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Dandy Ford and Walsh and the clinical features of bilateral vestibulopathy.

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Causative Factors and Epidemiology of Bilateral
Vestibulopathy in 255 Patients
Stephen G. Reich, MD1 and Dana Boatman-Reich, MD2
In their study of bilateral vestibulopathy, Zingler and colleagues1 employed standard bedside tests to screen for hearing loss: asking patients whether they had impaired hearing
and whispered speech. We recently showed that these and
other bedside tests are poor screening tools for detecting clinically significant hearing loss. In our study,2 asking patients
whether they had difficulty hearing and whispered speech
had sensitivities of only 0.27 (95% confidence interval,
0.19 – 0.37) and 0.46 (95% confidence interval, 0.36 – 0.56),
respectively, to detect a hearing loss of more than 40dB by
pure-tone audiometry. Yet, both of these tests had a high
specificity of 0.89 and 0.78, respectively, consistent with
Zingler and colleagues’ findings.1 Of the 255 patients these
authors tested, 80 had an abnormal bedside hearing test that
almost always (98%) was sensorineural based on pure-tone
audiometry. Given the poor sensitivity of bedside hearing
tests, it is likely that more patients in their sample had hearing loss, which may have had diagnostic importance, particularly in light of the relatively large number of patients for
whom no cause for bilateral vestibulopathy could be established. When it is important to know the status of a patient’s
hearing, we recommend performing an audiogram because
many patients who “pass” bedside hearing tests nevertheless
have a hearing loss.
1
Department of Neurology, University of Maryland Medical
System, and 2Department of Neurology, Johns Hopkins
University School of Medicine, Baltimore, MD
1. Zingler VC, Cnyrim C, Jahn K, et al. Causative factors and epidemiology of bilateral vestibulopathy in 255 patients. Ann Neurol 2007;61:524 –532.
2. Boatman DF, Miglioretti DL, Eberwein C, et al. How accurate
are bedside hearing tests? Neurology 2007;68:1311–1314.
DOI: 10.1002/ana.21242
Reply
Vera C. Zingler, MD and Michael Strupp, MD
We appreciate being given the opportunity to respond to the
comments of Drs Reich and Boatman regarding our recent
publication in Annals of Neurology.1 The authors2 refer to
their own study of 107 adults in which they report poor
sensitivity but good specificity of bedside tests for detecting
hearing impairment.
Our review included 255 patients who had been diagnosed to have a bilateral vestibulopathy (BV) in the 18 years
between 1988 and 2005 at the Department of Neurology of
the University of Munich. All patients underwent standard
bedside tests to determine hearing impairment, but only
those patients with pathological results (subjective hearing
impairment and pathological whispered voice test) received a
pure-tone audiogram (n ⫽ 80). This approach reflects the
common procedure in the clinic. Traditionally, neurologists
first use evidence from the patient history in combination
Annals of Neurology
Department of Neurology, University of Munich, Munich,
Germany
References
1. Zingler VC, Cnyrim C, Jahn K, et al. Causative factors and epidemiology of bilateral vestibulopathy in 255 patients. Ann Neurol 2007;61:524 –532.
2. Boatman DF, Miglioretti DL, Eberwein C, et al. How accurate
are bedside hearing tests? Neurology 2007;68:1311–1314.
DOI: 10.1002/ana.21277
Dandy, Ford, and Walsh, and the Clinical
Features of Bilateral Vestibulopathy
Douglas J. Lanska, MD, MS, MSPH
References
530
with bedside tests as part of the neurological examination to
screen for hearing loss. Of the 80 patients in our study who
were tested with an audiogram, 98% had sensorineural hypoacusis. This confirms the high specificity of clinical tests
and corresponds to Boatman and colleagues’2 data. We agree
with the authors’ comment2 that possibly more of our BV
patients had hearing loss, particularly when both the poor
sensitivity of bedside tests and the high prevalence of hearing
loss in older adults are considered. The hearing status of BV
patients is important, because we learned from our study1
that the BV patients with associated hearing loss differed in
many other aspects (eg, cause, manifestation of the disease,
clinical presentation) from the BV patients without hearing
loss. From our review1 we therefore initiated a program to
ensure that all patients with BV in our neurological dizziness
unit receive a pure-tone audiogram in addition to the clinical
neurophthalmological and neurootological testing. We would
also recommend such a program to other centers.
Vol 62
No 5
November 2007
In a recent editorial, Drs Leigh and Thurtell1 suggest (as
have others previously) that neurosurgeon Water Edward
Dandy (1886 –1946) at Johns Hopkins “was perhaps the
first to recognize that loss of vestibulo-spinal reflexes caused
imbalance that was prominent in darkness. . .[and] also
noted that loss of the vestibulo-ocular reflexes caused vision
to become blurred whenever the head moves rapidly.”1 Indeed, in 1941, Dandy2 described oscillopsia and imbalance
in the dark in patients with Ménière’s disease in whom he
had sectioned both vestibular nerves to alleviate vertigo: “Division of both vestibular nerves is attended by one rather
surprising after effect, jumbling of objects (visual) when the
patient is motion. As soon as the patient is at rest, the objects are again perfectly clear. The other disturbance is uncertainty when the patient is walking in the dark. Both of
these effects persist, though with gradual lessening in severity.” The syndrome of bilateral vestibulopathy is sometimes
called “Dandy’s syndrome” on this basis.
However, similar observations after bilateral vestibular
nerve section had been reported earlier, in 1936, by neurologist Frank Rodolph Ford (1892–1970) and neurophthalmologist Frank Burton Walsh (1895–1978) at Johns Hopkins in a surgical patient of Dandy’s.3 As noted on the Johns
Hopkins Department of Neurology and Neurosurgery Web
site,4 Ford “was the neurologist to Walter Dandy, and
formed a legendary relationship with Frank Walsh in Oph-
thalmology.” In their original report, Ford and Walsh3 state:
“During convalescence [following bilateral vestibular nerve
section] it became evident that a new series of symptoms had
developed. Objects seemed to move before his eyes unless his
head was kept perfectly still. Walking caused objects to
‘jump’ before his eyes to some extent. . .He was also very
unsteady in the dark.” Dandy had, in fact, not reported these
observations in his original report on this patient, although
the postoperative period was brief at the time of Dandy’s
report.5 Ford6 later summarized the observations he made
with Walsh in the 1930s: “Destruction of the vestibular apparatus on both sides in man produces a constant unsteadiness of station and gait which is exaggerated in the dark and
also by sudden movements of the head. There is also a striking inability to fix objects with the eyes when the head is in
movement so that the patients complain of objects seeming
to dance or oscillate before their eyes when they are walking
or riding in a car. This oscillation ceases as soon as the head
is held still.” Therefore, even though Dandy was recognized
as an outstanding diagnostician, it appears that Ford and
Walsh made the original observations in a convalescent patient of Dandy’s.
Veterans Affairs Medical Center, Tomah, and Department of
Neurology, University of Wisconsin School of Medicine and
Public Health, Madison, WI
References
1. Leigh RJ, Thurtell M. Vestibular areflexia: under the radar. Ann
Neurol 2007;61:499 –500.
2. Dandy WE. The surgical treatment of Meniere’s disease. Surg
Gynecol Obstet 1941;72:421– 425.
3. Ford FR, Walsh FB. Clinical observations upon the importance
of the vestibular reflexes in ocular movements: the effects of section of one or both vestibular nerves. Bull Johns Hopkins Hosp
1936;58:80 – 88.
4. Griffin JW. The first 80 years. Available at: http://
www.neuro.jhmi.edu/nrotrn/first80.html. Accessed August 8,
2007.
5. Dandy WE. The treatment of so-called pseudo-Ménière’s disease. Bull Johns Hopkins Hosp 1934;55:232–239.
6. Ford FR. A clinical classification of vestibular disorders: with differentiation of three syndromes and discussion of a common
form of vertigo induced by sudden movement of the head. Bull
Johns Hopkins Hosp 1950;87:299 –304.
DOI: 10.1002/ana.21238
Reply
R. John Leigh, MD and Matthew J. Thurtell, MB, BS
We thank Dr Lanska for pointing out that it was not Dr
Dandy, but rather his colleagues Drs Frank Ford and Frank
Walsh, who first recognized that oscillopsia during head
movement was a consequence of bilateral vestibular nerve
section. Thus, even for such a seasoned diagnostician as
Walter Dandy, the visual consequences of vestibular areflexia
slipped “under the radar.” By understanding how vision may
be compromised in such patients, and by conducting simple
bedside tests, neurologists should not miss the diagnosis. In
the words of the Bard: “For some must watch, while some
must sleep: So runs the world away.”2
Department of Neurology, Veterans Affairs Medical Center
and University Hospitals, Case Western Reserve University,
Cleveland, OH
References
1. Leigh RJ, Thurtell M. Vestibular areflexia: under the radar. Ann
Neurol 2007;61:499 –500.
2. Shakespeare W. 1602 Hamlet, Act III, Scene II.
DOI: 10.1002/ana.21272
Annals of Neurology
Vol 62
No 5
November 2007
531
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