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Учебники / Middle Ear Mechanics in Research and Otology Huber 2006

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may have advantages compared to tympanometry, there are still various methodological and ethical limitations.

In continuation of improving these methods a new approach has previously been introduced, where a transducer is connected directly to the mastoid cavity in human subjects [13]. This method has the advantage of recording the MEP behind an intact TM, and hence, also avoiding the additionalvolumeoftheearcanal[12].Preliminaryresultshavebeenreported, and the current study describes further improvements of this method and extends the preliminary findings illustrating its various possibilities.

2. Materials and Methods

2.1 Instrumentation

Apressuretransducerincludingasamplingunitwasconnectedtothemastoid cavity by a catheter in human adult volunteers. Pressure was measured with an ultra-small high resolution transducer (2mm diameter, Endevco 8507C1), which was equipped with temperature compensating electronics, so that absolute accuracy is better than 5Pa over 24 hours. Pressure range was ±4 kPa, and data were sampled at 10 Hz by the sampling unit with a resolution of 1Pa. The transducer was mounted in a small brass cylinder (9×30 mm) carried close to the bandage. The catheter connecting to the mastoid was 15 cm long with an outer/inner diameter of 3.5/2.0 mm.

Data from the sampling unit were sent to a PC over USB bus using a custom made program (Matlab 7.0), which also allowed to store patient data and to perform a first analysis. Acquisition was possible both directly on-line as well as from a data storage of up to 48 hours of pressure monitoring. The sampling unit measured 28×65×138 mm and was carried in a breast pocket.

282.2 Subjects and procedure

The study included results from 5 patients, who were referred to our department for parotidectomy, where the antero-lateral aspect of the mastoid is routinely exposed in order to identify the facial nerve. Hence, this area for accessing the mastoid was readily available, and a small hole could be drilled through the compact bone layer into the mastoid. The catheter was inserted and by suturing the connective tissue above the bone tightly, air tightness was ensured. Finally, the functioning of the system was checked under the otomicroscope by tapping gently on the tympanic membrane with a cotton stick resulting in recordable pressure peaks.

The subjects were otherwise healthy with no history of previous middle ear disorders and presented with normal otomicroscopy, tympanom-

etry and pure tone audiometry. The day after surgery the patient could be discharged with the equipment for monitoring at home being mobilized and in daily surroundings; on the second day the catheter was removed similarly to an ordinary drainage tube and the returning of the pressure to 0 Pa was observed. The experiment was approved by our Ethical Committee (2005/50).

3. Results

In Fig. 1 the functioning of the system is illustrated by immediate synchronous pressure peaks up to 950 Pa resulting from tapping the TM. In Fig. 2 the results from a Valsalva procedure are depicted also illustrating the correct function by the system. An immediate steep pressure increase up to 3 kPa was found; in some cases pressure peaks obtained were out of range, i.e. >4 kPa.

Fig. 1 Repeated synchronous pressure peaks recorded in response to tapping the TM after the pressure recording system has been mounted.

29

Fig. 2 Rapid pressure increase in response to Valsalva manoeuvre.

Fig. 3 Pressure equilibration of positive MEP in a step-wise pattern; arrows indicate swallowing followed by steeper decreases towards 0 Pa.

Fig. 4 Pressure equilibration of positive MEP with a constant slow decrease in pressure; left arrow indicate start of pressure decrease, while the right arrow indicate MEP becoming negative.

30In Fig. 3 equilibration of a positive MEP in a stepwise pattern is illustrated. Three distinct points with an M-shaped form characteristic for swallowing are found (not clearly seen at this time resolution) followed by subsequent steep pressure decreases. The MEP approaches to almost 0 Pa. This pattern is di erent from equilibration of a similar positive pressure found in Fig. 4. Theincreasedpressureseeninitiallyresultedfromanup-goingelevatortrip (31 m), which is followed by a constant pressure decrease; after 15 min the MEP becomes negative and decreases further on.

Fig. 5 In both graphs periodic pressure fluctuations at high resolution are illustrated. In the left graph the pressure amplitude is high around 20 Pa after Valsalva, while in the right graph the amplitude is only around 4 Pa during sleep (note identical ranges on axes in both graphs).

Fig. 5 demonstrates small pressure fluctuations seen at the high resolution in time and pressure. These fluctuations are explained by pulsatile pressure changes in the mucosa of the middle ear and mastoid. Hence, the heart rate can be calculated; in both graphs, 5–6 peaks appear during 6 s, and hence, the heart rate was 50 to 60 beats per min. The pressure amplitude of the left graph amounts to around 20 Pa occurring after a Valsalva maneuver; in the right graph the amplitude is only around 6 Pa occurring during sleep at night.

4. Discussion

The initial experiment by touching the TM repeatedly at the end of surgery ensured the correct function of the system, since pressure increments were immediately recorded by the transducer. Further, the prompt pressure increase seen related to the Valsalva maneuver also confirms its cor-

rect function. Moreover, at the end of the experiment, when the catheter 31 was removed from the mastoid cavity, the pressure returned to 0 Pa. These observations were made in all subjects.

The preliminary results from our 5 subjects included many data on various situations, but only a few of these have been illustrated here. The positive pressure equilibration seen in Figs. 3 and 4 showed two di erent ways of counter regulation of a positive MEP towards 0 Pa. In one case a stepwise pattern was found, where three steep decreases were preceded by M-shaped patterns characteristic for swallowing (Fig. 3). Hence, this could be attributed to swallowing with openings of the ET resulting in MEP approaching to ambient pressure. It should be noted that the M- shaped pattern was always found in relation to swallowing, but it was not

consequently related to the equilibration of a deviating MEP, and hence, to an actual ET opening.

In the other case the equilibration of a positive MEP was found to be gradual with a constant slope (Fig. 4). Hence, in this situation there were no apparent ET openings involved in the pressure decrease, and it seemed likelythatgasexchangewastakingplacewithanetabsorptionofgas.After 15 min the MEP became negative. This phenomenon also confirmed the tightness of the measuring system, since a pressure decrease explained by leakage would not show subsequent development of a negative MEP.

These observations suggest that pressure equilibration took place in two di erent ways: stepwise with ET openings and gradual due to gas exchange.Themagnitudeofthepositivepressuresishigheraround400Pain Fig. 3, while only 200 Pa in Fig. 4. It can be speculated that a more deviating MEP elicit counter regulation by more e cient ET openings, whereas smaller pressures are only regulated by gas exchange. However, individual di erences in ET and mastoid function may also play a role. The counter regulation of negative MEP is also interesting especially from a clinical point of view, and our current results have also shown such examples, which will be described in future studies.

The small periodic pressure changes seen at high resolution in time and pressure (Fig. 5) were found throughout all recordings; since their frequency was found to correspond to the heart rate, these changes have been attributed to pulsation in the mucosa [13]. Generally the amplitude was only 3–6 Pa, but in some cases it was higher up to 20 Pa (Fig. 5). Changes in the pulsation amplitude are likely to reflect alterations in the perfusion of the mucosa. Hence, the high amplitude found after Valsalva in Fig. 5 may be explained by a high perfusion rate resulting in increased gas absorption, and thus, an overall decreasing MEP as seen on the graph. Contrary, the smaller amplitude found during sleep (Fig. 5) may reflect a

32low perfusion rate and hence lower gas exchange rate. Further, the MEP is rather stable in this case, which corresponds to the low exchange rate.

The issue of an active role of the mastoid in MEP control has been questioned [14], but the current observations may imply the existence of an active counter regulation represented by controlled changes in the perfusion of the mastoid. Hence, the phenomenon is interesting for further investigationssubmittingthemiddleeartovariouspressurechallengesand recording the subsequent pressure changes including the high frequency signals explained by mucosa pulsation.

The overall monitoring of the MEP was successful in terms of the acquisition of large amounts of data, but the analysis of these is hampered at this stage, since we need to analyze in more detail distinct well defined ex-

periments in order to recognize the various pressure-related phenomena. Hence, we have not gone into a detailed description of this issue. Future experiments may include an automated pattern recognition analysis for a detailed detection of events related to the various phenomena.

Previousmethodsusedfordetailedlong-termmonitoringofMEPin- cludedsubjectswitheitheraTMperforationoraventilationtubeinserted, since the pressure is measured at the ear canal [12]. Our present approach accessing the mastoid included the bu ering e ect of the TM, which is important in its own passive way [15], but also may be very important, if a erent input from mechano-receptors in the TM plays a role in a central neural feedback control of the MEP [16]. Limitations of our method included its current application only in normal ears, and that patients with diseased ears often have sclerotic mastoids, which will complicate the accessibility of the mastoid. Further, damping of pressure changes between the compartments (middle ear and mastoid) could theoretically influence our results, but pressure gradients have been found to dissipate quickly in model experiments [17].

5. Conclusions

Preliminary results showed that our method demonstrated a high accuracy anddetailedrecordingsofMEPanditschangesinresponsetovariouspressure stimuli. These have to be corroborated and described in more detail, and methods for describing full monitoring of the MEP have to be worked out. On this basis, our method is likely to provide new information which is valuable for understanding the variations in MEP and its counter regulation. This is a prerequisite for the overall description of pressure regulation and the improvement of treatments for patients. The method was found safe, since no side e ects were observed.

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Acknowledgments

A grant from “Speciallæge Heinrich Kopp’s legat” made it possible to compensate our patients for any discomfort in participating in the experiments.

References

1.Zielhuis G. A., Rach G. H. and van-den-Broek P., The occurrence of otitis media with e usion in Dutch pre-school children. Clinical Otolaryngol 15 (1990) pp. 147–153

2.Gaihede M., Hald K., Nørgaard M., Wogelius P., Buck D. and Tveterås K., Epidemiology of pressure regulation. Incidence of ventilation tube treatments and its correlation to subsequent ear surgery. Proceedings of the 4th International Symposium on Middle Ear Mechanics in Research and Otology

3.Sadé J., Ar A., Middle ear and auditory tube: Middle ear clearance, gas exchange, and pressure regulation. Otolaryngol Head Neck Surg 116 (1997) pp. 499–524

4.Flisberg K., Ingelstedt S. and Örtegren U., On middle ear pressure. Acta Otolaryngol (Stochk) Suppl 182 (1963) pp. 43–56

5.Gaihede M., Middle ear volume and pressure e ects on tympanometric middle ear pressure determination: Model experiments with special reference to secretory otitis media. ANL 27 (2000) pp 231–239

6.Cinamon U. and Sadé J., Tympanometry versus direct middle ear pressure measurement in an artificial model: is tympanometry an accurate method to measure middle ear pressure? Otol Neurotol 24 (2003) pp. 850–853

7.Alper C. M., Banks J. M., Philp K. D. and Doyle W. J., Tympanometry accurately measures middle ear underpressures in monkeys. Ann Otol Rhinol Laryngol 112 (2003) pp. 877–884

8.Hergils L. G., Magnuson B. and Falk B., Di erent tympanometric procedures compared with direct pressure measurements in healthy ears. Scand Audiol 19

(1990) pp. 183–186

34 9. Buckingham R. A. and Ferrer J.L., Middle ear pressures in eustachian tube malfunction: manometric studies. Laryngoscope 83 (1973) pp. 1585–1593

10. Sadé J., Halevy A. and Hadas E., Clearance of middle ear e usions and middle ear pressures. Ann Otol Rhinol Laryngol Suppl 25 (1976) pp. 58–62

11. Takahashi H., Hayashi M. and Honjo I., Direct measurement of the middle ear pressure through the eustachian tube. Arch Otolaryngol 243 (1987) pp. 378–381 12. Tideholm B., Jönsson S., Carlborg B., Welinder R. and Grenner J., Continuous 24–hour measurement of middle ear pressure. Acta Otolaryngol (Stockh) 116

(1996) pp. 581–588

13. Dirckx J.J.J., Somers Th., Decraemer W.F., Govaerts P., O eciers E., Continuous pressure monitoring in the intact middle ear. In P. Magnan and A. Chays (eds.)

Cholesteatoma and ear surgery. (Label Production, Marseilles, France 2001) pp. 41–47

14. Doyle W. J., Middle ear pressure regulation. In J. J. Rosowski and S. N. Merchant (eds) The function and mechanics of normal, diseased and reconstructed middle ears. (Kugler, The Hague, the Netherlands 2000) pp. 3–21

15. Dirckx J. J. and Sadé J., Middle ear pressure regulation: basic research and clinical observation. Otol Neurotol 26 (2005) pp. 300–309

16. SamiS.,GaihedeM.,NielsenL.G.,andDrewesA.M.,Dynamicversusstaticpressure evoked potentials. Indications of central middle ear pressure regulation in humans. Proceedings of the 4th International Symposium on Middle Ear Mechanics in Research and Otology

17. Felding U. N., Banks J. M. and Doyle W. J., Middle ear gas exchange in the air phase. Acta Otolaryngol 123 (2003) pp. 808–811

35

DYNAMIC VERSUS STATIC PRESSURE EVOKED POTENTIALS. INDICATIONS OF CENTRALMIDDLE EAR PRESSURE CONTROL IN HUMANS

Saber A.K. Sami1,2, Michael Gaihede1, Lars-Gustav Nielsen1, Asbjørn M. Drewes2,3

Department of Otolaryngology, Head and Neck Surgery1, Center of Excellence in Visceral Biomechanics and Pain, Department of Gastroenterology2, Aalborg University Hospital, Hobrovej 18–22, DK 9000 Aalborg and Center for Sensory-Motor Interactions (SMI)3, Aalborg University, Frederiks Bajersvej 7D, DK 9220 Aalborg Ø, Denmark

Saber Sami A. K.: saber@smi.auc.dk

Michael Gaihede: mlg@rn.dk

Lars-Gustav Nielsen: lgn@dadlnet.dk

Asbjørn M. Drewes: drewes@smi.auc.dk

Corresponding author: Saber A. K. Sami

Keywords: auditory brainstem, middle ear pressure regulation, electroencephalography, signal analysis, source analysis

Purpose: In clinical practice, the presence of negative middle ear pressure (MEP) is very common and most often related to secretory otitis media. Although pathological

36changes in the tympanic membrane may be associated with impaired baroreceptor function, little is known about the middle ear’s active regulation of pressure. New information on these aspects would be of major significance in otological research. On this background we have designed a new experimental method for conducting pressure stimuli to the ear canal and investigated the corresponding multi-channel pressure-related evoked potentials (PREP) in humans. This was then compared with multi-channel auditory evoked potentials for the same subjects.

MaterialsandMethods:Theexperimentswereconductedbystimulatingthetympanic membrane initially with acoustic rarefaction click stimuli and afterwards with a novel computer controlled pressure triggering system for rapid synchronized pressure loads (≈3 kPa). In seven adult subjects the resulting brain evoked responses were recorded from 64 surface electrodes using a standard EEG cap. A full band EEG acquisition

method was adopted, signals were sampled at 20,000 Hz, and band-pass filtered between 150 and 3000 Hz.

Results:Thestudycomparedearlymulti-channelauditoryevokedpotentialstopressure- related evoked potentials. Although these waveforms are given in the same time scale, they di ered significantly. Source localization was adopted on a realistic head model to show the location of these early neural generators. The same time interval with the highestsignaltonoiseratiowasinvestigatedforeachcondition.Theacousticcondition showed activation of the lateral lemniscus while the pressure condition showed activation in medulla followed by the activity, which was generated by the cerebellum. Conclusions: In agreement with earlier studies in primates, our current findings showed an early activation of the brainstem in response to pressure stimulation of the TM and the middle ear. The additional activation of the cerebellum was assumed to play a role in controlling the activity of the Eustachian tube. Further studies along this line are likely to provide basic knowledge on the possible role of an overall neural control of the MEP.

1. Introduction

Despite much research, especially during the last decade, many of the central mechanisms of the human ear’s functions for both dynamic and quasi static pressures loads remains unknown. Due to its’ obvious pertinent role, dynamic pressure loads (i.e acoustic) and the subsequent neurophysiological mechanisms have been widely investigated. Among the well known methods are auditory evoked potentials (AEPs), which can be obtained by recording the electrical brain activity from the human scalp following an acoustic stimulus. The earliest AEPs, which arise within the first 10 ms following stimulus onset, were initially described by Jewett as auditory brainstem responses (ABR) [1].

Of the di erent latency scalp-recorded AEPs, most attention has focussed on refining the origins of the ABR, presumably because of its 37 valueinotoneurologicalinvestigations[2].AlthoughtheABRwasfirstdescribedmorethanaquarterofacenturyago,thenatureandlocationofthe generators of its waveforms are still not definitively understood [3]. The humanABRconsistsofaseriesofuptosevenwaveforms,whichhavebeen standardized in the International Federation of Clinical Neurophysiology guidelines.AlthoughABRshavebeenextensivelystudiedinanimals,there

is a great lack of functional data on the human brainstem origin of these waveforms.

Even though recordings of electrical brainstem activity have excellent temporal resolution, they have poor spatial resolution. Traditionally, ABR recordings have been limited to a maximum of three channels, ow-