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Objective. Evoked tympanic membrane displacement (TMD) measurements show a correlation with intracranial pressure (ICP). Attempts to use these measurements for non-invasive monitoring of ICP in patients have been limited by high measurement variability. Pulsing of the tympanic membrane at the cardiac frequency has been shown to be a significant source of the variability. In this study we describe a post processing method to remove the cardiac pulse waveform and assess the impact of this on the measurement and its repeatability. Approach. Three-hundred and sixteen healthy volunteers were recruited for evoked TMD measurements. The measurements were quantified by V m, defined as the mean displacement between the point of maximum inward displacement and the end of the stimulus. A sample of spontaneously pulsing TMDs was measured immediately before the evoked measurements. Simultaneous recording of the ECG allowed a heartbeat template to be extracted from the spontaneous data and subtracted from the evoked data. Intra-subject repeatability of V m was assessed from 20 repeats of the evoked measurement. Results with and without subtraction of the heartbeat template were compared. The difference was tested for significance using the Wilcoxon sign rank test. Main results. In left and right ears, both sitting and supine, application of the pulse correction significantly reduced the intra-subject variability of V m (p value range 4.0 × 10−27 to 2.0 × 10−31). The average improvement was from 98 ± 6 nl to 56 ± 4 nl. Significance. The pulse subtraction technique substantially improves the repeatability of evoked TMD measurements. This justifies further investigations to assess the use of TMD measurements in clinical applications where non-invasive tracking of changes in ICP would be useful.

Objective: Although previous studies have shown associations between patient symptoms/outcomes and the spontaneous tympanic membrane displacement (spTMD) pulse amplitude, the contribution of the underlying intracranial pressure (ICP) signal to the spTMD pulse remains largely unknown. We have assessed the relative contributions of ICP and arterial blood pressure (ABP) on spTMD at different frequencies in order to determine whether spTMD contains information about the ICP above and beyond that contained in the ABP. Approach: Eleven patients, who all had invasive ICP and ABP measurements in situ, were recruited from our intensive care unit. Their spTMD was recorded and the power spectral densities of the three signals, as well as coherences between the signals, were calculated in the range 0.1–5 Hz. Simple and multiple coherences, coupled with statistical tests using surrogate data, were carried out to quantify the relative contributions of ABP and ICP to spTMD. Main results: Most power of the signals was found to predominate at respiration rate, heart rate, and their harmonics, with little outside of these frequencies. Analysis of the simple coherences found a slight preference for ICP transmission, beyond that from ABP, to the spTMD at lower frequencies (7/11 patients at respiration, 7/10 patients at respiration 1st harmonic) which is reversed at the higher frequencies (2/11 patients at heart rate and its 1st harmonic). Both ICP and ABP were found to independently contribute to the spTMD. The multiple coherence reinforced that ICP is preferentially being transmitted at respiration and respiration 1st harmonic. Significance: Both ABP and ICP contribute independently to the spTMD signal, with most power occurring at clear physiological frequencies—respiration and harmonics and heart rate and harmonics. There is information shared between the ICP and spTMD that is not present in ABP. This analysis has indicated that lower frequencies appear to favour ICP as the driver for spTMD.

The tympanic membrane displacement test (TMDT) is an attempt to record intracranial pressure (ICP) reflective of an intracranial pulse pressure amplitude wave (IPPA) transmitted to the inner ear and tympanic membrane with a probe placed into the external ear canal. Twelve tinnitus patients, divided into two groups, who were resistant to attempts to achieve tinnitus control or relief were selected for the TMDT. The group 1 TMDT recordings were obtained on one session test date, and group 2 (n = 6) recordings were obtained sequentially on different session test dates. Patient selection with the medical audiologic tinnitus patient protocol (MATPP) identified all to have a nonpulsatile, predominantly central-type severe disabling subjective idiopathic tinnitus (SIT) resistant to attempts for tinnitus relief with instrumentation or medication. Associated complaints in all selected SIT patients included persistent ear blockage in the SIT ear, normal middle-ear function, controlled secondary endolymphatic hydrops in the SIT ear, sensorineural hearing loss of high frequency, hyperacusis, occasional vertigo, and central nervous system complaints of headache, head pressure, and cognitive interference in memory and/or speech expression. Clinical concern is for the presence of an increased ICP reflecting an idiopathic intracranial hypertension (IIH) which, if not identified and treated, may be a factor influencing the clinical course of this particular cohort of SIT patients, highlighted by persistent ear blockage and associated complaints as described.We set out to accomplish a number of goals: (1) To identify abnormal intracranial pulse pressure (IPPA ICP) with the extracranial TMD in a preselected particular cohort of SIT patients clinically suspected (by use of the MATPP) to have an abnormal ICP (i.e., IIH); (2) to identify the abnormal IPPA ICP as a positive indicator for IIH and as a factor - not an etiology - influencing the clinical course of SIT in a preselected cohort of SIT patients; (3) to identify with the TMDT in SIT patients spontaneous nonevoked recordings of intra-aural pressure and test-retest reliability of the TMDT; (4) to identify with the TMDT levels of normal and abnormal IPPA ICP in real time in the clinical course of SIT (i.e., an objective diagnostic and treatment monitor function of the TMD targeting ICP and IIH before and after treatment); (5) to attempt to establish a correlation of treatment efficacy, targeting preand post-ICP as a manifestation of IIH, with SIT subjective tinnitus relief; (6) to identify the limitations and complications of the TMDT; and (7) to share with the reader the evolution of a new science of brain pulsatility and a technology having a clinical application for otology and neurotology complaints of hearing loss, tinnitus, ear blockage, and vertigo. The results reported in the literature complement and alter conventional medical teaching focusing on brain pulsation, absolute intracranial pressure, and brain disease.The Southampton Tympanic Membrane Displacement Analyzer was used to record spontaneous intra-aural pressure waves in 12 SIT patients. Patients selected for the TMDT were divided into two groups: Group 1 (n = 6) recordings were obtained on one session test date, and group 2 (n = 6) recordings were obtained sequentially on different session test dates. Multiple recordings were attempted in all patients to identify test-retest reliability in both groups. An attempt for treatment and control of an elevated ICP with or without reduced cerebral compliance (CC) was recommended in 4 patients.With single and multiple recordings using the TMDT, the IPPA (i.e., ICP) was demonstrated to be abnormal and to fluctuate in the clinical course of 10 of the 12 predominantly central-type tinnitus patients (SIT): abnormal IIPA with reduced CC in 8 of 12 patients and normal IPPA with reduced compliance in 2 of 12. Tinnitus treatment results targeting ICP as a manifestation of IIH with Diamox were positive in the short term in 2 patients and incomplete in 3. The SIT relief is reflective of fluctuation in the ICP and the overall issue of multifactorial brain pulsatility.(1) The TMDT demonstrated repeated and consistent spontaneous nonevoked recordings of displacement of the tympanic membrane, reflective of intra-aural pressure, abnormal IPPA ICP in a preselected particular cohort of SIT patients clinically suspected to have an abnormal ICP (i.e., IIH). (2) Test-retest reliability of the TMDT was positive. (3) The results of the TMDT application for identification of an elevated ICP and reduced CC were positive in 10 of 12 particular preselected patients with nonpulsatile, predominantly central-type SIT resistant to attempts for tinnitus relief with instrumentation or medication. These positive findings support clinical and basic science investigations previously reported in the literature. (4) The clinical significance of these preliminary results of an elevated ICP in a particular cohort of SIT patients supports the clinical impression of the presence of an IIH and its influence on the clinical course and overall treatment of SIT. (5) A final conclusion as to the clinical significance of an elevated ICP and reduced CC for IIH and the diagnosis and treatment of tinnitus remains to be established.

Purpose: Raised intracranial pressure (ICP) is a potentially treatable cause of morbidity and mortality but tools for monitoring are invasive. We sought to investigate the utility of the tympanic membrane displacement (TMD) analyser for non-invasive measurement of ICP in children. Methods: We made TMD observations on normal and acutely comatose children presenting to Kilifi District Hospital (KDH) at the rural coast of Kenya and on children on follow-up for idiopathic intracranial hypertension at Evelina Children's Hospital (ECH), in London, UK. Results: We recruited 63 patients (median age 3.3 (inter-quartile range (IQR) 2.0-4.3) years) at KDH and 14 children (median age 10 (IQR 5-11) years) at ECH. We observed significantly higher (more negative) TMD measurements in KDH children presenting with coma compared to normal children seen at the hospital's outpatient department, in both semi-recumbent [mean -61.3 (95 % confidence interval (95 % CI) -93.5 to 29.1) nl versus mean -7.1 (95 % CI -54.0 to 68.3) nl, respectively; P = 0.03] and recumbent postures [mean -61.4 (95 % CI -93.4 to -29.3) nl, n = 59) versus mean -25.9 (95 % CI -71.4 to 123.2) nl, respectively; P = 0.03]. We also observed higher TMD measurements in ECH children with raised ICP measurements, as indicated by lumbar puncture manometry, compared to those with normal ICP, in both semi-recumbent [mean -259.3 (95 % CI -363.8 to -154.8) nl versus mean 26.7 (95 % CI -52.3 to 105.7) nl, respectively; P < 0.01] and recumbent postures [mean -137.5 (95 % CI -260.6 to -14.4) nl versus mean 96.6 (95 % CI 6.5 to 186.6) nl, respectively; P < 0.01]. Conclusion: The TMD analyser has a potential utility in monitoring ICP in a variety of clinical circumstances. © 2013 The Author(s).

Transcranial cerebral sonography (TCCS) is a noninvasive technique that allows the clinician to detect abnormal intracranial-inner-ear fluid interactions in terms of nanoliter tympanic membrane displacements. The displacements recorded in TCCS are evoked either by the acoustic stapedius reflex or spontaneous movements generated by intracranial cardiovascular or by respiratory pressure waves transmitted through the inner ear to the stapes and thence to the tympanic membrane. Analysis of the amplitude and direction of these displacements has enabled neurosurgeons and neurologists to estimate cerebrospinal fluid pressures in patients evaluated by TCCS. This procedure allows for applications in neurootology, particularly in those patients who present with symptoms of pulsating tinnitus, dizziness and imbalance, or hearing loss. This study describes the application of TCCS tests in a series of patients whose diagnoses included perilymphatic fistula and a variety of neurological conditions such as idiopathic intracranial hypertension, type I Arnold-Chiari malformation, sigmoid sinus thrombosis, hydrocephalus, and cerebrovascular malformations. We conclude that both raised intracranial pressure and abnormal intracranial pressure waves are associated with common neurootological symptoms, including tinnitus, dizziness, and hearing dysfunction. Furthermore, TCCS is a valuable addition to neurootologists' test batteries.

Address: 1Centre for Geographic Medicine Research, Kenya Medical Research Institute, Kilifi, Kenya, 2Department of Paediatrics and Child Health, Mulago Hospital/Makerere University Medical School, Kampala, Uganda, 3Department of Paediatrics, Imperial College, London, UK, 4Neurological Physics Group, Department of Medical Physics, Southampton University Hospitals NHS Trust, Southampton, UK, 5Clinical Neurosciences, Southampton University, Southampton, UK and 6Neurosciences Unit, Child Health Institute, University of London, London, UK