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PubMed2001

Vestibular diagnosis as prognostic indicator in sudden hearing loss with vertigo.

The majority of episodes of sudden hearing loss are caused by inner ear disorders, often accompanied by vertigo. The patterns of hearing loss usually influence the prognosis. The purpose of this study was to analyze vestibular diagnoses in sudden hearing loss with vertigo, and to correlate them with the recovery of hearing loss. The clinical records of 125 patients with sudden hearing loss were reviewed. Various vestibular evaluations were performed in 36 patients with vertigo. The vertigo in these patients was classified as normal, unilateral hypofunction, directional preponderance, benign paroxysmal positional vertigo (BPPV), non-specific or irritative. The initial and final pure-tone audiograms of these patients were compared. The distribution of vestibular diagnoses was unilateral hypofunction in 30.6% of patients, BPPV in 25.7%, normal in 19.4%, non-specific in 11.1%, directional preponderance in 8.3% and irritative in 8.3%. The recovery of hearing in patients with vertigo was significantly worse than in those without vertigo. The recovery of hearing in patients with spinning vertigo did not differ from that of patients with non-spinning vertigo. The recovery of hearing was worst in the BPPV group, especially in the high frequency range, followed by the unilateral hypofunction group, who showed hearing thresholds between those in the BPPV group and those in the normal vestibular function test group. This study suggests that the diagnostic classification of vestibulopathy is a useful prognostic indicator of hearing recovery in sudden hearing loss with vertigo. We conclude that otolithic and semicircular canal involvement may cause poor hearing results, especially in the high frequency range.

Adult↗
PubMed2004

Congenital morphological abnormalities of the distal vertebral arteries (CMADVA) and their relationship with vertigo and dizziness.

BACKGROUND: The aim of our study was to identify congenital morphological abnormalities of distal vertebral arteries (CMADVA) and their association with cerebral hypoperfusion leading to vertigo, and the role of MR and MRA in the diagnosis of vertebrobasilar (VB) abnormalities. MATERIAL/METHODS: 768 patients who complained of dizziness and/or vertigo were included in the study and evaluated by MR and MRA. CMADVAs were determined in 88 of the cases with no other explanation for vertigo and dizziness. 150 patients without dizziness or vertigo were used as a control group. The 3D TOF (Time- of- flight) MR angiographic technique was used. RESULTS: CMADVAs were detected in 88 of 768 patients (11.5%) with vertigo and/or dizziness. We also detected CMADVAs in 4 (2.7%) of 150 persons in the control group. The patients with abnormal vertebral artery findings were classified into ten categories. Lacunar infarcts in the brain stem were found in 8 patients after long-duration vertigo attacks. There was significant correlation between the control and vertigo groups in terms of CMADVA (p=0.0001). After excluding the control group, there was a significant relationship between CMADVA and vertigo and/or dizziness symptoms (p=0.0001). CONCLUSIONS: We believe that vertigo and dizziness associated with CMADVA is a real entity that deserves greater attention. For this reason, the vertebrobasilar system in these patients should be examined for CMADVA with MRA. This would enable us to take preventive measures against brainstem ischemia or at least elucidate the etiology of vertigo in these patients.

Adolescent↗
PubMed2004

Persistent vertigo following particle repositioning maneuvers: an analysis of causes.

OBJECTIVE: To analyze the causes of persistent vertigo following treatment with particle repositioning maneuvers (PRMs) in patients with benign paroxysmal positional vertigo. DESIGN: Prospective study of outcomes in patients with benign paroxysmal positional vertigo. STUDY SETTING: Outpatient clinic of a tertiary care referral center. PATIENTS: A sample of 90 consecutive patients with documented benign paroxysmal positional vertigo of the posterior semicircular canal who had persistent vertigo after at least 3 sessions of PRMs during a period of 2 weeks. INTERVENTION: Particle repositioning using a modified Epley maneuver. MAIN OUTCOME MEASURE: Persistent vertigo following at least 3 sessions of PRMs over a period of 2 weeks. RESULTS: Seven patients showed partial or no improvement following treatment. The causes subsequently determined included coincident horizontal canal positional vertigo (2 cases), Ménière's disease (2 cases), persistent posterior canal benign paroxysmal positional vertigo in association with cervical spondylosis (2 cases), and a posterior fossa meningioma (1 case). CONCLUSIONS: Patients with persistent or frequently recurring positional vertigo following treatment with PRMs should undergo detailed investigation to exclude coincidental pathology for which specific treatment is required. In patients in whom no coincident pathology requiring therapy is identified, treatment options other than the PRM already instituted should be considered.

Aged↗
PubMed2007

[Low frequency fluctuating hearing loss without labyrinthine vertigo--a genuine disease? A follow up study after 4 and 10 years].

BACKGROUND: Besides the typical attacks of dizziness, recurrent low-frequency sensory hearing loss--together with mostly low-frequency tinnitus--is also a characteristic sign of Menière's disease. It is therefore often assumed to be a prodromal sign of Menière's disease, even without dizziness. METHODS: During our longitudinal study, which was started in 1995, we reported that there were 81 patients with recurrent low-frequency hearing loss with no initial vertigo in the first suspense year of 1999. After a further 6 years, we investigated 46 (57%) of these original 81 patients in the second suspense year, 2005, for new components of vertigo, with the questions of development of Menière's disease and further development of the patients' hearing ability and psychic situation in mind. RESULTS: In all, 12 (26%) of the 81 former patients suffered from vertigo, but only 4 (9%) had developed the typical signs of full-blown Menière's disease with the typical labyrinthine vertigo. Of the 12 patients who suffered from vertigo, 6 (13% of the 81 with vertigo) were diagnosed with psychogenic vertigo, 1 (1%) suffered from benign and treatable paroxysmal positional vertigo and 1 (1%) had developed vertigo after acoustic neurinoma surgery. CONCLUSIONS: We conclude from our observations that, although almost every patient with Menière's disease suffers from recurrent low-frequency hearing loss, only a few patients with recurrent hearing loss develop Menière's disease. However, many patients with low-frequency sensory hearing loss develop anxiety leading to psychogenic dizziness in fearful expectation of "imminent" Menière's disease. We found that 26% of the patients had persisting bilateral normacusis in the low-frequency ranges, while 34% had unilateral hearing loss that was sufficiently severe to affect their lives and 39%, bilateral hearing loss; however, none of the patients became completely deaf.

Adolescent↗
PubMed2006

Clinical investigation on hypotensive patients with vertigo.

The aim of this study was to investigate the characteristic of hypotensive patients with vertigo. Twenty hypotensive patients with rotatory vertigo, 15 hypotensive subjects without vertigo, and 15 mitral valve prolapse subjects without vertigo underwent a battery of tests including audiometry, electronystagmography (ENG), and vestibular evoked myogenic potential (VEMP) test. The abnormal rates in terms of audiometry, eye tracking, optokinetic nystagmus, visual suppression, and caloric tests were 15, 35, 35, 10, and 42% for the first group; 13, 20, 33, 0, and 0% for the second group; and 7, 13, 60, 0, and 3% for the third group, respectively. Comparison of the first group with the other two control groups revealed that significant difference existed only in the abnormality of caloric responses. Fifteen (75%) of 20 hypotensive patients with vertigo having abnormal ENG results, asymmetric caloric responses, or delayed VEMPs were attributed to vertigo of central origin, possibly from ischemic disorder. In contrast, five patients (25%) had neither central signs in ENG nor abnormal VEMPs, but showing bilateral normal or hyperactive caloric responses were classified as autonomic dysfunction. After 3 months of medication, all patients with autonomic dysfunction had their vertigo and autonomic symptoms subsided, whereas 27% of the patients with ischemic disorder had vertigo persisted, showing a significant difference. In conclusion, hypotensive patients with vertigo could be due to either direct autonomic dysfunction or ischemic disorder mediated by autonomic deficits.

Adult↗
PubMed2007

Etiology of vertigo in children.

OBJECTIVE: To detect the most common causes of vertigo in children. METHODS: Fifty-four children (20 boys and 34 girls) aged 3-16 years, who presented with vertigo attacks during a 3-year period, were studied. A detailed medical history for vestibular symptoms and migraine was obtained from our patients or their parents. All patients underwent otolaryngologic, ophthalmologic and neurologic clinical evaluation. A detailed laboratory examination, including serologic tests for viral infections, was also obtained. Additionally, a complete audiological and neurotologic evaluation was performed. Computed tomography (CT) scans and magnetic resonance imaging (MRI) were obtained in selected cases. RESULTS: Viral infections, benign paroxysmal vertigo of childhood and migraine were the most common causes of vertigo accounting for approximately 65% of our patients. Otitis media, head trauma, benign paroxysmal positional vertigo, Meniere's disease and brain tumor were less common causes of vertigo. CONCLUSIONS: A peripheral type of vertigo was found in most cases. Diagnostic approach in vertigo in children should include a detailed history and clinical examination in conjunction with a test battery of audiological and neurotologic tests. When a central cause of vertigo is suspected an MRI or CT scan should be ordered.

Adolescent↗
PubMed1998

Vertigo.

Vertigo is a subtype of dizziness, which results from an imbalance within the vestibular system. This seminar focuses on three common presentations of vertigo: prolonged spontaneous vertigo, recurrent attacks of vertigo, and positional vertigo. The patient's history is usually the key to differentiation of peripheral and central causes of vertigo. The most common cause of vertigo, benign paroxysmal positional vertigo, can be cured with a simple positional manoeuvre. Other common causes of vertigo include vestibular neuritis, Ménière's syndrome, migraine, and vertebrobasilar insufficiency. Treatment should be directed at the underlying cause whenever possible, but antivertiginous and antiemetic drugs can suppress symptoms when a specific cause cannot be found. These drugs are generally not indicated for long-term daily use, however, since they may interfere with the normal compensation process.

Humans↗
PubMed1997

Otoneurologic evaluation of child vertigo.

In this study 282 children with vertigo are subdivided (according to previous experiences) into three large groups: (1) vertigo and cochlear diseases; (2) vertigo as an isolated symptom; and (3) vertigo and C.S.N. diseases. Due to the difficult etiopathogenetic investigation of the patients from the second group, the authors focused on that group as they are less studied, are without associated symptoms (deafness--first group; CNS diseases--second group) and where vertigo appears as an idiopathic and an isolated symptom. A careful anamnestic, clinical and instrumental analysis leads to the following observations: (1) in decreasing order of frequency we find the third group, followed by the first and finally by the second; (2) in spite of the overall lower incidence of the second group, this latter includes the paroxismal benign vertigo (PBV) which is overall the second most frequent vertiginous form (after vertigo due to cranial trauma). In this group the authors underline the reasonably high incidence of the iatrogenic syndromes, insisting on the need of their accurate prevention of these risks; (3) the authors confirm that, nowadays, a reliable etiopathogenetic cause of the apparently isolated vertigo (except for the ascertained iatrogenic forms) cannot be identified. Moreover, in spite of its frequency, PBV is the less known form of vertigo, of which we cannot give a certain diagnosis and which can be identified only the the exclusion of all the other known forms through instrumental and clinical observations.

Acoustic Impedance Tests↗
PubMed2005

Migraine-associated vertigo.

CONCLUSIONS: It is probably not wise to demand a temporal relationship between migraine symptoms and vertigo for the definition of migrainous vertigo. When recurrent vertigo attacks begin at an early age in a patient with normal hearing and migraine, there are few diagnoses other than migraine that need to be considered. OBJECTIVE: The clinical association between migraine and vestibular symptoms, such as dizziness, motion intolerance and spontaneous attacks of vertigo, is well documented. Recently, investigators have attempted to develop diagnostic criteria for this association. We hypothesized that there are multiple migraine-associated vestibular syndromes and studied a more homogenous subset of them (benign recurrent vertigo). MATERIAL AND METHODS: A structured interview was conducted over the telephone with 40 patients who presented to our neurotology clinic with benign recurrent vertigo and met the International Headache Society criteria for migraine. The structured interview was also conducted with 40 relatives of the patients who reported the same symptoms. RESULTS: A marked female predominance was found. Most of the patients had vertigo attacks lasting minutes or hours and most were completely free of dizziness between attacks. Imbalance and nausea typically accompanied the vertigo. However, in half of the cases, vertigo occurred without an association with headache.

Adult↗
PubMed2002

New approaches to the management of peripheral vertigo: efficacy and safety of two calcium antagonists in a 12-week, multinational, double-blind study.

OBJECTIVE: To evaluate the efficacy and safety profile of one 30-mg nimodipine oral tablet taken three times per day (one tablet with breakfast, one with lunch, and one with dinner) or one 150-mg cinnarizine verum oral capsule taken once each day with dinner for 12 weeks. STUDY DESIGN: Comparative in a double-blind, multinational pilot study. SETTING: Tertiary referral center. PATIENTS: A total of 221 patients met the study criteria; of that total, 181 adult patients completed the study, including 135 women and 46 men whose ages ranged from 20 to 80 years. INTERVENTIONS: Two calcium antagonists were used to treat vertigo (nimodipine, 89 patients; cinnarizine, 92 patients), and all patients were maintained on the same dosage regimen until they completed 12 weeks of treatment. Patients were evaluated at 2-and 4-week intervals; an additional evaluation was made at Week 14 to determine vertigo recurrence in the posttreatment period. MAIN OUTCOME MEASURES: The response was evaluated by using the vertigo severity index, a count of vertigo episodes in a given time period. Each episode is weighted according to its intensity. RESULTS: Nimodipine treatment decreased the incidence of moderate vertigo episodes by 78.8% and decreased severe vertigo episodes by 85.0%. Cinnarizine treatment decreased the incidence of moderate vertigo episodes by 65.8% and decreased severe vertigo episodes by 89.8%. Nimodipine and cinnarizine exhibited similar safety profiles. Only two patients withdrew from the study because of adverse events possibly related to the study drug. One patient withdrew from the cinnarizine group because of headache, and one patient withdrew from the nimodipine group because of lipothymia. CONCLUSION: These data confirm the marked efficacy of both nimodipine and cinnarizine in the treatment of vestibular vertigo.

Adult↗
PubMedDate not supplied

Why does vertigo become chronic after neuropathia vestibularis?

OBJECTIVE: Vertigo is one of the most frequent complaints in general medical practice and is often linked to psychiatric disorders. A longitudinal study of 67 patients with an acute vestibular disorder was undertaken to clarify if, after experiencing acute vestibular vertigo, certain patients have a higher likelihood of developing chronic, debilitating dizziness despite no evidence of a damaged peripheral vestibular system. METHOD: The severity of dizziness was determined in 67 patients with vestibular neuronitis, 6 months after their release from hospital, using the Vertigo Symptom Scale from Yardley et al. The intensity of anxiety directly after vertigo was experienced, body-related cognitions, illness coping, personality structure, and the recovery of the organ of equilibrium were recorded in order to explain the severity of vertigo that occurred after 6 months. The function of the organ of equilibrium was assessed by using a caloric test. RESULTS: Over a period of 6 months, 13 of the 67 patients (19.4%) reported continuing dizziness after neuropathia vestibularis. Eleven of the 13 patients showed high scores on a scale for measuring vertigo-related symptoms, which can be interpreted as being equivalent to anxiety. The variables of gender, catastrophic thoughts and a dependent personality accounted for 35% of why vertigo became chronic. CONCLUSION: Neuropathia vestibularis represents a risk factor for the development of chronic vertigo. Chronic vertigo after neuropathia vestibularis appears to be equivalent to anxiety and is partly conditional on catastrophic thoughts at the beginning.

Anxiety Disorders↗
PubMed2026

Exploring the mechanism of Acanthopanax in treating vertigo: A network pharmacology and molecular docking study.

Acanthopanax has therapeutic efficacy against vertigo; however, the underlying mechanism remains unclear. This study aimed to elucidate the mechanism by which Acanthopanax treats vertigo through integrated network pharmacology and molecular docking techniques, and retrieved all target genes of Acanthopanax for vertigo treatment from July to October 2025. Vertigo-related target genes were subsequently identified from public databases, including GeneCards and Online Mendelian Inheritance in Man. The intersection between Acanthopanax-derived targets and vertigo-related targets was analyzed to identify candidate target genes. Using the STRING platform, we constructed protein-protein interaction networks for the identified candidate targets and mined the core functional modules within these networks. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses were performed on candidate targets via the clusterProfiler package. A carp bile poisoning-liver injury target-pathway network was constructed via Cytoscape 3.8.2 software, network topology analysis was conducted, and the core components and targets were screened. The results found that A total of 295 candidate targets for the treatment of vertigo caused by Eleutherococcus senticosus were identified. Pathway enrichment analysis revealed that Eleutherococcus senticosus treatment for vertigo may be closely associated with pathways related to IL-17, TNF, phosphoinositide 3-kinase (PI3K)-Akt, p53, HIF-1, and Forkhead box O signaling. The core targets for the treatment of A. senticosus vertigo include TP53, AKT1, STAT3, TNF, and JUN. Network pharmacology and molecular docking studies suggest that A. senticosus may treat vertigo by regulating targets such as JUN, TNF, AKT1, STAT3, and STAT3 through pathways such as the IL-17, TNF, phosphoinositide 3-kinase-Akt, p53, HIF-1, and Forkhead box O signaling pathways. These mechanisms warrant further investigation in future o and in vitro studies.

Molecular Docking Simulation↗
PubMed1995

Sensorineural hearing loss with delayed onset of vertigo.

Sensorineural hearing loss with delayed onset of vertigo is a syndrome in which episodic vertigo arises in a person who has preexisting unilateral severe-to-profound sensorineural hearing loss. This syndrome has an ipsilateral form in which the vertigo arises from the poorer hearing ear and a contralateral form in which the aural symptoms arise from the better hearing ear. The existence of this syndrome has only been noted within the past two decades. This report details our clinical experience with 17 persons with the ipsilateral form of this disorder. The onset of the vertigo after the occurrence of the hearing loss was quite variable. It ranged from 1 to 60 years after the development of the hearing loss. The hearing loss occurred for several reasons. Most patients had hearing loss due to an unknown cause. The development of the vertigo and the timing of the onset of the vertigo were not related to the cause of the hearing loss. Bithermal caloric testing identified the offending labyrinth in most patients who underwent ablative vestibular surgery. Ablative vestibular surgery was performed in 13 of the 17 persons in this study because of disabling symptoms. In all 13 cases, the episodic vertigo was eliminated. Surgical treatment for sensorineural hearing loss with delayed-onset vertigo, as with all surgery for vertigo, should be based on the severity of the afflicted person's symptoms.

Adult↗
PubMed2001

Vertigo syndromes and mechanisms in migraine.

This paper attempts to define and categorize the vertigo associated with migraine. A retrospective chart review of 344 cases of vertigo identified 19 cases with headaches characteristic of migraine as per strictly defined criteria (International Headache Society, 1988). Four distinct types of vertiginous syndromes were noted. The commonest syndrome (Group I) manifested transient episodes of imbalance with additional momentary subjective rotary vertigo worsened by movement. The attacks lasted a few hours and evaluation in the inter-episode interval demonstrated no vestibular deficit. Group II manifested transient objective rotatory vertigo of from 10 minutes to a few hours but no demonstrable permanent vestibular deficit. Group III displayed symptoms and signs characteristic of benign paroxysmal positional vertigo (BPPV) and Group IV manifested a permanent unilateral labyrinthine weakness. Causation of vertigo by migraine was implied in 10 of 19 cases where the headache and vertigo occurred simultaneously and in two other cases where the vertigo improved with anti-migraine prophylactic treatment. Four distinct and characteristic vertigo syndromes have been noted with migraine. Their spectrum ranges from a transient reversible dysfunction to a more permanent destruction, and includes involvement of both the peripheral and the central vestibular systems.

Adolescent↗
PubMed1999

Intratympanic gentamicin for control of vertigo in Meniere's disease: vestibular signs that specify completion of therapy.

OBJECTIVE: To determine if a protocol of weekly intratympanic gentamicin injections administered until development of signs of unilateral vestibular hypofunction can alleviate vertigo while preserving hearing in patients with intractable vertigo caused by unilateral Meniere's disease. STUDY DESIGN: The study design was a prospective investigational protocol. SETTING: The study was performed in outpatients at a tertiary referral center. PATIENTS: Entry criteria included a diagnosis of "definite" Meniere's disease according to the 1995 report of the American Academy of Otolaryngology-Head and Neck Surgery (AAO-HNS), intractable vertigo despite optimal medical therapy, no symptoms suggestive of Meniere's disease in the contralateral ear and serviceable hearing in the contralateral ear. The outcomes of the first 34 patients who entered the protocol are reported. INTERVENTION: A buffered gentamicin solution was injected into the middle ear at weekly intervals until development of spontaneous nystagmus, head-shaking-induced nystagmus, or head-thrust sign indicative of vestibular hypofunction in the treated ear. MAIN OUTCOME MEASURE: The 1995 AAO-HNS criteria for reporting treatment outcome in Meniere's disease were used. The effects of treatment were assessed in terms of control of vertigo, disability status, hearing level, and quantitative measurement of vestibular function with caloric and rotatory chair tests. RESULTS: Vertigo was controlled in 91% of the patients. Profound hearing loss occurred as a result of gentamicin injection in one patient (3%). Intratympanic gentamicin was significantly less effective in controlling vertigo in patients who had previous otologic surgery on the affected ear. Recurrence of vertigo > or = 6 months after initially complete control was noted in seven patients (22%). Vertigo in six of these patients was eliminated by additional intratympanic gentamicin injections. CONCLUSIONS: Ending weekly intratympanic gentamicin injections when clinical signs of unilateral vestibular hypofunction appear can control vertigo in most patients. Hearing loss directly attributable to gentamicin is uncommon. Treatment outcome is best in patients who have not had previous otologic surgery.

Adult↗
PubMed2003

Effect of repetition of Semont's manoeuvre on benign paroxysmal positional vertigo of posterior semicircular canal.

If Semont's liberating manoeuvre does not lead to relief of symptoms in benign paroxysmal positional vertigo of posterior semicircular canal after the first session, it can be repeated once again, in refractory cases, whilst symptomatic patients after second manoeuvre require rehabilitation therapy Repeating Semont's manoeuvre several times has proven to progressively increase the percentage of cured patients or it may convert posterior semicircular canal forms to typical incomplete or lateral semicircular canal forms, hence requiring other manoeuvres to achieve vertigo resolution. Aim of study was to assess the effect of liberating manoeuvres repeated up to 4 times and to establish possible passages from one canal to the other during manoeuvres as well as percentage of cases refractory to this therapy, who would then need rehabilitation. Benign paroxysmal positional vertigo was diagnosed in 448 cases of whom 344 (76.8%) of the posterior semicircular canal, 20 (0.45%) the incomplete form of the posterior semicircular canal, 20 (0.45%) subjective positional vertigo and 74 of the lateral semicircular canal (4.2%). Right side was affected in 58.4% of cases, left in 34.5%, and bilateral in 7.1%. All 344 patients underwent Semont's liberating manoeuvre (1st manoeuvre) with first control after 48 hours: if symptoms (typical, atypical nystagmus or paroxysmal vertigo evoked by Dix-Hallpike's manoeuvre) persisted, Semont's liberating manoeuvre was repeated (2nd manoeuvre). In presence of lateral semicircular canal benign paroxysmal positional vertigo conversion, Lempert's manoeuvre was performed instead. Second control was performed after 48 hours and in cases of persistent typical, atypical or lateral semicircular canal nystagmus 3rd manoeuvre was performed. After further 48 hours, third control was carried out: symptomatic patients with typical forms were submitted to 4th manoeuvre, while typical incomplete forms or forms of the lateral semicircular canal underwent Lempert's manoeuvre. In conclusion, symptoms disappeared after 1st manoeuvre in 61.6% of cases; further manoeuvres, carried out in view of possible changes in semeiology of vertigo, increased the percentage of cured patients to 82.5% after the 2nd, 90.7% after 3rd and 94.1% after the 4th. Repeated positioning manoeuvres in benign paroxysmal positional vertigo led to a progressive increase in percentage of cured vertigo, at the same time, allowing detection of those cases converted to multicanal pathology, hence offering the possibility to proceed with appropriate liberating manoeuvres.

Adult↗
PubMed2006

[Neurootological manifestation of migrainous vertigo].

OBJECTIVE: To analyzed the characteristics of migrainous vertigo (MV), a kind of paroxysmal vertigo, in order to demonstrate the extent of damage and dysfunction in MV and to judge whether MV is peripheral or central vertigo. METHODS: Twenty-two cases of acute (5 cases) or subacute (17 cases) MV were examined with oto-neurological tests, spontaneous nystagmus, positional nystagmus and auditory tests. RESULTS: There were 6 males and 16 females. Among those patients, 15 had migraine, 17 motion sickness, 15 family history of migraine or motion sickness, 1 visual aura, 7 motion intolerance (vertigo from head movement and body movement), 4 photophobia, 6 phonophobia and 5 vertigo from insomnia and emotion. There were likely to have vertigo in menstrual period in 2 cases. The duration of vertigo lasted from minutes to days. For pure-tone audiometric, 9 were normal which from mild to moderate hearing loss. Three cases had abnormal high frequency ABR bilaterally and 10 abnormal unilaterally. Subjective visual vertical were normal in all of the cases. Vestibular evoked myogenic potentials were abnormal in 14 cases (13 had low amplitude and 1 had longer latency of P13 wave). Bithermal caloric test was abnormal in 3 cases and 11 had abnormal ocular movement (9 with low gain of optokinetic nystagmus, 1 with overshoot in saccade and 1 with vertical nystagmus after head shaking), in which 10 had abnormal high frequency ABR and 1 was normal. CONCLUSIONS: MV could be peripheral or central vertigo and MV should be included in the differentiation of peripheral and central vertigo.

Adolescent↗
PubMed2001

[Vertigo as a symptom of migraine].

EPIDEMIOLOGY: Since both migraine and vertigo are common complaints in clinical practice they may coincide in an individual patient just by chance. There are, however, numerous patients with vestibular symptoms caused by migraine, accounting for 6-8% of diagnoses in specialized dizziness clinics. CLINICAL MANIFESTATION: Migraine-associated vertigo is a vestibular disorder which manifests itself with spontaneous or positional rotational vertigo or dizziness induced by head motion. The vertigo may occur without accompanying headache and may last from seconds to several weeks. DIAGNOSIS: Migraine-associated vertigo can be diagnosed according to the following criteria: 1. recurrent vestibular symptoms, 2. migraine according to the criteria of the International Headache Society, 3. migrainous symptoms during the vertigo such as headache, photophobia, phonophobia, scintillating scotoma or other auras, 4. exclusion of other causes. PATHOPHYSIOLOGY: The mechanism of migraine-associated vertigo is still obscure. Several hypotheses relating to the pathophysiology of migraine have been proposed: cortical spreading depression, regional changes in brain perfusion, release of neurotransmitters and paroxysmal dysfunction of ion channels. Clinical findings suggest both central and peripheral vestibular involvement. THERAPY: Treatment is based on the repertoire of acute and prophylactic medications that are used for migrainous headaches. Controlled studies on the treatment of migraine-associated vertigo are still lacking.

Age Factors↗