BENIGN PAROXYSMAL
POSITIONAL VERTIGO AND STRESS: A CASE HISTORY
OF A PATIENT, TREATED
WITH ANTISTRESS DRUGS (updated March 2004).
Renato Cocchi, a neurologist and a medical
psychologist
Summary
The case history of a 75-years old woman
suffering from Benign Paroxysmal Positional Vertigo (BPPV) which comes out
during situations of physical stress, is reported. The patient did non have any
hypertension, diabetes, labyrinthine infections, vascular dysfunction of the
vertebral arteries, etc. It is supposed that the BPPV can rise even from
labyrinthine excess of glutamate, as a following of the stress.
The woman had therapy with antistress
drugs for one year with much reduction of the vertigo episodes, which
reappeared during the great heat of the summer 2003. So they required
therapeutic adjustments. Although not exhaustive, the stress-linked glutamergic
suggestion could allow the overcoming of many incongruities of the cupololithiasis
explanation.
Key words: BPPV, stress, glutamate, antistress drug therapy.
Drug modulation of stress reactions
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The Benign Paroxysmal Positional Vertigo
(BPPV) is a syndrome that features short-lasting, but violent and relapsing
crisis of objective vertigo, instigated by particular movements of the head in
the space, and it is accompanied, in mostly cases, from primarily rotatory
nystagmus. Its course is usually favourable. (Kim and Amed‚e, 2002).
Short summarized etiopathogenesis and the
clinical frame.
From the clinical point of view the crisis
of vertigo rises up suddenly, usually at night or in the mornings ( Vannucchi
and coll. 1994). They last some about ten seconds as the maximum, have
intensity increase to a peak and decrement (the paroxysm), have rotatory
features, with intense contemporary neurovegetative reactions like nausea,
vomit, pallor, perspiration, and sometimes diarrhea.
Costanzo, Ciniglio Appiani and Catania, 1995
said that the vertigo did never rise up spontaneously - a questionable
statement for live personal experience -, even if, generally, the crisis is
switched by particular movements:
- the passage from the standing to the
reclining position;
- turning from a side to the other in the
bed;
- the passage from the reclining to the
standing position as the leaving the bed;
- movements of the head from forward to
backward and vice versa. From that comes the specification of
"positional"
The same assumed position from patient
laying in bed, points out the suffering labyrinthine channel (Lopez-Escamez and
coll., 2002).
This syndrome, although benign, disturbs
greatly the patient, and it is affirmed that it gains poor benefits from the
medical therapy.
It results instead much sensitive to the
rehabilitative physical therapy, that, in the BPPV of peripheral origin,
exploits some simple but specific manoeuvres that presuppose the repositioning
possibility of wandering otolithes' fragments into the endolymph. This is a
fact, as for otolithic wandering fragments, that is very probable after cranial
traumas.
The BPPV etiological classification often
follows the criteria of the probable and the possible because we cannot surely
go up again to the causal agent in most cases.
The BPPV more frequent forms are the idiopathic
ones (from 38% to 68%, following Cipparrone et al., 1985, Blessing et al.,
1986). They show an incidence peak after the fifth decade of life and the
female gender prevalence with F/M ratio 2:1 (Baloh and coll., 1987, Katsarkas
and Kirkham, 1978). That has done suspect, between others, about the importance
of hormonal factors able to alter the exchange mechanism of CA salts of the
otolithes and of factors as compatible with the maculas ageing.
We should consider in fact that in these VPPB
idiopathic forms, a varying rate of subjects, about 30%, showed a reduction of
the caloric bilaterally response to the thermal stimulation. This drives to
suppose the existence of a labyrinthine lesion not limited to the posterior
semicircular channels (Baloh and coll., 1987).
Particularly in elderly persons we have to
pay attention even to the vascular causes, which count in a varying rate, from
6% to 11% (Baloh and coll., 1987, Katsarkas and coll., 1978, Pagnini et al.,
1982). That so, because the labyrinth, as for the back cerebral circle, may
justify the onset of the vertigo when it is present vertebra-basilar arteries'
insufficiency.
A BPPV peculiar form follows the occlusion
of the anterior vestibular artery ( Lindsay and Hemenway, 1956 ). It usually
came out in elderly patients with an isolated intense unilateral labyrinthine
dizzy crisis without hypoacusia and alterations of the CNS, with progressive
regression within several weeks, followed then by the onset of a same side
persistent BPPV.
We need to consider, in the vascular genesis
of the illness, those situations of systemic vascular risk (heart failure,
diabetes, polycythemia, carotid arteriosclerosis, important cardiac
arrhythmias) associate or not to hypertension.
We remember besides, to list, the
post-traumatic BPPV, the post]-infectious, which follow inflammatory processes
of the intern ear, the iatrogenic ones and the secondary ones to the neurinomas
of the acoustic nerve, those during multiple sclerosis, in meningiomas, and in
the vit B12 deficit, in the macroglobulinemia, even if all these are not
precisely idiopathic.
For the pathogenesis, now it prevails the
hypothesis that the BPPV has a peripheral origin and has links to abnormal
conditions of the same labyrinth.
In spite of some observations related to the
presence of paroxysmal positional nystagmus, even if atypical, reported during
pathologies of the CNS, it is however common opinion to consider the typical
BPPV as of peripheral origin. Among its causal hypotheses, those more creditable
are two: the cupulolithias of Schuknecht (1962) and the canal lithiasis of
Parnes and McClure, 1992.
The trouble could have been induced by the
presence, on the dome or in the light of the posterior semicircular canal or of
the lateral channel, of things of elevated density and specific gravity,
probably of otolithic nature. Eventually however none of both invoked as
explanatory mechanisms had incontestably evidence. Welling and coll., 1997,
found, during therapeutic surgical interventions, that the otolithic fragments
were only present in 8/26 patients with BPPV, but even that such fragments did
non appear in the 73 patients without BPPV.
The hypothesis of the canal lithiasis
succeeds however to justify in more convincing way the effectiveness of the
physiotherapeutic manoeuvres of liberating.
Both invoked mechanisms could play a
contemporary role in some persons.
Current therapies.
The BPPV therapy is thought nearly
exclusively physiotherapy ( von Brevern et al., 2002). The drug therapies with
against dizziness drugs and drugs inhibiting of the nausea and/or the vomit can
have a supporting use, aiming to decrease the accompanying symptom of the
vertigo mainly during the physiotherapy, but they cannot be considered specific
tools.
In the pass the patient was recommended to
assume the switching position till to the exhaustion of the symptomatology (a
habituation technique). The manoeuvre currently more used, is that of Semont,
1988, which however it is only helpful when the symptom has its origin from the
posterior canal. For the vertigo of the lateral canal the patient is
recommended to stay in forced decubitus on the healthy side for 8-10 hours
(Vannucchi and coll., 1994). Otherwise, the manoeuvres of Baloh and coll., 1993
or Lempert and Tiel-Wilck, 1996, are performed.
What are the results of the crp technique?
Following the first CRP procedure, more than 80% of patients no longer
experience vertigo or nystagmus. Patients who do not respond to the first CRP
and undergo a second or third procedure have an overall success rate of greater
than 90%. Patient who fail after three attempts with CRP undergo further
diagnostic evaluation with ENG and rotary chair testing.
For the invalidating paroxysmal vertigo that
is not resolved with liberating manoeuvres, surgical solutions were proposed.
The intervention invented by Gacek, (1995), currently much in use, pointed out
the selective section of the singularis nervus, which has its origin to level
of the ampule of the posterior semicircular canal. On the other hand there is
the intervention of selective occlusion of the posterior semicircular canal, as
proposed by Parnes and McClure (1990). The auditory function did not have any
damage in both cases.
Troubles of the balance, like in moving the
body to and fro, can profit only partially of the repositioning manoeuvres.
Therefore they can be more tied to the chronic feeling of dizziness observed in
these patients (Giacomini et al., 2002).
We have however to remember that not all the
patients can be given the repositioning manoeuvres. So it happens, for example,
to whom suffering from cervical or thoracic spine pathology, and to fewer that
do not absolutely respond to them (Banfield et al., 2000).
In these latter patients, they asserted that
vestibular habituation retains a useful role and good results in the treatment
of BPPV
One personal experience of BPPV had me done
to rise doubts that stress had links with it (see:
www.stress-cocchi.org/news3.htm ).
An outpatient's BPPV female convinced me
that not only the stress was surely involved, but perhaps it could be at least
a very important cofactor.
Therefore I shall report here the case of
BPPV in an elderly woman, which I treated, primarily, with an antistress drug
therapy.
The case history.
Female, 76 years old at the first visit.
Since three months she is suffering from
fits of objective vertigo during which she has the impression to see the things
turning anticlockwise. Her dizziness last perhaps one-two minutes [??] and it
depends on the head position. The attacks can rise up even in the bed, and with
shut eyes. During an attack, insurgent with shut eyes, she had the clean
feeling that her eyes "turned on their own" (probable nystagmus ).
Till now, she had five episodes in total. The attacks not have scheduled preference,
in the mornings or in the afternoon.
Soon before the dizzy attack she had a
feeling of heat that came from feet to the head.
She remembers that at the beginning of the
first episode she was surely under stress.
An US-doppler of the carotid arteries showed
thickening of the middle-intimate layer without any hemodynamics lesion
currently meaningful + normal permeability and orientation of the cerebral
arteries.
As a widow, she lives by herself, and she is
a very active person. She doesn't have intrusive thought, nor depression. She
sleeps about 5-6 hours every night, but the sleep is troubled for difficulty to
falling asleep, some nighttime awakening and waking up again early-morning.
Rarely she slobbers during the sleep.
Her appetite is normal, with normal
greediness for sweets, meat or cube broth. Her bowel function runs well. She
has reduced right hearing since many years attributed to otosclerosis but not
reduced to the left ear, without any tinnitus, Not hypertension reported,
neither diabetes.
Therapy: Oxazepam 15mg; thiamine 67.5mg +
pyridoxine 67.5mg + 250mcg cyanocobalamin; clothiapina 3.3mg; betahistine
bichloride, 16mg.
This is the first checkup after one
month of drug therapy, with reduced dizziness. One only dizzy episode, of short
duration, insurgent at the end of two days of physical stress, and stopped
after nemisulide tablets 100mg x four ( totally 400mg).
Meanwhile she had done specific examinations
( tympanic objectivity, audiometer examination, vestibular examination, eyes
motility examination, and thermo-stimulation) with normal results, but
bilateral neuri-sensorial hypoacusia, - then not conduction hypoacusia, which
is from otosclerosis -, more accentuated for high frequencies. The dizzy
episodes were related to vascular impairment, without any current sign of
vestibular failure.
Her sleep is much improved and more restful.
No more feeling of heat raising the body, but, lately some nausea in the
mornings, for which she is eating less.
Therapeutic variation: carbamazepine 100mg.
A second checkup made three months and half since the beginning of
the therapy. She did not have any dizziness, only some preludes when she is
tired, and then she stops what she is doing and she puts herself on rest. With
her eyes shut, she had the feeling that her eyes were turning by themselves.
She sleeps very well, with 7-8 hours continuous sleep a fact that she did not
remember since a long time. She has the impression to do better, with good
appetite, regular bowel function.
She underwent a check CAT of the brain
without contrast, and its referral was absolutely normal.
The betahistine bichloride stopped.
Third checkup, after one year from the starting of the drug
therapy. Since about half July 2003, during a heat summer without any rain, she
had a BPPV episode at night, during her sleep. Carbamazepine dosing decreased
to 200mg/die and hydrochloride betahistine had 16mg/die resumption.
Till the end of August she had then one
episode every week, heat summer persisted, then the episodes spaced out and
disappeared at the end of September. They had always intermittent episodes of
short lasting (2-3 hours in the total) as compared to what she had to beginning
of the drug therapy, which can last even whole days, even if always in an
intermittent way.
Her drug compliance did get worse and she
stopped in following times carbamazepine, oxazepam and betahistine
hydrochloride. Then she had a light BPPV crisis in December, and an other of
the same type, to the end of January, both in the mornings.
Now she thinks that they can increase for
frequency, severity and lasting. She had to increase the clotiapine to
6.6mg/die because she was losing her sleep.
As for feeding, intestinal emptying, and
hypoacusia she did not observe any variation, also for illnesses from winter
cooling.
Therapeutic variation (daily doses, by the
oral via): Bromazepam 0.75mg; clotiapine 6.6mg; betahistine hydrochloride 8mg;
thiamine 75mg + pyridoxine 75mg + cyanocobalamine 250mcg. Besides them, I
prescribed a compound of vitamins and mineral salts, 1 capsule x week.
Discussion.
Some elements of this case drive to the fact
that we are dealing with a pure idiopathic form of BPPV. Namely they are the
gender, the patient's age, links with the head's movements, no relationships
with general or brain vascular troubles, not diabetes presence, the lack of
positive signs following specific examinations of the auricular-vestibular
district.
The same patient clearly pointed out the
stress component either in coming out of the first episode, either when of the
sixth episode appeared, during drug therapy, or early signs of dizziness, at
once abortive, later on. Even the relapse of the summer 2003, in presence of
great sultry heat, goes with the stress, in this type case, of a physical type.
To this amount of stress we had to add, as
further supply, that one derived from the sleep trouble.
The current combination of gender and age,
in its turn, would have been an index of a smaller ability to react adequately
to the stress, for which the stressful action became greater even for reduced
resistance.
There is still another datum that, as for
me, is meaningful. She has been and she is an overactive woman, which could
correspond to a constitutional balance with a certain prevalence of brain
glutamate and peripheral acetylcholine.
Her overactivity should have been a
consummating behaviour for the one and for the second, then like a behavioural
selfmedication aiming to maintain balanced an already precarious state.
The reported hypoacusia from presumed
otosclerosis, in fact it was denied as a conduction hypoacusia. As the
audiometer examination showed, it was bilateral neurosensorial hypoacusia, of
which a glutamergic overstimulation could have been a not secondary cause.
On the other hand there is the noise stress
the reactions of which, as in all stress reactions, may go throughout the
neurochemical pathway GABA-glutamate (Horger and Roth, 1995).
It is to remember that the hypoacusia from
noise is even of neurosensorial type.
Therefore she may have been a woman with
greater constitutional easiness to the glutammergic overfuncion from stress,
for stopping or reducing the transformation of the glutamate into GABA.
Her summer relapse in 2003 starting when she
was sleeping, can suggest an other share of glutamate hyperfunction, because
the reduced turnover of this neurotransmitter, due to reduced sensory
afferences during the sleep.
Of the rest, her body does not show any
mechanism to increasing the intake of precursors of glutamate and GABA. The
glucose introduction ( through the sweets ) and that of the glutamine ( through
the meat or the cube broth) are in fact are both normal.
The stress reactions may be different from
an individual to another and they depend from constitutional factors,
hereditary and acquired. Among them the particular moment of the biological
cycle of a living organism can affect in heavy way the stress reactions.
The more understandable exemplum is the
aging as a condition of reduced response to the stress ( You, 1996; Pike and
coll. 1997; Friedman and Irwin, 1997; for the cows, see Garcia-Belenguer and
coll. 1996).
Interesting still the elements that drive
thinking about the stress as a cause the onset of the same BPPV:
- the age as risk factor;
- the gender, even if to a lesser extent, as
a risk factor.
- the sudden coming out;
- the presence of possible not specific
symptoms of vagal and parasympathetic activation by stress (nausea, vomit,
perspiration, and sometimes diarrhea);
- the impossibility that the famous
wandering fragments of otolites form immediately before the dizzy episode;
- in post trauma dizziness, the vertigo
episode is not immediate, as the possible otolitic fragmentation, but to
distance, and the post traumatic syndrome is a syndrome of stress.
- the greater nighttime or early-morning
frequency of BPPV, when the glutamate, as principal neurotransmitter of the
sensory afferent pathways, has less turnover.
On the drug modulation of the stress
reaction I come back to the attempt of rational explanation previously given in
a detailed way ( see: www.stress-cocchi.net/Drugs3-it.htm).
According to what then I wrote, the main
points on which we can act by drugs, as base intervention, are:
- increasing type A GABAergic inhibition;
- decreasing type B GABAergic inhibition;
- increasing the GAD stimulation;
By themselves, these interventions drive
even to:
- diminution of the cortisol incretion and
of the peripheral adrenergic compensation for reduced activation of the
hypothalamus-hypophysis-corticosuprarenal axis (Buckingham, 1998; Schedlowski
and Schmidt, 1996 ), even if not much evident in this patient;
- diminution of the possible glutamate
excess because its greater transformation into GABA.
I used her for those tasks:
- a low dosing benzodiazepine, to act on the
type A GABAergic receptor.
- a brain Ca** antagonist, the
carbamazepine, to decrease the type B GABAergic inhibition (Crowder and
Bradfors, 1987).
- pyridoxine, that stands as cofactor of all
decarboxylases, including the GAD, that favours the transformation of the
glutamate into GABA.
When the GABA synthesis gets up, the brain
glutamate goes down, and, at the same time, is reducing the hypothalamus
stimulation of the dorsal nucleus of the vague and of the nucleus of the
solitary tract, which are the starting points of the parasympathetic answers in
stress conditions (Brann, 1995).
About betahisine, by now there is not
evidence for its benefits (James and Burton, 2001).
It is trivial that a polytherapy of this
type has modest chances to become standard protocol, because the individual
characteristics of reactions to stress are either constitutional either linked
to the particular moment of own biological life. The aging - I still remember
it -, reduces thresholds of stress.
It is sure that one-year drug therapy is not
very significant, but it is hard to say that the patient has could have
improved by herself. The BPPV has this characteristic, but that may say of any
treatment of it.
Two facts do this answer doubtfully: 1. Early
dizziness signs are still reappearing, and always in stress conditions. 2.
There was an improvement of the neurosensorial hypoacusia, a trouble I
connected to the glutamate excess due stress, even ageing stress ( see:
www.stress-cocchi.net/News9.htm ). The patient was at all unaware of this
possible result.
A new event appeared lately. The poor
compliance, with the patient stopping important drugs for the therapy
rationale, as for the stress hypothesis, makes all even less verifiable than is
already the BPPV in itself.
The role of the stress in the BPPV is all to
understand. Undoubtedly such a role exists anyhow, but we need to see if it is
primary or secondary. What pertains to the otolitic fragments is not of the all
clarified.
Zucca et al., 1998, suggested that these
fragments dissolve in endolymph within about 20 hours, and suggested that this
be the reason for spontaneous recovery of the BPPV. They speculate that lack of
spontaneous recovery might be related to increased calcium levels in the endolymph,
trapping of otolitic fragments, or ongoing production of loose fragments. The
explanation for lack of spontaneous recovery remains obscure, and it remains
within peripheral pathology, a fact that the stress hypothesis would make it at
least more complicated.
Tirelli and coll. 2001, asserted that the
CRM is effective even without a diagnosis of BPPV. That is to say although
indirectly, that the CRM might be a placebo manoeuvre, or that improvement
might be in part related to the passage Of time (see Zucca et al., 1998) rather
than the CRM.
The CRPs would even have an indirect effect,
with sectoral consummation of the excess of glutamate. Since this old technique
of habituation worked and still works, it gives us much to think.
Conclusion.
The idea that the Benign Positional
Paroxysmal Vertigo implicates even stress answers doesn't have to seem
bewilders, because every illness elicits even stress answers. The case treated
with antistress drug therapy for one year, relapsed for about two months and
half, during the great summer heat of 2003. Even this, as all the precedents,
followed then a situation of physical stress.
Owing to the compliance to the therapy by
the patient, after the critical summer relapse ran out, even one-year drug
therapy is few for a fleeing illness like the VPPB is. A glutamate excess, as
the byproduct of the stress, is an explanation less complicated and able to
overcome the difficulties of the peripheral theory of the BPPV.
The case will come however periodically
up-to-date.
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Posted on Internet on June 2003: Copyright by Renato Cocchi
2003.
Author's address: dr Renato COCCHI, via Rabbeno, 3
42100 Reggio Emilia
renatococchi@libero.it