In the acute period, the goal of drug therapy for vertigo is suppressing the sensation of vertigo, preventing vomiting and helping restore normal balance. Intravenous injection of NaHCO3 is effective against the sensation of vertigo. Since histamine H1-receptors are involved in vomiting that is associated with vertigo, antihistamines could prevent it. Benzodiazepines may restore normal balance by stimulating the initial develop-ment of vestibular compensation, in addition to their antianxiety effects. In the chronic period, vasodilators such as diphenidol or betahistine could prevent recurrent attacks of vertigo. Benzodiazepines may act on the limbic system and relieve psychotic triggering of vertigo attacks. Meniere's disease, in which the primary pathology is endolymphatic hydrops, is specifically managed by an osmotic diuretic, isosorbide. Steroids may be helpful in patients with vestibular neuronitis.
Vestibular compensation consists of the following stages: the inhibition of the contralesional medial vestibular nucleus (contra-MVe) activities at the acute stage after unilateral labyrinthectomy (UL) and the recovery and maintenance of the ipsilesional MVe (ipsi-MVe) spontaneous activities at the chronic stage after UL. In this paper, we reviewed molecular mechanisms of vestibular compensation in the central vestibular system by means of several morphological and pharmacological approaches in rats. Based on our examinations, we propose the following hypothesis. At the acute stage after UL, the activated neurons in the ipsi-MVe project their axons into the flocculus to inhibit the contra-MVe neurons via NMDA receptor, nitric oxide (NO), acetylcholine (Ach) and/or GABA-mediated signaling, resulting in the restoration of balance between intervestibular nuclear activities. At the chronic stage after UL, the flocculus depresses the inhibitory effects on the ipsi-MVe neurons via protein phosphatase 2A (PP2A) β, protein kinase C (PKC) and/or glutamate receptor (GluR) δ-2, to help the recovery and maintenance of the ipsi-MVe activities.
The secondary phase of paroxysmal positional nystagmus was observed in five patients with paroxysmal positional vertigo. In all five, positional and/or positioning rotary nystagmus appeared for 20 to 30 seconds in the head-hanging and/or the lateral head position with a short latency of crescendo and decrescendo in character, associated with vertiginous sensation, and it was followed by the secondary phase nystagmus involving rotation to the opposite direction for more than 45 seconds in the same head position. Head MRI or head CT findings were normal in 4 cases, but a small pontine infarction was detected in one patient. There was no other evidence of ear disease, and neurological examination revealed nothing abnormal even in the patient with the pontine lesion in MRI. The secondary phase of BPPV is clinically rare and it is still unknown whether the origin is peripheral or central. Review of the literature introduced that the secondary phase of BPPV might be caused by movements of debris in the posterior semicircular canal, abnormal function in short term adaptation, or other transient dysfunction of the central nervous system.
Basal lamina (BL) anionic sites are considered to act as negative charge barriers that contribute to the selective permeability of electrically charged macromolecules and ions in the labyrinth. Transmission electron microscopy was used to study the effects of acute furosemide administration on the basal lamina (BL) anionic sites in the stria vascularis, dark cell area, and the endolymphatic sac using cationic polyethyleneimine (PEI, M.W. 1800). Albino guinea pigs with normal Preyer's reflex were used in this study. Furosemide (80 mg/kg. B.W.) and physiological saline was administered intravenously via the axillary vein to each animal in the experimental and control groups, respectively. After 20 min, auditory bullae were removed and processed for histological evaluation. A marked enlargement of the intercellular space was observed in the stria vascularis. No marked edematous change was observed in the epithelium in the dark cell area. PEI distribution was significantly decreased on the capillary BL in the stria vascularis and on the subepithelial BL in the dark cell area. These findings suggest that the water and ionic transport system in the stria vascularis may be different from that in the dark cell area. No significant difference of the PEI distribution was observed on the subepithelial BL in the endolymphatic sac. These findings suggest that furosemide severely alters the distribution of the anionic sites in the strial capillary BL and in the subepithelial BL in the dark cell area but not in the subepithelial BL of the endolymphatic sac. Hence, we propose that the charge barrier may not be injured in the endolymphatic sac following the administration of furosemide.
We report a patient with vertigo and sudden hearing loss due to acute disseminated encephalomyelitis (ADEM). A 17-year-old male complained of sudden hearing loss in the right ear and dizziness subsequent to symptoms resembling those of a common cold. To his recall, he had never manifested any previous neurological disturbances. Audiometric testing revealed severe sensorineural hearing loss in his right ear and mild sensorineural hearing loss in his left ear. In addition, a short increment sensitivity index (SISI) test was positive bilaterally. Neuro-otological examinations revealed horizontal-rotating nystagmus and upbeat nystagmus on positional and/or positioning nystagmus tests. Although pursuit eye movement was normal, the optokinetic nystagmus was impaired and fast-phase velocity of the nystagmus was reduced. Caloric tests revealed severe hypofunction bilaterally. MRI showed patchy high-intensity areas in the pons, left frontal lobe, left superior frontal gyrus, and left parietal lobe on T2-weighted and FLAIR (fluid attenuated inversion recovery) images. Based on the history, physical examinations, laboratory tests, and MRI findings for this patient, he was diagnosed as having ADEM with bilateral inner ear lesions. This patient was considered to be an unusual case of ADEM complicated with cochlear and vestibular signs. To our knowledge, such a case has not been previously reported.
This study investigated the relationship between magnitude of body sway and competence in older persons living in a community. The subjects were 637 older adults (males 263, females 374) aged 67 to 91 years living in Nangai Village in Japan. The subjects stood stationary and upright on a force platform with their feet together (Romberg stance) for 20 seconds with wearing shoes with eyes open and eyes closed. Body sway length and body sway area were calculated as magnitude of body sway. Competence was tested by TMIG Index of Competence. In this index, competence involved three constructions: Instrumental Self-Maintenance, Intellectual Activity, and Social Role. The relationship between all of the 4 indexes of magnitude of body sway and the Instrumental Self-Maintenance Score was significant. The relationship between magnitude of body sway with eyes open and the Social Role Score was significant. The relationship between magnitude of body sway and the Intellectual Activity Score was not significant. The Competence Score was significantly related to magnitude of body sway with eyes open. The magnitude index that showed the highest relation to competence was body sway area with eyes open.
Linear acceleration (CF) caused by centrifugal force results in ocular deviation and change in spatial orientation. Thirteen healthy human subjects and one labyrinthine defective (LD) subject were exposed to CF to examine the change in spatial orientation and eye position. CF was applied by rotating the subject at a 90 cm off-center position (eccentric rotation). Constant angular velocities of 80, 100, 120 and 140 deg/sec depicted CF of 0.18 to 0.55 G. CF was introduced in two chair positions as it affects along the inter-aural (X) or naso-occipital (Y) axes. Subjects were asked to adjust an LED bar to a perpendicular position while the chair was rotated in the darked room. Judgement for visual vertical was very accurate when the chair was stationary (with deviation of the bar within 1.1 degrees). Under CF along the X-axis, judgement for subjective perpendicular changed (i.e., toward the center of rotation). Amplitude of the tilting angle significantly increased as a function of CF (ANOVA, p<0.05). However, no significant change in bar deviation was found in one LD subject during the rotation. Also, CF along the Yaxis did not cause any significant deviation of the bar in healthy volunteers. Eye movement during eccentric rotation was analyzed by using an infrared video camera and computer analyzing system. Torsional eye deviations with amplitudes of 0.1 to 1.5 degrees were detected under CF along the X-axis. Under CF along the Y-axis, upward eye deviations with amplitudes of 1.6 to 3.2 degrees were detected. As the amplitude of eye deviation was very small in both conditions, it is assumed that the gain of otolithocular reflex had only a small gain. The linear acceleration acting upon the head had a larger influence upon spatial orientation than upon the oculomotor system.
Although the interrelations between dizziness and various psychological factors have been well reported, the effectiveness of various therapies in reducing dizziness has received much less attention. In a previous study, we reported that group psychotherapy was effective in improving the condition of patients suffering from dizziness. In this study, we investigated the environmental factors which may have caused the dizziness of eighty-six patients. Probable causes for their dizziness included a dysfunctional family (30%), work- or job-related stress (31%), and mental illness (23%). Difficulty with human relations and anxiety were the most common factors exacerbating symptoms of dizziness. Group psychotherapy was found to be effective in helping these patients reduce their dizziness.
The possibility of inducing physiological changes of otoliths by applying sinusoidal linear acceleration for a long time was investigated. Changes in otolith function were examined by analysis of cognition changes in the gravitational axis as spational orientation. Namely, the effects of functional changes of otoliths caused by linear acceleration on cognition of gravitational axis was analyzed, and the relation of otoliths to the spatial orientation was examined. In consequence, we found that cognition of the gravitational axis in linear acceleration in a lying position was lower than that in a sitting position. This could be attributed to the difference in the direction of the acceleration applied to the head (otolith). These results suggested that otoliths possibily participate in the formation of spatial orientation because cognition of the gravitational axis was lowered by applying linear acceleration.
To determine whether neurosteroids suggested to be present in the brain act on MVN neurons, we electrophysiologically examined the effects of dehydroepiandrosterone sulfate (DHEAS), a neurosteroid, on the neuronal activity of the medial vestibular nucleus (MVN) in cats anesthetized with α-chloralose. Single neuronal activity in the MVN was extracellularly recorded using a glass-insulated silver wire microelectrode attached to a seven-barreled micropipette. Each micropipette was filled with DHEAS (5 mM), γ-aminobutyric acid (GABA 1 M) or NaCl (5 mM). These chemicals were microiontophoretically applied to the immediate vicinity of the target neuron being recorded. The effects of these chemicals were examined on type I neurons, identified by responses to horizontal and sinusoidal rotations. Microiontophoretic application of DHEAS did not affect the spontaneous and rotation-induced firings, but reduced rotation-induced inhibition, which is known as commissural inhibition, in 8 of 15 type I neurons examined. Moreover, microiontophoretically-applied DHEAS in dose of 100 nA decreased GABA-induced inhibition on type I neurons. These findings suggests that DHEAS reduced the commissural inhibition to type I neurons by attenuation of GABA effects.