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A simplified diagnostic approach to dizziness in children.

The objective of the study was to validate the effectiveness of a questionnaire and computer-assisted algorithm in diagnosing children with dizziness or vertigo. Dizziness and vertigo are common complaints in children, causing an extensive, often unnecessary evaluation. A pediatric "dizziness questionnaire" was designed and a computer-assisted algorithm was developed to facilitate the diagnostic task. A retrospective medical record review was conducted on all children presenting to the clinic for dizziness or vertigo throughout a 2-year period. The information was used by one investigator to complete the questionnaire and by the other, the algorithm. The two diagnoses thus obtained were compared by the third investigator to the medical record diagnosis. Sixty-two records were reviewed. The final diagnoses were migraine (39%), benign paroxysmal vertigo (15%), vestibular neuronitis (14%), and anxiety (13%). In 57 patients (92%), the questionnaire-derived diagnosis was identical to the medical record diagnosis. In 52 patients (84%), the algorithm-derived diagnosis matched the medical record diagnosis. The questionnaire and computer-assisted algorithm are reliable diagnostic screening tools for children with dizziness or vertigo. When these tools combined provide a clear-cut diagnosis, no further evaluation is necessary.

Adolescent↗

A neural correlate for vestibulo-ocular reflex suppression during voluntary eye-head gaze shifts.

The vestibulo-ocular reflex (VOR) is classically associated with stabilizing the visual world on the retina by producing an eye movement of equal and opposite amplitude to the motion of the head. Here we have directly measured the efficacy of VOR pathways during voluntary combined eye-head gaze shifts by recording from individual vestibular neurons in monkeys whose heads were unrestrained. We found that the head-velocity signal carried by VOR pathways is reduced during gaze shifts in an amplitude-dependent manner, consistent with results from behavioral studies in humans and monkeys. Our data support the hypothesis that the VOR is not a hard-wired reflex, but rather a pathway that is modulated in a manner that depends on the current gaze strategy.

Animals↗

Roles of fibroblast growth factor 2 during innervation of the avian inner ear.

The importance of individual members of the fibroblast growth factor gene family during innervation of the vertebrate inner ear is not clearly defined. Here we address the role of fibroblast growth factor 2 (FGF-2 or basic FGF) during development of the chicken inner ear. We found that FGF-2 stimulated survival of isolated cochlear and vestibular neurons during distinct phases of inner ear innervation. The potential neurotrophic role of FGF-2 was confirmed by its expression in the corresponding sensory epithelia and the detection of one of its high-affinity receptors in inner ear neurons. Finally, we have analysed the potential of the amplicon system based on defective herpes simplex virus type 1 (HSV-1) vectors to express FGF-2 in cochlear neurons. Overexpression of FGF-2 in cochlear neurons resulted in neuronal differentiation demonstrating the presence of biologically active growth factor. This study underlines the potential of FGF-2 to control innervation and development of sensory epithelia in the avian inner ear. Furthermore, amplicon vectors may provide a useful tool to analyse gene function in isolated neurons of the vertebrate inner ear.

Animals↗

[Rare differential diagnosis in "vertigo" symptoms].

The diagnosis of vestibulocochlear nerve and statoacoustic organ lesions is based on the symptoms vertigo, hearing loss and tinnitus. The most common diseases are vestibular neuronitis, Ménière's disease, benign positional vertigo and sudden hearing loss. 6 patients are presented, complaining of at least one of the symptoms vertigo, hearing loss or tinnitus. They were suspected of suffering from a peripheral audiovestibular disease when admitted to the clinic, but all of them revealed other pathologies. A careful history and step-wise otoneurologic diagnostics including clinical examination, otoneurologic testing, audiologic tests, electronystagmography, acoustic evoked potentials and imaging techniques finally resulted in the correct diagnosis.

Adult↗

[High-resolution computed tomography in diseases of the inner ear].

High-resolution CT of the petrous bone was carried out in 259 patients with clinically diagnosed abnormalities of the inner ear; in some the lesions were bilateral. In 62 patients (approximately 20%), the scans showed findings which related to the signs and symptoms. Patients with hearing loss and vestibular neuronitis showed no abnormalities. Amongst the remaining patients, the most common findings were acoustic neuromas (17 cases), cochlear otospongiosis (14 cases), malformations (13 cases) and tumours or cholesteatomas of the labyrinth (13 cases) as well as single rare isolated lesions.

Cochlear Diseases↗

Influenza A virus infection of human Schwann cells in vitro.

OBJECTIVES: Sudden sensorineural hearing loss, vestibular neuronitis, vocal fold paralysis and Bell's palsy have been associated with a viral etiology, due to the infection of nerve cells. The goal of this research was to ascertain whether Schwann cells can support infection with human influenza A virus and thereby represent a plausible alternative site for virus-host interaction. Viral infection of Schwann cells may lead to secretion of inflammatory mediators, leukocyte recruitment, demyelination and nerve damage. MATERIAL AND METHODS: Cultured human Schwann cells were exposed to human influenza A virus. Infection was assayed at various times post-inoculation (0, 24, 48 and 72 h) using light microscopy, immunocytochemistry and influenza A virus-specific reverse transcriptase polymerase chain reaction (RT-PCR). A group of unexposed cells served as controls. RESULTS: Following exposure to the virus, vacuolization, cellular expansion and detachment from the dish were seen as early as 24 h post-inoculation. The exposed cells demonstrated positive immunocytochemical staining for influenza A virus antigen at 24, 48 and 72 h. Using RT-PCR, a sharp rise in influenza A virus-specific mRNA was detected. CONCLUSIONS: Human Schwann cells can be infected with human influenza A virus. Further studies will assess the inflammatory response in this model.

Cell Transformation, Viral↗

Which comes first? Psychogenic dizziness versus otogenic anxiety.

SUMMARY: OBJECTIVE To investigate the hypotheses that physical neurotologic conditions may trigger anxiety disorders (otogenic pattern of illness), that psychiatric disorders may produce dizziness (psychogenic pattern), and that risk factors for these syndromes may be identified. STUDY DESIGN Retrospective review of all patients (N = 132) treated at a tertiary care balance center from 1998 to 2002 for psychogenic dizziness with or without physical neurotologic illnesses. METHODS All patients underwent comprehensive neurotologic and psychiatric evaluations with attention to the longitudinal course of symptoms and risk factors for psychopathology. Patients were grouped according to the condition first causing dizziness. Risk factors were compared across groups. RESULTS Three equally prevalent patterns of illness were found: anxiety disorders as the sole cause of dizziness (33% of cases), neurotologic conditions exacerbating preexisting psychiatric disorders (34%), and neurotologic conditions triggering new anxiety or depressive disorders (33%). Panic disorder and agoraphobia were significantly more prevalent than less severe phobias in the first two groups, whereas the opposite pattern existed in the third group (P <.0001). More patients in the first two groups had risk factors for anxiety disorders (P <.05). Depression was not a primary cause of dizziness in any patient. Vestibular neuronitis, benign paroxysmal positional vertigo, and migraine were the most common neurotologic conditions. CONCLUSIONS These data support the hypothesis that physical neurotologic conditions may trigger psychopathology as often as primary anxiety disorders cause dizziness. A third pattern appears to be equally common wherein physical neurotologic conditions exacerbate preexisting psychiatric illnesses. Individuals at risk for anxiety disorders may be more likely to have primary psychopathology.

Adolescent↗

Migrainous vertigo: development of a pathogenetic model and structured diagnostic interview.

PURPOSE OF REVIEW: Vestibular symptoms occur frequently in patients with migraine. This review refines recently proposed diagnostic criteria for migraine-related vestibular symptoms, and develops a pathophysiological model for the interface between migraine and the vestibular system. RECENT FINDINGS: The epidemiological link between migraine and vestibular symptoms and signs suggests shared pathogenetic mechanisms. Links between the vestibular nuclei, the trigeminal system, and thalamocortical processing centers provide the basis for the development of a pathophysiological model of migraine-related vertigo. During the last year, several studies have increased understanding of the relationship between migraine and vestibular symptoms. A study of motion sickness and allodynia in migraine patients supports the importance of central mechanisms of sensitization for migraine-related vestibular symptoms. A study has demonstrated effective treatment of vertigo with migraine therapy. The identification of migrainous vertigo, however, is hampered by a lack of standardized assessment criteria for both clinical and research practices. The application of published criteria for the diagnosis of migrainous vertigo allows the development of a standardized, structured assessment interview. SUMMARY: An understanding of the relationship between migraine and the vestibular system increases knowledge of the pathogenesis of both migraine and vertigo. In addition, studies have identified successful treatment, with standard migraine therapies, of vestibular symptoms in patients with both migraine and vertigo. The use of a standardized assessment tool to identify this unique population of patients will help future studies to test both the pathological model and effective treatment options.

Cerebral Cortex↗

Aging, opioid-receptor agonists and antagonists, and the vestibulosympathetic reflex in humans.

Animal studies indicate that opioids inhibit the firing rate of vestibular neurons, which are important in mediating the vestibulosympathetic reflex. Furthermore, this inhibition appears to be greater in more mature rats. In the present study, we tested the hypotheses that opioids inhibit the vestibulosympathetic reflex in humans and that endogenous opioids contribute to the age-related impairment of the vestibulosympathetic reflex. These hypotheses were tested by measuring muscle sympathetic nerve activity (MSNA), arterial blood pressure, and heart rate responses to otolith organ engagement during head-down rotation (HDR) in young (24 +/- 2 yr old) and older (63 +/- 2 yr) subjects before and after administration of either an opioid-receptor antagonist (16 mg naloxone in 9 young and 8 older subjects) or an opioid-receptor agonist (60 mg codeine in 7 young and 7 older subjects). Naloxone did not augment the reflex increase in MSNA during HDR in young (Delta7 +/- 2 vs. Delta4 +/- 2 bursts/min and Delta81 +/- 23 vs. Delta60 +/- 24% change in burst frequency and total MSNA before and after naloxone, respectively) or older subjects (Delta2 +/- 2 vs. Delta1 +/- 2 burst/min and Delta8 +/- 7 vs. Delta8 +/- 9% before and after naloxone). Similarly, codeine did not attenuate the increase in MSNA during HDR in young (Delta8 +/- 1 vs. Delta7 +/- 2 bursts/min and Delta53 +/- 4 vs. Delta64 +/- 16% before and after codeine) or older subjects (Delta6 +/- 4 vs. Delta3 +/- 3 bursts/min and Delta38 +/- 21 vs. Delta33 +/- 20%). Mean arterial blood pressure and heart rate responses to HDR were not altered by either naloxone or codeine. These data do not provide experimental support for the concept that opioids modulate the vestibulosympathetic reflex in humans. Moreover, endogenous opioids do not appear to contribute the age-associated impairment of the vestibulosympathetic reflex.

Adult↗

Morphological correlates of response dynamics and efferent stimulation in horizontal semicircular canal afferents of the toadfish, Opsanus tau.

1. We used the intraaxonal labeling technique to study correlations between the terminal dendritic morphology of horizontal semicircular canal primary afferents and their response dynamics to sinusoidal head rotation and combined electrical stimulation of central efferent vestibular neurons. Thirty-eight canal afferents were identified by their sensitivity and phase of response to rotation between 0.1 and 1.0 Hz (+/- 10 degrees/s) and were subsequently labeled with horseradish peroxidase or biocytin. The afferent's dendritic field and synaptic specializations in the neuroepithelium of the crista were examined under light microscopy. 2. Rate and regularity of background discharge of the afferent were not correlated with its axon diameter or relative location of its dendritic field in the crista. 3. Response sensitivity of the afferent to rotation was correlated both with the relative location of its dendritic field in the crista and with the number of terminal endings it possesses. Afferents having low sensitivities, slow dynamics, and few terminal endings supply the peripheral portions of the crista; afferents with higher sensitivities, faster dynamics, and greater number of terminal endings supply the more central portions. It is suggested that the differences in sensitivity among the afferents reflect principally the variations in both the cupular dynamics along the crista and the number of possible hair cell contact sites in the neuroepithelium. 4. Response phase of the afferent was correlated only with the extent of its dendritic processes along the transverse axis of the crista. Afferents having transversely oriented dendritic fields had less phase lags relative to acceleration than did those having a more longitudinally oriented dendritic field. 5. Efferent stimulation produced a change in both the afferent's discharge rate and its response sensitivity to rotation. Afferents discharge rate and its response sensitivity to rotation. Afferents having a centrally located dendritic field and acceleration afferents, defined by their response to rotation, were the most affected by efferent stimulation. These results suggest that efferent innervation is either directed toward, or most efficacious in, the central regions of the crista and that it may select specific hair cell-afferent complexes.

Animals↗

Herpes simplex polyganglionitis.

Evidence suggests that many cranial nerve syndromes, such as migraine headache, acute vestibular neuronitis, globus hystericus, carotidynia, acute facial paralysis (Bell's palsy), and Meniere's disease, are caused by the neurotropic herpes simplex virus (HSV). Because transitory cranial nerve dysfunction during acute HSV infection can be asymptomatic but often occurs in conjunction with mucocutaneous vesicles, we tested five subjects with herpes labialis for cranial nerve dysfunction. Four of the subjects had hypesthesia of the trigeminal nerve (which recurred in two); four, hypesthesia of the glossopharyngeal nerve; and two, hypesthesia of the second cervical nerve. Three of the subjects had positional or spontaneous nystagmus (which recurred in one); one of the subjects had a unilateral, decreased caloric response of 50%. Unilateral weakness of the cricothyroid muscle or the palate occurred in three of the subjects (and recurred in one). Volitional electromyograms were normal in all the subjects, but two of the subjects had increased facial nerve latency (which recurred in one). Similar findings of an acute, transitory nature should suggest to the clinician a viral polyganglionitis caused by HSV infection.

Adult↗

Acute superior laryngeal nerve palsy: analysis of 78 cases.

Acute superior laryngeal palsy is often clinically unrecognized and frequently overlooked. Yet, this motor paralysis occurs more frequently than facial paralysis. Like acute facial paralysis, superior laryngeal palsy often occurs as part of a cranial polyneuritis that is probably related to herpes simplex virus reactivation. Rotation of the larynx and shortening of one vocal cord have been found in such diverse syndromes as vestibular neuronitis, migraine and tension headaches, unexplained cough, tinnitus aurium, globus hystericus, and carotidynia. Electromyographic studies suggest that laryngeal spasm may be caused by faulty regeneration of the superior, rather than the recurrent, laryngeal nerve.

Acute Disease↗

Diagnosis of vestibular imbalance in the blink of an eye.

BACKGROUND: In a recent study, the authors found that blinks in healthy volunteers always triggered ocular torsion quick phases during dynamic roll movements of the head. On the basis of this observation, they hypothesized that blinks in patients with a vestibular tone imbalance would also trigger torsional quick phases. METHODS: Using video-oculography with a fixation target, the authors recorded the ocular torsion position of the left eye of 37 participants while they made voluntary blinks once every 6 to 10 seconds. The participants were recruited from four groups: two age groups of healthy volunteers with a mean +/- SD age of 32 +/- 4 (n = 9) and 65 +/- 11 y (n = 9); patients with a unilateral vestibular disorder in an acute state (n = 12, 53 +/- 17 y); and those in a persisting state in which spontaneous nystagmus had already faded (n = 9, 65 +/- 13 y). RESULTS: In the control groups of healthy volunteers, blinks triggered no or only small quick phases on the order of 0.1 deg. In both patient groups blinks always triggered quick phases with significantly higher amplitudes of 1.85 +/- 1.02 deg and were followed by exponentially decaying slow-phases with time constants on the order of 1 to 2 seconds. Patients in the persisting state clearly differed from patients in the acute state in that their torsional spontaneous nystagmus had already vanished due to vestibular compensation. But surprisingly, these two groups did not show a large difference in terms of the effect of blinks on ocular torsion. The authors always observed torsional quick phases with the upper pole of the eye beating away from the side of the lesion. CONCLUSIONS: Blinks are able to trigger torsional quick phases in patients with both acute and persisting vestibular disorders. The side of the impairment can be determined from the direction in which the eye is rotated after a blink. Thus, ocular torsion recordings during blinks can be used as a simple clinical test for a vestibular tone imbalance, particularly during a persisting failure in which spontaneous nystagmus has resolved and can therefore no longer be used for diagnosis.

Adult↗

Ephrin A/EphA controls the rostral turning polarity of a lateral commissural tract in chick hindbrain.

Most post-crossing commissural axons turn into longitudinal paths to make synaptic connections with their targets. Mechanisms that control their rostrocaudal turning polarity are still poorly understood. We used the hindbrain as a model system to investigate the rostral turning of a laterally located commissural tract, identified as the caudal group of contralateral cerebellar-projecting second-order vestibular neurons (cC-VC). We found that the caudal hindbrain possessed a graded non-permissive/repulsive activity for growing cC-VC axons. This non-permissiveness/repulsion was in part mediated by glycosyl-phosphatidylinositol (GPI)-anchored ephrin A. We further demonstrated that ephrin A2 was distributed in a caudal-high/rostral-low gradient in the caudolateral hindbrain and cC-VC axons expressed EphA receptors. Finally, perturbing ephrin A/EphA signalling both in vitro and in vivo led to rostrocaudal pathfinding errors of post-crossing cC-VC axons. These results suggest that ephrin A/EphA interactions play a key role in regulating the polarity of post-crossing cC-VC axons as they turn into the longitudinal axis.

Animals↗

Histamine in the treatment of vertigo.

The vasodilating properties of histamine were the basis for histamine treatment of episodic vertigo and other inner ear dysfunctions. The successes obtained led to the development of betahistine: an orally active histamine analogue; its general pharmacology resembles that of histamine. Animal pharmacology experiments proved that betahistine increases cerebral blood flow and probably also affects vestibular neurons. From clinical studies, it appears that betahistine is an effective agent for the symptomatic treatment of Meniere's syndrome. Efficacy has also been shown in the treatment of patients suffering from paroxysmal vertigo.

Animals↗

Stage-assessment of the progress of continuous vertigo of peripheral origin by means of spontaneous and head-shaking nystagmus findings.

The stages of continuous vertigo of peripheral origin were classified into nine categories according to the findings of spontaneous nystagmus (SPN) and head-shaking nystagmus (HSN). The patients analysed were 18 with vestibular neuronitis, 6 with sudden deafness and 6 with unilateral inner ear disorders. 1) Irritative SPN (Stage I) was rarely encountered. 2) SPN of the paralytic type (Stage II) was usually observed in the period less than one month after the onset of diseases. 3) HSN directed toward the intact side with or without a reversal phase (Stages III-2 and III-1, respectively) were the common types of central compensation. 4) The progress of recovery to complete cure (Stage V) was usually rapid once it had actually begun. 5) During the process of recovery, HSN could disappear transitorily (Stage III-3), or be directed toward the affected side without a reversal phase (Stage III-5). Spontaneous recovery nystagmus (Stage IV) could also occur. 6) About 40% of patients recovered to Stage V within about 4 months after the onset of vertigo, but about 30% of patients remained in Stage III-1 or III-2 even after 4 months.

Adolescent↗

The aetiology of dizziness and how to examine a dizzy patient.

Dizziness embraces various sensations of spatial disorientation. A common symptom, it has been experienced by at least one third of the population by the age of 65. Peripheral causes include disorders of the labyrinth and vestibular nerve such as Ménière's disease, benign paroxysmal positional vertigo, acute vestibulopathy (vestibular neuronitis) and acoustic neuroma. The most common lesions of the central nervous system that cause dizziness are infratentorial ischaemia, mechanical trauma, multiple sclerosis and cerebellar atrophy. Other aetiological factors include intoxications, psychogenic causes, cervical problems and cardiovascular diseases. The history and physical examination are the cornerstones of the search for the cause of dizziness. The most valuable otological methods are electronystagmography and audiometry. Of the clinical neurophysiological methods, brainstem auditory evoked potentials are more useful than electroencephalography. Computed tomography and magnetic resonance imaging should be used when a CNS disorder is suspected.

Dizziness↗

Immunohistochemical localization of glycine receptors and a linked polypeptide in the goldfish brain.

Three monoclonal antibodies were used to examine with immunocytochemistry the distribution of the glycine receptors and the related 93kd polypeptide in the adult goldfish brain (Carassius auratus). One immunoglobulin recognizes the 48kd strychnine-binding subunit of the receptor and the two others bind to the peripheral 93kd polypeptide which is coupled to the receptor molecules. Immunofluorescent spots were visualised with all three antibodies on the somatic and dendritic membrane of the cells. A differential intensity of immunofluorescence was detected in the three different brain regions examined: the brainstem, the cerebellum and the telencephalon. For both proteins, the highest fluorescence was observed in the brainstem, particularly on reticular and vestibular neurons. In the cerebellum both the density and the intensity of labelling was low. At the level of the Mauthner cell, an identified bulbar command neuron, the distribution of glycinergic receptors was identical with that of the 93kd polypeptide. Both subunits were visualized on the somatic and dendritic membrane up to their extremities. These proteins appear to be co-localized in neurons other than the Mauthner cell, since they are always co-expressed in the same brain region. Their distributions are comparable with that observed in the mouse and rat nervous system as reported from autoradiographic localization of [3H]strychnine binding.

Animals↗