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Objective Tinnitus in Benign Intracranial Hypertension: An Update
Abstract
Previously, the authors reported that objective pulsatile tinnitus can be the major or only manifestation of benign intracranial hypertension. This report updates the authors' experience with 31 patients managed over the past 7 years.
Benign intracranial hypertension should be suspected in all patients with pulsatile‐objective tinnitus, especially when the patient is a young, obese female with headaches and/or visual disturbances. Papilledema and small ventricles or an empty sella on computerized tomography are almost diagnostic. The diagnosis is confirmed by elevated spinal fluid pressure on lumbar puncture. In such patients, angiography is not indicated. Furosemide and acetazol‐amide are very effective. Ligation of the internal jugular vein is contraindicated.
... 19,20 Similar to other arterial-phase PT etiologies, tinnitus caused by ICA stenosis does not improve on digital pressure or head rotation. 21 Atherosclerotic disease in the petrous carotid can be managed medically, with antiplatelet medications, or with angioplasty and stenting for patients with severe or symptomatic stenosis. 22 Improvement in PT has been reported after successful stenting of the petrous ICA. ...
... 92,111 IIH is associated with PT; headache; papilledema; visual obscurities; palsies of the fifth, sixth, and seventh nerves; and pseudosensorineural hearing loss. 21,112 Approximately 50% of patients with IIH will have PT, typically presenting with unilateral PT. 113 The exact pathophysiology connecting IIH and PT remains unknown, but the proposed mechanisms include turbulent flow through venous sinuses that are compressed by increased intracranial pressure ( Figure 6). 114 In addition, recent studies suggest a correlation between sigmoid sinus wall abnormalities and PT in patients with IIH. ...
Traditionally in the domain of the otolaryngologist, pulsatile tinnitus (PT) has become increasingly relevant to neurosurgeons. PT may prove to be a harbinger of life-threatening pathology; however, often, it is a marker of a more benign process. Irrespectively, the neurosurgeon should be familiar with the many potential etiologies of this unique and challenging patient population. In this review, we discuss the myriad causes of PT, categorized by pulse-phase rhythmicity.
... Pulsatil tinnitus transvers sinüs darlığına bağlı olarak tek veya iki taraflı olabilir (Boddu et al., 2016). Pulsatil tinnitusun yanı sıra kulakta dolgunluk, düşük frekans da olan sesleri duymada sıkıntı, vertigo, kulak ve burundan BOS sızıntısı görülebilen bulgulardandır (Sismanis et al., 1990). ...
... Additionally, the frequency spectrum of the first heart sound is primarily distributed in the low frequency range of 50-200 Hz (24). Specifically, in the cases of SS-Div/SS-Deh, it has been proven that pulse-synchronous acoustic characteristics are relatively low sound pressure levels within low-frequency range (19,26). Expanding upon the improvement of LFHL in these previous studies, our study is meaningful in that the improvement in audiometric profiles can be visualized with the help of our new examination method and thus PTA with manual neck compression may aid in confirming a venous origin of PT and predicting a favorable surgical outcome. ...
Venous pulsatile tinnitus (PT) is characterized by an auditory perception of pulse-synchronous sound, suppressed by compression of the ipsilateral internal jugular vein. We sought to determine the preoperative prognostic significance of the effect of ipsilateral neck manual compression on the PT loudness and audiometric changes in patients with sigmoid sinus dehiscences (SS-Deh) and diverticula (SS-Div) by comparing postoperative improvements in ipsilateral low-frequency hearing loss (LFHL) in pure-tone audiogram (PTA) and PT symptoms. Twenty-two subjects with PT originating from SS-Deh/Div were recruited. Air-conduction hearing thresholds were measured using PTA at three time points: twice preoperatively (with neutral neck position and with ipsilateral manual compression of internal jugular vein) and once at 3-months postoperatively with neutral neck position. We defined a positive neck compression effect as a threshold improvement of ≥ 10 dB HL at 250 or 500 Hz after manual neck compression. All but two subjects presented with ipsilateral LFHL in the neutral position. The average hearing threshold in the neutral position markedly improved after manual neck compression, indicating that LFHL originated from the masking effect of venous PT. All subjects had subjective improvements in PT and LFHL after sigmoid sinus surgeries, confirming that LFHL resulted from the masking effect of PT. Additionally, improvement of LFHL after neck compression could be regarded as a positive prognostic indicator after surgery. Collectively, elimination of PT loudness and improvement of LFHL with manual compression over the ipsilateral neck may suggest the venous origin of the PT and predict a favorable outcome following repair of SS-Deh/SS-Div.
... The objectification of venous pulsatile tinnitus (PT), a common form of objective tinnitus characterized by selfperception of the pulse-synchronous extradural sinus flow sound, has recently been increasingly documented [3][4][5][16][17][18][19], of which the trans-external auditory canal and Doppler ultrasound-recording techniques are the commonly implemented methodologies to capture in vivo acoustic characteristics of PT [9,11,[13][14][15]. It has been suggested that analyzing the frequency features of PT has a high potential for differentiating the vascular type [13]. ...
Objective:
Venous pulsatile tinnitus (PT) has received increasing attention recently. As analyses of psychophysical and neuropsychological dimensions of venous PT are lacking, this study aimed to quantitatively and qualitatively investigate the correlation among audiometric, hydroacoustic, and subjective outcomes in patients with PT.
Methods:
Fifty-five venous PT patients, with or without sigmoid sinus wall anomalies (SSWAs), were subdivided into SSWAs (n = 30) and non-SSWAs (n = 25) groups. Audiometric and hemodynamic evaluations were assessed. Questionnaires including the Tinnitus Handicap Inventory, Hospital Anxiety and Depression Scale (HADS), and Athens Insomnia Scale (AIS) were deployed to evaluate the psychological impacts of PT.
Results:
Among 55 subjects, PT frequency-related pure-tone audiometry (PTA) was significantly different between ipsilesional non-PT frequency-related PTA (p < 0.01), ipsilateral jugular vein compression PTA (p < 0.01), and contralesional ear PTA (p < 0.01). In contrast with the pulsatility index and flow velocity, bilateral EOET and flow volume were significantly different (p < 0.01). Of the 3 questionnaire types, there was a strong correlation between HADS anxiety and AIS scores (r = 0.658, p < 0.01). The duration of PT was not correlated with subjective outcomes, and there was no statistical significance found among audiometric, hemodynamic, and subjective outcomes between SSWAs and non-SSWAs groups.
Conclusions:
(1) The duration of PT was irrelevant to the increase of PTA. (2) Venous PT is the perception of vascular flow sound, in which hydroacoustic characteristics can be highly independent. (3) Anxiety, depression, and sleep disorders commonly prevail among PT patients.
Purpose
The purpose of this study was to explore the ophthalmological involvement in diagnosed cases of Idiopathic Intracranial Hypertension (IIH).
Methods
Case series of all patients diagnosed with IIH from October 2012-2014 at the Neurology Department of Amrita Institute of Medical Sciences were prospectively analysed. Analysis was done for 35 patients who fulfilled the updated diagnostic criteria.
Results
80% of the patients were women with a mean age of 34.5. The chief complaint was a throbbing headache in 85.7%.The least common complaints were tinnitus, phonophobia, and photophobia, and one patient had right facial paresis. All patients had well-preserved visual acuity. 30 patients had normal extraocular movements, bilateral abduction restriction was found in 4 patients, and one was reported to be with third and sixth nerve paresis. 22 patients were in Obese class I. CSF opening pressure was elevated in all patients. 80% had Grade 1 papilledema. Enlargement of blindspot and peripheral constriction of fields were commonly seen. 41.4% of patients showed inferior RNFL thickness to be the most affected. A statistically significant association was found between the grade of papilloedema and the visual field.
Conclusion
All our patients had papilledema clinically, with well-preserved central vision. Visual field defects were found, which showed a positive correlation with the severity of papilledema, showing the visual field to be a sensitive indicator. Contrary to expectation, an increase in RNFL on OCT was not a universal finding in our patients despite clinically observable papilledema.
Superior semicircular canal dehiscence (SSCD) is an example of a “third mobile window” (TMW) condition resulting from dehiscence of middle fossa bone over the superior semicircular canal [1]. While not as well characterized as SSCD, other foci of otic capsule dehiscence have also been described, including the posterior semicircular canal, vestibular aqueduct, internal auditory canal, carotid canal, and fallopian canal [2–7]. TMWs allow aberrant sound and energy transfer through the inner ear, leading to classic findings of mixed hearing loss, autophony and vestibular dysfunction. Less specific symptoms, including pulsatile tinnitus, headache, hyperacusis and visual disturbance, may also be present, resulting in difficulty distinguishing TMW conditions from other entities, including migraine variants and idiopathic intracranial hypertension (IIH) [8].
While superior semicircular canal dehiscence (SSCD) is relatively well-known in the medical community, there are many other sites of otic capsule dehiscence (OCD) which create a third mobile window resulting in third window syndrome (TWS). Over the past quarter century, there has been tremendous expansion of the depth of our knowledge and understanding of TWS; however, the identification of lesser-known sites of OCD remains an important diagnostic and therapeutic challenge. This is all the more so as in our experience TWS, including SSCD, remains under-diagnosed. Therefore, the development of a unitary anatomical-clinical and radiological classification would be an important step for a better understanding of these pathologies by neurotologists, otologists, neurologists, auditory-vestibular specialists, otolaryngologists, and neuroradiologists. Thus, the probability of being left without an etiological diagnosis in case of “mysterious” pseudo-conductive hearing loss, with or without obvious associated vestibular phenomena, should become lower. Furthermore, due to the progressive increase in new reported variants of OCD, the characterization of the anatomical structures involved, as well as the size and location of the TW, has become essential for a better understanding of the various mechanisms associated with this pathology. This allows us not only to systematize the different known variants but also to propose new, eventually less invasive or more pathophysiological therapeutic strategies. Based on the experience of the authors of this chapter, who have considered not only personal case studies but also other relevant publications on the subject, this chapter is the result of collaborative collegial work.KeywordsThird mobile window abnormalitiesOtic capsule dehiscenceCochlear-meningeal dehiscenceCochlear-vascular dehiscence
Objective:To probe the clinical characteristics of diagnosis and therapy of vascular pulsatile tinnitus（PT） associated with sigmoid sinus-mastoid. Methods:Retrospectively analyzed the clinical data of the hospitalized 45 PT patients of an ear surgeon in one hospital between January 2013 to January 2020, and observed the effectiveness with surgery and non-surgery therapy. Surgical procedures include reconstruction the bone wall of sigmoid sinus by transmastoid approach and ligation of mastoid emissary vein. Non-surgery therapy includes anti-anemia therapy and observation. All patients have been followed-up in ENT outpatient. Results: Of 45 cases, female：male was 43：2, the mean age was 42.7 years old. The other PT patients were the subjective tinnitus except two females were the objective tinnitus. Of 40 cases, 38 patients underwent transmastoid approach to reconstructed sigmoid sinus bone wall, including 6 patients with the ligated mastoid emissary vein at the same period.The other 2 cases with the ligated mastoid emissary vein only.Five cases were treated by non-surgery therapies, including 2 cases anti-anemia therapy and 3 cases observation. The longest follow-up period was seven and a half years, the shortest was six months. One case was lost to follow up. The total cure rate was 80.0%（36/45），the surgery cure rate was 82.5%（33/40）, the non-surgery cure rate was 60.0% （3/5）. Conclusion:The pathophysiologic mechanism of the PT is still complex and unclear until now. However, the following conditions probably play an important role in the etiology: female, common features of anatomy anomalies, hemodynamic variations. It is a key point to confirm the responsible site or the main cause of the PT . Although the surgery is relatively simple, the effect is remarkable and no major postoperative complications，surgery could not be a only choice.
Objective
This study aimed to quantitatively and qualitatively evaluate the hydroacoustic changes from “presence” to “disappearance” of pulsatile tinnitus (PT) with the extraluminal compression surgical technique. The recent issues of concern pertaining to the hydroacoustic characteristics of sigmoid sinus wall anomalies and distal transverse sinus stenosis (dTSS) were discussed.
Methods
This study was based on a retrospective case series. Seventy-seven patients with PT and transverse-sigmoid sinus enlargement with or without transverse-sigmoid sinus junction anomalies and transverse sinus stenosis (TSS) who had undergone extraluminal compression surgery under local anesthesia were included. Management of intractable intraoperative challenges and techniques for reversal extraluminal compression were introduced. Anatomical measurements, intraoperative color-coded Doppler ultrasonography, spectro-temporal analysis, and computational fluid dynamics were employed to analyze the hydroacoustic characteristics of PT.
Results
The efficacy of the extraluminal compression technique was evident with the significant reduction in peak turbulent kinetic energy, vorticity, and mean pressure gradient at the transverse-sigmoid junction, resulting in over 20% reduction in PT amplitude. dTSS is a common finding in patients with PT exhibiting transverse-sigmoid sinus enlargement. Patients with dTSS presented with significant differences in hemodynamic characteristics as compared to those without. Linear regression analysis showed that the flow disturbance (turbulent kinetic energy and vorticity) was closely associated with the degree of dTSS, whereas the flow amplitude was not related to the degree or location of TSS. Low-pulsatory vortex flow at the transverse-sigmoid junction was visualized during an intraoperative color-coded Doppler examination, and the displayed low-frequency PT sound corresponded to the patients’ subjective perception of PT.
Conclusion
(1) A reduction of over 20% of the flow-induced noise is the therapeutic goal of extraluminal compression technique. Since reductions in the magnitude of hemodynamic parameters, including turbulent kinetic energy, vorticity, and mean pressure gradient, render the flow-induced noise inaudible, besides sigmoid sinus wall anomalies, it is likely that PT develops from the aggregation of flow-based pathologies. (2) Although dTSS and diverticulum may greatly affect the hemodynamics at the transverse-sigmoid junction, in contrast to dehiscence, dTSS and diverticulum may not be the limiting factors for PT development.
Thirty-six patients with benign intracranial hypertension (BIH) were reviewed. Follow-up was obtained on 33 patients (91%) after a mean period of years. Precipitating factors were found in 27 patients (75%). On admission, 5 patients had retro-ocular pain, especially on eye movements, a complaint not yet described in BIH. Seven patients had nystagmus, two of them horizontal positional nystagmus. It is questionable whether all signs in BIH are caused by the raised CSF pressure.
• The prognosis for vision in most patients with pseudotumor cerebri is excellent; however, visual loss, which is the only serious complication, may occur either early or late in the course of the disease. A group of 57 patients was followed up five to 41 years with visual fields, visual acuity, and fundus photographs. Blinding visual loss or severe visual impairment in one or both eyes occurred in 14 patients, and in seven patients, this occurred months to years after the initial symptoms. Systemic hypertension was a significant risk factor for visual loss in patients with pseudotumor cerebri, and blindness occurred in eight of 13 patients who were hypertensive. Despite suggestions that blind spot measurement is useful for following up patients with this condition, we believe that sequential quantitative perimetry gives more complete information and is essential to rational decision making in the treatment of pseudotumor cerebri.
Tinnitus is a frequent presenting symptom. Tinnitus that is rhythmic and synchronous with the patient's heartbeat is rare. Pulsatile tinnitus may be the only symptom of life-threatening and treatable diseases. The presence of hearing loss or vertigo focuses the diagnostic evaluation. The cause of pulsatile tinnitus may be found on otoscopic examination. Audiologic assessment and enhanced computed tomography often contribute to the diagnosis. Increased intracranial pressure should be excluded with a fundoscopic examination. Arteriography is required to diagnose life-threatening and treatable lesions in the presence of normal otoscopy, audiologic assessment, and enhanced computed tomography.
Pulse-synchronous tinnitus is probably due to turbulent blood flow in or around the temporal bone. The anatomy of temporal bone blood supply is reviewed. Eight examples of tinnitus are presented to illustrate the spectrum of lesions that will produce this symptom and the role of angiography in its investigation.
The occurrence of vascular perturbations in the tympanogram in association with glomus tumors has previously been noted in the literature. We have broadened the scope of this method of diagnosis in the study of 3 glomus tympanicum and 3 glomus jugulare tumors, 1 dehiscent high jugular bulb, 1 aberrant carotid artery in the middle ear and 2 cases of pulsatile tinnitus of vascular origin. Analysis of illustrative tympanograms at standard and at increased sensitivity (x 20) obtained in these cases are presented. The following factors as they relate to the mechanism of recording the vascular perturbations are presented: air pressure and/or presence of fluid in the middle ear; compliance of the tympanic membrane and ossicular chain as affected by the mass, size and degree of vascularity of the mass and presence of extraneous sounds. A new method of recording the vascular perturbations utilizing a time-base generator affixed to an X-Y plotter is described. It is the purpose of this study to demonstrate the utility of obtaining tympanograms at standard and at increased sensitivity in the evaluation of vascular middle ear lesions and tinnitus of vascular origin.
Few conditions are seen as commonly by the otologist and are more poorly understood than subjective tinnitus. Tinnitus has been reported in as high as 80% of patients seen in an otolaryngology practice. This symptom is especially marked in patients with a hearing problem and can be so severe that it becomes incapacitating. Careful diagnosis and classification of tinnitus is important for understanding of the problem. Identification of the frequency and intensity of masking, using a tinnitus analyzer, is useful in selecting the form of treatment. Analysis of the history, physical findings and the use of special electrocochleography and brain stem evoked response audiometry help to identify the site of lesion, which may be within the cochlea, cochlear nerve, cochlear nucleus, brain stem, midbrain or auditory cortex. Specific disease entities should be identified and treated. Lesions of the end-organ or cochlear nerve can be treated when necessary by translabyrinthine or middle cranial fossa section of the cochlear nerve. Tinnitus from cervical nerve lesions can be treated by rhizotomy. The use of a hearing aid or introduction of a sound with a tinnitus masker has been found to be 82% effective in suppressing tinnitus. Maskers can be combined with a hearing aid in some cases. The pathogenesis of tinnitus is discussed, but the method of action of tinnitus relief by auditory stimulation is still unclear. A thoughtful and complete examination with our new diagnostic tools and the judicious selection of therapy now makes it possible to give relief to the majority of patients suffering with disturbing tinnitus.
An unusual case presenting to the otolaryngologist as pulsatile tinnitus is discussed. Fowler points out that the circulatory response to anemia is increased cardiac output. There is associated tachycardia and increased arterial pulse pressure. Because of this increased flow state and turbulence, systolic bruits, venous hums, and "capillary" pulsations are found. This increased flow state is perceived in the ear as a transmitted pulsatile tinnitus. The successful treatment of this patient's pernicious anemia corrected the hyperdynamic circulatory state, and resulted in disappearance of her tinnitus.
Carotid arteriograms on three patients with unilateral pulsatile tinnitus demonstrated an ipsilateral atypical trigeminal artery extending from the cavernous portion of the internal carotid artery to form the posterior inferior cerebellar artery. Illustrations and a dissection of a human fetus with a similar finding show this artery crossing the cochlear nerve near its insertion in the pons. Evidence is presented suggesting that neurovascular compression of the eighth nerve is the source of pulsatile tinnitus in these patients.