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PubMed2003

[A study of factors influencing intensity and annoyance in vertigo or dizziness].

For 74 men and 123 women averaging 52.5 years of age with vertigo and dizziness, we recorded the age, gender, vertigo type, duration of illness, concomitant symptoms, and vestibular and psychological test results and used a 100 mm horizontal visual analog scale (VAS) to quantitatively assess sensation intensity and annoyance in vertigo or dizziness. Factors influencing these 2 quantitative assessment parameters were analyzed by stepwise multiple regression analysis. Factors influencing sensation intensity were nausea or vomiting as a concomitant symptom, duration of vertigo or dizziness (within a day), and first episode onset. Intensity of sensation to vertigo or dizziness, self-rating depression score (SDS), and gender (female) were selected as significantly influencing annoyance. These results suggest that rational care of significant factors that involve the intensity and annoyance in vertigo is essential to treating patients with vertigo or dizziness.

Adult↗
PubMed1999

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.

Bone Cements↗
PubMedDate not supplied

[Diagnosis of common causes of vertigo using a structured clinical history].

The structured clinical history is the most sensitive test for diagnosing vertigo. Its diagnostic effectiveness on the first visit was analyzed and key signs and symptoms with high predictive value for common causes of vertigo were identified. One hundred outpatients who complained of dizziness or loss of balance were evaluated using a structured clinical interview. Each questionnaire was examined independently by three blinded investigators, who assigned a diagnosis and identified the elements of the history that figured most prominently in the diagnosis. The gold standard was defined as independent selection of the same diagnostic category by all three investigators. A first-visit diagnosis was obtained in 40% of patients (95% confidence interval 30-50%): 38% women and 42% men. Causes included benign positional paroxysmal vertigo (BPPV, 13 patients), headache-associated vertigo (9), Meniere disease (7), cervical vertigo (3), psychiatric dizziness (2), post-traumatic vertigo (2), vertebro-basilar transient ischemic attack (1), vestibular neuritis (1), convulsive seizure (1), and presyncope (1). The best predictors of BPPV were the precipitating mechanism (specificity [SP] 100%), positional nystagmus (sensitivity [SE] 90%, SP 63%), and the Dix-Hallpike test (SE 82%, SP 71%). Elements predictive of headache-associated vertigo were duration of the attack (minutes) and a personal history of headache (both, SP 100%). Other predictors were facial hypoesthesia (SE 92%, SP 47%) and associated neurological disease (SE 82%, SP 58%).

Adult↗
PubMed2000

[Pitfalls in the diagnosis of benign paroxysmal positional vertigo].

Benign paroxysmal positional vertigo (BPPV) is a common but often unrecognized cause of treatable vertigo. Possible causes of misdiagnosis of BPPV were studied by review of the records of 191 patients referred to our neurology clinic; 36 were identified as having BPPV not previously diagnosed. On referral the patients carried the following diagnoses: unspecified dizziness/vertigo (33%), transient ischemic attacks (28%), cervicogenic vertigo (19%), psychogenic dizziness/vertigo (11%), and others (8%). The paroxysmal nature of the vertigo and position-precipitating factors were not spontaneously reported by 31%. Atypical, even bizarre, symptoms including dizzy sensations were reported by 19%, and neck pain and headache were cardinal symptoms that accompanied vertigo. The Dix-Hallpike maneuver, which is essential for the diagnosis of BPPV, was not performed in any of the patients prior to referral. 30 (83%) experienced complete resolution of signs and symptoms after the first physical treatment session. We conclude that non-paroxysmal, non-positional vertigo does not rule out BPPV. Atypical and even bizarre complaints of dizziness, as well as neck pain and headache could be cardinal symptoms of BPPV. The Dix-Hallpike maneuver is mandatory in those complaining of dizziness and vertigo.

Adult↗
PubMed2002

[Diagnostic evaluation of "acute" vertigo].

Numerous studies of outpatients have been effected with the object of evaluating the role of the different causes of vertigo, and these have clearly evidenced the importance of the individual disciplinary sectors and, consequently, of the clinicoinstrumental exams necessary in order to reach the correct etiopathogenetic interpretation of the dizzy syndrome. We report the experience of a retrospective study carried out in 310 patients suffering from dizziness who were sent to us from the Emergency Room with a generic diagnosis of "acute vertigo". A detailed medical history was taken in every case, after which the patients underwent a series of otoneurological examinations which enabled us to situate each in the ambit of a vestibular pathology (central and/or peripheral) or to schedule him for a series of specialized exams, the indication of which was drawn directly from the characteristics of the clinical examination and medical history associated with the vertigo symptomatology. Of the 157 cases (50.6%) with otoneurological signs compatible with a vestibular involvement, 77 presented positional paroxysmal vertigo, 34 had an acute peripheral vestibulopathy, and 32 manifested sufferance of the central vestibular structures. In 137 patients, the otoneurological exam was negative and further investigations led to the identification of a psychogenic form in 54 cases, a cardiovascular disease in 31 cases, and a neurological disorder in 24 cases. Our data highlights the fundamental role of the anamnestic approach and the objective examination with particular reference to the search for nystagmic evidence that enabled us to make a definitive diagnosis in an elevated number of cases. In the remainder, we proceeded to perform various instrumental examinations, at times upon the request of the other specialists involved in the management of the vertigo patient. By means of a structured and detailed medical interview, it was possible to obtain useful information that directed our investigation towards a clear distinction between extravestibular and vestibular forms. In this way, furthermore, the same information was able to supply a whole series of clinical indicators of fundamental importance in identifying the most suitable specialist for the clinical picture under examination. A detailed knowledge of the different pathologies (vestibular and extravestibular) capable of causing acute vertigo appears to us to be of fundamental importance if the patients sent from the Emergency Room is to be properly evaluated. From the above, one may see how fundamental a multidisciplinary approach is in appraising the vertigo patients, enabling the correct diagnosis to be reached rapidly and economically, as demonstrated by the results obtained by our group, in which we failed to reach a precise diagnostic conclusion in only 5% of the cases.

Acute Disease↗
PubMedDate not supplied

What is vertigo?

Vertigo is one of the types of dizziness with dysequilibrium, presyncope and lightheadedness. But what does vertigo mean? Vertigo indicates a sensation of false movement (generally described like a rotation) but sometimes the patient can describe it like a sensation of tilt. Instead, the word dizziness indicates a sensation of disturbed relation to surrounding objects in space with feelings of rotation or whirling characteristic of vertigo as well as non-rotatory swaying, weakness, faintness and unsteadiness characteristic of giddiness. In our review we describe, after brief considerations about functional anatomy of the vestibular system, the most important cause of vertigo considering the duration of the symptom; moreover we underline the importance of anamnesis and of the objective examination for a correct differential diagnosis of a dizzy patient. As to objective examination we describe the most important characteristics of nystagmus, that is the only objective sign in vertigo, of central and peripheral origin. At last we consider the most efficacious therapies, like as medications (specific and aspecific), surgery (conservative and destructive) and rehabilitation, in relation the characteristics and the causes of vertigo.

Age Factors↗
PubMed2005

Treatment of vertigo.

Vertigo is the illusion of motion, usually rotational motion. As patients age, vertigo becomes an increasingly common presenting complaint. The most common causes of this condition are benign paroxysmal positional vertigo, acute vestibular neuronitis or labyrinthitis, Ménière's disease, migraine, and anxiety disorders. Less common causes include vertebrobasilar ischemia and retrocochlear tumors. The distinction between peripheral and central vertigo usually can be made clinically and guides management decisions. Most patients with vertigo do not require extensive diagnostic testing and can be treated in the primary care setting. Benign paroxysmal positional vertigo usually improves with a canalith repositioning procedure. Acute vestibular neuronitis or labyrinthitis improves with initial stabilizing measures and a vestibular suppressant medication, followed by vestibular rehabilitation exercises. Meniere's disease often responds to the combination of a low-salt diet and diuretics. Vertiginous migraine headaches generally improve with dietary changes, a tricyclic antidepressant, and a beta blocker or calcium channel blocker. Vertigo associated with anxiety usually responds to a selective serotonin reuptake inhibitor.

Diagnosis, Differential↗
PubMed2005

[Analysis of select diagnostic examination results and their connection with cervical vertigo diagnosis].

Cervical spine spondylotic changes are known to cause vertigo, but diagnostic criteria are not established. The aim of present study was to asses diagnostic value of classical radiologic, electronystagmographic (ENG) and transcranial doppler ultrasonographic (TCD) examinations in cervical vertigo diagnostic process. Forty patients with vertigo lasting more than 6 months with radiological evidence of cervical spondylosis participated in the study. All patients had ENG and TCD with neck rotation test. Cervical vertigo was diagnosed in patients with positive neck rotation test in: TCD examination (15% decrease of vertebral artery flow) and/or ENG examination (cervical nystagmus). We diagnosed cervical vertigo in 65% of patients. Multivariate model of logistic regression analysis showed that the best statistical predictors of cervical vertigo were: asymmetry of vertebral artery flow in TCD (OR: 92.2; 95% CI: 6,2-1381) and presence of osteophytes and discopathy in radiological examination (OR: 64.1; 95% CI: 1,3-1107). The transcranial doppler ultrasonographic examinations seems to be useful for diagnosing cervical vertigo.

Adult↗
PubMed2006

[Hearing evaluation in patients with vertigo].

INTRODUCTION: Vertigo is one of the most frequent and disturbing sensations that the practicing otolaryngologist is called upon to treat. Vertigo is the illusory sensation of motion. True vertigo is caused by pathology in the peripheral end organ, the vestibular nerve, and the pathways that connect them in the brainstem and rarely, in the cortex. AIM: The aim of this study was to evaluate hearing in people with vertigo according to the etiology of balance disorders. The study comprised 127 patients treated in our clinic between 1999 and 2004, 88 women and 39 men (254 ears) aged 24-90 years. The average age was 56. METHODS: Hearing tests (pure tone audiometry, speech audiometry, impedance audiometry, auditory brainstem responses, OAE) as well as vestibular function tests (electronystagmography, rotational chair tests, caloric tests) were performed. In order to evaluate the nature of vertigo radiological diagnostics (head and cervical computer tomography, vascular diagnostics using Doppler sonography) was performed. RESULTS: Audiometric testing showed impaired hearing in 71 of 127 subjects. Among 73 patients with vertigo of vascular origin caused by vertebrae-basilar insufficiency, bilateral cochlear lesion was noticed in 33 cases and unilateral in 9. In 8 patients with cervical ankylosing spondylitis 3 had cochlear hearing loss (1--unilateral, 2--bilateral). CONCLUSIONS: In our group of patients with vertigo in the most of cases the hearing loss was on cochlear origin.

Adult↗
PubMed1987

[New aspects of differential vertigo diagnosis in childhood].

Eight cases of vertigo in childhood are reported. Four of them suffered from benign paroxysmal vertigo, and the other four from atypical migraine. History of a head injury and attacks of vertigo lasting only a few seconds are typical of benign paroxysmal vertigo. These children are older than 4 years and the vertigo is of peripheral origin. Vertigo due to atypical migraine is frequent in young children up to 4 years of age, shows a longer duration of vertigo (more than 1 min) and is of central origin.

Adolescent↗
PubMed1994

[Benign paroxysmal positional vertigo. Diagnosis, course, physiopathology and treatment].

The benign paroxystic positional vertigo (BPPV) is defined by brief attacks of rotational vertigo and concomitant rotatory-linear nystagmus, triggered by rapid extension and by lateral head tilt toward the affected ear. Cupulolithiasis of the posterior semi-circular canal from one inner ear is responsible of this peculiar type of positional vertigo. Definition diagnostic criteria are based upon the time history of the burst of rotational vertigo associated with the typical positioning nystagmus induced by rapid position changes from the setting to the head hanging right or left position during the Nylen-Barany maneuver. The nystagmus, which is a torsional nystagmus of the eye-balls rolling on the orbit's ground toward the affected and undermost ear, begins a few seconds after the head tilt, is best seen with Frentzel's glasses, preventing the suppression of the nystagmus by fixation, and the repetition of the maneuver will result in everlasting symptoms. According to the largest series of the literature the BPPV is the most frequent recognized cause of vertigo, with more than 30% of the cases of vertigo, explored in a dizziness clinic. In half of the cases, a peculiar etiology can be found, such as head trauma, ototoxic drug, or viral labyrinthitis, with a sex-ratio of one. On the contrary the sex-ratio among the idiopathic forms of BPPV is of two females for one male. The prognosis of BPPV is benign because of its recovery within weeks or months, either spontaneously, or after the liberatory maneuver. In rare cases, the vertigo recurs or persists for months or years. For some very handicapping BPPV, a surgical treatment can be proposed.

Adult↗
PubMed1995

Reliability of examination data in the diagnosis of benign paroxysmal positional vertigo.

A practical clinical view of the reliability of the data obtained in the several steps of the examination procedure is discussed to obtain an objective basis for the selection of patients with provoked vertigo (benign paroxysmal positioning vertigo [BPPV]) in view of treatment of this type of vertigo by rehabilitation therapy. Clinical experience supports the concept that the diagnosis has to be based not only upon a typical history, but also upon the presence of a reproducible vertigo and paroxysmal positional nystagmus (ppn). Such a ppn can be reproduced not only as a "classic" nystagmus by the Dix-Hallpike maneuver, but also as a positional nystagmus and vertigo during electronystagmographic recording in the position tests and in the vestibular habituation training (VHT)-test battery (a battery of 19 maneuvers applied for defining the adequate exercises in the rehabilitation treatment of BPPV). The ppn is not a constant reproductible sign in every patient, and in some, only one of these tests confirms the BPPV. This experience is confirmed by the analysis of the reviewed data in 95 patients, which showed that one third of the patients described their vertigo in a rather atypical way, whereas further testing revealed a BPPV. In this way any absolute reliability of history has to be denied. In fact, only the finding of a ppn is conclusive for confirming BPPV. However, as in former experiences, here too, the presence of such a ppn appeared not to be a constant datum, so that in some patients more than one examination was necessary to come to a reliable diagnosis. Patients in whom only vertigo could be reproduced, never confirmed by nystagmus, were excluded as an atypical ppv group.

Adolescent↗
PubMed1996

[Vertigo as an atypical symptom of intraspinal cord tumor].

Vertigo is an unpleasant sensation of movement of the subject or of his surroundings. There are many causes of vertigo. Traditionally these are divided into 'central' and 'peripheral'. It is unusual to find it as a symptom of myelopathy. We describe the case of a 67 year-old woman with no significant previous clinical history who complained of the sudden onset of vertigo a few hours previously, which worsened on turning her neck towards the left. On examination, the vertigo recurred on turning her neck to the left after a latent period of a few seconds together with the appearance of ipsilateral conjugated nystagmus, which gradually disappeared. On neurological examination, there was amyotrophy of both arms with weakness, considerably reduced reflexes, except for clonus of the left wrist. There was slight paraparesia with bilateral cutaneoplantar flexion and a level of sensitivity at C2-C3. The sensitivity disorder was more marked in the arms with a bilateral distribution approximately at C5-C7 affecting predominantly thermoanalgesia. Cervical MRI showed a mass consistent with ependymoma. This was removed surgically 2 weeks after admission. The findings of the intraoperative biopsy confirmed the radiological diagnosis. The vertigo improved one week after admission, although the patient died of pneumonia one month after operation. Despite the vertigo was an atypical symptom, it was the clue that led to the diagnosis. Hypotheses about the cause of vertigo are discussed.

Aged↗
PubMed1998

[Vertigo and dizziness related to platelet aggregability].

Platelet aggregates were measured in 82 cases with vertigo and dizziness and 60 cases with additional symptom of headache (so-called cervical vertigo). Results showed that patients with vertigo and dizziness had increased aggregability and patients with cervical vertigo were within normal range (p < 0.0001). 53 cases of these with vertigo and dizziness were administrated platelet aggregation inhibitors (mainly ticlopidine). After 1 approximately 2 weeks, most of patients became symptom free, and at this time platelet aggregates of these patients were suppressed to within normal range. Then patients were followed with chronological measurements of platelet aggregates. During this time, aggregabilities were attempted to be kept within the normal range, thus dose of platelet aggregation inhibitor was controlled depending on the result of aggregability. Also patients were encouraged to show good drug compliance by being informed of sudden increasing aggregability. One patient experienced recurrence of vertigo after ceasing the medicine. This study demonstrates that platelet aggregation may increase in most of patients with not only vertigo but also dizziness in whom administration of a platelet aggregation inhibitor is effective. It also stresses that chronological measurements of platelet aggregations are important to control the dose of medication.

Adult↗
PubMed1998

Intracranial tumors mimicking benign paroxysmal positional vertigo.

Benign paroxysmal positional vertigo is a common type of vertigo seen by the otolaryngologist; however, intracranial tumors can mimic benign paroxysmal positional vertigo in their presentation. A review of patients seen in the Department of Otolaryngology at The Ohio State University between July 1992 and August 1996 identified five patients with intracranial pathologic conditions mimicking benign paroxysmal positional vertigo. These patients were first seen with episodic vertigo associated with positional change. Failure of the symptoms to respond to the particle repositioning maneuver or the finding of associated auditory or neurologic symptoms prompted further evaluation by magnetic resonance imaging of the brain, which revealed intracranial pathologic conditions including two meningiomas, a vestibular schwannoma, a glioma, and a lipoma. These findings suggest that patients seen with symptoms like those of benign paroxysmal positional vertigo who do not show improvement after undergoing the particle repositioning maneuver or those who describe associated auditory or neurologic symptoms should have magnetic resonance imaging done to rule out intracranial pathologic conditions. Additionally, benign paroxysmal positional vertigo and intracranial tumors may coexist.

Adult↗
PubMed1993

Vestibular nerve disorder in patients suffering from sudden deafness with vertigo and/or vestibular dysfunction.

Vestibular nerve disorder (VND) in cases suffering from sudden deafness with vertigo was studied. Between 1987 and 1991, we observed 46 patients suffering from sudden deafness with or without vertigo, who had undergone the caloric test and galvanic body sway test (GBST). Twenty-seven patients had vertigo and canal paresis (CP) upon the caloric test, 6 vertigo without CP and 13 CP without vertigo. VND was detected in 12 of the 46 patients. All those with VND had vertigo and CP upon the caloric test, 12/27 (44%). The degree of hearing loss in those with VND was significantly (p < 0.05) more severe and their recovery of hearing loss was poorer than in patients without VND. These results indicate that VND is a common finding in cases of sudden deafness with vertigo especially in those with severe hearing loss.

Caloric Tests↗
PubMed1998

Homeopathic vs conventional treatment of vertigo: a randomized double-blind controlled clinical study.

OBJECTIVE: To compare the efficacy and safety of a homeopathic remedy (Vertigoheel, Heel Inc, Albuquerque, NM) vs betahistine hydrochloride (active control) in the treatment of patients with vertigo of various origins in a confirmative equivalence trial. DESIGN: Randomized (1:1) double-blind controlled clinical trial. SETTING: Fifteen study centers (general practice) in Germany between November 1995 and November 1996. SUBJECTS: A total of 119 patients with vertigo of various origins (from whom 105 patients could be analyzed as intended per protocol). MAIN OUTCOME MEASURES: Frequency, duration, and intensity of vertigo attacks. RESULTS: Both homeopathic and conventional treatments showed a clinically relevant reduction in the mean frequency, duration, and intensity of the vertigo attacks. The therapeutic equivalence of the homeopathic remedy and betahistine was established statistically. CONCLUSIONS: Concerning the main efficacy variable, therapeutic equivalence between the homeopathic remedy and betahistine could be shown with statistical significance (confirmative analysis). Both remedies reduced the frequency, duration, and intensity of vertigo attacks during a 6-week treatment period. Also, vertigo-specific complaints were significantly reduced in both treatment groups.

Adolescent↗
PubMed2003

Posterior semicircular canal dehiscence: a morphologic cause of vertigo similar to superior semicircular canal dehiscence.

The aim of this study was to assess imaging findings of posterior semicircular dehiscence on computed tomography and to evaluate incidence of posterior and superior semicircular canal dehiscence in patients presenting with vertigo, sensorineuronal hearing loss or in a control group without symptoms related to the inner ear. Computed tomography was performed in 507 patients presenting either with vertigo ( n=128; 23 of these patients suffered also from sensorineuronal hearing loss), other symptoms related to the inner ear, such as hearing loss or tinnitus ( n=183) or symptoms unrelated to the labyrinth ( n=196). All images were reviewed for presence of dehiscence of the bone, overlying the semicircular canals. Twenty-nine patients had superior semicircular canal dehiscence. Of these patients, 83% presented with vertigo, 10% with hearing loss or tinnitus and the remaining 7% with symptoms unrelated to the inner ear. In 23 patients dehiscence of the posterior semicircular canal was encountered. Of these patients, 86% presented with vertigo, 9% with hearing loss or tinnitus and 5% with symptoms unrelated to the inner ear. Defects of the bony overly are found at the posterior semicircular canal, in addition to the recently introduced superior canal dehiscence syndrome. Significant prevalence of vertigo in these patients suggests that posterior semicircular canal dehiscence can cause vertigo, similar to superior semicircular canal dehiscence.

Case-Control Studies↗