 hour after the blast,
and LOC for 30 minutes. Documented TBI diagnosis 850.11 (mild
Impression: peripheral hearing loss and tinnitus.
Primary diagnosis: 389.18 (sensorineural hearing loss)
Secondary diagnoses: 388.31 (tinnitus, subjective)
907.0 (late effect of intracranial injury without skull
Veteran receives ongoing auditory rehabilitation for auditory
problems dating back to an in-theater motor vehicle accident
occurring in Iraq 2 months ago. Documented mild TBI. Veteran is
being seen by audiologist.
Primary diagnosis: V57.89
Secondary diagnosis: 388.45 (acquired central auditory processing
907.0 (late effect of intracranial injury without skull
Veteran reports history of IED blast exposure during
deployment in Iraq. Documented LOC of 60 minutes and poor recall
of events for 2 days afterward. Documented TBI diagnosis 850.12
(moderate TBI). He complains of persistent difficulty listening,
paying attention, remembering information, following verbal
multistep instructions, and hearing in background noise.
Impression: Central auditory manifestations of TBI
Primary diagnosis: 388.45 (acquired central auditory
Secondary diagnosis: 907.0 (late effect of intracranial injury
without skull fracture)
About the Author
Kyle C. Dennis is an audiologist currently assigned as a
rehabilitation planning specialist in the National Audiology and
Speech Pathology Program Office for the Department of Veterans
Affairs. Dr. Dennis received a master's of science degree
from Tulane University in 1977 and a PhD from Northwestern
University in 1987. He has written and coauthored numerous
publications and papers, and is a frequent presenter on a broad
range of topics, including evidence-based practice, productivity,
clinical issues, and coding.
This article first appeared in the Vol. 8, No. 4, July/August
2009 issue of
ASHA Access Audiology.