Hydromechanical interactions of the intracranial and intralabyrinthine fluids
In Proceeding of the Sixth International Tinnitus Seminar, Cambridge 1999
Intracranial pressure as a generator of aural noises: Improved
differential diagnosis will facilitate effective treatments
Consultant Scientist Director, Non-invasive Intracranial Assessment Unit (NIPA), Medical Physics Department, Southampton University Hospital, Southampton SO16 6YD
intracranial hypertension, dizziness, Ménière’s, fluctuating hearing, headache,
Raised cerebral fluid pressure (intracranial hypertension) often results in tinnitus, vertigo
and sometimes a hearing loss, which may be irreversible. In cases where the expected
headache and papilleodema are absent, patients with intracranial hypertension are likely to
be referred to the otolaryngological clinic for investigations of the audiovestibular
symptoms, yet these patients are rarely cross-referred to neurology.
A multi-centre study which is supported by 'Defeating Deafness -- the Hearing ResearchTrust' is currently underway. This study aims to more clearly define the characteristics ofthe tinnitus, vertigo, aural fullness and hearing loss found with intracranial hypertension.
From this work a questionnaires and objective clinical tests such as made by the 'TMDCerebral and Cochlear Pressure Analyser' will be combined to provide an ‘At Risk Profile’to facilitate cross-referral of patients with intracranial hypertension to neurology.
Certain aspects of this multi-centre study are discussed. Two case studies highlightinappropriate diagnosis of intracranial hypertension as otological disorders. Low frequencytinnitus of a pulsatile and/or 'whooshing' 'sea-like' nature appears to be the key symptomfor diagnosing intracranial hypertension and in many cases may be the only definingsymptom. The existence of a cohort of mostly female patients with these symptoms, whichare due to undiagnosed intracranial hypertension, has both a cost implication for the healthservice and is a 'quality of life' issue for the individual. Correct diagnosis of intracranialhypertension in the otolaryngological clinic is important to avoid ineffective treatments. Italso allows recognised treatments and management regimes to applied which shouldprovide the patient with total relief from audiovestibular symptoms.
It is recognised that raised cerebral fluid pressure (intracranial hypertension) often resultsin aural noises, dizziness and sometimes a hearing loss, which may be irreversible. It isapparent that patients with intracranial hypertension are being missed in virtually allotology clinics, since the few centres which look to identify these patients, find them.
Currently in nearly all cases the condition will be wrongly diagnosed as being a ‘Ménière’slike’ or a non-specific inner ear disorder which may include tinnitus as the primarysymptom. Yet this condition is treatable if correctly diagnosed, with often a completeremission of the audiological symptoms.
There is a particular interest in the audiovestibular symptomatology of patients with acondition known as Benign Intracranial Hypertension (BIH) also known as pseudotumourcerebri or idiopathic intracranial hypertension . How do we differentiate these patientswith this condition from those with an actual otological disease process? How common isthis problem and what are the referral patterns? What are the effective diagnosis andtreatment regimes? What are the underlying mechanisms for this disorder and inparticular the intracranial-labyrinthine interactions?
A multi-centre UK study funded by ‘Defeating Deafness - the Hearing Research Trust’ isbeginning to address some of these questions. This collaborative action includes: - theNIPA (Non-invasive Intracranial Pressure Assessment) Unit, Southampton; theDepartment of Neuro-Otology, National Hospital for Neurology and Neurosurgery, London;the Academic Department of Neurosurgery and the Department of Neuro-Otology,Addenbrooks, Cambridge; the Queens Medical School and Institute of Hearing Research,Nottingham.
These centres will research the exact nature of the symptomatology and utilise a non-surgical method of assessing the cerebral and cochlear fluid pressure on patients withproven intracranial hypertension (the MMS-11 TMD Cerebral and Cochlear PressureAnalyser). The aims are: - (1) to advance our understanding of inner ear physiology bytesting the hypothesis that ‘Connectivity between the cerebral and cochlear fluids isassociated with specific forms of tinnitus, vertigo and hearing loss’
(2) to provide an ‘AtRisk Profile’ to help all major audiology and neuro-otology clinics identify and successfultreat patients with this condition.
This paper provides a résumé of the methods being employed in this multi-centre trial andillustrates the importance of this work in terms of two patients who were wronglydiagnosed as having otolaryngological disorders and where later found to have BIH.
The Clinical Study
In the current multi-centre trial, patients with confirmed raised intracranial pressure and inparticular with BIH are being cross-referred from neurology/neurosurgery to the audiologyand neuro-otology centres of the participating hospitals. A full neurological assessment ismade on these patients and BIH is diagnosed on the basis of absent cerebral lesion andtumours, normal ventricle appearance, cerebrospinal fluid (CSF) of normal compositionand abnormal high CSF on lumbar puncture. A complete assessment of visual acuity,visual fields and enlarged blind spots is also made and papilloedema is almost alwayspresent.
Once diagnosed as BIH, these patients undergo an audiological assessment and adetailed questionnaire is administered by the researching clinician to assess the natureand severity of any tinnitus, dizziness, head and aural fullness, hearing deficits, visualobscurations, headache and the patient's general feeling of wellbeing.
A non-invasive measurement of the cochlear pressure is made using the 'MMS-10/11 TMDCerebral and Cochlear Pressure Analyser' which is also used to quantify the level ofcardiovascular noise being emitted from the external ear canal [2,3,4]. Cerebral tocochlear fluid connectivity is also assessed by inducing a change in intracranial pressureby moving the patient from a sitting upright to supine position [5,6]. A correspondingchange in cochlear pressure is assumed to represent a patent fluid pathway between thecerebral and cochlear fluids. The relationship between the change in pressure with postureand the existence of tinnitus and cardiovascular activity in a particular ear will be
investigated to see if a patent cerebral-cochlear fluid pathway is a prerequisite for havinglow frequency tinnitus, and possibly stimulation of the cochlea directly by cerebral pressurewaves.
The aim is to test up to 48 patients with BIH, with each of the 4 centres contributing about12 patients. In addition, the symptom questionnaire devised for the BIH patients has alsobeen answered by an age and gender matched control group of 60 normal femalesubjects. These subjects have undergone a full TMD cerebral/cochlear pressure, hearingand tympanometric assessment.
To date 60 normal female controls and 10 BIH subjects with proven intracranialhypertension have been tested at Southampton. It is not possible to draw definiteconclusions at the current time, nevertheless, the findings to date are in generalagreement with the earlier Southampton study which included 34 BIH patients . In thisearlier study an open fluid connection between the cerebral and cochlear (perilymphatic)fluids could be demonstrated using the ‘TMD Cerebral and Cochlear Fluid PressureAnalyser’ in 29 patients. Of these patients 16 (55%) complained of tinnitus which wasunilateral in 6 (21%) cases and it was bilateral in 10 (34%) cases. As in the current series,if tinnitus exists it is principally of a low frequency nature with pulsatile characteristics insome instances.
Comparing these findings with the normative data, none of the 60 normal femalesquestioned reported daily headaches, low frequency or pulsatile tinnitus as found in most,but not all of the BIH patients.
The multi-centre study seeks to investigate the premise that patients with intracranialhypertension are being seen for otological conditions, but are not being cross referred toneurology. Of the 10 patients seen in the current series, it is interesting to note that 2patients were being seen by ENT consultants who were treating the patients forotolaryngological disorders. In both cases, only by chance the patients visited theiropticians for a regular check-up, and the opticians fortunately identified papilloedema andimmediately referred them to our Wessex Neurological Centre where BIH was confirmed.
The first case is an slightly over-weight 18 year old female who had been studying for her
A levels when one morning she woke up with a 'whooshing' tinnitus in her left ear
(November 1997). This was described as being like 'a fast train' noise which was
incidental with her heart beat. She noticed that the tinnitus stopped when turning her
head, but became worse with physical activities such as squash. The 'whooshing' tinnitus
was always present and frequently interfered with daily activities and sleep. She did not
have any balance problems, no sensations of pressure or fullness, and no significant
The patient's GP referred her to an ENT consultant so that the pulsatile tinnitus could beinvestigated further (15/01/98). The ENT consultant found no clinical abnormalities andthe audiogram was normal. The CT scan was normal and it was decided to undertake aneurological vascular examination.
About 8 months after the start of the condition the patient visited her optician for a regularcheck-up and he found bilateral papilloedema (25/06/98). She was immediately referredto our Wessex Neurological Centre where the TMD technique was used to provide a non-invasive assessment of the intracranial pressure and to assess patency of the cerebral-cochlear fluid pathways (26/06/98). There appeared to be a cerebral-cochlearconnection in the left ear where the tinnitus was present but not the right ear which waswithout tinnitus. A lumbar puncture gave an excessive opening pressure of 46 cm ofsaline. The CSF composition, cell count, glucose and protein were all normal and BIH wasdiagnosed. Interestingly she commented that the tinnitus was no longer present 2 to 3weeks after the lumbar puncture.
The patient was managed on oral diuretics, Frusemide (40 mg per day), for 4 weeks andthen a repeat lumbar puncture showed that the CSF pressure was still raised at 38 cmsaline. At this time 10ml of CSF was withdrawn which brought the pressure down to 26cm saline. The papilleodema still was present (14/08/98). A course of steroid (30mg perday Prednisolone) was taken for 1 week and then Frusemide was continued. Ten weekslater there was no papilloedema and the fundi were normal (20/10/98). The openinglumbar puncture pressure was lower, but still abnormally high at 29.5 cm. These findingswere repeated after a further 10 weeks following a continuing course of Frusemide (40mgalternative days).
The diuretic was discontinued and when she was reviewed this year her optic disks werenormal (12/05/99). At this time TMD assessment of intracranial pressure was used so asto avoid further lumbar puncture, and this indicated there had been a significant reductionin CSF pressure although this pressure may still be greater than normal. The tinnitus wasno longer continuous and only occurred 3 to 4 times per month. The character of thetinnitus had changed from the 'train-like' whooshing tinnitus to an occasional less intrusivemuffled 'whooshing'. On the basis that the optic disks were normal, the patient has nowbeen discharged and will be review by her GP at regular intervals.
This patient is a 35 year old female civil servant who was first referred by her GP to an
ENT consultant because of a sensation of aural pressure in both ears, a low frequency
fluctuating hearing loss, vertigo and tinnitus which was described as a 'buzzing' (6/01/97).
The vertigo was episodic, objective and rotary. Vertigo attacks occurred every few weeks
and these could sometimes last all day. The vertigo was accompanied by the tinnitus.
The patient felt nauseous during these attacks and vomited on a number of occasions.
The patient was reviewed later in 1997 by the ENT consultant who found that a mild lowfrequency hearing loss had developed over a period of 11 months since the lastaudiogram as shown in figure 1. The other symptoms remained largely unchanged andthe patient complained that she found the blockage of her ears extremely irritating(14/11/97). Neither Beconase® nor topical steroids improved the condition that wasconsidered to be related to nasal obstruction. The consultant considered the condition tobe due to persistent Eustachian tube function with nasal obstruction. ENT surgery wasundertaken in terms of trimming of turbinates to clear the nose and septoplasty.
Following this surgery the symptoms continued but were less severe. However, 16months later the patient was admitted into hospital due to a sudden onset of headache andnausea (16/03/98). The dizziness was now occurring regularly, particularly in themorning. There did not appear to be papilleodema and the CT scan was normal.
Following investigation the patient was discharged and was prescribed Serc®, 16 mg perday for 1 month.
In February 1999 the patient visited her optician who found papilleodema and immediatelyreferred her to the Wessex Neurological Centre (9/02/99). At this time she reportedheadaches with visual disturbances, vomiting and diarrhoea. These attacks lasted up to 1hour and were sometimes accompanied by 'bright flashing lights'. Over the past 12 monthsthe rotary vertigo had become less severe and now only lasted about 10 minutes,however, she now had periods when she became unsteady on her feet and had a moregeneral feeling of dizziness. This was described 'as feeling drunk' and she frequently'bumped into things'. Absent acoustic stapedial reflexes precluded TMD assessment.
Over the past 3 months she had noticed a change in her vision in terms of transientblindness which lasted a few seconds and sometimes blurring which lasted a few minutes.
She also commented that her night vision had deteriorated and had a feeling of 'bruising'behind her eyes. On investigation bilateral papilleodema and field defects were found.
Lumbar puncture found a raised CSF pressure of 28 cm saline. The diagnosis of BIH wastherefore made (10/02/99). The condition is not responding to medication(Acetazolamide) and a lumbar-peritoneal shunt with possibly optic nerve fenestration isbeing considered.
Discussion and conclusion
It is evident that the otolaryngological symptoms associated with intracranial hypertensioncan include tinnitus, dizziness, vertigo, a hearing loss which may fluctuate, and asensation of aural fullness. Depending on the combination and exact nature of thesesymptoms, intracranial hypertension may be misdiagnosed as Ménière’s disorder, non-specific labyrinthine disorders, Eustachian tube dysfunction and even nasal obstruction.
Correct differential diagnosis depends on identifying the underlying signs and symptoms ofintracranial hypertension, however, this is seldom possible, even by those experienced inneurology, without reverting to lumbar puncture. The situation is even more complex sincewe know that most cases intracranial hypertension will occur without the expectedpressure-specific headache and papilloedema will either not be present or will goundetected. This may leave the otolaryngological symptoms as the main reason forreferrals from the GP to the specialist consultant.
The two cases presented in this paper are good examples of the above. Both were initiallyreferred by their GPs to an ENT consultant to investigate a 'whooshing' tinnitus in the firstcase and in the second case a combinations of tinnitus, dizziness and sensations of auralpressure. With the first patient, one of the key symptoms of intracranial hypertension,headache, was not present and with the second patient, headache was initially notconsidered to be significant and at a later stage was considered to be nothing more thanmigraine. Although headaches are the most common symptom found with intracranialhypertension they are not infrequently absent, mild or non-specific. Also headachesoften accompany vertiginous episodes or tinnitus. Rassekh and Harker (1992) report that22% of Ménière’s patients suffer from migraine and this increases to 81% for those withso-called vestibular Ménière’s .
Visual problems and papilleodema are further important pointers to underlying intracranialhypertension. However, in one of the few otolaryngological clinics where BIH is regularlydiagnosed, Sismanis found that only 4/20 (20%) of patients reported actual visualproblems . It is also recognised that the absence of papilleodema may not be taken toindicate the absence of raised intracranial pressure . Furthermore, papilleodema isunlikely to be seen in cases where abnormal pressure is episodic in nature. It is reportedthat clinically significant changes in the fundus which are recognisable as papilleodema
are only apparent in a minority of patients (5-10%) with raised intracranial pressure, andthen only after a prolonged period of several days or even weeks .
The actual prevalence of undiagnosed intracranial hypertension existing in the GP practiceor the otolaryngological clinic is as yet unknown. The generally accepted low incidence of1 case of BIH per 100,000 population per year cited by Wall and George cannot be takenas representative of undiagnosed intracranial hypertension which is likely to besignificantly more common in certain groups of the population for a number of reasons. Firstly, the condition mostly affects women within the age range of 14 to 45 andthere will be a cohort of women patients in which the condition is never correctlydiagnosed. Secondly, the diagnosis of BIH largely depends on a referral forpapilleodema. However, as described above, for each patient with papilleodema therecould be 10 or more patients with intracranial hypertension without papilleodema. Addedto this, unless the visual condition is progressive, detection of papilleodema may be aperchance event dependent on a visit to a vigilant optician -- of the first 10 BIH patientsseen in the latest series half have been referred to neurology from opticians. Selfreferral by the patient is also highly unlikely, because papilleodema normal goes unnoticedunless a significant visual deficit has developed.
Correct diagnosis of intracranial hypertension in the otolaryngological clinic is important asrecognized treatments and management strategies should provide the patient with totalrelief from audiovestibular symptoms [1,9]. Treatments include dietary management interms of weight loss if appropriate and restricted salt intake. Medication includes diureticssuch as Diamox often in combination with a short 1 week course of a steroid. Surgicaltreatments have been used for treating the audiovestibular symptomatology and includecerebrospinal fluid drainage by either repeated lumbar puncture or lumbar-peritonealshunts . As our understanding of intracranial/inner fluid interactions improves we arebeginning to see the advent of new surgical treatments such as the posterior fossacochlear aqueduct occlusion procedure which appears to relieve certain forms of tinnitusand vertigo .
The current multi-centre study aims to more clearly define the characteristics of thetinnitus, vertigo, aural fullness and hearing loss found with intracranial hypertension, figure2. From this a strategy will be developed whereby questionnaires and objective clinicalmeasurements such as the TMD technique can provide an ‘At Risk Profile’ to help identifypatients with intracranial hypertension and to allow cross-referral to neurology. Ifavailable, the TMD technique is valuable for reducing the need for lumbar puncture byproviding a non-invasive alternative for assessing changes in intracranial pressure withsymptoms and treatment, figure 3. Since patients with treated intracranial hypertensionremain 'at risk' of further occurrences, then the TMD technique is also proving valuable forproviding pressure assessments with long term patient reviews
Low frequency tinnitus of a pulsatile and/or 'whooshing' 'sea-like' nature appears to be thekey symptom for diagnosing intracranial hypertension and in many cases may be the onlydefining symptom. This finding concurs with the observations made by other severalauthors who consider that tinnitus and intracranial pressure generated aural noises maybe a better indication of increased intracranial pressure than headache or visualobscurities, and indeed may be the only manifestation of this condition [9,14]. If present,gentle compression of the internal jugular vein will often reduce the intensity of the tinnitusor even cause a complete cessation. Likewise, in cases of unilateral tinnitus, turning thehead to the ipsilateral side will often reduce or abolish the tinnitus. In the opinion ofSismanis, idiopathic intracranial hypertension, glomus tumors and carotid atherosclerosisare the most common aetiologies for pulsatile tinnitus seen in the otolaryngological clinic.
It is now recognised that the misdiagnosis of intracranial hypertension is not just occurringin otolaryngology. Recent studies show that patients with intracranial hypertension arebeing referred to headache clinics and the condition is being missed because of one of thekey symptoms, papilloedema, is absent. In a recent study conducted at the HoustonHeadache Clinic all patients with refractory chronic daily headache underwent lumbarpuncture even though they did not have papilloedema. Of the 85 patients, 12 (14%) werefound to had raised CSF pressure . In a later case-control study, 25 patients withrefractory chronic daily headaches were selected on the basis that they had raised CSFpressure without papilloedema. These were compared with 60 patients with similarheadaches who had normal CSF pressure. It was concluded that pulsatile tinnitus was thestrongest indicator for intracranial hypertension without papilloedema .
The existence of a cohort of mostly female patients with undiagnosed intracranialhypertension has both a cost implication for the health service and is a 'quality of life' issuefor the individual. It should be remembered that besides the symptoms described above,intracranial hypertension is normally associated with a general feeling of malaise anddulling of memory. These are disabling conditions and are often described by the patientas 'not feeling in this world' or 'feeling in a constant daze'. These symptoms alone may beso severe as to be incapacitating and to make it impossible for the patient to continue withhis/her occupation. Failure to diagnose intracranial hypertension, therefore, hassignificant implications for the quality of life of the patient. If tinnitus is the only well definedsymptom, then the apparent degree of incapacitation with this symptom may be perplexingto the clinician and there may be a danger of the patient being labelled as psychosomatic.
The outcome of the current UK multi-centre study should provide a better understanding ofthe pathophysiology of the audiovestibular symptomatology of intracranial hypertension,and whether this is as a direct consequence of connectivity between the cerebral andcochlear fluids [18,19]. By providing an 'At Risk Profile’ to help identify patients withintracranial hypertension, the current 'Defeating Deafness' sponsored study will provide thefoundation for future work to establish the prevalence and referral patterns forundiagnosed intracranial hypertension. This in turn should lead to more effectivetreatment with the likelihood of complete relief from various audiovestibular disorders forcertain patients.
I wish to thank 'Defeating Deafness', Hearing Research Trust for supporting this research.
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Figure 1: Audiogram for a 35 year old patient with
intracranial hypertension which shows a mild low
frequency hearing loss
Figure 2: A Typical Profile for Sub-clinical Intracranial Hypertension
Predominantly female - at least 4 to 1, female/male ratio. The patient may be 20% or moreoverweight.
Likely to be suffering from a low frequency tinnitus which will be described as 'hum', 'roaring','whooshing'
or perhaps 'sea like'
with sometimes characteristics which are synchronous withthe heart beat. About 60% of patients will report tinnitus and of these about 60-70% (36-42%of total) will be of a low frequency type. In cases of unilateral tinnitus, gentle compression ofthe internal jugular vein will often result in a reduction in the intensity of the tinnitus or even acomplete cessation. Likewise turning the head to the ipsilateral side will often reduce thetinnitus.
Most patients will report a mild imbalance or 'unsteadiness on their feet'. About 40% of thosewith tinnitus will be suffering some form of objective vertigo. This will be described asepisodes when the 'room appears to move' and this can last for several minutes andsometimes hours. This is often not fully developed rotary vertigo. The feeling is oftenassociated with nausea, but only infrequently vomiting.
The patient will be suffering from a malaise which will often be associated with a'deterioration in memory', 'mental slowing' or 'dulling of mind'. The patient will commonlyreport headaches, however, in most cases these headaches will be mild, sometimesdescribed as a 'dull'
headache. The headache may be associated with a pressure or fullnesssensations in the head, ears or behind the eyes.
If investigated, papilloedema will only probably be found in less than 10% of cases.
Interestingly, although visual deficits are often found, these or visual disturbances frequentlygo unreported by the patient. If these occur, they may include 'greying'
whichmay occur - as with other symptoms - with change of posture and subsequently last forseveral minutes.
Low frequency and/or fluctuating hearing losses are also symptoms, but only rarely aresignificant enough to be noticed by patients.
The most distinguishing associations of intracranial hypertension are probably 'female'
and'low frequency and/or pulsatile tinnitus'.
Nevertheless, if this latter symptom alone was takenfor a 'clinical screen'
for this condition, then we would expect to miss over 50% of thepatients.
Figure 3: Clinical Use of the TMD Technique
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