Neurotologic Consequences of Blast Injury


Injury secondary to blast exposure is the most frequent battlefield injury seen in Iraq and Afghanistan.  In the civilian world blast exposure at job sites is increasingly more common.   Individuals exposed to blast describe a classic “inward then outward” sensation which is associated with the blast pressure wave.   This blast pressure wave can be best modeled experimentally with a Friedlander wave [27], shown from an experimental shock tube  in Figure 1. This pressure produces a barotraumas capable of damaging tissues throughout the body. 

 It is important to realize that the damage done within the body can occur without any obvious outward signs of trauma [15, 23].  We consider many of the signs and symptoms encountered in the Neurotology clinic as a combination of primary and secondary consequences of blast exposure.  Acoustic trauma or labyrinthine concussion can be considered as primary blast injury, but later developing features are viewed as secondary or collateral damage from recovery processes.

Figure 1
Figure 1
Experimental Friendlander wave produced in the blast simulation tube shown in Figure 2.  The wave in black shows the standard Friedlander wave overpressure (positive)-underpressure (negative) sequence.  It was recorded at the distal end of the illustrated animal holding area.  The waveform in red was recorded when a larger aperture distal section was added (not shown). 
Barotrauma can be produced by both the positive and negative pressure components

Neurotologic consequences are among the most common because of the relative lack of protection of the ears and head from the propagating blast wave.  Much of the literature to date on blast exposure has focused on the effects of blast on hearing or the tympanic membrane [5, 14, 22, 28].    While there are dozens of studies on this subject, much of the data were derived from mass casualties at single events, when it was hard to collect a standard set of data on all patients.  Moreover, the very nature of blast makes it difficult to study because the effects will be dramatically affected by the patient’s distance from the blast and orientation towards the blast, environmental features (e.g., alcoves) that produce reflection and resonance of the blast wave, the strength of the blast itself, and the patient’s previous otoneurologic and head trauma history.

Lastly, many of the studies suffer from reporting only a single time point after the blast so that there is not a great deal of knowledge of symptom progression over time.  We will initially discuss data examining patients at various time points after blast exposure, followed by a description of the underlying basic science that is consistent our clinical observations.  The presentation of clinical data prior to experimental data is intentional.  Translational research requires parallel investigations such that the basic science drives that clinical work and the clinical work drives the basic science. Our primary goal is to understand and ameliorate human clinical conditions; animal models provide contextual information for gleaning deeper clinical insight.

Clinical findings of blast exposure

We examined three separate groups of patients at three different time points after blast exposure [12]. The acute group was composed of 81 individuals seen within 72 hours of blast in theatre, the subacute group was composed of 25 individuals who were composed of 42 individuals who were seen 4-30 days after blast at our tertiary care facility at Naval Medical Center San Diego (NMCSD), and the chronic group was seen 30-360 days after blast exposure at NMCSD. The number of patients represents a very small percentage of our clinics experience with this group of patients but was limited by collection time and the need to find patients with only blast damage and no recent blunt injury.  The individuals in theatre were evaluated with a clinical exam and an Otogram hearing test (Tymapni Inc., Houston, TX). 

Those seen at NMCSD underwent an extensive vestibular evaluation including a clinical exam, standard audiometery, rotational chair test (Neurokinetics Inc, Pittsburgh, PA and Micromedical, Inc. IL) and computerized dynamic posturography (Neurocom Inc., Clackmas, OR).  The neurotologic symptoms of the three groups are shown in table one.  Dizziness (in the form of unsteadiness or feeling off balance) is the most common symptom at all time points.   In fact, dizziness is also the most frequent sequela of mild traumatic brain injury in this group of patients at all time points as well.   The prevalence of clinically significant hearing loss and vertigo increased over time.  It is interesting to note that the 70% of individuals who reported tinnitus initially also complained of hearing loss but the audiometer only confirmed hearing loss in a total of 1/3 of the group.  While the rate of tinnitus stays the same, the acute group did complain of much louder tinnitus than the other two groups. The hearing loss seen in this group of individuals was all sensorineural in type.  We do see conductive loss from ossicular damage but

Table 1




Hearing Loss

















The literature reports a significant variability in symptoms with sensorineural hearing loss (SNHL) rate varying from as low 49% to as high as 78% and dizziness rates from as low as 15% to as high as 98%. [2, 4, 20, 21]   Much of this variability is likely due to a variety of factors including the type of blast, the victims distance from the blast, the amount of protective equipment worn by the individuals, and other victim specific issues including previous blast exposures. Equally important is the components of the work-up. 

We showed much higher rate of reported hearing loss in our early group than actually had hearing loss on testing.  Conversely, it is often the case that if individuals are simply asked if they feel dizzy (often while sitting or lying down) they will not report the disorder because they have not “tested” their legs enough to realize that they are unsteady.  In addition, we feel that it is important to take a careful clinical history since we differentiate between unsteadiness and hearing loss in our blast patients.  Lastly the reports in the literature fail to document multiple time points most occurring either immediately after the exposure or many months later. The mix in outcomes may be due to the different time points as well.  In summary, the literature agrees that dizziness/vertigo, hearing loss, and tinnitus are common after blast exposures but differs widely about the relative rates of each.

The presence of tympanic membrane perforations in minority of patients is a common element in studies that examined patients in the acute time period after blast exposure.  The frequency of perforation varied from as low as 16% to as high as 29%. [10, 17, 28].  Interestingly it was not always the case that those studies who judged acute to be within the first few hours had higher perforation rates that those that looked at patients a few weeks later.  This may seem to be a contradiction since all of the studies report relatively high rates of spontaneous perforation healing.  However, the ability to detect small perforations may not be available in the field setting meaning the studies done very early may have missed perforations that were easier to see in the tertiary care setting.  Given the barotrauma nature of the blast event it is surprising that tympanic membrane perforations are not more common.  This may be in part to a high rate of missed perforations in the acute population (often evaluated on scene) and a subsequent healing that obscures the original perforation. 

Basic Science neurotologic consequences in blast injury

Classical neuropathologic signs of concussive brain injury include subdural hematoma,  cerebral contusion, and subarachnoid hematoma [6].  Signs and symptoms of  subdural hematoma can emerge in acute, subacute or chronic stages after injury [6], even at relatively long intervals after the original insult.  Although radiological findings are generally subclinical in mild TBI, there is increasing interest in more subtle vascular findings such as dilation of perivascular spaces [13].  The recent confirmation of transmission of a blast wave to the brain [3, 19, 25], both directly and indirectly via vasculature, implies that the blast wave injury to intracranial tissues (brain, vasculature and meninges) may be similar to effects in other soft tissues. 

Tissues such as the lung, liver, kidney, heart and GI tract show blast injury features that  include local plasma extravasation (local edema), local hemorrhage (including perivascular ring hemorrhage), disseminated intravascular coagulation (a term that includes microthrombi in small vessels) and introduction of air emboli [27].  Depending upon location (e.g., in an extension of the subdural space such as the velum interpositum, Meckel’s cave, cochlear aqueduct and transverse cerebral fissure) and time of onset, these cellular injuries could easily elude clinical detection with standard imaging protocols.

Studies employing a single, relatively low-level shock wave exposure have provided evidence for cellular damage in central nervous system that may be associated with blast-induced mTBI.  Studies of hearing impairment, on the other hand, have used 50-100 presentations of shock waves or impulse sound to demonstrate acoustic trauma-like effects to cochlear vasculature and cochlear hair cells [7-9, 16, 22, 23].  Although single blast exposure studies have used different species, different exposure intensities and different methods of shock wave presentation, some common principles for effects of low level exposures seem to be emerging.

Recent basic research studies provide further histopathological evidence of the inner ear effects of low intensity (10-18 psi) blast overpressure (BOP) exposures.  The blast pressure wave exposures were performed in a 30” cast aluminum tube (10” outer and 8” inner diameter) compression chamber at Naval Medical Center, San Diego.  The tube houses an adjustable reservoir chamber that releases a compressed air volume ranging from 1570 to 7850 cm3 through a PVP film diaphragm.  A second 15-inch long tubular portion attaches to the wave generation chamber and serves as the animal exposure and holding area (Figure 2).  A 1.6 hp compressor (Sears Inc) produces up to 175 PSI in the compression chamber. Between the reservoir chamber and the animal holding area is a variable aperture that holds the PVP film diaphragm. 

Figure 1
Figure 2 
Blast pressure simulator (exposure tube) at Naval Medical Center San Diego. See text for detailed description.

The input to peak output pressures are linear over the range of 0 – 100 PSI, and the velocity of the BOP wave was measured at 1221 feet/sec at six inches from the compression chamber aperture.   Anesthetized adult female Sprague-Dawley rats were placed horizontally in the holding/exposure area and tethered to a removable wire rack either six or 12 inches from the film diaphragm.  The head faced the blast source.  The blast overpressure (BOP) wave is measured with Tucker Davis Technologies (TDT) System 3 and Endevco pressure transducers (model 8510B-200) rated for 200 PSI and electronic conditioners interfaced with a computer. Figure 1 (right panel) shows an example of an overpressure/underpressure Friedlander wave generated by this system   after survival times of 2 hours (n=3), 24 hours (n=3), 3 days (n=1), 7 days (n=3), 21 days (n=3) and 42 days (n=3) after BOP exposure, the rats were euthanized and perfused with paraformaldehyde fixative.  

A sham control group (anesthetized, but not blast exposure) was also used.  The skinned heads were decalcified, embedded in paraffin and sectioned serially at 6-8 microns in the horizontal plane.  Sets of every fiftieth section were stained with hematoxylin and eosin for histopathologic analysis.  At survival times through 7 days, 8/10 rats showed red blood cell ghosts and hematoma in the scala tympani of at least one ear, particularly in proximity to the cochlear aqueduct (Figure 3).  Lymphocytes and macrophages were found occasionally within these aggregates (Figure 4).    Their location suggests an origin from the cochleovestibular vein, near its junction with the inferior petrosal sinus. 

Figure 1
Figure 3. 
Photomicrographs of horizontal sections through the inner ears of four rats after blast exposure. The paraffin-embedded sections were stained with hematoxylin and eosin. The Friedlander wave peak is noted in pounds per square inch (PSI) and the survival time is noted in hours (h) or days (d) for each animal. Small hematoma regions within the perilymph (scala tympani) are indicated with arrows; examples are shown at higher resolution in Figure 4. The round window membrane (RW) and cochlear aqueduct (CA) are also indicated.

Figure 1
Figure 4. 
Higher magnification photomicrographs of regions of hemorrhage in the scala tympani after blast exposure. Note erythrocyte ghosts and infiltrated inflammatory cells. The calibration bar represents 20 microns.

A light protein exudate was commonly present within the perilymph of both scalae tympani and vestibuli. For the longer survival times (21 and 42 days), only 1/6 rats showed evidence of hematoma in the perilymph, but one of the negative rats showed extensive spiral ganglion cell degeneration the apical third of the cochlea. We suggest that these pathological features are linked to persistent or worsening audiovestibular symptoms.  Further, because the perilymph is confluent with the cerebrospinal spinal fluid, these pathologic findings are a form of subarachnoid hematoma. 

The strong evidence of hemorrhage within the perilymph at lower level blast overpressure exposures has the potential to provide new insights into warfighter clinical health presentations after relatively mild blast exposure. Even small amounts of autologous blood in the scala tympani can affect hearing permanently [24].  Because the perilymph is confluent with cerebrospinal fluid through the cochlear aqueduct, an intracochlear hemorrhage is, also, by definition, a subarachnoid hemorrhage, which is a likely contributor to the headache and dizziness that are the hallmarks of acute and subacute blast-related mTBI [11].  

There is also increasing recognition that subarachnoid hemorrhage can contribute to both early and delayed mechanisms of secondary brain injury, including vasospasm, transient ischemia, oxidative stress, excitotoxicity, cortical spreading depression, microcirculatory dysfunction and delayed thromboembolism [1, 18, 26].   These secondary factors can contribute to delayed neuronal insult and apoptotic cell death.  Further, the responses to these insults could explain the observation of dilated perivascular spaces in the brain of some individuals with mTBI [13]. 


The frequency of blast exposure and consequent blast injury in the recent wars in Southwest Asia has allowed us to draw a more accurate clinical picture of the impact of blast on the ears and related structures.  A clinical picture has emerged that shows that headache and otological signs of injury to the auditory and vestibular system are among the most common findings after blast exposure/injury.  Motivated by these findings, histopathological studies were conducted to more closely examine the effects of blast in small mammals.  These studies suggest that small intracochlear hemorrhages and embolus formation may contribute to headache and audiovestibular symptoms in blast-induced mTBI.  These studies motivate clinical examination of the value of balance and auditory testing as sentinels for the presence of mild traumatic brain injury after blast wave exposure.

The close relationships of the basic science findings with the clinical picture provide us a paradigm to establish an iterative research environment where the basic science findings allow drive clinical solutions and clinical issues drive basic science experiments. True translation can best be achieved by close communication of clinicians and scientists and with projects aimed at answering the most critical questions and providing the most timely patient and disease orientated solutions to improve public health and welfare.


  1. J. Cahill, J.W. Calvert and J.H. Zhang, Mechanisms of early brain injury after subarachnoid hemorrhage, J. Cereb Blood Flow Metab 26 (2006), 1341-1353.
  2. K.M. Cave, E.M. Cornish and D.W. Chandler, Blast injury of the ear: clinical update from the global war on terror, Military Medicine 172 (2007), 726-730.
  3. M. Chavko, W.A. Koller, W.K. Prusaczyk and R.M. McCarron, Measurement of blast wave by a miniature fiber optic pressure transducer in the rat brain, J. Neurosci. Methods 159 (2007), 277-281.
  4. S.A. Fausti, D.J. Wilmington, F.J. Gallun, P.J. Myers and J.A. Henry, Auditory and vestibular dysfunction associated with blast-related traumatic brain injury, J Rehabil Res Dev 46 (2009), 797-810.
  5. R.J.N. Garth, Blast injury of the auditory system: a review of mechanisms and pathology, J. Laryngol. Otol. 108 (1994), 925-929.
  6. J.G. Greenfield, Traumatic lesions of the central nervous system, in: Neuropathology, J.G. Greenfield, W.H. McMenemy, A. Meyer andR.M. Norman eds., Edward Arnold Co., London, 1958, pp. 408-440.
  7. P.R. Hamernik, J.H. Patterson and R.J. Salvi, The effect of impulse intensity and the number of impulses on hearing and cochlear pathology in the chinchilla J Acoust Soc Am 81 (1987), 1118-1129.
  8. P.R. Hamernik, J.H. Patterson, G.A. Turrentine and W.A. Ahroon, The quantitative relation between sensory cell loss and hearing thresholds, Hearing Res 38 (1989), 199-212.
  9. P.R. Hamernik, G.A. Turrentine and C. Wright, G,.  , Surface morphology of inner sulcus and related epithelial cells of the cochlea following acoustic trauma, Hearing Res 16 (1984), 143-160.
  10. C.D. Harrison, V.S. Bebarta and G.A. Grant, Tympanic membrane perforation after combat blast exposure in Iraq: a poor biomarker of primary blast injury, J. Trauma 67 (2009), 210-211.
  11. M.E. Hoffer, C.D. Balaban, K.R. Gottschall, B.J. Balough, M.R. Maddox and J.R. Penta, Blast exposure: vestibular consequences and associated characteristics, Otology & Neurotology in press (2009).
  12. M.E. Hoffer, C.D. Balaban, K.R. Gottschall, B.J. Balough, M.R. Maddox and J.R. Penta, Blast exposure: vestibular consequences and associated characteristics, Otology & Neurotology 31 (2010), 232-236.
  13. M. Inglese, E. Bomsztyk, O. Gonen, L.J. Mannon, R.I. Grossman and H. Rusinek, Dilated perivascular spaces: hallmarks of mild traumatic brain injury, AJNR Am J Neuroradiol 26 (2005), 719-724.
  14. J.H. Jensen and P. Bonding, Experimental pressure induced rupture of the tympanic membrane in man, Acta Otolaryngol. 113 (1993), 62-67.
  15. K. Kato, M. Fujimura, A. Nakagawa, A. Saito, T. Ohki, K. Takayama and T. Tominaga, Pressure-dependent effect of shock waves on rat brain: induction of neuronal apoptosis mediated by a caspase-dependent pathway, J Neurosurg 106 (2007), 667-676.
  16. B. Kellerhalls, Acoustic trauma and cochlear microcirculation, Adv. Oto-Rhino Laryngol. 18 (1972), 91-168.
  17. D. Leibovici, O.N. Gofrit and S.C. Shapira, Eardrum perforation in explosion survivors: is it a marker of pulmonary blast injury?, Ann Emerg Med 34 (1999), 168-172.
  18. R.L. Macdonald, R.M. Pluta and J.H. Zhang, Cerebral vasospasm after subarachnoid hemorrhage: the emerging revolution, Nature Clin Prac Neurol 3 (2007), 256-263.
  19. D.F. Moore, A. Jerusalem, M. Nyein, L. Noels, M.S. Jaffee and R.A. Radovitzky, Computational biology--modeling of primary blast effects on the central nervous system, NeuroImage 47 (2009), T10-T20.
  20. R. Mrena, R. Pääkkönen, L. Bäck, U. Pirvola and J. Ylikosk, Otologic consequences of blast exposure: a Finnish case study of a shopping mall bomb explosion, Acta Otolaryngol. 124 (2004), 946-952.
  21. B.I. Nageris, J. Attias and R. Shemesh, Otologic and audiologic lesions due to blast injury, J Basic Clin Physiol Pharmacol. 19 (2008), 185-191.
  22. J.H. Patterson and P.R. Hamernik, Blast overpressure induced structural and functional changes in the auditory system, Toxicology 121 (1997), 29-40.
  23. G.R. Price, H.N. Kim, D.J. Lim and D. Dunn, Hazard from weapons impulses: histological and electrophysiological evidence, J Acoust Soc Am 85 (1989), 1245-1254.
  24. A. Radeloff, M.H. Unkelbach, J. Tillein, S. Braun, S. Helbig, W. Gstöttner and O.F. Adunka, Impact of intrascalar blood on hearing, Laryngoscope 117 (2006), 58-62.
  25. A. Saljo, F. Arrhen, H. Bolouri, M. Mayorga and A. Hamberger, Neuropathology and pressure in the pig brain resulting from low-impulse noise exposure, J. Neurotrauma 25 (2008), 1397-1406.
  26. F.A. Sehba and J.B. Bederson, Mechanisms of acute brain injury after subarachnoid hemorrhage Neurological Research 28 (2006), 381-398.
  27. D.D. Sharpnack, A.J. Johnson and Y.Y.I. Phillips, The pathology of primary blast injury, in: Conventional Warfare: Ballistic, Blast, and Burn Injuries R.F. Bellamy andR. Zajtchuk eds., Borden Institute, Office of the Surgeon General, Department of the Army, Bethesda, MD, 1991, pp. 271-294.
  28. M.S. Xydakis, V.S. Bebarta, C.D. Harrison, J.C. Conner and G.A. Grant, Tympanic-membrane perforation as a marker of concussive brain injury in Iraq, New England Journal of Medicine 357 (2007), 830-831.