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Year: 2006  Vol. 10   Num. 2  - Abr/Jun - (8º) Print:
Section: Original Article
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Vestibular Rehabilitation in Subclavian Steal Syndrome
Author(s):
Daniela Affonso Moreira1, Juliano Marcelo de Nadai2, Edson Carlos Miranda Monteiro3
Key words:
Subclavian steal syndrome. Dizziness. Vestibular rehabilitation. Imbalance. Vestibular function tests.
Abstract:

Introduction: The subclavian steal syndrome is an unusual pathology that presents with vertigo, syncope and visual disturbances, which are often precipitated by exercises involving upper extremity. These symptoms are caused by retrograde flow of blood through the vertebral artery to the subclavian artery. Objective: To report a clinic case of subclavian steal syndrome, aspects of pathophysiology, diagnosis and efficacy of treatment with a neurotological approach by vestibular rehabilitation. Case Report: A 56 years old male patient with previous diagnosis of subclavian steal syndrome was referred to us for vestibular rehabilitation. His complaints after the surgical treatment of the subclavian steal syndrome were dizziness, tinnitus and imbalance. The patient recovered 85% 6 months after the beginning of the treatment. Conclusion: The improvement of this case was a summation of various factors in which the vestibular rehabilitation had a crucial role being useful and complementary to the post-surgery treatment.

INTRODUCTION

Irrigation of labyrinth, of vestibulocochlear nerve, of hearing and vestibular pathways of brainstem and cerebellum come from vertebrobasilar system. Its implication can cause ischemia on labyrinth, on brainstem or on both (1).

Subclavian artery arises directly from aortic arches at left and from brachiocephalic trunk at right. Vertebral artery, the first and most important branch from subclavian artery, goes in posterior and medium way into traversed process foramen of the cervical vertebra (C1).Vertebral arteries go through marrow anterior surface, forming basilar artery at the level of the pons. This single formation provides blood to upper spinal cord, marrow, cerebellum, labyrinth, cochlea, thalamus, occipital cortex and parts of temporal lobe (2) and transports about 30% of the cerebral irrigation (3).

Subclavian steal syndrome and cerebral circulation disorder are due to subclavian artery occlusion between its origin in the aorta and the origin of vertebral artery (3). Because of the reduction on pressure from subclavian artery in a distal manner to obstruction, blood runs in a anterograde way through contralateral vertebral artery, achieves basilar artery and goes down in a retrograde way through ipsilateral vertebral artery, in order to supply collateral circulation to upper extremity. In this way blood supply is taken from basilar system and it can endanger total and local brain blood flow (4).

Subclavian coronary steal syndrome is an uncommon organic alteration, occurring from 0.4% (5) to 3.4% (6) especially in men at their 60s in the proportion of 3:1 (7).

Heidrich (1968) divided clinical manifestations of subclacian steal in four symptom groups: plainly cerebral, cerebral associated to arm complaint, only arm-related complaint and asymptomatic cases. 75% of patients had cerebral manifestations with dizziness, headache (43%), visual disorder (35%), syncope (25%), ataxia (11%), speech disorder (11%), hearing loss (8.3%), sleep disorder (4,2%) and 15% had arm complaint (7).

Lawson et al (1979), when studying 35 patients with occlusion of subclavian, observed 31 of them (88%) with central-nervous-system-related symptoms, 14 (45%) with syncope, vertigo and ataxia due to vertebrosilar insufficiency. In 20 patients (64%), symptoms could be clearly classified as vertebrosilar, and included headache, blurred visio, diplopia (double vision) and dizziness (8).

Smith et al (1994) followed 59 patients with secondary symptoms of subclavian steal syndrome for 14 years, and observed that the most common symptoms were vertigo, syncope and weakness (9).

There is a lack on subclavian steal syndrome issue in the literature, but the studies done show that although there are different symptoms from these patients, the physical exam is a trustful method of screening for such disease.

Weak pulse or considerable differences from pulse amplitude and from blood pressure between upper limbs can be subclavian-steal-syndrome-related, but the definite diagnosis is by arteriography (2). Few cases reported presented hearing and vestibular tests and warn us on frequent labyrinth symptoms found on elderly people who can present this type of disease as other alterations coming from brain (2).

Surgical treatment is recommended in order to easy symptoms and to improve intracranial blood flow. A positive response could be observed in 94% of patients submitted to surgery, and only 6% did not have any results, presenting dizziness as isolated symptoms (8).

The target of this study is to present a case of subclavian steal syndrome and the description of its clinical and therapeutical process due to the relation between vertebrobasilar and vestibular systems associated to lack in the literature with a multiple otoneurological approach.


CASE REPORT

Male, 56-year-old patient, married, hypertense and overweight. He started with double vision (diplopia) occurrences as a symptom in different situations such as televisions or cars one above the other, followed by fluctuation feeling and instability. His condition developed to irregular vertigo and paleness lasting about 30 minutes. Vertigo symptoms presented slowly progressive, developing to a new condition of rotatory dizziness associated to nausea, indisposition and blurred vision followed by drop-attacks after physical effort.

He was sent to emergency department and it was found a difference from the measure of arterial blood pressure found in upper limbs associated to syncope. Thus, patient was hospitalized under vascular surgery care, and subclavian steal syndrome as diagnosis hypothesis. This was confirmed after doing the echo Doppler and carotid angiography performance and vertebrobasilar system.

He, then, was submitted to a surgical treatment with anastomosis (shunt) between left common carotid artery and left subclavian artery. Patient improved and post-surgery angioresonance showed success on blood flow recovery by left subclavian artery.

Ten months after surgery, patient reported that vertigo and diplopia had stopped, but not dizziness and indisposition. He went to ENT department of our service complaining of non-rotatory dizziness, with variable intensity and stable frequency, nausea, blurred vision, constant indisposition and fluctuation feeling. Together with those, he also reported aura completeness and bilateral tinnitus like infrequent whistling, more intense in left ear, associated to syncope. He reported as worse symptoms when bending head downwards and when in high and crowded places, and improving those symptoms when remained seated with closed eyes. He presented signs of depression and insecurity, memory problems, concentration and social contact.

Everything started with general physical exam, static and dynamic balance test, cerebellar test and otoneurological exam. Static balance tests (Romberg, Romberg-Barré and Unterberger) presented oscillated alteration and lateral punction for both sides, more intense with closed eyes. Dynamic tests had positive results and the cerebellar ones were normal. Audiological evaluation showed hearing loss from 6000 Hz, with bilateral descending configurations, tympanometric curve type A and reflexes from contralateral estapedial muscle in bilateral way. Computed Vectoeletronistagmography exam had normal result.

It was done a treatment using medicine with calcium canal blocker (cinarizine 25mg VO every 8 hours), direct vasodilator (piracetam 400 mg VO every 8 hours), anticholinergic antihistaminic (dimenhydrinate 50 mg VO every eight hours), antiaggregate and flow modulator on microcirculation (Egb 761- 120 mg VO every 12 hours).

Due to light and insufficient improvement of symptoms, patient was sent to program of vestibular rehabilitation, following the protocol established by our service.

Vestibular Rehabilitation Process

The patient used to go to clinic once a week for 30-45-minute section. The exercises (a series of 10 repetitive movements) were supervised in office and performed at home from 2 to 3 times a day.

Firstly, patient was explained about labyrinth and its physiology, was oriented about caffeine reduction replacing it by decaffeinated coffee and a proper diet, as he reported drinking 10 to 12 cup of coffee per day and eating fat and spicy food.

He started doing eye, head, trunk and relaxing exercises, selected by Cawthorne & Cooksey protocol (1946) (10). Head movement exercises caused a feeling of heaviness and as a consequence a feeling of instability.

Brandt-Daroff and Dix-Hallpike maneuvers were used as complementary exercises. Along time, it was noticed an improvement on dizziness as for intensity, though frequency remained the same as well as tinnitus.

Exercises which aimed stimulation of vestibuloocular reflex were also done, including optokinetic stimulation using optokinetic drum on horizontal, vertical and oblique plan lasting 10 to 15 minutes at the end of each section, trying to reduce symptoms caused by kinetosis. In the beginning, patient reported discomfort and instability on optokinetic stimulation, and later had normal movements.

Quitting medication started according to gradual improvement of vertigo and tinnitus. The exercises of static and dynamic balance gain based on Associazione Otologi Ospedalieri Italiani protocol (AOOI) were recommended due to complaint of instability during walking.

Along rehabilitation process, patient reported 70% of improvement in 3 months. He occasionally presented few-minute-lasting indefinite indisposition. In these situations, he was monitored by a doctor through a hearing gadget in order to better know what was happening to him, with special attention to sleeping, eating and psychological state, which doctor and patient talked about.

After 6 months, he improved 85% over vestibular and psychic aspects. Therefore, with symptoms improvement, patient himself quit exercises, went to coffee drinking and irregular diet, what caused the back of symptoms although less intense.

There were new recommendations and at the moment he is well in general terms. He started reducing caffeine, walking for half an hour introducing therapy exercises adjusted to gym. His life has improved in both physical and psychological terms. He is taking cinarizine associated to piracetam once a day and has no more crises.


DISCUSSION

We can observe a large amount of otoneurological symptoms in the reported case of subclavian steal syndrome, probably coming from a defficiency of vertebrobasilar system.

The reduction of blood flow in vertebrobasilar system can come from vertigo crises, instability, unbalance, falls, incoordenation, hearing loss, tinnitus, mental confusion, headache, pre-syncope, syncope, allucination or vision failure, diplopia, dysarthria, dysphagia, etc. It can happen as an intermittent way, in which symptoms arise with positional changes of head and/or body that reduce blood flow to labyrinth (1).

In the reported case, patient started with diplopia and violent vertigo of short duration associated to nausea, sudoresis and drop-attacks. These symptoms are caused by ischemia from other areas provided by posterior circulation. Balance was endangered by blood supply.

Acute occlusion of arterial system and its collateral circulation cause hemiplegia and unilateral sensorial deficit. If occlusion develops slowly, it can occur cerebral ischemic attacks type ´drop-attacks´, situation in which individual loses muscular tonus and falls, though not losing consciousness (3).

Vectoeletronistagmography exam did not show any evidence of unilateral hypofunction and oculomotor abnormality. Balance tests added valuable information in relation to disfunction, as vestibular-spinal reflex were evaluated in such cases.

In the balance tests, patient showed estatic posture instability, observed in Romberg and Romberg-Barré tests. Although in an inefficient way, he can use vestibular information in order to keep a standing position. Besides, he presented dynamic posture instability with cephalic rotation when walking. Before this, exercises which caused a gradual sensorial conflict between vestibular, visual and proprioceptive information were selected. Then we chose more complex exercises, which would cause more sensorial conflict.

Thus, before a sensorial conflict, a repetitive stimulation leads a process of adaptation, called habituation. That is why patient was encouraged and guided to strictly follow exercises, even if they might cause a worsening feeling. In this way, compensation is more effective when conflict situation is presented in a repetitive way.

Compensation is the functional recovering mechanism of body unbalancing caused by vestibular lesion. It occurs in vestibular nuclei of brainstem and is optimized by neural plasticity phenomenon which increases synaptic efficiency, making inactive synapsis work and creating a large number of it (11).

The association of medication and exercises of vestibular rehabilitation speeds up the vestibular compensation process, and this is the target of any treatment for vestibular pathology.

One of the main aspects when starting treatment is to clarify patient on vestibular function and on pathology prognosis. We believe that all and any patients should obtain enough information and orientation, so s/he is able to know what it is happening and to have more acceptances to treatment.

Understanding or having knowledge about the function of balance system and compensation process, which occurs after vestibular lesion, reduces patient's anxiety and help the understanding of causes, meaning and control of symptoms (12).

We would say that not only a correct performance of physical exercises is convenient, but also a change in the life style, in relation to caffeine use, fat and spicy food, family and work problems, depression and discouragement feelings and sedentariness.

Unproper diet, alimentary indiscipline and some other habits can also affect hearing and vestibular functions or worsening of otoneurological problems (13).

Therefore, changing life style or even a simple correction on diet is not so easy. As a habit is part of life, it is necessary a big effort by patient and professionals.

Labyrinthic symptoms went up and down, and this can be explained by the compensation and decompensation process of the vestibular system.

The negative and extensive impact on quality of life caused by dizziness was a factor that called our attention during vestibular rehabilitation therapy. The feeling of sleeping and wakening with indisposition caused an implication on everyday life, interfering on family, work, heath and leisure.

In this way, a vicious cycle started between otoneurological and psychological symptoms, though dizziness cased insecurity such as depression and panic feelings, with negative impact on quality of life. At the same time, stress, anxiety and fear caused an increase on instability feeling and then led to physical insecurity such as unbalancing and instability.

Possible psychosomatic interpretations can lead to such conception that anxiety or suffering can cause or intensify dizziness, and also can lead to a hypothesis that a particular personality feature can predispose people to any dizziness complaint, or even to develop organic disorders which may cause vertigo (14).

We insist on the importance of a personalized vestibular rehabilitation to supply individual needs, providing then physical and psychological security when performing body movements and activities which require body balance.

The improvement with therapy might happen due to multifactor neural adaptations, sensorial replacement, functional recovery from vestibuloocular and vestibular-spinal reflexes, adaptation to different habits, change of life style and psychological effect with recovery of physical and psychological security (15).

We believe the clinical condition improvement occurred due to different factors, such as corrections of bad habits and diet, change of life style and medication associated to personalized vestibular rehabilitation. A multidisciplinary team and disease clearance to patients in relation to medical and therapeutical treatment are important to achieve treatment success in a more effective way.


FINAL COMMENTS

We believe that clinical improvement from the current case of subclavian steal syndrome has been a sum of different factors, with correct diagnosis, surgery and all orientations and therapeutical process, in which vestibular rehabilitation has an important role.

Thus, vestibular rehabilitation proved to be a powerful and efficient therapeutical way on treating subclavian steal syndrome after surgery.


BIBLIOGRAPHY

1. Ganança MM, Caovilla HH, Munhoz MS, Silva ML, Settani FA, Ganança CF. Insuficiência vertebrobasilar. eM: Silva ML, Munhoz MS, Ganança MM, Caovilla HH. Quadros clínicos otoneurológicos mais comuns. São Paulo: Atheneu, 2000. p.71-9.

2. Shapiro SL. Otologic aspects of the subclavian steal syndrome. Eye Ear Nose Throat Mon, 1971, 50(3):94-6.

3. Becker W, Naumann HH, Plaltz CR. Otorrinolaringologia Prática - diagnóstico e tratamento. 2ª edição. Rio de Janeiro: Editora Revinter, 1999.

4. Whittemore AD, Mannick JA. Sindrome do Sequestro da Subclávia. Em: Sabiston DC, Lyerly HR. Tratado de Cirurgia - As bases biológicas da Prática Cirúrgica Moderna. 15ª edição. Rio de Janeiro: Guanabara Koogan, 1998. p.1566-70.

5. Gutierrez GR, Mahrer P, Aharonian V, Mansukhani P, Bruss J. Prevalence of subclavian artery stenosis in patients with peripheral vascular disease. Angiology, 2001, 52:189-94.

6. Lobato EB, Kern KB, Bauder-Heit J, Hughes I, Sulek CA. Incidence of coronary-subclavian steal syndrome in patients undergoing noncardiac surgery. J Cardiothorac Vasc Anesth, 2001, 15:669-92.

7. Heidrich H. Subclavian steal syndrome. Arch F Kreislaufforschung, 1968, 57:190-5.

8. Lawson JD, Petracek MR, Buckspan GS, Dean RH. Subclavian Steal: Review of the clinical manifestations. South Med J, 1979, 72(11):1369-73.

9. Smith JM, Koury HI, Hafner CD, Welling RE. Subclavian steal syndrome. A review of 59 consecutive cases. J Cardiovasc Surg, 1994, 35(1):11-4.

10. Cooksey FS. Rehabilitation in vestibular injuries. Proc Royal Soc Med, 1946, 39:273-8.

11. Caovilla HH, Ganança MM. Reabilitação vestibular personalizada. Em: Ganança MM, editor. Vertigem tem cura? São Paulo: Lemos Editorial, 1998. p.197-225.

12. Yardley L. Overview of psychologic effects of chronic dizziness and balance disorders. Otolaryngol Clin North Am, 2000, 33(3):603-16.

13. Ganança MM, Munhoz MS, Caovilla HH, Silva ML, Ganança FF, Perracini MR, et al. Conceitos e algoritmos terapêuticos. Em: Ganança MM, Munhoz MS, Caovilla HH, Silva ML. Condutas na vertigem. São Paulo: Grupo Editorial Moreira Jr, 2004. p.55-103.

14. Yardley L, Luxon LM, Haacke NP. A longitudinal study of symptoms, anxiety and subjective well-being in patients with vertigo. Clin Otolaryngol, 1994, 19:109-16.

15. Ganança FF, Ganança CF, Caovilla HH, Ganança MM. Como manejar o paciente com tontura por meio da reabilitação vestibular. São Paulo: Janssen, 2000.












1. Fonoaudióloga Specialist Audiology by IEAA; Responsible for the sector from the Institute Otoneurology Promur.
2. Medical Ex-resident in Promur Institute of Otolaryngology.
3. Master and Doctor of Otolaryngology by UNIFESP-SP; Coordinator of Residence in Promur Institute of Otolaryngology.

Institution: Multidisciplinary Institute of Rehabilitation Programme (PROMUR).
Correspondence: Daniela Moreira Affonso - Hunter Street, 409 - Sao Paulo / SP - CEP 02073-000 - Phone: (11) 6901-0776 / 9967-6947 -- E-mail: daffmoreira@hotmail.com

Article received on 3 October 2005. Article accepted with modifications on January 10, 2006.
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