1. No category

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Vo l u m e 4 , N u m b e r 1 , 2 0 0 6
CONTENTS
Review Article
Role of Cinnarizine in Peripheral
Vertigo
2
Prof. Ramesh C Deka and Dr. C.Venkatakarthikeyan
Original Articles
Managing Cogan’s Syndrome
5
Dr. George Thomas
Migrainous Vertigo
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Dr. Aru Handa and Dr. K.K. Handa
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Journal Scan
4
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Balance performance and self-perceived
handicap among dizzy patients in primary
health care
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Canalolithiasis of the superior semicircular
canal: an anomaly in benign paroxysmal vertigo
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The minimal ice water caloric test compared
with established vestibular caloric test
procedures
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Can Migraine Damage the Inner Ear?
Drop attacks in elderly patients secondary to
otologic causes with Meniere's syndrome
15
Quiz
16
Advisory Board
Chief Advisor:
International Advisors:
Dr. R.C. Deka, Delhi
Dr. Michel Ballester, France
Dr. W.J. Oosterveld, The Netherlands
Dr. Anirban Biswas, Kolkata
Dr. Milind V. Kirtane, Mumbai
Dr. B.K. Roychaudhuri, Kolkata
Dr. Mohan Kameswaran, Chennai
Dr. Babu Manohar, Chennai
Dr. P.L. Dhingra, Delhi
Dr. G.V.S. Rao, Hyderabad
Dr. Santanu Banerjee, Kolkata
Dr. H. Ganpathy, Chennai
Dr. T. Ramadas, Chennai
Dr. K. K. Ramalingam, Chennai
V e r t i g o
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Review Article
Role of Cinnarizine in Peripheral
Vertigo
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elastic, increases their deformability,
decreases blood viscosity and allows
the erythrocytes to pass more readily
through narrowed blood vessels to
deliver oxygen to compromised tissues.
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Cinnarizine, a piperazine derivative, is a
H1 antihistamine. It antagonizes noradrenaline, nicotine and angiotensin. It
is also a calcium channel blocker.
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Prof. Ramesh C Deka1 and
Dr. C. Venkatakarthikeyan2
1Chairman, 2Assistant Professor
Department of Otolaryngology
All India Institute of Medical Sciences
New Delhi
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Cinnarizine is found to be very effective
in both central and peripheral vertigo
(The usual dose for patients with
peripheral vertigo is 25 mg, one tablet
three times daily.) The maximum recommended dosage should not exceed
225 mg (9 tablets) daily.1 As the effect
of cinnarizine on vertigo is dosedependent, the dosage should be
increased progressively. Cinnarizine
has been shown to suppress post-rotatory dizziness and nystagmus. Cinnarizine inhibits contractions of vascular
smooth muscle cells by blocking calcium channels and exerts anti-vasoconstrictive action. Cinnarizine also inhibits
the calcium influx into the red blood
cells (RBCs), makes the cell wall more
Based upon mechanism of activation,
three general classes of calcium channels have been identified:
• Voltage-operated calcium channels (VOCCs)
• Receptor-operated calcium
channels (ROCCs)
• Second messenger-operated
calcium channels (SOCCs)
VOCCs have been extensively studied and subcategorized into six distinct channel subtypes — L, T, N, P, Q
and R. Cinnarizine is a selective Ttype calcium channel inhibitor. As a Ttype calcium channel antagonist, cin-
Cinnarizine also inhibits the calcium influx into the red blood cells
(RBCs), makes the cell wall more elastic, increases their
deformability, decreases blood viscosity and allows the erythrocytes
to pass more readily through narrowed blood vessels to deliver
oxygen to compromised tissues
2
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As a T-type calcium channel antagonist, cinnarizine has
advantages over L-type calcium channel antagonists which affect
the audio-visual node function or inotropy of the cardiac muscle
at therapeutic doses
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metabolites of cinnarizine are eliminated in the urine and two-thirds in the faeces. The plasma protein binding of cinnarizine is 91%. Cinnarizine may cause
drowsiness and impaired concentration, which may be aggravated by
simultaneous intake of alcohol or other
central nervous system depressants.
Trial comparing the combination of cinnarizine 20 mg/dimenhydrinate 40 mg
with dimenhydrinate 50 mg, or betahistine dimesylate 12 mg, in randomised
order at 1-week intervals suggests that
it exerts only a minor effect on vigilance
not significantly different from betahistine which is commonly described as a
non-sedating antivertiginous drug.5
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narizine has advantages over L-type
calcium channel antagonists which
affect the audio-visual node function
or inotropy of the cardiac muscle at
therapeutic
doses.
Cinnarizine
appears to function centrally also by
mitigating excessive increases in
intracellular calcium, thereby avoiding
cerebral vasoconstriction and cerebral hypoxia. A double-blind study by
Pianese et al showed that cinnarizine
decreased severe vertigo episodes
by 89.8% compared to 85% by
nimodipine.2 Cinnarizine is a very
effective drug in the acute phase of
many of the peripheral vestibular disorders like Méniére's disease, benign
paroxysmal
positional
vertigo,
vestibular neuronitis, perilymph fistula,
temporal
bone
fractures,
labyrinthine fistula, vertigo due to
vestibulotoxic drugs, vascular loop
compression and labyrinthine artery
occlusion. Cullen et al demonstrated
significant reduction in the induced
nystagmus with cinnarizine and compared it with betahistine which did not
have any significant effect on induced
nystagmus.3 Animal studies suggested that the calcium channel blockers
effectively reduced the duration of
spontaneous nystagmus in rabbits,
accelerated the vestibular compensation in partially hemi-labyrinthectomised
guinea
pigs
and
decreased the amplitude of rotatory
nystagmus after occlusion of a vertebral artery in dogs.4
The peak plasma level of cinnarizine is
achieved in 2–3 hours. Plasma half-life
is 4–6 hours. Cinnarizine is completely
metabolised; about one-third of the
V e r t i g o
Headaches and gastrointestinal ailments
have been observed less frequently. Skin
reactions and cholestasia are rare.
Although significant progress has been
made in the management of vertigo
with very good molecules like cinnarizine, more knowledge is yet to be
acquired pertaining to the pathogenesis of different conditions causing vertigo, especially of peripheral vestibular
origin which helps in forming a logical
and effective therapeutic approach.6
REFERENCES
1.
2.
3.
http://home.intekom.com/pharm/janssen/stugeron.html
Pianese CP, Hidalgo LO, Gonalez RH,
Ponce CE, Ramirez AM, Moran LM.
New approaches to the management of
peripheral vertigo: Efficacy and safety of
two calcium channel antagonists in a
12-week, multinational, double blind
study. Otol Neurotol 2002;23(3):357–63.
Cullen JR, Hall SJ, Allen RH. Effect of
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6.
et al. Influence of three antivertiginous
medications on the vigilance of
healthy volunteers. Int J Clin Pharmacol
2003;41:171–81.
Deka RC. Management of vertigo:
Present status and directions in the new
millenium. Vertigo Update Millenium
Issue 2000;4(3):4–5.
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betahistine dihydrochloride compared
with cinnarizine on induced vestibular
nystagmus. Clin Otolaryngol 1988;
14:485–7.
Olesen J. Calcium entry blockers in the
treatment of vertigo. Ann NY Acad
Sci 1988;522:690–7.
Schneider D, Kiessling B, Wieczorek M,
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Hansson EE, Mansson NO, Hakansson A
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Balance performance and self-perceived handicap
among dizzy patients in primary health care*
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Objective. To study the diagnostic panorama at a primary health care centre where the physiotherapist is specialized in dizziness. To study balance
measures of dizzy patients as well as measures of self-perceived handicap
and to analyse whether these measures correlate. Design. Retrospective
study of computerized medical records. Setting. A primary health care centre in Malmo, Sweden. Subjects. A total of 119 patients with dizziness, 73
women and 46 men, aged from 22 to 90 years. Main outcome measures.
Diagnoses according to specified criteria. Four balance measures: tandem
standing, standing on one leg, walking in a figure of eight, and walking heel
to toe on a line. The Dizziness Handicap Inventory (DHI). Results. Six different groups of diagnoses were found: multisensory dizziness, peripheral
vestibular disorder, dizziness as a symptom caused by whiplash-associated
disorder, unspecific dizziness, phobic postural vertigo, and dizziness of cervical origin. The group with multisensory dizziness performed poorer on the
balance measures than the other groups. The group with phobic postural
vertigo had the highest total scores on DHI, while the vestibular group had
the lowest total score. Subjects over 65 years old had more disturbances in
balance, but a lower level of self-perceived handicap, than subjects aged 65
or younger. DHI did not correlate with any of the balance measures.
Conclusions. Self-perceived handicap, measured with DHI, and disturbed
balance measured with clinical methods, do not necessarily correlate.
Elderly patients with dizziness seem to have more disturbances in balance
than younger patients but a lower level of self-perceived handicap.
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*Scand J Prim Health Care 2005;23(4):215–20.
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Original Article
Managing Cogan’s Syndrome
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Dr. George Thomas
Consultant Audiological Physician &
Neurotologist
Coimbatore Speech Hearing Neurotology
Centre
457B, Dr Nanjappa Road
Gandhipuram, Coimbatore
neuritis, glaucoma, dry eye ptosis, etc.1
Cogan’s syndrome is generally considered as an autoimmune disease
despite the frequent lack of direct
immunological evidence. The efficacy
of steroid treatment in the acute phase
provides a compelling argument for this
hypothesis. Histological study of temporal bone from a patient who had suffered from Cogan’s syndrome and later
died of another pathology revealed that
the lesions were similar to those usually found in other autoimmune diseases
such as acute labyrinthitis with inner
ear tissue atrophy, endolymphatic
hydrops, diffuse fibrosis and neural
degeneration.2
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INTRODUCTION
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Cogan’s syndrome was first described
as a clinical entity in 1945 by David
Cogan, an ophthalmologist. Cogan’s
syndrome is defined as nonsyphilitic
interstitial keratitis (inflammation of the
eye) and bilateral audio-vestibular
symptoms. This is a rare disease characterised by progressive bilateral hearing loss and may lead to total deafness
in 40–60% of reported cases. The
symptoms of hearing fluctuation, tinnitus and vertigo may resemble
Méniére’s disease. Attacks of dizziness
are severe and they are usually accompanied by ataxia. The initial symptoms
pertain to the eye in about 37% of the
patients and warrant a slit-lamp examination. The cochlea-vestibular symptoms present themselves initially in
only about 30% of the patients. Cogan’s
syndrome can occur in children wherein it is particularly difficult to recognise.
“Atypical” Cogan’s syndrome is the
association of the typical hearing symptoms with other ocular signs including
scleritis or episcleritis, retinitis, optic
V e r t i g o
The vestibular system in Cogan’s syndrome is affected days or weeks before
the cochlear system.3,4 Most often
vestibular damage goes undetected,
unless clinical examination and instrumental vestibular testing are performed. Cochlear damage is better
documented than that of vestibular system.5 Ocular manifestations include
conjunctivitis, photophobia and red-
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Investigations revealed that his erythrocyte sedimentation rate (ESR) and creactive proteins were grossly elevated.
His serum IgG and serum IgA were
also found to be increased, while
serum IgM was normal. Blood studies
including rheumatological tests, serum
fluorescent treponemal antibody (FTAABS) absorption test, were negative.
Electrocardiogram (ECG) and computerised tomography (CT) scan were normal. Audiogram revealed bilateral
severe mixed hearing loss.
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Cogan’s syndrome is an inflammatory
disease not always restricted to the
eyes and the inner ear. The systemic
manifestations can occur any time
between two months to seven years.6
On the contrary, systemic manifestation
may be the first and only manifestation
of Cogan’s syndrome for a long period,
and this may delay diagnosis. The systemic manifestations are basically
attributable to systemic vasculitis of
small, medium and large vessels.7
Cogan’s syndrome should not be considered as a disorder strictly limited to
the eyes and inner ear and a long-term
cardiac follow-up examination should
be regularly performed to promptly
detect complications.8,9
and normal toward the right. The
patient was unable to stand on a plain
surface even with his eyes open. There
were no other abnormalities of cranial
nerves. Motor sensation and examination were normal. The patient had a
wide-based and unsteady gait.
Romberg’s test was negative. Tandem
Romberg
demonstrated
fall.
Untenberger’s stepping test showed a
deviation to the right.
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ness in eyes. These symptoms must
alert the ophthalmologist and a slitlamp examination is mandatory to look
for interstitial keratitis, which represents
the most typical lesion of ocular disease in Cogan’s syndrome and is used
to confirm the diagnosis.
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CASE REPORT
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A 23-year-old adult male presented
with complaints of progressive bilateral
hearing loss, bilateral tinnitus continuous in nature and vertigo/disequilibrium
(a feeling of being pushed down) related to rapid head movement and on
ambulation. He had visual problems
and his refractory error was corrected
with glasses. While walking on uneven
surfaces, he complained of bobbing
oscillopsia. Slit-lamp examination
revealed bilateral interstitial keratitis.
He had undergone bilateral cataract
surgery and also appendectomy in the
past.
Neurotological examination revealed
left beating nystagmus in the primary
position that worsened on left lateral
gaze. There was a left beating posthead-shake nystagmus. The head
thrust test was abnormal toward the left
6
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Word recognition score: 70% on the
right, 60% on the left. Tympanometry:
Bilateral “A type” curve with absent
acoustic reflexes.
Auditory brainstem response (ABR):
No signs suggestive of retrocochlear
pathology.
Electronystagmography (ENG): Bilateral hypoactive labyrinths with a
directional preponderance to the right
and
a
low
fixation
index.
The presence of spontaneous nystagmus and abnormal postural control on
physical examination indicates a
vestibular imbalance and the patient
notes a bilateral hearing impairment.
These findings support the idea of bilateral otological disease. Given the information available from the history, the
differential diagnosis for the patient’s
condition is broad. However, the progressive nature of the illness and the
associated complaints of bilateral hear-
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MANAGEMENT
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Cogan’s syndrome is a disorder characterised by auditory and vestibular
dysfunction that most often is bilateral
and is thought to be produced by the
damage mediated by both cellular and
humoral immune mechanisms.10,11 The
patient was started on corticosteroids
such as prednisolone, 1 mg/kg/day for
a period of two months followed by a
tapering dose and then by a maintenance dose. During this time, he experienced an improvement in hearing
especially in his ability to understand
speech, and a slight improvement in
balance. Surprisingly, the bobbing
oscillopsia had completely disappeared. Vertigo and ataxic attacks continued at occasional intervals. For
these, the patient was started on cinnarizine 25 mg t.i.d. for a week during
attacks, which effectively reduced his
vertiginous spells. This effect can be
attributed to cinnarizine since it suppresses the labrynthine excitability.12
Direct action of cinnarizine on hair cells
should also be considered, as molecular mechanisms contribute to the therapeutic effects of cinnarizine in vertigo.13
The patient underwent vestibular reha-
bilitation treatment after his acute vertiginous symptoms subsided. It is well
known that patients with bilateral
vestibular reduction generally have a
more serious balance problem and a
worse prognosis than those with unilateral vestibular loss. Many of the principles that underlie the vestibular rehabilitation of patients with unilateral
vestibular loss also apply to patients
with bilateral vestibular loss, but there
are several special considerations: the
recovery is usually slower; sensory
substitution is the primary means of
rehabilitation, which was difficult in our
patient since his labyrinth and vision
were affected and we had to rely on his
somesthetic projections; exercises may
be needed for a longer time; visual
input (proper lighting) is critical; and a
cane or a walker may provide a great
deal of help, especially early in the
rehabilitation process. Following this
regime, the patient showed remarkable
progress in his gait-related activities.
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ing loss render some diagnoses more
likely than others. Méniére’s disease,
ototoxicity, neurosyphilis, HIV infection,
Lyme’s disease, autoimmune inner ear
disease, Cogan’s syndrome, bilateral
acoustic neuroma associated with neurofibromatosis and otosclerosis are all
possible. Based on the history, physical
examination, laboratory testing and the
association of interstitial keratitis along
with the bilateral otological disease
impairing both cochlear and vestibular
functions, a diagnosis of Cogan’s syndrome was made.
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Regarding the troublesome tinnitus
bothering him and causing sleep disturbances, habituation therapy in the
form of tinnitus retraining therapy
(TRT), based on the neurophysiological model by Jastreboff and Hazell,14
was instituted.
Stress and anxiety, the silent killers, are
the most common psychopathological
complaints associated with vertigo and
tinnitus. The co-morbidity of vertigo, tinnitus, hearing loss and stress/anxiety is
very high. Physical and mental instability always leads to increasing psychological insecurity. It is therefore very
important to give the patient emotional
support and psychological counseling
to prevent depression and panic
attacks.
For vertigo and ataxic attacks, the patient was started on
cinnarizine 25 mg t.i.d. for a week during attacks, which effectively reduced his vertiginous spells
V e r t i g o
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CONCLUSION
5.
6.
7.
8.
9.
10.
11.
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The patient has been fitted with bilateral hearing aids; his balance functions
are stabilised with regular vestibular
rehabilitation therapy. His tinnitus is well
under control. He is under a maintenance dose of steroids and cinnarizine
during acute episodes of vertigo.
Cochlear implant has been offered to
him in case his hearing deteriorates
further. He attends to his job and routine housework. It is mandatory that
Cogan’s syndrome be familiar to otorhinolaryngologists, ophthalmologists,
paediatricians and family physicians as
delayed diagnosis can be deleterious to
the inner ear and visual neurosensory
organs attributable to delayed steroid
treatment.
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Diagnosis of Cogan’s syndrome is
often missed or delayed because it is a
rare disease and its clinical signs at
onset are not specific (banal conjunctivitis). This is dangerous for the
patients because steroid treatment
should begin as early as possible to
allow functional restoration of inner ear
and eyes before irreversible lesions
develop.
drome:
A
preliminary
report.
Otolaryngol Head Neck Surg 1983;91:
24–32.
Rosen E, Newark NJ. Interstitial keratitis
and vestibulo-auditory symptoms following vaccination. Arch Opthalmol
1949;41:2–31.
Pleyer U, Baykal HE, Rohrbach JM, et
al. Cogan’s syndrome: Too often detected too late? A contribution to early diagnosis of Cogan 1 syndrome. Klin
Monatsbl Augenheilkd 1995;207:3–10.
McDonald TJ, Vollertsen RS, Younge
BR. Cogan’s syndrome: Audiovestibular
involvement and prognosis in 18
patients. Laryngoscope
1985;95:
650–4.
Dillion MJ. Rare vasculitis syndromes.
Ann Med 1997;29:175–9.
Cheson BD, Bluming AZ, Alroy J.
Cogan’s syndrome: A systemic vasculitis. Am J Med 1976;60:549–55.
Cogan DS. Syndrome of nonsyphilitic
interstitial keratitis and vestibuloauditory
symptoms. Arch Opthalmol 1945;
33:144.
Veldman JE, Roord JJ, O’Conor AF,
Shea JJ. Autoimmunity and inner ear
disorders: An immune complex mediated sensorineural hearing loss. Laryngoscope 1984;94:501.
Griffiti AJ. Biological and clinical aspects
of autoimmune inner ear disease. Yale
J Biol Med 1992;65:17–28.
Philipszoon AJ. Influence of cinnarizine
on the labyrinth and on vertigo. Clin
Pharmacol Ther 1962; 3(2):184–90.
Arab SF, Duwel P, Jungling E, et al.
Inhibition of voltage-gated calcium
currents in type II vestibular hair cells
by cinnarizine. Naunyn Schmiedebergs Arch Pharmacol 2004;369
(6):570–5.
Jastreboff PJ, Hazell JWP, Graham RL.
Neurophysiological model of tinnitus:
Dependence of the minimal masking level
on treatment outcome. Hearing Research
1994;80:216–32.
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REFERENCES
2.
3.
Grasland A, Pouchot J, Hachulla E, et
al. Typical and atypical Cogan’s syndrome: 32 cases and review of the literature.
Rheumatology
2004;43:
1007–15.
Schuknecht HF, Nadol JB Jr. Temporal
bone pathology in a case of Cogan’s
syndrome. Laryngoscope 1994;104:
1135–42.
Hugues GB, Kinney SE, Barna BP, et al.
Autoimmune reactivity in Cogan’s syn-
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V e r t i g o
13.
14.
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Migrainous Vertigo
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Dr. Aru Handa* and Dr. K.K. Handa**
*Senior Consultant
Department of ENT
Moolchand Medcity
New Delhi.
**Associate Professor
Department of ENT
All India Institute of Medical Sciences
New Delhi
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Diagnostic criteria
The diagnostic criteria proposed to
classify a patient as a patient of
migrainous vertigo are as follows:
•
Recurrent episodic vestibular
symptoms of at least moderate
severity.
•
One of the following:
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Vertigo, headache and their combination
are very common symptoms. Vertigo is
defined as a subjective sense of imbalance. It is a symptom and not a disease.
Dysfunction in different organs can give
rise to a feeling of imbalance and
headache. In a patient presenting with
headache and vertigo, the physician
should try to ascertain if the two are related or independent of each other and if the
headache is because of migraine.
• Migrainous symptoms during
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two or more attacks of vertigo.
There is enough evidence which links
vertigo to migraine. The prevalence of
migraine is about 50% in patients having Mèniére’s disease. Patients of
benign paroxysmal positional vertigo
(BPPV) also complain more frequently
of migraine than controls. On the other
hand, vertigo has been noted frequently in patients of migraine. Vertigo associated with migraine or migrainous vertigo is now a well established entity.
• Migraine-precipitants before
vertigo in more than 50% of
attacks.
• Response to migraine medications in more than 50% of
attacks.
• Current or previous history of
one of the migraine forms
defined by International
Headache Society (IHS)
MIGRAINOUS VERTIGO
Migrainous vertigo is a type of migraine
in which vertigo may be the prevailing
or sole symptom.1
V e r t i g o
Knowledge of different migraine presentations is essential for understanding migrainous vertigo. Different forms
of migraine proposed by are:
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•
1.1 Migraine without aura
(Common migraine). It is the most
common form of presentation. It is
characterised
by
recurrent
headaches associated usually with
nausea, vomiting, photophobia and
phonophobia. Hyperacusis is common in migraine and may differentiate it from other ear disorders. The
disorder, which begins in childhood,
is seen commonly in females and
runs in families.
•
1.2 Migraine with aura. This type
can be categorised in to the following:
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This condition is relatively common in older patients. The aura
could be in the form of vertigo. In
the recurrent attacks of vertigo
not accompanied or followed by
headache and not explained by
any vestibular pathology, a probable diagnosis of migraine-related vertigo is made provided that
there is a past or family history of
migraine.
• 1.2.6 Migraine with acute onset
aura. The aura develops fully
within four minutes.
•
1.3 Opthalmoplegic migraine.
The headaches are associated with
paresis of the cranial ocular nerves.
•
1.4 Retinal migraine. The aura
symptoms are visual in nature and
monocular.
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•
1.5 Childhood periodic syndromes that may be precursors to
or associated with migraine.
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(Classic migraine). It is usually
accompanied with aura of
reversible neurological symptoms followed by headache.
When the neurological symptoms
are vestibular, patients may have
vertigo, tinnitus and decreased
hearing.
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• 1.2.1 Migraine with typical aura
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• 1.5.1 Benign paroxysmal verti-
aura. The aura lasts for more
than 60 minutes but less than
one week.
go of childhood (BPV). It is
characterised by episodes of
dysequilibrium, anxiety, often
with nystagmus and vomiting, but
normal neurological and electrocephalographic findings. Common age of presentation is
between 1–4 years.
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• 1.2.2 Migraine with prolonged
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• 1.2.3
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Familial
hemiplegic
migraine. It is a rare childhood
condition in which headache is
associated with hemiparesis.
• 1.2.4 Basilar migraine. It originates from the brainstem or from
both occipital lobes. Bickerstaff
was the first to describe basilar
artery migraine which is also
called Bickerstaff syndrome. This
is characterised by an aura of
scotomata, transient blindness,
vertigo, decreased hearing, tinnitus, ataxia, dysarthria or
decreased level of consciousness followed by throbbing
headache.
• 1.2.5 Migraine aura without
headache. The aura symptoms
are not followed by headache.
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V e r t i g o
• 1.5.2 Alternating hemiplegia of
childhood (AHC). A rare neurological disorder with frequent
temporary episodes of paralysis
of one side of the body (hemiplegia) usually beginning before the
age of 18 months. One form of
AHC occurs primarily at night,
when a child awakens, and is
apparently related to migraine.
These children have no other
mental or neurological impairments. Treatment with flunarizine,
a calcium channel blocker, may
help to reduce the severity and
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duration of attacks of paralysis.
1.6 Complications of migraine
• 1.6.1 Status migrainous. It is
the term used to describe
migraine attacks that persist for
days with a headache-free interval of more than four hours.
These attacks may result in complications such as dehydration.
This may be with or without aura.
• 1.6.2 Migrainous infarction. In
PATHOPHYSIOLOGY
It is very important to elicit history of
headache in patients presenting primarily with vertigo, as headache may go
unnoticed due to dizziness spell and
patient may not relate the two together
due to time difference. In some patients
headache may be absent during an
acute attack, so other migrainous features have to be looked for by thorough
history taking.
w
w
w
.b
m
gd
e
si
gn
The pathophysiology of migrainous vertigo is not fully understood. It is believed
that a migrainous aseptic inflammation
creates a central sensitivity that
spreads from the trigeminal to the
vestibular system. But vertigo in
migrainous vertigo has been seen to
present both as a central and a peripheral vestibular disorder. In cases of
peripheral vertigo, it is presumed that
patients with migraine suffer recurrent
damage to inner ear due to ischaemia
caused
by
migraine-associated
vasospasm. The vascular insult in turn
causes vertigo.
co
m
this type, neuroimaging results
are abnormal and one or more
aura symptoms last for more than
a week.
There are no diagnostic tests to confirm migraine-associated vertigo.
Detailed history taking is the key to
evaluation and diagnosis. The usual
presentation of migrainous vertigo is
that of spontaneous or positional vertigo. Patients may present with varied
degrees of dizziness accompanied by
migrainous symptoms or provoked by
migraine triggers. Episodes of vertigo
vary in duration lasting between few
seconds to a day or even weeks.
Dizziness may present as an aura or
during headache-free interval or it may
appear after the headache episode.
ch
.
•
plained of vertigo. Vertigo was noted as
an aura in 8 patients, during the
headache in 25 patients, between the
headaches in 19 patients and after the
headache in one patient.
te
Vertigo-December1.qxd
CLINICAL PRESENTATION
Patients of migraine classically have
throbbing headaches but also frequently experience visual and vestibular
symptoms. In some patients, vertigo
may be the dominant presenting symptom and in these patients, the possibility of migrainous vertigo should be
considered. 25–35% of all migraine
patients may have episodic vertigo. In
1984, Kayan and Hood reported
increase in the frequency of vertigo in
migraine patients as compared with
tension headaches.2 He observed that
out of 200 patients of migraine, 53 comV e r t i g o
Auditory symptoms are less than
vestibular, but when present are bilateral. Low frequency nonprogressive sensorineural hearing loss has also been
reported in up to 31% of unselected
patients of migraine with incidence of
hearing loss increasing to 80% in
patients with basilar migraine.
Migraine-associated vertigo in seen
more commonly in females compared
to males with the majority of patients in
the age group of 30–45 years. Patients
often have history of motion sickness,
and in females, dizziness may be more
common during the menstrual cycle.
Individual or family history of migraine
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4:49 PM
Page 12
is common in patents with migrainerelated vertigo. To help the patient
understand the importance of trigger
factors, it is necessary to find out history of precipitating factors causing vertigo associated with migraine, e.g.,
stress, certain foods, hypoglycaemia
and menstrual cycle.
Migraine and Mèniére’s disease may
co-exist. Therefore, all patients having episodic vertigo, fluctuating
hearing loss, ear fullness and tinnitus characterising Mèniére’s disease
should be treated appropriately for
it, even if there is a history of
migraine.
When the patients of migrainous vertigo are examined during acute attack of
vertigo, the nystagmus may be absent
or very minimal, and when present, it is
more often a vertical beating nystagmus. Neuroimaging is normal in these
cases.
Benign paroxysmal positional
vertigo
.b
w
w
Méniére’s disease
m
gd
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ch
.
si
gn
It is sometimes difficult to distinguish
vertigo of peripheral vestibular origin
and vertigo caused by migraine.
Migraine headache may be masked by
severe symptoms of vertigo or there
may be vertigo associated with
migraine but without headache. The following should be considered in the differential diagnosis.
te
DIFFERENTIAL DIAGNOSIS
co
m
BPPV is accompanied by typical nystagmus and vertigo lasting for few a
seconds, which can be elicited by certain head movements in Hallpike
manoeuvres. The treatment is aimed at
adaptation rehabilitative exercises and
manoeuvers aiming at removing the
particles from posterior semicircular
canal and relocating them in the
vestibule. BPPV has no relation to
benign paroxysmal vertigo (BPV) of
childhood. In the latter, there are sporadic spells of severe rotational vertigo
accompanied by pallor, sweating, anxiety and vomiting lasting for a few minutes. This condition is usually seen in
early childhood but disappears as the
child grows. BPV of childhood is a
migraine variant and most of these children have a family history of migraine.
w
Symptoms of migrainous vertigo are
very similar to Mèniére’s disease. The
differentiating features of migrainous
vertigo are:
• The duration of symptoms in
migrainous vertigo may be more
than 24 hours.
• Tinnitus is usually mild and
never bothersome.
• Hearing loss is usually low frequency, may be fluctuant but is
nonprogressive.
• Migrainous vertigo may be associated with other visual symptoms.
• Family history of migraine may
be present.
12
V e r t i g o
Other causes of vertigo to be considered
as differential include recurrent vestibular
neuronitis, labyrinthitis and vertigo of
central causes, viz., vertebrobasilar
insufficiency, multiple sclerosis, craniovertebral junction abnormality, cerebellar pontine angle lesion in patients with
unilateral tinnitus and/or hearing loss.
TREATMENT
Management includes avoiding trigger factors such as stress, certain
foods, oestrogen replacement therapy and oral contraceptives. In the
event of severe acute attacks of vertigo with migraine, vestibular suppressants may be given as drugs
V i e w p o i n t
Page 13
used for relief of headache in
migraine usually are not effective in
relieving vertigo.
REFERENCES
SUGGESTED READING
Crevits L, Bosman T. Migraine-related vertigo: Towards a distinctive entity. Clin
Neurol Neurosurg 2005; 107(2):82–7.
Ishiyama A, Jacobson K.M, Baloh R.W.
Migraine and benign positional vertigo.
Ann Otol Rhinol Laryngol 2000;109
(4):377–80.
Lee H, Lopez I, Ishiyama A, Baloh R.W. Can
migraine damage the inner ear? Arch
Neurol 2000:57(11):1631–34.
Lempert T, Neuhauser H. Migrainous vertigo. Neurologic Clin North Am 2005;23
(3):715–30.
Von Brevern M, Zeise D, Neuhauser H,
Clarke AH, Lempert T. Acute migrainous
vertigo: Clinical and oculographic findings. Brain 2005;128 (2):365–74.
.b
m
gd
e
si
gn
Bajwa ZH, Sabahat A. Pathophysiology,
w
w
Canalolithiasis of the superior semicircular canal: an
anomaly in benign paroxysmal vertigo*
w
1.
2.
ch
.
While patients of peripheral vertigo
respond very well to vestibular suppressants (cinnarizine), patients of vertigorelated migraine need specific therapy
for migraine prophylaxis. In frequent
attacks of vertigo with migraine, prophylactic therapy with calcium channel
blockers (flunarizine), tricyclic antidepressants (aminotriptyline) and beta
blockers can be considered. This is indicated, if the attacks of migrainous vertigo are very frequent and severely effect
patient’s lifestyle. In case of doubt, trial
of medical treatment of migraine can be
both diagnostic as well as therapeutic, if
patient responds to treatment.
Clinical Manifestations, and Diagnosis
of Migraine in Adults. Up To Date online.
2005.
Kayan A, Hood JD. Neuro-otological
manifestations of migraine. Brain
1984;107:1123.
m
4:49 PM
co
27/12/05
te
Vertigo-December1.qxd
Schratzenstaller B, Wagner-Manslau C, Strasser G, Arnold W
According to the canalolithiasis theory, benign paroxysmal positional
vertigo (BPPV) is caused by gravity-dependent movements of otoconial
debris that collects in the endolymph of the posterior semicircular canal.
Other parts of the vestibular organ are rarely affected, and it is mainly the
horizontal canal that is affected by this atypical form of BPPV.
Canalolithiasis of the superior semicircular canal must be considered an
anomaly because the superior semicircular canal is the highest point of the
vestibular organ and debris normally cannot collect in this special location.
Until now, BPPV of the superior canal has mainly been dealt with theoretically in the literature. The authors present three patients with canalolithiasis
of the superior semicircular canal and offer direct proof of the condition
using high-resolution 3D MRI.
*Acta Otolaryngol 2005;125(10):1055–62.
V e r t i g o
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Page 14
Can Migraine Damage the
Inner Ear?*
Lee H, Lopez I, Ishiyama A, Baloh RW
RESULTS
Auditory and vestibular symptoms and
signs are common in patients with
migraine, yet little is known about the
pathogenesis of these symptoms and
signs.
The brain and cerebrovasculature were
normal. The left cochlea showed prominent fibrosis consistent with an old
infarction. The right inner ear showed
hydrops, with relatively good preservation of the hair cells in the cochlea, saccular macule, and cristae of the semi-circular canals. However, the utricular macule was denuded of hair cells.
co
ch
.
te
si
gn
OBJECTIVE
w
w
.b
m
gd
e
To perform clinicopathological correlation in a patient with migraine, sudden
deafness, and delayed endolymphatic
hydrops.
METHODS
m
BACKGROUND
w
A
patient
with
long-standing
migraine with aura developed sudden hearing loss in the left ear at the
age of 50 years and Méniére’s disease on the right side at age 73. At
age 76, he had a flurry of sudden
drop attacks typical of otolithic crisis.
He died of unrelated causes at age
81. The brain and temporal bones
were removed approximately 24
hours after death. The cochlea and
vestibular end organs were dissected after the surrounding bone was
carefully removed.
14
V e r t i g o
CONCLUSIONS
The sudden left-sided deafness likely resulted from ischaemia, possibly
due
to
migraine-associated
vasospasm. Presumably, the right
ear suffered only minimal damage
when the patient was 50 years old,
but this damage later led to the
development of delayed endolymphatic hydrops on the right. Otolithic
crises are thought to result from
pressure changes across the utricular macule. We speculate that loss of
hair cells in the utricular macule
resulted from a collapse of the utricular membrane onto the macule.
*Arch Neurol 2000;57(11):1631–34.
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Page 15
The minimal ice water caloric test compared with
established vestibular caloric test procedures*
Schmal F, Lubben B, Weiberg K, Stoll W
gd
e
si
gn
te
ch
.
co
m
Caloric testing of the vestibular labyrinth is usually performed by classical
caloric test procedures (CCTP) using water warmed to 30°C and 44°C. Ice
water irrigation (4°C) is usually not performed, although it might be useful as a
bedside test. To verify the validity of the Minimal Ice Water Caloric Test
(MIWCT), comparative video-oculographic investigations were performed in 22
healthy subjects using ice water (0.5 ml, 1.0 ml, 2 ml), CCTP, and cold air (27°
C). Frequency, amplitude, slow phase velocity (SPV), the onset, and the duration of nystagmus were documented. After addition of three ice cubes, the
temperature of conventional tap water (16°C) fell within 13 min to 4°C. In pessimum position the subjects demonstrated no nystagmus response. Compared
to CCTP, MIWCT was associated with a significantly later onset of nystagmus
and a significant prolongation of the nystagmus reaction. In contrast to air stimulation (27°C), a significant Spearman's correlation was noted between
MIWCT (1 and 2 ml) and established CCTP in respect of essential nystagmus
parameters (frequency, amplitude and SPV). Furthermore, MIWCT (0.5 and 1
ml) showed a higher sensitivity and specificity with regard to the detection of
canal paresis based on Jongkees' formula compared to stimulation with air 27°
C. Thus, MIWCT appears to be a suitable procedure for bedside investigation
of vestibular function outside the vestibular laboratory, e.g. in a hospital ward,
where bedridden patients with vertigo occasionally require vestibular testing.
m
*J Vestib Res 2005;15(4):215–24.
w
w
.b
Drop attacks in elderly patients secondary to otologic
causes with Méniére’s syndrome or non-Méniére
peripheral vestibulopathy*
w
Lee H, Yi H A, Lee SR, Ahn BH, Park BR
Many neurologists are unaware of the drop attacks that may occur from an inner
ear dysfunction especially in the elderly. We studied the clinical features and
results of quantitative audiovestibular tests in six elderly patients (>65 years of
age) who presented with drop attacks attributable to an inner ear pathology.
Group was divided into Méniére's syndrome (4) or non-Méniére peripheral
vestibulopathy (2). Standard dizziness questionnaire and quantitative
audiovestibular function testing were performed. Episodes were described as a
sudden push to the ground in four or a violent illusionary movement of environment leading to a fall in two. All cases gave a history of prior vertiginous episodes
and vestibular testing revealed unilateral caloric paresis. Ipsilateral hearing loss
was documented in four cases. Our results suggest that otologic causes should
be considered in the differential diagnosis of the drop attacks in the elderly, even
if the symptoms and signs were not consistent with Méniére's syndrome.
*J Neurolog Sci 2005;232(1-2):71–6.
V e r t i g o
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Ve r t i g o QUIZ
7
Cinnarizine inhibits the calcium influx
into the red blood cells thereby causing
What percentage of patients of
Cogan’s syndrome suffers from
total deafness?
a)
b)
c)
d)
50–70
40–60
20–40
10–30
8
In which of the following peripheral
vestibular disorders cinnarizine is
indicated?
Which system is affected first in
case of Cogan’s syndrome?
a)
b)
c)
d)
a)
b)
c)
Vestibular system
Cochlear system
Both at the same time
None of the above
gd
e
Who made the neurophysiological
model on which tinnitus retraining
therapy (TRT) is based?
Bernard Gersh
Abernethy and Kaplan
Jastreboff and Hazell
None of the above
w
a)
b)
c)
d)
w
w
.b
5
Macular degeneration
Diabetic retinopathy
Xerophthalmia
Interstitial keratitis
m
a)
b)
c)
d)
9
si
gn
The most typical lesion of ocular
disease in Cogan’s syndrome
used to confirm the diagnosis is
10
Which one of the following is not a
central cause of vertigo?
a)
b)
c)
d)
Cinnarizine, a piperazine derivative, antagonizes the following:
Vertebrobasilar insufficiency
Multiple sclerosis
Recurrent vestibular neuronitis
Craniovertebral junction abnormality
Which one of the following should
not be considered in the differential
diagnosis of migrainous vertigo?
a)
b)
c)
6
Benign paroxysmal positional
vertigo
Perilymph fistula
Vascular loop compression
and labyrinthine artery occlusion
All of the above
te
d)
4
Cell wall to be more elastic
Increase in their deformability
Decrease in blood viscosity
All of the above
m
a)
b)
c)
d)
3
Bickerstaff
George Thomas
Carole Kenner
Deborah Harris
Noradrenaline
Nicotine
Angiotensin
All of the above
co
a)
b)
c)
d)
2
a)
b)
c)
d)
Who was the first to describe basilar artery migraine?
ch
.
1
d)
Méniére’s disease
Cerebellar pontine angle
lesion
Benign paroxysmal positional
vertigo
Migrainous infarction
The correct answers will be announced in the next issue. Please give your completed puzzle
to our representative on or before 30 April 2006 and enroll in a draw for a prize.
Answers to the Quiz given in Volume 3, Issue 4, 2005
1. a
2. d
3. d
4. d
5. b
6. c
7. d
8. b
9. b
10. b
Vertigo Viewpoint welcomes reader contributions to this series in the form of review
articles, original articles or interesting and unusual case studies.
Kindly email the articles to v.reddy@elsevier.com
16
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