Inner ear innervation is regulated by growth factors including neurotrophins. Neurotrophins include nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3), and neurotrophin-4/5 (NT-4/5). Each of the neurotro-phins selectively binds to the high affinity receptors designated as TrkA for NGF, TrkB for BDNF and NT-4/5, and TrkC for NT-3, whereas all neurotrophins bind to the low affinity receptor designated as p75. BDNF and NT-3, but not NGF or NT4/5, are expressed in most sensory epithelia of the inner ear. TrkB and TrkC, but not TrkA, are expressed in cochlear and vestibular ganglia. Analyses of mice lacking BDNF revealed a marked reduction of afferent innervation by vestibular ganglion cells. By contrast, a marked loss of cochlear ganglion cells occured in mice lacking NT-3. No deficits in cochlear or vestibular structures occur in mice lacking either NGF or NT-4/5. Moreover, nearly complete loss of both vestibular and cochlear ganglion cells is shown in double mutant mice lacking both BDNF and NT-3. These observations indicate that BDNF and NT-3 play crucial roles in the development and maintenance of afferent innervation of the inner ear. Local application of neurotrophins may be useful for the treatment of hearing loss.
Thirty-two patients with idiopathic unilateral auditory and/or vestibular symptoms (19 females and 13 males, mean age of 62.2 years) were evaluated with T2—weighted MR images (MRI). MRI of 18 patients with sudden deafness or vestibular neuronitis (10 females and 8 males, mean age of 54.9 years) were used as controls. Displacement of the basilar artery from the midline were assessed at the level of the internal auditory meatus in the axial view. The displacement was ipsilateral to the symptoms in 26 (81.3%) and contralateral in 6 (18.7%) of 32 patients, whereas it was ipsilateral to the lesion in 4 (22.2%), contralateral in 7 (38.9%) and not recognized in 7 (38.9%) of 18 control patients. Statistical analysis revealed that the patients with idiopathic unilateral auditory and/or vestibular symptoms had ipsilateral displacement of the basilar artery at a significantly high incidence, which may have developed as a result of ipsilateral dolichoectasia due to sclerotic change of the vertebrobasilar artery, leading to a unilateral lesion such as neurovascular compression or chronic blood flow change of the 8th cranial nerve or inner ear.
The axonal projections of 34 anterior canal (AC)-activated excitatory secondary vestibular neurons to the mesodiencephalon were studied electrophysiologically in cats. AC-related neurons were identified by monosynaptic activation elicited by electrical stimulation of the vestibular nerve and activation following nose-down rotation of the animal's head. Single excitatory neurons were identified by antidromic activation following electrical stimulation of the contralateral medial longitudinal fasciculus and oculomotor nucleus. The axonal projections of the identified neurons were then studied by systematic, antidromic stimulation of the mesodiencephalon. Ten of the 34 AC-related excitatory neurons were antidromically activated from the superior rectus (SR) subdivision of the oculomotor nucleus, central gray, interstitial nucleus of Cajal, dorsomedial part of Forel's field H and ventrobasal complex of the thalamus. In three other AC neurons, antidromic activation was examined only for the INC, but not for the thalamus. In the remaining 21 AC neurons, antidromic activation was obtained from the SR subdivision, but not from more rostral areas. These results suggest that AC-related excitatory neurons give off axon collaterals to the premotor areas to generate vertical eye movements and the thalamus concerning perception of vestibular sensation.
This study investigated age-related changes of magnitude of body sway in older persons living in a mainstream community. The subjects were 637 older adults (263 males, 374 females) aged 67 to 91 years, living in Nangai Village in Japan. The subjects, while wearing shoes, stood stationary and upright on a force platform with their feet together (Romberg stance) for 20 seconds with their eyes open and 20 seconds with eyes closed. Body sway length and body sway area were calculated as magnitude of body sway. Body sway length and body sway area increased with age. Values for body sway length and body sway area with eyes open were significantly lower than those with eyes closed. Values of body sway length in the female group were significantly lower than those in the male group. Body sway area in the female group was almost equal to that in the male group.
We used saccade latency in a visually guided saccade task as an index to examine the effects of sound stimulation. A light-emitting diode (LED) was embedded in a dome-shaped screen. DC electro-oculography (EOG) was used to record eye movements. Sound stimuli were delivered from a speaker at the center of the dome or from headphones or speakers on either side. The task was to maintain visual fixation at the dome center while the LED was on (overlap paradigm). LEDs on either side of the target at 20° were illuminated 20-50 times per session, and control data were obtained without sound stimulation. When sound stimuli were delivered from the speaker at the center of the dome every 10 ms between Target ON -200 to +200 ms, the latency was shortened between Target ON -200 to + 60 ms. When the sound stimulation from the speaker and the target were on the same side (the ortho condition), the latency was even shorter, in the target were on the opposite side (the anti condition), there was less shortening of the latency. These data suggested that sound simulation causes the loss of attention when a subject is asked to pay attention to a central fixation point, and results in brief eye movement towards the target spot.
A 56-year-old man complained of a hearing loss and tinnitus in his right ear after short intense exposure to a high level of sound. Although he had no complaints of vertigo or dizziness, his neuro-otological examination revealed apogeotropic direction changing type of positional nystagmus. An audiogram showed right high-frequency sensorineural hearing loss. An eye tracking test (ETT) and an optokinetic nystagmus (OKN) test showed no abnormalities. A caloric test showed normal responses in both ear sides. One week after the exposure to a high level of sound, the positional nystagmus completely disappeared. Apogeotropic direction changing type of positional nystagmus is generally considered to be a phenomenon observed in patients with central vestibular lesion. However, physical examination and laboratory tests of this patient suggested that he suffered from only a peripheral vestibular impairment. From these results, apogeotropic direction changing type of positional nystagmus observed in this patient resulted from an impair-ment of the peripheral vestibular system.
We have observed some severe cases of Meniere's disease with continuous or recurrent vertigo attacks. There are many factors that can make vertigo patents difficult to manage. One of the most important factors is neurotic depression. The most prominent symptom of neurotic depression is sleep disturbance, especially waking up many times at night. When you diagnose a vertigo patient as having neurotic depression, I recommend prescribing the antidepressant amitriptyline (10 mg at night). If this is not effective, you may use a dose of 20 mg to 75 mg. The case of symptoms such as vertigo or general fatigue, you may prescribe maprotiline (10 mg after breakfast); if this not effective, increase the dose to 30 mg every morning, afternoon, and night. If the case is especially severe, change maprotiline to dosulepin (75 mg). In the most severe cases try lofepramine (30 mg to 90 mg). If the patients are not in a depressive state, or take an overdose of the antidepressant, they often have nightmares or have resting tremors in their hands. When you observe such symptoms, stop the antidepressant therapy immediately.