Evaluation of vestibular functions in children with vertigo attacks. (25/306)

AIM: To examine vestibular system functions in children with episodic vertigo attacks. METHODS: Thirty four children (20 males) aged 4-18 years with paroxysmal dizziness and/or vertigo attacks were evaluated. A medical history for vestibular symptoms and migraine was taken. Vestibular and auditory functions were assessed. RESULTS: Chronic headache attacks consistent with migraine were reported in 12 children and motion sickness was reported in 30. Family history in first degree relatives was positive for migraine in 29 children and for episodic vertigo in 22. Electronystagmography and videonystagmography showed two types of nystagmus: spontaneous vestibular nystagmus (41%) and benign paroxysmal positional nystagmus (BPPN) (59%). The first type of nystagmus was assessed as a sign of vestibulopathy and the patients with BPPN were diagnosed as having benign paroxysmal positional vertigo (BPPV). Audiometric examination in four cases revealed bilateral sensory neural hearing loss in low frequencies. Pure tone averages in 30 cases were within normal ranges; however low frequencies in 28 of them were approximately 10 dB lower than high frequencies. Unilateral caloric responses diminished in eight children. CONCLUSIONS: Peripheral vestibular problems in childhood present in a wide spectrum, which varies from a short episode of dizziness to a typical vestibular attack with fluctuating sensory neural hearing loss or episodes of BPPV. A considerable number of these vestibular problems might be related to the migraine syndrome.  (+info)

Postural vertigo and positional nystagmus. (26/306)

Oscillation of the eyes of a patient when the head is placed in a certain position is objective evidence to support a complaint of postural vertigo-dizziness when the head is tilted forward or upward or turned to one side or the other. Since positional nystagmus may be difficult to evoke and may be elicited at one time and not at another, it is important to make repeated tests, lest a causative lesion be overlooked. Vertigo in such cases may be caused by pathologic change in the eighth peripheral nerve or in the central vestibular pathways. Sometimes no organic disease is observable even though positional nystagmus validates a complaint of vertigo. In such instances the patient should be assured that he does not have a progressive disease and be advised against activity in which dizziness would be hazardous.  (+info)

The practical management of dizziness. (27/306)

THE PROBLEM OF DIZZINESS IS GREATLY SIMPLIFIED IF: (1) A definite routine is followed in the history taking and the steps of the examination; (2) the examination is done in two stages; and (3) a simple classification is used in cases of dizziness of vestibular origin whereby three groups are distinguished on the basis of localization of the origin. The etiologic diagnosis is thereby narrowed down to a relatively few possibilities.The treatment consists of measures to relieve the symptoms and to reverse the underlying disease which produced the symptoms.  (+info)

DIZZINESS AND HEAD INJURY. (28/306)

Dizziness, whether vague or specifically rotational, is a common sequel to head injury, and is often postural. One hundred and sixty-five patients with this symptom were examined. The simple posture tests employed to detect positional nystagmus are described. This physical finding was present in one-quarter of the entire group, and in nearly one-half of cases of longitudinal fracture of temporal bone. In such cases, it is an objective finding that corresponds precisely to the patient's complaint of vertigo.Transverse fracture of temporal bone destroys the inner ear in both cochlear and vestibular parts. Longitudinal fracture is commoner and causes bleeding from the ear; inner-ear damage is usually minor.In the rare cases where persisting postural vertigo and positional nystagmus are disabling, relief of the symptom may be achieved by vestibular denervation of the affected side.  (+info)

The neurologic aspects of vertigo: analysis of 400 cases. (29/306)

Of almost 8,000 patients referred for neurological consultation, 6.1 per cent had "dizziness" as a presenting complaint. Dizziness is a nonspecific complaint, used loosely to describe funny feelings in the head or lightheadedness by anxious or depressed patients; or it may mean vertigo-a hallucination of movement of self or surroundings in horizontal, rotatory or vertical direction. An analysis of 400 cases showed the complaint "dizziness" to be functional in about 25 per cent of patients. The cause in the remaining cases varied from epilepsy from cortical lesions, to lesion of the brain stem, such as tumors, vascular insufficiency, and multiple sclerosis, or to the peripheral neurone from Meniere's disease, and vestibular neuritis. Leading the patient out in a description of the kind of dizziness he feels may give clues that will help differentiate between true vertigo and functional disorder, particularly when considered against the information that is obtained in neurological examination.  (+info)

Mutations in the COCH gene are a frequent cause of autosomal dominant progressive cochleo-vestibular dysfunction, but not of Meniere's disease. (30/306)

The COCH gene is the only gene identified in man that causes autosomal dominantly inherited hearing loss associated with vestibular dysfunction. The condition is rare and only five mutations have been reported worldwide. All affected families showed a similar progressive hearing loss and vestibular dysfunction. Since Meniere's disease-like symptoms have also been described in some families, it was suggested that COCH mutations might be present in some patients diagnosed with Meniere's disease. In this study, using a Japanese population, we performed a COCH mutation analysis in 23 patients from independent families with autosomal dominant hearing impairment, four of whom reported vestibular symptoms, and also in 20 Meniere's patients. While a new point mutation, A119 T, was found in a patient with autosomal dominant hearing loss and vestibular symptoms, no mutations were found in the Meniere's patients. Like all other previously identified COCH mutations, the mutation identified here is a missense mutation located in the FCH domain of the protein. The current mutation is located in close spatial proximity to W117, in which a mutation (W117R) had previously been associated with autosomal dominant hearing loss. Model building suggests that, like the W117R mutation, the A119 T mutation does not affect the structural integrity of the FCH domain, but may interfere with the interaction with a yet unknown binding partner. We conclude that mutations in the COCH gene are responsible for a significant fraction of patients with autosomal dominantly inherited hearing loss accompanied by vestibular symptoms, but not for dominant hearing loss without vestibular dysfunction, or sporadic Meniere's disease.  (+info)

Diagnosis and management of benign paroxysmal positional vertigo (BPPV). (31/306)

There is compelling evidence that free-floating endolymph particles in the posterior semicircular canal underlie most cases of benign paroxysmal positional vertigo (BPPV). Recent pathological findings suggest that these particles are otoconia, probably displaced from the otolithic membrane in the utricle. They typically settle in the dependent posterior canal and render it sensitive to gravity. Well over 90% of patients can be successfully treated with a simple outpatient manoeuvre that moves the particles back into the utricle. We describe the various techniques for this manoeuvre, plus treatments for uncommon variants of BPPV such as that of the lateral canal. For the rare patient whose BPPV is not responsive to these manoeuvres and has severe symptoms, posterior canal occlusion surgery is a safe and highly effective procedure.  (+info)

Phobic postural vertigo: a new proposed entity. (32/306)

BACKGROUND: Dizziness and vertigo can be a complaint in various psychiatric conditions where it usually constitutes only one of the features of the syndrome. Lately, a somatoform disorder characterized by almost mono-symptomatic dizziness and unsteadiness has been described. Since phobic postural vertigo usually presents without anxiety or other psychological symptomatology, patients with this condition seek help at neurologic and otolaryngologic clinics where they are often misdiagnosed as suffering from organic vertigo. OBJECTIVES: To present the clinical features of 55 consecutive patients diagnosed with phobic postural vertigo at our clinic during 1998-2002. METHODS: We conducted a retrospective review of patients' medical records and report two typical cases for illustration. RESULTS: The patients presented with complaints of unsteadiness with or without dizziness, and attacks of sudden veering that caused them to grasp for support. Accompanying anxiety was admitted by only 5% and vegetative symptoms were reported in 18%. In 16% the symptoms resulted in avoidance behavior. A stressful life event or an unrelated somatic disease triggered the onset of PPV in 35% of patients, whereas a vestibular insult preceded the symptoms in 13%. The mean duration of symptoms was 26.7 +/- 39.1 months (range 0.5-20 years). In 72% of patients the symptoms resolved after the psychological mechanism of their symptoms was explained to them; 24% improved with antidepressant treatment (selective serotonin reuptake inhibitors or tricyclic antidepressants), and only in 4% did the symptoms persist. CONCLUSIONS: Since PPV is a frequently encountered diagnosis at some specialized dizziness clinics, familiarity with this entity resulting in early diagnosis can avoid unnecessary examinations and lead to effective treatment.  (+info)