Auditory thrombosis represents a catastrophic neurotological emergency characterized by the acute occlusion of the arterial blood supply supplying the inner ear, culminating in rapid neuroepithelial ischemia and sudden functional loss. Because the membranous labyrinth is supplied by terminal microvessels lacking adequate collateral circulation, prompt clinical recognition is essential to differentiate peripheral vestibulopathy from impending posterior circulation infarction.
Auditory Thrombosis
1. Concise Definition
Auditory thrombosis is the acute thrombotic or thromboembolic occlusion of the internal auditory artery (labyrinthine artery) or its parent vessels within the vertebrobasilar circulation, leading to sudden, severe ischemia and subsequent infarction of the auditory and vestibular structures of the inner ear. The condition clinically manifests as an acute neurotological crisis marked by precipitous unilateral sensorineural hearing loss, intense rotational vertigo, tinnitus, and postural instability.
Pathophysiologically, the disorder constitutes an end-organ ischemic stroke localized to the cochleovestibular apparatus. Due to the high metabolic demand of the organ of Corti and the stria vascularis, even brief interruptions in arterial microperfusion deplete cellular adenosine triphosphate (ATP), abolish the endocochlear potential, and cause irreversible cellular injury across the neuroepithelium.
Within the broader spectrum of cerebrovascular pathology, auditory thrombosis occupies a critical diagnostic juncture. It can occur as an isolated microvascular phenomenon or serve as a harbinger of catastrophic stroke within the territory of the anterior inferior cerebellar artery (AICA) or the main basilar trunk.
2. Etymology & Linguistic Origin
The term “auditory thrombosis” is a compound medical designation rooted in classical Greek and Latin anatomical nomenclature. The adjective “auditory” derives from the Latin verb audire, meaning “to hear,” transitioning into Late Latin as auditorius (pertaining to the sense of hearing) before entering modern English medical vernacular during the sixteenth and seventeenth centuries.
The noun “thrombosis” originates directly from the ancient Greek word thrombōsis (θρώμβωσις), signifying “curdling” or “clotting,” which itself stems from thrombos (θρώμβος), denoting a lump, curd, or blood clot. In clinical nosology, the condition is frequently referred to interchangeably as internal auditory artery (IAA) thrombosis, labyrinthine artery thrombosis, or labyrinthine infarction.
Historically, early neuroanatomists referred to the primary vascular conduit as the arteria auditiva interna before the Nomina Anatomica standardized the term to arteria labyrinthi (labyrinthine artery) to better reflect its dual supply to both the cochlear and vestibular divisions of the inner ear.
3. Pronunciation & Grammatical Form
Pronunciation: Phonetically transcribed in the International Phonetic Alphabet (IPA) as /ˈɔː.dɪ.tər.i θrɒmˈboʊ.sɪs/ in British English, and /ˈɔː.də.tɔːr.i θrɑːmˈboʊ.sɪs/ in American English.
Grammatical Form: It is a singular, uncountable noun phrase. The term functions syntactically as a clinical entity or pathological diagnosis. Its plural formulation, rarely invoked due to the focal nature of the event, is “auditory thromboses” (/θrɒmˈboʊ.siːz/).
Adjectival modifications incorporate the associated clinical concepts, such as “thrombotic auditory ischemia” or “post-thrombotic vestibulocochlear impairment.” In formal medical documentation, practitioners commonly specify anatomical precision by recording “acute thrombosis of the left internal auditory artery” or “thrombotic labyrinthine infarction.”
4. Detailed Conceptual Explanation
To fully grasp the mechanics of auditory thrombosis, one must understand the unique microvascular anatomy and extreme metabolic vulnerability of the human inner ear. The labyrinth is supplied almost exclusively by the internal auditory artery (IAA), a delicate vessel that arises most commonly from the loop of the anterior inferior cerebellar artery (AICA), or less frequently, directly from the lower third of the basilar artery. The IAA traverses the internal acoustic meatus alongside the facial (CN VII) and vestibulocochlear (CN VIII) nerves, subsequently bifurcating into the common cochlear artery and the anterior vestibular artery.
Crucially, the internal auditory artery is a terminal end-artery. Unlike the brain parenchyma, which benefits from anastomotic redundancies via the circle of Willis and pial arteriolar collateral networks, the inner ear possesses virtually no effective collateral vasculature. When a thrombus forms in situ—frequently over an ulcerated atherosclerotic plaque—or lodges as an embolus within the lumen of the IAA, downstream capillary perfusion ceases almost instantaneously.
The metabolic architecture of the cochlea is extraordinarily demanding. The stria vascularis, a specialized epithelial bilayer lined with Na+/K+-ATPase pumps, actively generates and maintains the endocochlear potential (+80 to +100 mV) that drives hair cell transduction. Interruption of blood supply leads within seconds to acute anoxia, precipitous drop of ATP levels, and the collapse of the endocochlear electrical gradient. Without this ionic driving force, the stereocilia of both inner and outer hair cells lose their capacity to depolarize in response to mechanical acoustic stimulation.
Concurrently, cellular ischemia induces massive excitotoxic intracellular calcium accumulation, generation of reactive oxygen species (ROS), cytotoxic cellular edema, and eventual apoptotic or necrotic cell death. The vestibular sensory receptors within the ampullae of the semicircular canals and the maculae of the utricle and saccule undergo identical ischemic cascades, precipitating acute unilateral peripheral vestibular deafferentation. The functional consequence is an immediate, catastrophic disruption of sensory input to both the primary auditory cortex and the brainstem vestibular nuclei.
5. Historical Development
The concept that sudden neurotological symptoms could arise from vascular thrombosis emerged progressively over the past two centuries. Prior to the mid-nineteenth century, acute episodes of profound vertigo and deafness were almost universally classified as cerebral apoplexy or central epileptic events. In 1861, French physician Prosper Ménière revolutionized the field by demonstrating that apoplectiform vertigo originated not within the cerebral hemispheres, but within the peripheral semicircular canals and cochlea, postulating that sudden hemorrhagic or vascular disruptions within the temporal bone produced acute crises.
During the early twentieth century, European otologists, including Politzer, Alexander, and Siebenmann, conducted pioneering micro-dissections of temporal bones, mapping the course of the internal auditory artery and theorizing that occlusive vascular disease was an underappreciated cause of sudden idiopathy. However, definitive experimental validation came in the late 1950s through the landmark studies of H. B. Perlman, R. S. Kimura, and C. Fernandez. By surgically occluding the internal auditory artery in animal models, they meticulously documented the acute electrophysiological demise of the cochlea, confirming that microvascular ligation eradicated cochlear microphonics within minutes and caused profound histologic necrosis within hours.
The modern era of clinical recognition blossomed with the evolution of stroke neurology in the 1980s and 1990s. Clinicians such as Robert W. Baloh and subsequent neurotologists delineated the syndrome of AICA infarction, establishing that ischemic stroke within the posterior circulation frequently presented with audiovestibular signs. Over the past two decades, extensive neurotological investigations by researchers such as Hyung Lee and Ji-Soo Kim have utilized high-resolution diffusion-weighted magnetic resonance imaging (DWI-MRI) and video-oculography, systematically demonstrating that auditory thrombosis often acts as a prodromal herald to major stroke within the vertebrobasilar territory.
6. Theoretical Foundations
Auditory thrombosis is conceptualized within several robust medical and physiological frameworks: the terminal vascular bed model, neurovascular metabolic coupling, and the posterior circulation thromboembolic paradigm.
The terminal vascular bed model dictates that tissues supplied by end-arteries lack physiological defense mechanisms against acute occlusion. Because the labyrinthine microvasculature does not receive retrograde perfusion from adjacent dural or petrous arteries, occlusion of the primary vessel establishes an ischemic core with virtually non-existent penumbral rescue capacity. Consequently, the temporal therapeutic window for rescuing ischemic cochlear hair cells is markedly narrower than that observed in ischemic cerebral cortex.
From the perspective of neurovascular coupling and bioenergetics, the inner ear operates on strict homeostatic control of endolymphatic fluid balance. The endolymph exhibits a high potassium concentration ([K+] ∼ 150 mM) and extremely low sodium concentration ([Na+] ∼ 1 mM). This unique electrochemical environment requires continuous enzymatic pumping across the strial capillary network. Ischemic interruption of this metabolic cascade triggers rapid ionic equilibrium across cellular membranes, terminating auditory transduction well before structural cell death occurs.
Finally, the posterior circulation thromboembolic framework situates auditory thrombosis as a localized manifestation of systemic vascular disease. It reflects Virchow’s triad: endothelial injury (atherosclerosis of the vertebral or basilar arteries), hemodynamic alteration (hypoperfusion or turbulent flow at arterial branch points), and hypercoagulability. Thrombi may originate in situ due to local microatheroma at the orifice of the IAA, or propagate from upstream sources such as vertebral artery dissection, basilar atheroma, or cardiogenic emboli.
7. Key Components, Types & Dimensions
Auditory thrombosis can be categorized by the specific anatomical level of vascular occlusion, its underlying pathophysiological mechanism, and the resulting clinical syndrome:
- Isolated Internal Auditory Artery (IAA) Thrombosis: Complete occlusion restricted exclusively to the main trunk of the labyrinthine artery before its terminal bifurcation. This produces profound pan-labyrinthine infarction involving the entire cochlea, horizontal and superior semicircular canals, and the utricle and saccule.
- Common Cochlear Artery Occlusion: Selective thrombosis affecting the branch supplying the main cochlear spiral and the vestibulocochlear branch. Patients experience severe sudden sensorineural hearing loss with selective loss of low-frequency saccular or posterior canal function, often with partial sparing of horizontal canal function.
- Anterior Vestibular Artery (AVA) Occlusion: Selective thrombosis of the artery supplying the ampullae of the horizontal and superior semicircular canals, the utricular macula, and a small part of the saccule. This manifests as acute vestibular syndrome with severe rotational vertigo and nystagmus, but with completely preserved hearing, clinically mimicking vestibular neuritis.
- Main Cochlear Artery Thrombosis: Focal microthrombosis localized past the branching of the vestibulocochlear vessel, resulting in isolated severe-to-profound deafness and intense tinnitus in the absence of acute vestibular signs.
- Territorial AICA Infarction with Auditory Artery Thrombosis: Occlusion of the parent anterior inferior cerebellar artery at or proximal to the origin of the labyrinthine artery. This combines labyrinthine infarction with brainstem and cerebellar strokes, causing lateral pontine signs, ipsilateral facial numbness, ipsilateral Horner syndrome, cerebellar ataxia, and contralateral sensory loss.
- Hemodynamic Hypoperfusion Microthrombosis: Low-flow state thrombosis occurring secondary to severe basilar artery stenosis, subclavian steal syndrome, or profound systemic hypotension, in which microvascular sludging and thrombus formation settle in the terminal labyrinthine circulation.
8. Examples & Illustrative Cases
To contextualize how auditory thrombosis presents across diverse patient cohorts, consider the following representative clinical scenarios:
Case 1: The Impending Vertebrobasilar Stroke. A 64-year-old male with a history of long-standing hypertension, type 2 diabetes mellitus, and cigarette smoking presents to the emergency department with acute, spontaneous vertigo, accompanied by immediate loss of hearing and high-pitched roaring tinnitus in his right ear. On physical examination, he demonstrates spontaneous left-beating horizontal-torsional nystagmus and an abnormal right head impulse test, typical of peripheral vestibular hypofunction. An initial non-contrast head CT is unremarkable. Forty-eight hours later, he develops severe dysarthria, right-sided facial weakness, and profound right-sided limb dysmetria. Repeat MRI with diffusion-weighted imaging reveals acute infarction of the right middle cerebellar peduncle and lateral lower pons in the distribution of the AICA. In retrospect, the initial isolated auditory thrombosis was the prodromal sentinel event of progressive basilar artery branch atheromatous disease.
Case 2: Isolated Microvascular Thrombosis. A 58-year-old female with hyperlipidemia and previously undetected paroxysmal atrial fibrillation awakens with profound unilateral left deafness, violent spinning vertigo, nausea, and persistent vomiting. Neurological examination is entirely negative for cranial neuropathies, limb ataxia, sensory loss, or motor deficits. Pure-tone audiometry confirms severe sensorineural hearing loss across all frequencies on the left. High-resolution 3-Tesla brain MRI reveals no central brainstem or cerebellar infarction. However, high-resolution inner ear 3D-FLAIR sequences demonstrate faint high-signal hyperintensity within the left fluid spaces of the cochlea and vestibule, indicative of acute labyrinthine infarction secondary to isolated cardiogenic thromboembolism of the left internal auditory artery.
9. Measurement & Assessment
Evaluating suspected auditory thrombosis requires a multimodal diagnostic approach combining bedside neurotology, formal audiological measurement, and advanced neuroimaging. Because standard cranial imaging may fail to resolve micro-infarctions of the inner ear, clinical assessment plays an indispensable role.
At the bedside, the HINTS examination (Head Impulse, Nystagmus, Test of Skew) is the gold standard clinical algorithm for differentiating peripheral inner ear dysfunction from central posterior circulation stroke. In an isolated internal auditory artery thrombosis, the exam paradoxically displays “peripheral” characteristics: a positive (abnormal) horizontal head impulse test toward the affected ear, unidirectional horizontal-torsional nystagmus that intensifies on looking in the direction of the fast phase (following Alexander’s law), and an absence of skew deviation. However, because auditory thrombosis is frequently accompanied or rapidly followed by central ischemia, serial evaluations are critical.
Formal audiological and vestibular evaluations quantify the extent of neuroepithelial damage:
- Pure-Tone Audiometry (PTA): Documents the depth and configuration of hearing loss. Auditory thrombosis characteristically produces a severe-to-profound flat or high-frequency sloping sensorineural hearing loss with markedly reduced speech discrimination scores.
- Video Head Impulse Testing (vHIT): Measures the vestibulo-ocular reflex (VOR) gain across all six semicircular canals individually, identifying specific deficit patterns corresponding to the anterior vestibular or common cochlear branches.
- Vestibular Evoked Myogenic Potentials (VEMPs): Cervical VEMPs (cVEMP) evaluate saccular and inferior vestibular nerve integrity, whereas ocular VEMPs (oVEMP) evaluate utricular and superior vestibular nerve function, enabling topographical localization of ischemic injury within the labyrinth.
- Caloric Irrigation: Documents unilateral horizontal semicircular canal paresis, showing characteristic hyporesponsiveness on the affected side.
Neuroimaging protocols should employ 3-Tesla MRI incorporating diffusion-weighted imaging (DWI), apparent diffusion coefficient (ADC) mapping, and three-dimensional fluid-attenuated inversion recovery (3D-FLAIR). While conventional DWI readily detects territorial cerebellar or pontine infarction, isolated labyrinthine infarction requires targeted thin-slice inner ear sequences. Gadolinium-enhanced or unenhanced 3D-FLAIR sequences may reveal high-signal intensity or failure of fluid signal suppression in the affected labyrinth within hours to days of thrombosis, reflecting breakdown of the blood-labyrinth barrier or ischemic micro-hemorrhage. Magnetic resonance angiography (MRA) or CT angiography of the head and neck is indicated to evaluate patency of the basilar and vertebral arteries.
10. Applications & Practical Significance
The clinical and operational significance of diagnosing auditory thrombosis extends across emergency medicine, vascular neurology, otolaryngology, and primary care. The central clinical mandate is the rapid distinction between a benign inflammatory condition (such as viral labyrinthitis) and an acute vascular event capable of escalating into catastrophic brainstem infarction.
In acute clinical settings, sudden sensorineural hearing loss combined with vertigo should be treated as a transient ischemic attack (TIA) or minor ischemic stroke until proven otherwise, especially in patients with vascular risk factors (hypertension, hyperlipidemia, diabetes, tobacco use, or atrial fibrillation). Establishing an early diagnosis allows for immediate therapeutic intervention, including:
- Acute Revascularization: In highly selected cases presenting within narrow therapeutic windows (typically under 4.5 hours from symptom onset) alongside evolving territorial signs, intravenous thrombolysis with tissue plasminogen activator (tPA) or endovascular thrombectomy of a parent basilar artery occlusion may be considered.
- Secondary Stroke Prevention: Initiation of antiplatelet therapy (e.g., aspirin, clopidogrel, or dual antiplatelet therapy) or therapeutic anticoagulation (in cases of confirmed cardioembolic disease) to prevent thrombus propagation or subsequent strokes within the posterior fossa.
- Hemodynamic Optimization: Strict avoidance of aggressive blood pressure reduction during the hyperacute phase to preserve collateral micro-perfusion to the bordering vascular territories of the brainstem.
- Vestibular Rehabilitation: Following acute stabilization, customized physical therapy leveraging neuroplasticity facilitates central vestibular compensation for permanent unilateral peripheral vestibular hypofunction.
11. Research & Empirical Evidence
Substantial empirical literature supports the pathophysiology and clinical course of auditory thrombosis. A critical body of research led by Kim, Lee, and Baloh has established that acute audiovestibular loss is the single most common prodromal presentation of anterior inferior cerebellar artery territory infarction. In systematic cohorts analyzing patients with AICA stroke, up to 80% exhibited profound combined auditory and vestibular loss, and nearly 10% presented with isolated sudden hearing loss and vertigo days to weeks prior to the manifestation of brainstem or cerebellar infarction.
Pathological confirmation of isolated internal auditory artery thrombosis in humans has historically been constrained by the difficulty of obtaining early postmortem temporal bone specimens. However, landmark clinicopathological correlative studies have documented selective necrosis of the membranous labyrinth. These histological examinations revealed complete atrophy of the organ of Corti, marked cellular loss within the spiral ganglion, and extensive fibrocystic obliteration of the fluid spaces of the cochlea, while demonstrating variable, patchy sparing of the saccule and posterior semicircular canal ampulla. This observed pattern aligns with the anatomical hypothesis that inferior vestibular branches may occasionally receive subtle collateral contributions from the posterior meningeal or petrosal microvasculature.
Epidemiological registry studies have corroborated these biological findings. Large-scale retrospective cohort studies tracking patients presenting with sudden sensorineural hearing loss have demonstrated a significantly elevated hazard ratio for subsequent ischemic stroke—particularly within the vertebrobasilar territory—over the following five years compared to matched controls without sudden auditory deficits. This excess risk is most pronounced among individuals over 50 years of age exhibiting preexisting cardiovascular comorbidities.
12. Cultural & Cross-Cultural Considerations
The clinical approach to auditory thrombosis exhibits considerable variance across global healthcare environments, governed primarily by differences in diagnostic infrastructure, subspecialty cross-collaboration, and regional stroke protocols. In healthcare systems with integrated acute stroke care pathways, such as those found in tertiary hospitals across North America, parts of Europe, and East Asia, patients presenting to emergency departments with acute vertigo and hearing loss increasingly undergo comprehensive HINTS examinations by vascular neurologists alongside immediate neuroimaging.
Conversely, in many primary care settings worldwide, sudden hearing loss accompanied by vertigo is routinely misdiagnosed as acute labyrinthitis, benign paroxysmal positional vertigo (BPPV), or Ménière’s disease. These patients are frequently managed with oral corticosteroids or antihistamines and referred for outpatient otolaryngology visits weeks later. By that time, the therapeutic window for acute vascular intervention or secondary stroke mitigation has elapsed. Global health advocacy organizations have emphasized the implementation of unified neurotology triage education to standardize the recognition of acute audiovestibular signs as potential vascular stroke equivalents.
13. Criticisms, Debates & Limitations
Despite substantial clinical advances, several controversial areas and diagnostic limitations persist regarding auditory thrombosis:
The foremost clinical controversy centers on the etiology of “idiopathic” sudden sensorineural hearing loss (ISSNHL). While many otologists maintain that the vast majority of ISSNHL cases stem from viral cochleitis or autoimmune reactions, vascular neurologists argue that a significant proportion represents occult, undiagnosed microvascular thrombosis of the terminal branches of the internal auditory artery. Because ordinary clinical MRI cannot directly visualize vessels with a caliber smaller than 200 micrometers, verifying isolated microvascular thrombosis in vivo remains challenging, resulting in potential diagnostic underestimation.
Another contentious issue involves therapeutic protocol selection. Standard otolaryngological guidelines recommend high-dose systemic or intratympanic corticosteroids for sudden sensorineural hearing loss. However, if the underlying pathology is microvascular thrombosis, steroids may be ineffective or potentially counterproductive by increasing blood pressure and blood glucose levels in patients with metabolic vascular disease. Conversely, administering full-dose anticoagulation or thrombolytic therapy carries substantial intracranial and systemic hemorrhagic risks that may outweigh potential benefits when imaging cannot confirm an occluded vessel.
Finally, there is an ongoing debate regarding the diagnostic specificity of the HINTS protocol when applied by non-expert clinicians. While trained neurotologists achieve high sensitivity and specificity in distinguishing peripheral from central vertigo using HINTS, general emergency physicians often display high rates of misinterpretation, underscoring the urgent need for automated, objective video-oculographic devices in emergency settings.
14. Related Terms & Distinctions
To ensure diagnostic clarity, auditory thrombosis must be systematically differentiated from related otological and neurological entities:
- Viral Labyrinthitis: An acute inflammatory condition of the inner ear caused by viral infection. While it presents with combined sudden hearing loss and acute vertigo identical to auditory thrombosis, it typically occurs in younger individuals, often follows a systemic viral illness, and is unassociated with vascular risk factors or central neurological signs.
- Vestibular Neuritis: Inflammation of the vestibular division of cranial nerve VIII. Unlike auditory thrombosis, vestibular neuritis selectively affects the vestibular system; auditory function is completely preserved, and pure-tone audiometry remains strictly normal.
- Ménière’s Disease: An inner ear disorder characterized by endolymphatic hydrops. It causes episodic vertigo, fluctuating low-frequency hearing loss, tinnitus, and aural fullness. Crucially, Ménière’s disease is recurrent and episodic, resolving between attacks, whereas auditory thrombosis produces an abrupt, non-fluctuating, and typically permanent deficit.
- AICA Stroke: An infarction involving the territory of the anterior inferior cerebellar artery. Auditory thrombosis is often an early component or branch manifestation of AICA stroke, but full territorial AICA infarction presents with prominent central neurological signs, including cerebellar ataxia, facial numbness, Horner syndrome, and gaze-evoked nystagmus.
- Acoustic Neuroma (Vestibular Schwannoma): A benign, slow-growing neoplasm of the vestibulocochlear nerve. It generally causes progressive, insidiously worsening unilateral high-frequency sensorineural hearing loss, asymmetric speech discrimination decline, and mild dysequilibrium, rather than the catastrophic apoplectic onset characteristic of acute thrombosis.
15. Summary / Key Takeaways
Auditory thrombosis is a life-altering vascular crisis characterized by the acute occlusion of the internal auditory artery or its parent vessels, depriving the terminal microcirculation of the membranous labyrinth of oxygenated blood. Because the inner ear is uniquely susceptible to ischemic injury and lacks collateral arterial anastomoses, interruption of blood flow leads to rapid, irreversible damage to cochleovestibular hair cells, causing sudden sensorineural deafness and intense acute vertigo.
Clinically, auditory thrombosis must be treated as a potential vascular warning sign. It frequently heralds an impending, extensive posterior circulation ischemic stroke in the territory of the anterior inferior cerebellar artery. Timely assessment through rigorous bedside neurotological testing (HINTS protocol), urgent audiological measurement, and high-resolution neuroimaging is essential to stabilize the patient, initiate appropriate antiplatelet or anticoagulation protocols, and mitigate the risk of catastrophic cerebrovascular events.
Ultimately, prompt recognition of auditory thrombosis bridges the critical gap between otology and vascular neurology. Identifying acute audiovestibular deficits as potential indicators of posterior circulation ischemia ensures early diagnosis, preserves life-saving interventions, and helps optimize patient recovery and rehabilitation.
References
- Baloh, R. W. (1998). Vertigo of vascular origin. Neurologic Clinics, 16(2), 455–470. https://pubmed.ncbi.nlm.nih.gov/9531174/
- Kim, J. S., & Lee, H. (2009). Inner ear dysfunction due to vertebrobasilar ischemic stroke. Seminars in Neurology, 29(5), 534–540. https://pubmed.ncbi.nlm.nih.gov/19834866/
- Lee, H., & Cho, Y. W. (2003). Auditory disturbance as a prodrome of anterior inferior cerebellar artery infarction. Journal of Neurology, Neurosurgery & Psychiatry, 74(12), 1644–1648. https://pubmed.ncbi.nlm.nih.gov/14638883/
- Mazzoni, A. (1972). Internal auditory artery supply to the petrous bone. Annals of Otology, Rhinology & Laryngology, 81(1), 13–21. https://pubmed.ncbi.nlm.nih.gov/5013098/
- Perlman, H. B., Kimura, R. S., & Fernandez, C. (1959). Experiments on temporary obstruction of the internal auditory artery. The Laryngoscope, 69(6), 591–613. https://pubmed.ncbi.nlm.nih.gov/13665977/