Vertigo Syndromes Research Articles

Co-morbidities of vertiginous diseases

BackgroundCo-morbidities of vertiginous diseases have so far not been investigated systematically. Thus, it is still unclear whether the different vertigo syndromes (e.g. benign paroxysmal positional vertigo (BPPV), Meniere's disease (MD), vestibular migraine and phobic vertigo (PPV)) have also different spectrums of co-morbidities.MethodsAll patients from a cohort of 131 participants were surveyed using a standardised questionnaire about the co-morbidities hypertension, diabetes mellitus, BMI (body mass index), migraine, other headache, and psychiatric diseases in general and the likelihood of a depression in particular.ResultsWe noted hypertension in 29.0% of the cohort, diabetes mellitus in 6.1%, migraine in 8.4%, other headache in 32.1%, psychiatric diseases in 16.0%, overweight and obesity in 33.6% and 13.7% respectively, as well as a clinical indication for depression in 15.9%.ConclusionIn general, we did not detect an increased prevalence of the co-morbidities diabetes mellitus, arterial hypertension, migraine, other headache and obesity compared to the general population. There was an increased prevalence of psychiatric co-morbidity in patients with PPV, and the prevalence of hypertension was elevated in patients with MD.

Vertigo as a Symptom of Migraine

Migraine and vertigo are common disorders, affecting about 14% and 10%, respectively, of the general population. If migraine and vertigo were unrelated, the expected comorbidity would be 1%, whereas recent epidemiological studies indicate that 3.2% of the population have both migraine and vertigo. The excess comorbidity may be attributed to two factors: 1) vertigo syndromes (including Menière's disease, benign paroxysmal positional vertigo, and anxiety-related dizziness) that are more common in migraineurs than in controls and 2) vestibular migraine (VM) (vertigo as a symptom of migraine.) VM presents with attacks of spontaneous or positional vertigo lasting seconds to days. Headaches are often absent during acute attacks, but other migrainous features such as photophobia or auras, may be present. Like migraine headaches, VM triggers include stress, sleep deprivation, and hormonal changes. During acute attacks, there may be central spontaneous or positional nystagmus and, less commonly, unilateral vestibular hypofunction. In the symptom-free interval, vestibular testing shows mostly minor and nonspecific findings. The pathogenesis of VM is uncertain, but migraine mechanisms may interfere with the vestibular system at the labyrinth, brainstem, and cerebral cortex. Treatment includes vestibular suppressants for acute attacks and migraine prophylaxis for patients with frequent recurrences. However, treatment efficacy has not been validated by properly controlled clinical trials. VM does not fit into the 2004 International Headache Society Classification, in which "basilar-type migraine" must have at least two posterior circulation manifestations; isolated vertigo would not satisfy this criterion.

Why Do Subjective Vertigo and Dizziness Persist over One Year after a Vestibular Vertigo Syndrome?

The overlap and interlinkage of dizzy symptoms in patients with psychiatric and vestibular vertigo/dizziness disorders is the subject of an ongoing debate. In a one-year follow up in 68 patients with vestibular vertigo syndromes, the persistency of vertigo and dizziness symptoms was examined and correlated with vestibular parameters and results from a psychiatric evaluation. Patients with vestibular migraine showed poorest improvement of vertigo and dizziness symptoms over time. In addition, patients who developed anxiety or depressive disorder after the onset of the vestibular disorder showed poor improvement and high persistency of symptoms.

Neurovascular Compression Syndrome of the Eighth Cranial Nerve: Myth or Reality

Background and Aim: There is evidence that NCS of the eighth cranial nerve can cause a paroxysmal and persistent vertigo syndrome with or without tinnitus and hearing loss. In 1984, Jannetta et al introduced the term “disabling positional vertigo” for this situation and reported successful treatment by vascular decompression techniques. Brandt and Dieterich (1990) proposed that the term “vestibular paroxysmal” be used instead and suggested four characteristic features of the syndrome: (1) short attacks of rotational to-and-fro vertigo lasting seconds to minutes, (2) attacks frequently dependent on particular head positions and modification of the duration of the attack by changing head position (“disabling positional vertigo”), (3) hyperacusis or tinnitus permanently or during the attack, and (4) measurable auditory or vestibular deficits by neurophysiological methods. A lot of controversy exists in the literature about the diagnosis of the NCS, and the evolution in MRI and MRA techniques have elucidated the cases. Case Report: We report on a case of NCS in a 30-year-old woman who experienced short attacks of rotational vertigo combined with head movements. Full neurotological evaluation showed no measurable deficits, and MRI revealed a vascular loop of the AICA going deeply against the fundus of the eighth cranial nerve. Conclusions: It seems that although it is relatively rare and there is still no unanimous opinion in the literature about the pathogenesis and the diagnosis of the syndrome, NCS cannot be underestimated as a cause of vestibular disorders.

Epidemiology of vertigo, migraine and vestibular migraine

Both migraine and vertigo are common in the general population with lifetime prevalences of about 16 % for migraine and 7 % for vertigo. Therefore, a concurrence of the two conditions can be expected in about 1.1 % of the general population by chance alone. However, recent epidemiological evidence suggests that the actual comorbidity is higher, namely 3.2 %. This can be explained by the fact that several dizziness and vertigo syndromes occur more frequently in migraineurs than in controls including benign paroxysmal positional vertigo, Meniere's disease, motion sickness, cerebellar disorders and anxiety syndromes which may present with dizziness. In addition, there is increasing recognition of a syndrome called vestibular migraine (VM), which is vertigo directly caused by migraine. VM affects more than 1 % of the general population, about 10 % of patients in dizziness clinics and at least 9 % of patients in migraine clinics.Clinically, VM presents with attacks of spontaneous or positional vertigo lasting seconds to days. Migrainous accompaniments such as headache, phonophobia, photophobia or auras are common but not mandatory. Cochlear symptoms may be associated but are mostly mild and non-progressive. During acute attacks one may find central spontaneous or positional nystagmus and, less commonly, unilateral vestibular hypofunction. In the symptom-free interval, vestibular testing adds little to the diagnosis as findings are mostly minor and non-specific. In the absence of controlled studies, treatment of VM is adopted from the migraine sphere comprising avoidance of triggers, stress management as well as pharmacotherapy for acute attacks and prophylaxis.

Psychiatric morbidity and comorbidity in different vestibular vertigo syndromes

High rates of coexisting vestibular deficits and psychiatric disorders have been reported in patients with vertigo. Hence, a causal linkage between the vestibular system and emotion processing systems has been postulated. The aim of this study was to evaluate the impact of vestibular function and vestibular deficits as well as preexisting psychiatric pathologies on the course of vestibular vertigo syndromes over 1 year. This interdisciplinary prospective longitudinal study included a total of 68 patients with vestibular vertigo syndromes. Four subgroups were compared: benign paroxysmal positioning vertigo (BPPV, n=19), vestibular neuritis (VN, n=14), vestibular migraine (VM, n=27), and Menière's disease (MD, n=8). All patients underwent neurological and detailed neurootological examinations as well as two standardized interviews and a psychometric examination battery at five different times (T0-T4) over 1 year. The prevalence of psychiatric disorders at baseline (T0) did not differ between the four subgroups. Only patients with VM showed significantly higher rates of psychiatric disorders (p=0.044) in the follow-up over 1 year. Patients with a positive history of psychiatric disorders before the onset of the vestibular disorder had significantly increased rates of psychiatric disorders compared to patients with a negative history of psychiatric disorders (T1: p=0.004, T3: p=0.015, T4: p=0.012). The extent of vestibular deficit or dysfunction did not have any influence on the further course of the vestibular disease with respect to the development of psychiatric disorders. A positive history of psychiatric disorders is a strong predictor for the development of reactive psychiatric disorders following a vestibular vertigo syndrome. Especially patients with vestibular migraine are at risk of developing somatoform dizziness. The degree of vestibular dysfunction does not correlate with the development of psychiatric disorders.

Validation of the German version of the Vertigo Symptom Scale (VSS) in patients with organic or somatoform dizziness and healthy controls

The objective of this study was to validate the German version of the Vertigo Symptom Scale (VSS) and to determine its ability to differentiate the type, frequency, and severity of balance disorders. The scale (34 items) was designed by Yardley and coworkers and has been already validated in its English and Spanish versions. 98 patients with organic vertigo syndromes, 90 patients with somatoform (psychogenic) dizziness and 56 healthy controls were evaluated with the VSS and additional standardized questionnaires regarding distress (SCL-90R), quality of life (SF-36), anxiety and depression (HADS). In order to differentiate organic from somatoform dizziness all patients underwent detailed clinical neurological and vestibular neurophysiological testing. The two identified subscales 'vertigo and related symptoms' (VER) and 'somatic anxiety and autonomic arousal' (AA) had good internal consistencies (Cronbach's alpha: VER 0.79; AA 0.89). Test-retest correlations were r = 0.75 for VER and r = 0.75 for AA. VER could discriminate well between dizziness patients and healthy controls. AA discriminated moderately between somatoform and organic dizziness. We found close relations between the AA scale and different measures of emotional distress. Correlations between VER and measures of emotional distress were weaker. The German version of the VSS has good reliability and validity in the detection of different vertigo syndromes. Measurement of anxiety symptoms can be helpful to identify patients with somatoform dizziness.

Psychiatric comorbidity in different organic vertigo syndromes

A high degree of psychiatric disorders has repeatedly been described among patients with organic vertigo syndromes and attributed to vestibular dysfunction. Yet almost no investigations exist which differentiate between various organic vertigo syndromes with regard to psychiatric comorbidity. The following prospective, interdisciplinary study was carried out to explore whether patients with different organic vertigo syndromes exhibit different psychological comorbidities. 68 patients with organic vertigo syndromes (benign paroxysmal positioning vertigo (BPPV) n = 20, vestibular neuritis (VN) n = 18, Menière's disease (MD) n = 7, vestibular migraine (VM) n = 23) were compared with 30 healthy volunteers. All patients and control persons underwent structured neurological and neuro-otological testing. A structured diagnostic interview (-I) (SCID-I) and a battery of psychometric tests were used to evaluate comorbid psychiatric disorders. Patients with VM and MD showed significantly higher prevalence of psychiatric comorbidity (MD = 57%, VM = 65%) especially with anxiety and depressive disorders, than patients with VN (22%) and BPPV (15 %) compared to normal subjects (20 %). These elevated rates of comorbidities resulted in significantly elevated odds-ratios (OR) for the development of comorbid psychiatric disorders in general (for VM OR = 7.5, for MD OR = 5.3) and especially for anxiety disorders (for VM OR = 26.6, for MD OR = 38.7). As a consequence, a structured psychological and psychometric testing and an interdisciplinary therapy should be proceeded in cases with complex and prolonged vertigo courses, especially in patients with VM and MD. Possible reasons of these unexpected results in VM and MD are discussed.

Migrainous Vertigo

Patients with migraine frequently have hypersensitivity to light, sound, and smell. In addition to these hallmark features of migraine, patients often describe vestibular complaints ranging from true vertigo to less specific symptoms of dizziness, unsteadiness, and head motion intolerance. Over the last two decades a number of studies have stressed the association of migraine with vestibular and ocular motor disorders. Migraine may be a most common cause of various forms of episodic vertigo, but definite diagnostic criteria for migraine related vertigo are still lacking. As migrainous vertigo is an evolving entity, terminology is confusing and generally accepted diagnostic criteria are not established. The interrelations of migraine and dizziness can be classified into seven categories: (1) vertigo as an aura of migraine-basilar type migraine, (2) episodic vertigo attack without typical temporal relationship to migraine headache-migraine equivalent, (3) vertigo/dizziness during migraine attack, (4) susceptibility of motion sickness in migraine patients, (5) CACNA1A gene mutation and migraine-familial hemiplegic migraine, episodic ataxia type 2, (6) well defined vertigo syndromes that are not caused by migraine but show a statistical association with migraine-Meniere's disease, BPPV, (7) non-vestibular dizziness in migraine patients-psychiatric comorbidity, antimigraine medication. Each part of categories will be discussed.

Autonomic Nervous System Function in Chronic Dizziness

The goals of this study were to validate the clinical diagnosis of autonomic dizziness as a cause of chronic nonvertiginous dizziness that may be exacerbated by physical exertion or orthostatic challenges, estimate its prevalence in a tertiary referral population, and investigate the usefulness of three autonomic challenges as objective tests for this condition. Laboratory investigation of autonomic activity. Tertiary care balance center. Fifteen men and women with symptoms indicative of autonomic dizziness. Subjects with other causes of dizziness, histories of syncope, or psychiatric disorders were excluded. Autonomic tests included 45 minutes of head upright tilt (HUT), 20 minutes of 5% CO2 inhalation and then HUT, and 2 minutes of voluntary hyperventilation and then HUT. Patterns of cardiovascular and respiratory responses and subjective ratings of dizziness, autonomic symptoms, and anxiety during autonomic challenges. Twelve subjects had evidence of autonomic dysfunction, including 10 with abnormal heart rate, blood pressure, or respiratory responses to HUT. Two other subjects had prolonged hypocarbia after voluntary hyperventilation. Many of these abnormalities would have been missed by current autonomic testing paradigms. In one subject, CO2 inhalation revealed latent anxiety. In two subjects, the presence of high symptom ratings without objective autonomic dysfunction prompted a successful search for other diagnoses. Study results validated the clinical syndrome of autonomic dizziness. Autonomic testing protocols may have to be updated to detect clinically relevant abnormalities in patients with dizziness.

Central vestibular disorders

Dizziness or vertigo is an erroneous perception of selfmotion or object-motion as well as an unpleasant distortion of static gravitational orientation. It is caused by a mismatch between the vestibular, visual, and somatosensory systems. Thanks to their functional overlap, the three systems are able to compensate, in part, for each other's deficiencies. Thus, vertigo is not a well-defined disease entity, but rather a multisensory syndrome that results when there is a pathological dysfunction of any of the stabilizing sensory systems (e.g., central vestibular disorders, peripheral vestibular diseases with asymmetric input into the vestibular nuclei). This article provides an overview of the most important and frequent forms of central vestibular vertigo syndromes, including basilar/vestibular migraine, which are characterized by ocular motor, postural, and perceptual signs. In a simple clinical classification they can be separated according to the three major planes of action of the vestibulo-ocular reflex: yaw, roll, and pitch. A tonic imbalance in yaw is characterized by horizontal nystagmus, lateropulsion of the eyes, past-pointing, rotational and lateral body falls, and lateral deviation of the perceived straight-ahead. A tonic imbalance in roll is defined by torsional nystagmus, skew deviation, ocular torsion, tilts of head, body, and the perceived vertical. Finally, a tonic imbalance in pitch can be characterized by some forms of upbeat or downbeat nystagmus, fore-aft tilts and falls, and vertical deviation of the perceived straight ahead. The thus defined syndromes allow for a precise topographic diagnosis as regards their level and side.

Neuro-otological emergencies

Physicians find acute vertigo a diagnostic challenge. This article review recent evidence outlining the clinical presentation of acute central and peripheral dizzy syndromes and suggest when clinicians may consider acute neuro-imaging. Recent evidence highlights the difficulty that acute vertigo may sometimes pose to the clinician. For example, migrainous vertigo may have oculomotor abnormalities suggestive of either central neurological or peripheral vestibular dysfunction. Furthermore, vertebrobasilar stroke syndromes may mimic peripheral disorders such as vestibular neuritis, or when there is hearing involvement may be misdiagnosed as Meniere's disease. In addition to the need for identifying serious conditions in acute vertigo, recent evidence suggests that early steroid treatment in vestibular neuritis may improve long term outcome. Further trials regarding symptomatic outcome are required, however, before routine use of steroids can be recommended in this condition. Recent findings have not made the assessment of acute vertigo any easier for the nonspecialist. Although the commonest vertigo syndromes are benign, serious conditions such as stroke may masquerade as a peripheral labyrinthine disorder and conversely benign conditions such as migrainous vertigo may have clinical characteristics of central disorders. These findings re-emphasize the need for a thorough clinical evaluation of the acutely dizzy patient.

The Genetics of Vertigo

Vertigo is a common principal complaint among patients seen by primary care physicians, neurologists, and otolaryngologists. The most common causes of recurrent episodes of vertigo are benign inner ear disorders, but central nervous system disorders must be excluded. Several common vertigo syndromes are now known to be familial, a feature distinguishing them from other common causes of vertigo. Familial vertigo has been recognized in patients with isolated recurrent attacks of vertigo, genetic deafness syndromes, and in patients with neurological disorders. Although susceptibility loci and mutations have been identified, genetic heterogeneity is common in all familial vertigo syndromes. Research in these disorders has advanced the understanding of vertigo pathophysiology but much remains to be known. This article provides an overview of the clinical features, genetic analyses, and treatment strategies for these disorders.

Interaction of somatoform and vestibular disorders

Background: The high coincidence of organic vestibular and somatoform vertigo syndromes has appeared to support pathogenic models showing a strong linkage between them. It was hypothesised that a persisting vestibular...

Ménière's Disease Review 2005

Ménière's disease (MD) is a complex, multifactorial disorder of the inner ear that is the most common cause of the syndrome of episodic vertigo combined with fluctuating hearing loss. In spite of a century of investigation, the etiology and pathophysiology of MD remain controversial and incompletely understood. Among the factors that have contributed to these controversies are the absence of (1) a validated clinical test, (2) an appropriate animal model, and (3) a specific treatment. Nonetheless, physicians are able to assist MD patients with a variety of tailored, symptom-specific medications and therapies. Given that the vertigo induced by MD, in general, is self-limited, the long-term outlook for balance function is good. The same cannot be said for the hearing dysfunction of MD.

Clinical Implications of a Mathematical Model of Benign Paroxysmal Positional Vertigo

Benign paroxysmal positional vertigo (BPPV) is the most commonly diagnosed vertigo syndrome. It is caused by movement of detached otoconia within the inner ear (canalithiasis) or otoconia adherent to the cupula (cupulolithiasis). A mathematical model incorporating fluid dynamics of BPPV, which results in the following insights, has been developed recently: (1) The characteristic latency of BPPV is explained by movement of detached otoconia through the ampulla, as pressure caused by moving otoconia is negligible until otoconia enter the narrow duct of the semicircular canal. Typical otoconia move at a rate of 0.2 mm/s, or about 1% of the circumference of the canal each second. (2) Particle-wall interactions can account for the considerable variability in duration and latency of BPPV. (3) Dispersion of a clump of otoconia creates more rather than less nystagmus. Thus, dispersion is not a viable explanation of fatigability. (4) Cupulolithiasis is predicted to cause a far weaker nystagmus than canalithiasis. (5) Inertial effects of treatment maneuvers cause negligible movement of otoconia.

0937 Vertigo syndromes associated with Earthquake in Georgia

Georgia experienced strong earthquake, after this event the amount of patients with vestibular symptoms increased. Study evaluates 60 outpatients (51 females, 9 males) aged from 18 to 85 years old who applied at outpatient clinics with vestibular complaints in the initial weeks following the earthquake. BPPV and PPV are the most common causes of vertigo. "Idiopathic" BPPV is the cause of BPPV in 50-70% of cases. Head trauma, vestibular neuritis, Meniere disease, migraine are the most common causes of "secondary" BPPV. (PPV) syndrome characterized by dizziness, subjective disturbance of balance and by perception of illusory body perturbations, usually triggered by perceptual stimulus. PPV frequently associated with anxiety symptoms in patients with obsessive-compulsive type personality. The study revealed "Idiopathic" BPPV in 49 cases and "secondary" types BPPV in 11 cases. 37 previously documented histories of BPPV patients had features typical for posterior semisercircular canal BPPV and 23 patients experienced subjective disturbance symptoms like BPPV, but there were no abnormal responses in their vestibular testing. It is assumed that earthquake could manifest psychogenic vertigo with panic attacks, anxiety, agoraphobia, PPV and could provoke a transition from organic vertigo to PPV. It is concluded that psychological stress play an important role in occurring "secondary" BPPV, earthquake may trigger exacerbation of "secondary" BPPV and could be provoked factor to developing psychogenic vertigo, mostly PPV.

Evaluation and management of the dizzy patient

Balance in man is a sophisticated and complex mechanism comprised of sensory inputs from the vestibular apparatus, vision, and proprioception. These pass into the central nervous system (CNS), are integrated...

Dizziness.

The article gives an overview of the most frequent forms of vertigo, that are of peripheral-labyrinthine, central-vestibular, psychogenic, or physiologic origin. Dizziness or vertigo is a result of a mismatch between 3 sensory systems: the vestibular, the visual, and the somatosensory systems. These systems are mutually interactive and redundant in that orientation and balance are guided by simultaneous reafferent cues. The functional ranges of the systems overlap, thus permitting them to compensate in part for each other's deficiencies. Vertigo is not a well-defined disease entity, but rather a multisensory syndrome induced either by stimulation of the intact sensorimotor system by motion (eg, physiologic vertigo as in motion sickness or height vertigo), or by pathologic dysfunction of any of the stabilizing sensory systems (eg, peripheral vestibular as in vestibular neuritis, or central vestibular as in vertebro-basilar ischemia). The core region in vestibular vertigo syndromes is the vestibulo-ocular reflex, a 3-neuron arc that mediates the information of the semicircular canals and otoliths via the vestibular nerve and vestibular nucleus to the ocular motor nuclei (VI, IV, III) and the supranuclear integration centers in the ponto-mesencephalic brain stem. Clinical phenomena characteristic for physiological and pathologic vertigo syndromes include postural, perceptual, oculomotor, and vegetative syndromes, which manifest with ataxia, nystagmus, vertigo, and nausea. Thus, the clinical testing must include examinations of postural, perceptual, oculomotor, and vegetative dysfunctions.

Neurological and somatoform vertigo syndromes

Vertigo is one of the most common cardinal symptoms encountered in the practice of general medicine and after headache the most frequent major complaint in neurology. The various vertigo syndromes should be differentiated according to organic and somatoform manifestations. Unfortunately, somatoform vertigo disorders are often not included in the differential diagnosis or be-latedly considered, which delays the diagnosis. This compounds the tendency of vertigo disorders to rapidly become chronic and frequently results in severe impairment of the patient's quality of life, even precipitating early retirement and incurring high costs for health care systems. Hence, in cases of complex vertigo disorders, early interdisciplinary cooperation is both helpful and essential during diagnostic work-up to include signs of somatic and psychosomatic origin.