Cases reported "Vertigo"

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1/25. A surgical case of atypical aortic coarctation using cardiopulmonary bypass.

    We report a 44-year-old woman with atypical aortic coarctation accompanied by cerebral artery disease. She was hospitalized for vertigo. An extra-anatomic bypass between the ascending aorta and abdominal aorta was performed using partial cardiopulmonary bypass under moderate hypothermia to reduce the after load of the left ventricle and maintain cerebral blood flow and cerebral perfusion pressure. The postoperative course was uneventful and there was no postoperative neurological deficiency.
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2/25. Superior semicircular canal dehiscence: a new cause of vertigo.

    There are many known causes of vertigo, but many cases remain unexplained. sound-induced, pressure-induced, or positional vertigo caused by bony dehiscence of the superior semicircular canal into the middle cranial fossa is a newly described etiology of vertigo. Three case studies of patients with CT evidence and surgical confirmation of bony dehiscence of the superior semicircular canal with variable presentations are described. The history, symptoms, CT findings, vestibular studies, and method of surgical repair are presented. Two patients had disabling vertigo and one had no vestibular symptoms. All underwent exploration via a middle cranial fossa approach with repair of the dehiscence. The bony dehiscence of the superior semicircular canal of the asymptomatic patient was identified and closed at the time of an encephalocele repair procedure. All patients did well postoperatively and both patients with vertigo improved. Bony dehiscence of the superior semicircular canal may cause vertigo or be asymptomatic and should be added to the differential diagnosis of vertigo.
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3/25. Superior canal dehiscence syndrome.

    OBJECTIVE: To present the symptoms, signs, and findings on diagnostic tests of patients with the superior canal dehiscence syndrome and to describe the surgical procedures used to treat the dehiscence in five patients. DESIGN AND SETTING: Prospective study of a series of patients identified as having this syndrome at a tertiary care referral center. patients AND RESULTS: Seventeen patients with vertigo, oscillopsia, or both evoked by intense sounds or stimuli that caused changes in middle ear and/or intracranial pressure were identified over a 4-year period. The evoked eye movements had vertical and torsional components, with the direction corresponding to the effect of the stimuli in causing excitation (Valsalva against pinched nostrils, tragal compression, sounds) or inhibition (Valsalva against a closed glottis or jugular venous compression) of the affected superior semicircular canal. Thirteen (76%) of these patients also experienced chronic dysequilibrium that was often the most debilitating symptom. Dehiscence of bone overlying the superior semicircular canal on the affected side was confirmed with computed tomographic scans in each case. Surgical procedures through the middle fossa approach to plug or resurface the superior canal were performed in five patients (canal plugging in three cases and resurfacing of the dehiscence without plugging in two). The debilitating symptoms resolved or improved after the procedures. Signs of vestibular hypofunction, without loss of hearing, were noted in one patient after plugging of the superior canal and in one other patient after resurfacing of the canal. CONCLUSIONS: The superior canal dehiscence syndrome is identified based on characteristic symptoms, signs, and computed tomographic findings. The clinical presentation and findings can be understood in terms of the effect of the dehiscence on the physiology of the labyrinth. The syndrome is a treatable cause of vestibular disturbance.
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4/25. Continuous vertigo and spontaneous nystagmus due to canalolithiasis of the horizontal canal.

    The authors present a patient with benign paroxysmal positional vertigo of the right horizontal semicircular canal who developed persistent vertigo with spontaneous horizontal nystagmus to the left and caloric hypoexcitability on the right after a head shaking maneuver. Both spontaneous nystagmus and canal paresis resolved after repeated shaking of the head. The most probable mechanism of this type of vertigo is plugging of the horizontal canal by otoconial particles with a negative endolymph pressure between plug and cupula.
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5/25. Unpredictable hearing loss after intratympanic gentamicin treatment for vertigo. A new theory.

    A new hypothesis is advanced suggesting that unpredictable cases of profound hearing loss after intratympanic gentamicin treatment (IGT) may be caused by decreased patency of the communication routes between the inner ear and the cerebrospinal fluid, primarily of the cochlear aqueduct. A tympanic displacement analyzer, which can indirectly analyze inner ear and intracranial pressure changes and can also evaluate the efficiency of communication between these two compartments, was used. Two cases are presented: in the first, a patient who became deaf after IGT showed signs of decreased patency of the communication routes with the tympanic membrane displacement (TMD) test; in the second, a patient without hearing damage after IGT had efficient communication evaluated by the TMD test. These preliminary findings are in accordance with the proposed pathophysiology. If future clinical studies confirm the present theory and findings, it may prove possible to predict and prevent deafness after IGT and possibly also after systemic aminoglycoside treatment.
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6/25. Vestibular-evoked myogenic potentials in the diagnosis of superior canal dehiscence syndrome.

    patients with superior canal dehiscence (SCD) syndrome have vertigo and oscillopsia induced by loud noises and by stimuli that result in changes in middle ear or intracranial pressure. We recorded vestibular-evoked myogenic potentials (VEMP responses) in 10 patients with SCD syndrome. The diagnosis had been confirmed in each case by evoked eye movements and by high-resolution CT scans of the temporal bones that showed a dehiscence overlying the affected superior canal. For the 8 patients without prior middle ear disease, the VEMP threshold from the dehiscent ears measured 72 /- 8 dB NHL (normal hearing level) whereas the threshold from normal control subjects was 96 /- 5 dB NHL (p < 0.0001). The VEMP threshold measured from the contralateral ear in patients with unilateral dehiscence was 98 /- 4 dB NHL (p > 0.9 with respect to normal controls). Two patients with apparent conductive hearing loss from middle ear disease, and SCD, had VEMP responses from the affected ears. In the absence of dehiscence, VEMP responses would not have been expected in the setting of conductive hearing loss. These findings confirm earlier studies demonstrating that patients with SCD syndrome have lowered VEMP thresholds. Conditions other than SCD syndrome may also lead to lowered VEMP thresholds. Rather than being based upon a single test, the diagnosis of SCD syndrome is best established when the characteristic symptoms, signs, VEMP response, and CT imaging all indicate SCD.
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7/25. rupture of the round window membrane.

    A perilymph leak into the middle ear through a ruptured round window membrane results in the symptoms of hearing loss, tinnitus and vertigo, either singly or in combination. The case histories of thirteen patients with such a fistula are described, these patients having in common a predisposing incident which had led to a rise of C.S.F. pressure. Symptomatology and the results of investigation are analysed and operative technique and results discussed. While it appears that vertigo uniformly responds very satisfactorily to operative treatment the improvement in hearing loss and tinnitus is more difficult to predict.
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8/25. Autonomic failure mimicing dopamine agonist induced vertigo in a patient with macroprolactinoma.

    A 68-year-old man presented with general fatigue, increasing adynamia, weakness, vertigo and recurrent syncope. Six weeks earlier the diagnosis of a macroprolactinoma had been established based on a greatly elevated prolactin concentration (161 170 micro U/l) and MR-evidence of a 3.5 cm measuring pituitary mass. The patient had been started on cabergoline (1.5 mg weekly). Orthostatic hypotension due to the dopamine agonist was considered very likely and carbergoline therapy was stopped. However, there was no relief of the symptoms and further syncopes followed. Testing of blood pressure and heart rate regulation, selective testing of postganglionic cardiac neurons with [ 123 J] metaiodobenzylguanidine scintigraphy provided evidence of grossly impaired neurogenic cardiovascular regulation due to failure of postganglionic efferent sympathetic activity. This is characteristic for pure autonomic failure. The patient was treated symptomatically with high fluid intake, compression stockings, fludrohydrocortisone (0.1 mg o.d.s.), piroxicam (20 mg o.d.s.) and etilephrin (10 mg q.d.s.), which enabled him to cope with daily activities without syncope. This case shows that vertigo in a patient with macroprolactinoma is not always related to drug therapy but may be related to other causes.
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9/25. The problem of dizziness and syncope in old age: transient ischemic attacks versus hypersensitive carotid sinus reflex.

    In the elderly, a transient ischemic attack (TIA) and a hypersensitive carotid sinus reflex (HCSR) often co-exist and can pose a diagnostic challenge. Seven cases are presented. HCSR is a relative condition; besides increased irritability of the receptor or target organs, susceptibility of the nerve center to ischemia probably is induced by a slow heart rate or low blood pressure in any patient with pre-existing occlusive cerebrovascular disease. dizziness and syncope of this type represent hemodynamic TIA in contrast to thromboembolic TIA. The carotid sinus massage test is recommended for differentiating the two types of TIA; the treatments differ. At present there is no uniform management that can be applied to either TIA or HCSR routinely. Therefore, treatment should be approached on an individual basis, keeping in mind the different pathophysiologic factors operating in the specific patient.
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10/25. Chiari-I malformation in two fighter pilots.

    This report describes two cases of Chiari Malformation Type I (Chiari-I) in fighter pilots of the Turkish air Force. Chiari-I is a congenital malformation characterized by herniation of cerebellar tonsils through the foramen magnum. patients have symptoms and signs related to dysfunction of the brainstem, spinal cord, and cerebellum. They generally are symptomatic in the earlier years of life. However, asymptomatic cases can eventually become symptomatic in later years. Symptoms can be provoked by increasing intracranial pressure (Valsalva or straining). We report on two pilots with Chiari-I malformation who had no symptoms or signs in their daily activities. Furthermore, these pilots had successfully completed physiological training, including centrifuge training, without any symptoms. However, they suffered from headache, neck spasms, and/or disequilibrium under Gz during flight training sorties. The clinical presentation, diagnosis, treatment, possibility of acquired cases, and aeromedical disposition of Chiari malformations are discussed.
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