Kyle C. Dennis, PhD
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. Government.
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 following:
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.
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 short time.
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 caution because:
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 mild TBI is inappropriately used to describe unresolved brain injury and concussion is a more apt description. The terms concussion and mild TBI 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 heart attack 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 week.
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:
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.
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, immediately following the event:
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 blast injuries.
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 the event:
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 Stratification
|Normal structural imaging||Normal or abnormal structural imaging||Normal or abnormal structural imaging|
|LOC=0–30 minutes||LOC > 30 minutes and < 24 hours||LOC > 24 hours|
|AOC=a moment up to 24 hours||AOC > 24 hours. Severity based on other criteria|
|PTA=0–1 day||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 breached.
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 (Concussion)
|1||No LOC; PTA < 5 minutes||No LOC; confusion without amnesia||Transient confusion; no LOC;
Concussive symptoms resolve < 15 minutes
< 5 minutes;
PTA > 30 minutes
|No LOC; confusion with amnesia||Transient confusion; no LOC;
Concussive symptoms last > 15 minutes
|3||LOC > 5 minutes;
PTA > 24 hours
|Any LOC||Any LOC either brief (seconds) or prolonged (minutes)|
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 mental disorders).
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 stress disorders.
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 should not 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 persistent 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 condition.
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 conditions.
TBI symptoms generally fall into one or more of the three following categories:
(Note that these signs and symptoms are typical of each category but are not an exhaustive list of all possible signs and symptoms.)
The following are typical symptoms seen in TBI:
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 listed below:
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 evaluation rehabilitation.
Audiologists may see a wide variety of symptoms related to 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 characteristics.
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 sound.
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 Ménière'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.
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 that is 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 disorders:
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 auditory-specific 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 techniques.
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.
The 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 duplicate counting.
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 acute stage.
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:
(The Chronic and Subacute terms are not defined by ICD-9-CM [late effects].)
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:
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. ICD-9-CM 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. ICD-9-CM 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, 851–854 series).
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 initial visit 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 neuropsychologist.
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 effect" code.
The term late effect is a misnomer. Injury late effects are residuals that persist after the acute stage of the injury and include sequelae that may occur 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 fracture
907.0-Late effect of intracranial injury without skull fracture
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 procedure).
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 TBI).
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 fracture)
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 disorder)
907.0 (late effect of intracranial injury without skull fracture)
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 processing disorder)
Secondary diagnosis: 907.0 (late effect of intracranial injury without skull fracture)
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. Contact him at Kyle.Dennis@va.gov.
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