|Year : 2018 | Volume
| Issue : 3 | Page : 191-193
Increased intracranial tension and cochleovestibular symptoms: an observational clinical study
Badr E Mostafa, Hesham A.A El-Sersy, Tarek A Hamid
Department of Otorhinolaryngology, Head and Neck Surgery, Faculty of Medicine, Ain Shams University, Cairo, Egypt
|Date of Web Publication||16-Aug-2018|
Badr E Mostafa
75 El Nozha Street, Heliopolis, 11361 Cairo
Source of Support: None, Conflict of Interest: None
Objectives Meniere’s disease is thought to be pathophysiologically due to increased pressure in the endolymphatic spaces leading to distortion of the sensory elements. As the inner ear fluids are in direct and indirect contact with cerebrospinal fluid (CSF), it was hypothesized that changes in CSF hydrodynamics could affect inner ear fluid pressures.
Patients and methods This study was conducted on 150 patients presenting with benign increased intracranial tension diagnosed by Dandy’s criteria and by radiological data. All patients were subjected to a detailed vertigo questionnaire and underwent comprehensive clinical, audiological, and vestibular testing to detect any vestibular abnormalities.
Results Of the studied patients, 38 (25.3%) (34 females and four males) presented with audiovestibular symptoms: ear fullness and/or hearing loss, tinnitus, attacks of vertigo, and instability. Some patients reported atypical positional or motion-induced vertigo. A total of 13 patients presented with sensorineural hearing loss (SNHL). Clinical head impulse test (HIT) was positive in 30 patients, abnormal caloric test results in 24 patients, and 12 had positive Dix–Hallpike test results. All patients with audiovestibular symptoms were previously treated with betahistine (24 mg, three times a day) with poor response. Patients with abnormal test results were shifted to acetazolamide+betahistine. Thirty patients had a dramatic response on both audiological and vestibular manifestations.
Conclusion Changes in CSF pressure significantly affect inner ear fluids in some patients. Symptoms and tests may mimic Meniere’s disease, and we recommend evaluating patients with atypical Meniere’s disease (MD), especially early bilateral affection and/or poor response to conventional therapy, for increased intracranial tension (ICT). Further testing of other cochlea-vestibular functions in these patients is under way.
Keywords: crebrospinal fluid, intracranial tension, Meniere’s disease, vertigo
|How to cite this article:|
Mostafa BE, El-Sersy HA, Hamid TA. Increased intracranial tension and cochleovestibular symptoms: an observational clinical study. Egypt J Otolaryngol 2018;34:191-3
|How to cite this URL:|
Mostafa BE, El-Sersy HA, Hamid TA. Increased intracranial tension and cochleovestibular symptoms: an observational clinical study. Egypt J Otolaryngol [serial online] 2018 [cited 2019 Mar 22];34:191-3. Available from: http://www.ejo.eg.net/text.asp?2018/34/3/191/239106
| Introduction|| |
Proper function of the inner ear depends on the delicate balance between inner ear fluids. It is thought that symptoms can arise from the pressure differential between the endolymph and perilymph leading to distortion of the neural bearing membranes and thus dysfunction of the system. Abnormal endolymph accumulation is called endolymphatic hydrops and leads to the syndrome tagged Meniere’s disease or variants thereof . It can also lead to changes in middle ear compliance, cochlear microphonics, and DPOAE ,,,,,. Perilymphatic pressure is directly transmitted to the endolymph via the thin Reissner’s membrane; the pressure difference between endolymph and perilymph is less than 0.5 mmHg, and both perilymphatic and endolymphatic pressures can be considered equivalent to the inner ear pressure ,. Intracranial pressure (ICP) has been shown to influence the perilymphatic pressure ,,, because the cranial cerebrospinal fluid (CSF) and inner ear intralabyrinthine fluid communicate through three routes: the vestibular aqueduct, the cochlear aqueduct, and the internal auditory canal ,. Consequently, inner ear pressure can mirror ICP, and this may play a key role in inner ear pressure regulation and fluid homeostasis and may be related to inner ear diseases ,.
The hypothesis was whether differential changes in pressure of the inner ear fluids due to transmission of ICP via naturally occurring channels can mimic symptoms of endolymphatic hydrops. It may be then possible that in a subset of patients with clinically diagnosed Meniere’s disease (MD), raised ICP can be transmitted to the inner ear and cause their symptoms ,.
| Patients and methods|| |
This study was conducted on 150 patients presenting with benign increased intracranial tension diagnosed by Dandy’s criteria and by radiological data (clinical, fundus and MRI). All patients were subjected to a detailed audiovestibular questionnaire. In addition, they underwent a pure tone and speech audiometry, impedencemetry, and a comprehensive clinical and instrumental vestibular testing to detect any vestibular abnormalities.
The study was approved by the Ain Shams University Faculty of Medicine IRB (Approval number ENT-7124/2014). The approval includes an informed consent, approved and regulated by the IRB.
| Results|| |
There were 92 females and 58 males (65% females) aged 6–67 (mean age 43) years. Of the studied patients, 38 (25.3%) (34 females and four males) presented with audiovestibular symptoms: ear fullness and/or hearing loss, tinnitus, attacks of vertigo, and instability. Some patients reported atypical positional or motion-induced vertigo. Some comorbidities were also recorded: hypertension (17), diabetes (9), and hyperlipidemia (6). A total of 80 (53.3%) patients had papilledema. However, in the group with audiovestibular symptoms, only five (13.1%) had papilledema (grade I/II).
Pure tone audiometry
Pure tone and speech discrimination tests were performed. All results were normalized for age and comorbidities. There were 20 patients with normal hearing, and 13 with sensorineural hearing loss (SNHL) (four bilateral). The hearing loss was predominantly low tone in 8 [mean 32 dB (bilateral in 3)] and flat in 5 [mean 40 dB (1 bilateral)]. In five patients there was a mean conductive hearing loss of 23.5 dB (with no other causes).
Clinical positive head impulse test (HIT) result was seen in 30 [videao head impulse test (vHIT) was unavailable at the time] patients, abnormal caloric test results were seen in 24 [canal paresis (CP) 16 unilateral and eight bilaterally reduced] patients, and 12 patients had positive Dix–Hallpike test result, with four typical of posterior canal benign paroxysmal positional vertigo (BPPV) and eight geotropic variable. Other oculographic tests and CDP were all normal.
The patients with cochleovestibular symptoms were referred to one of the authors (H.A.S.) who was blinded to the primary diagnosis. The clinical picture is suggestive of an atypical peripheral cochleovestibular lesion. The assumption was that it was some form of endolymphatic hydrops or Meniere’s disease. The patients were started on betahistine (24 mg, three times a day) for a trial period of 4 weeks and asked to report back. All patients had a partial albeit unsatisfactory response with persistence of vestibular symptoms and ear fullness.
After the run-in period, acetazolamide was added as 250 mg, three times a day, for 2 weeks. In 30 patients, there was complete disappearance of the sense of fullness and of any vestibular symptoms. In one patient, the low tone loss was normalized. In the remaining eight patients, the sense of fullness disappeared with a subjective improvement of hearing (but no change on the audiological pattern). Vestibular symptoms were reported to be greatly diminished without any interference with daily activities.
The medications were continued for 8 weeks after which dosage reduction was tried (betahistine and acetazolamide twice daily). In 17 (44.7%) patients, symptoms recurred and we reverted back to the high dose. Twelve patients regained their favorable symptomatic response, whereas the remaining five had a persistence of their symptoms. In those patients, other symptoms and signs of uncontrolled IICP persisted, and they were planned for further neurosurgical management. We plan to review them after their drainage procedures.
| Discussion|| |
Inner ear pressure differentials can cause symptoms related to functional neurosensory disruption . Induced changes in perilymphatic pressure can cause changes in measurable inner ear parameters such as DPOAE SP, CM, or AP/SP ratios by postural changes or by changes in middle ear pressure ,,,,,. Due to the direct pressure transmission between endolymphatic and perilymphatic spaces, pressure changes in either system directly affects the whole inner ear. Endolymphatic hydrops (clinically manifested as MD) and perilymphatic hypertension can thus potentially cause the same clinical manifestations. Due to the natural connections between the CSF spaces and the perilymph [endolymphatic duct, cochlear aqueduct and internal auditory meatus (IAM)], it is theoretically possible that in some patients changes in CSF pressure can be directly transmitted to the perilymph and cause EH-like disease ,,,. In this cohort of 150 patients with BIH, there were 38 (25.3%) patients with audiovestibular symptoms. Testing suggested a peripheral cochleovestibular dysfunction. Thirty (78.9%) patients responded favorably to measures to lower intracranial fluid pressures using acetazolamide. There was a recurrence of symptoms on dosage reduction, suggesting a true positive effect of the drug in this subset of patients. Of notice is that the proportion of patients with audiovestibular symptoms with concomitant papilledema is much lower than the studied population suggesting a differential effect on the inner ear and eye due to hitherto unspecified causes.
| Conclusion|| |
Some patients with a clinical history suggestive of endolymphatic hydrops may have secondary perilymphatic hydrops due to increased ICP. This may in part explain the response of some patients with diagnosed MD to diuretics which may act by modulating ICP rather than acting directly on the inner ear ,,. Further diagnostic measures should then be warranted (MRI, fundus examination and perimetry, and possibly measurement of ICP) to check whether they can be liable to visual loss, CSF leaks, or other central neurological dysfunction .
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Merchant SN, Adams JC, Nadol JB. Pathophysiology of Meniere’s syndrome:are symptoms caused by endolymphatic hydrops. Otol Neurotol 2005; 26:74–81
Macrae JH. Effects of body position on the auditory system. J Speech Hear Res 1972; 15:330–333.
Yoshida M, Uemura T. Transmission of cerebrospinal fluid pressure changes to the inner ear and its effect on cochlear microphonics. Eur Arch Otorhinolaryngol 1991; 248:139–143.
Salt AN, DeMott JE. Longitudinal endolymph movements and endocochlear potential changes induced by stimulation at infrasonic frequencies. J Acoust Soc Am 1999; 106:847–856.
Franz B, Anderson C. Effect of static middle-ear and intracranial pressure changes on differential electrocochleographic response. Int Tinnitus J 2008; 14:101–107.
Traboulsi R, Poumarat G, Chazal J, Avan P, Mom T, Ranchon-Cole I, Traboulsi S. The estimation of the time constant of the human inner ear pressure change by noninvasive technique. Model Simul Eng 2009; 2009:8.
Voss SE, Agedoke MF, Sheth KN, Horton NJ, Rosand J, Shera CA. Detecting changes in intracranial pressure using ear-canal reflectance and otoacoustic emissions. Hearing Research as part of the MEMRO group of manuscripts 2009; 1–28.
Nakashima T, Watanabe Y, Yanagita N. The effect of round window membrane rupture on endolymphatic and perilymphatic pressures. Arch Otorhinolaryngol 1987; 244:236–240.
Takeuchi S, Takeda T, Saito H. Pressure relationship between perilymph and endolymph in guinea pigs. Acta Otolaryngol 1990; 109:93–100.
Hara A, Salt AN, Thalmann R. Perilymph composition in scala tympani of the cochlea: influence of cerebrospinal fluid. Hear Res 1989; 42:265–272.
Carlborg BIR, Konradsson KS, Carlborg AH, Farmer JC, Densert O. Pressure transfer between the perilymph and the cerebrospinal fluid compartments in cats. Am J Otol 1992; 13:41–48.
Valk WL, Wit HP, Albers FW. Effect of acute inner ear pressure changes on low-level distortion product otoacoustic emissions in the guinea pig. Acta Otolaryngol 2004; 124:929–936.
Warmerdam TJ, Schroder FH, Wit HP, Albers FW. Perilymphatic and endolymphatic pressures during endolymphatic hydrops. Eur Arch Otorhinolaryngol 2003; 260:9–11.
Ciuman RR. Communication routes between intracranial spaces and inner ear: function, pathophysiologic importance and relations with inner ear diseases. Am J Otolaryngol 2009; 30:193–202.
Marchbanks JC. Hydrodynamical interactions of the intracranial and intralabyrinthine fluids. In: Ernest A, Marchbanks R, Samii M, editors. Handbook of intracranial and intralabyrinthine fluids: basic aspects and clinical applications. Berlin, Germany: Springer; 1995.
Carlborg BI, Farmer JC Jr. Transmission of cerebrospinal fluid pressure via the cochlear aquaduct and endolymphatic sac. Am J Otolaryngol 1983; 4:273–282.
Portier F, de Minteguiaga C, Racy E, Huy PT, Herman P. Spontaneous intracranial hypotension: a rare cause of labyrinthine hydrops. Ann Otol Rhinol Laryngol 2002; 111:817–820.
Nakashima T, Sone M, Teranishi M, Yoshida T, Terasaki T, Kondo M et al.
A perspective from magnetic resonance imaging findings of the inner ear: relationships among cerebrospinal, ocular and inner ear fluids. Auris Nasu Larynx 2012; 39:345–355.
McCall AA, Ishiyama GP, Lopez IA, Bhuta S, Vetter S, Ishiyama A. Histopathological and ultrastructural analysis of vestibular endorgans in Meniere’s disease reveals basement membrane pathology. BMC Ear Nose Throat Disord 2009; 9:4.
De Kleine E, Wit HP, van Dijk P, Avan P. The behavior of spontaneous otoacoustic emissions during and after postural changes. J Acoust Soc Am 2000; 107:3308–3316.
Saxena RK, Tandon PN, Sinha A, Kacker SK. Auditory functions in raised intracranial pressure. Acta Otolaryngol 1969; 68:402–410.
Gordon AG. Endolymphatic hydrops and CSF pressure. J Neurosurg 1984; 60:1332–1334.
Chomicki A, Sakka L, Avan P, Khalil T, Lemaire JJ, Chazal J. Derivation of cerebrospinal fluid: consequences on inner ear biomechanics in adult patients with chronic hydrocephalus. Neurochirurgie 2007; 53:265–271.
Pogodzinski MS, Shallop JK, Sprung J, Weingarten TN, Wong GY, McDonald TJ. Hearing loss and cerebrospinal fluid pressure: case report and review of the literature. Ear Nose Throat J 2008; 87:144–147.
Ferrary E, Sterkers O. Mechanisms of endolymph secretion. Kidney Int Suppl 1998; 65:S98–S103.
Thirlwall AS, Kundu S. Diuretics for ’Ménière’s disease or syndrome. Cochrane Database Syst Rev 2006; 3:CD003599.
Van de Heyning PH, de Valck CFJ, Boudewyns A, Cammaert T, Casteleyn S, Deggouj N et al.
Meniere’s disease. B-ENT 2007; 3(Suppl 6):11–20.