Auditory plasticity has been noticed by success of cochlear implant surgery. Since patients with acquired deafness who lost hearing absolutely on the way of life, can hear voice, environmental sounds and understand conversation again, we wonder how their brain mechanism changes biologically. No auditory stimuli climb up central auditoy pathway in patients with complete loss of hearing. Then, probably, neurons or synapses must be modified from aspects of biochemistry, pharmacology, physiology and morphology. Neurons or synapses may be reorganized after cochlear implant surgery, again. As long as we observe patients with cochlear implant, successful conditions of recovery of hearing seem to be younger ages or shorter periods of loss of hearing and normal psychology at the time of surgery. In this review, items of background which are related to auditory development, plasticity and regeneration are described. For example, development of hearing and language of congenital and acquired deafness in children, unilateral or bilateral hearing aid fittings, hearing aid in elderly peoples and central auditory processing in central auditory disorders are discussed. Auditory plasticity is an important and interesting field for research in basic and clinical medicine.
In this review, different meanings of the term “auditory plasticity” are defined and some important dimensions of plasticity are discussed. After providing this framework, two studies on the developmental plasticity of cortical frequency maps are presented. The first explores effects of neonatal, partial cochlear deafferentation on the development of cochleotopic or tonotopic maps in auditory cortex. The second deals with the effects of auditory augmentation on tonotopic frequency maps in primary auditory cortex. In this latter study, kittens were reared in an acoustic environment containing a dominant 8kHz signal, and were subsequently found to develop an overrepresentation of the 8-12kHz region of the tonotopic map in primary auditory cortex. A brief discussion of possible mechanisms is given.
It has been widely held that the mammalian central nervous system (CNS) lacks regenerative capacity but that is not true. Studies over the past twenty years have provided convincing evidence for the occurrence of marked regeneration of mammalian CNS pathways and the formation of neural connections between the brain of host animals and grafted embryonic brain structures. Years of pessimism about the failure of regeneration of the mammalian CNS are consequently giving way to new optimism for repairing of injured brains and spinal cords. In neural repairing there are two fundamental problems. One is how to prove the occurrence of regeneration and the other is how to promote regeneration. The proof of regeneration is paradoxical because it requires evidence for the severance of axons that is no longer existent when regeneration occurred. The fibers in continuity at the time of examination have always been doubted for the possibility that they were spared from severance. This is the reason why the occurrence of regeneration has so long been discredited and why the Advisory Task Force of the National Institute of Neurological and Communicative Disorders and Stroke proposed criteria for evaluating spinal cord regeneration experiments (Exp. Neurol., 69, '80).Without firm foundation of evidence endeavors of neural repairing would become'a house built on sand'like wise the various surgical and pharmacological therapies that had been repeatedly advocated since the turn of century and condemned totally. Current endeavors to repair spinal cord injury can be classified into four categories: 1) employment of a peripheral nerve segment or Schwann cells as conduit of CNS axons, 2) blockade of neurite growth inhibitory factor by antibody (IN-1) and enhancement of axonal outgrowth by neurotrophin-3, 3) transplantation of embryonic CNS structures to supplement neurons and also to provide positional and guiding cues for axons that are contained in glia and extracellular matrix, and 4) transplantation of stem cells derived from the adult brain. At the moment reparable neural connections in these endeavors are mostly very restricted in the amount and extension. If the restriction is broken and neural connections similar to normal can be reconstructed, then, remarkable functional restoration would be expected. In fact, albeit only in neonatal rats, we succeeded in replacing spinal cord segments with embryonic homologous structures and proved the reconstruction of neural connections across the graft that were hardly distinguishable from normal and that the animals could walk, run, and climb with almost normal hind-forelimb coordination. Achievement of such results in adult rats after contusion injury would open up the door to clinical application. The prospects of the endeavors in this regard are discussed.
Recovery of auditory function after damage to the central auditory pathway would be achievable if the neural connections can be restored histologically. The present study is the first report of successful regeneration of the central auditory pathway after transection in the rat central auditory pathway. Functional recovery of hearing by the regenerated pathway was confirmed by the auditory brain stem response. Thus, the present findings contradict the widely held view that the mammalian central auditory system cannot be restored once being damaged. These findings suggest the possibility that similar restoration can be achieved in humans.
Administration of vanadate or ouabain on the round window did not produce a significant change in the position of Reissner's membrane, but ouabain produced more adverse effects on the cochlear and vestibular sensory cells and limbus spiralis. Pressure application to hydropic animal ears through the external auditory canal elicited nystagmus at lower pressure in comparison to normal ears. Maxzide (potassium sparing diuretic) treatment had no effect on the development of endolymphatic hydrops. Perforation of the tympanic membrane or a tube insertion into the bulla was effective to inhibit growth of hydrops.
CBP-15, a small and acidic calcium-binding protein in the organ of Corti of the guinea pig found by Senarita et al (1995), was qualitatively analyzed using the cochleae of the guinea pigs, rats and mice in this study. Partial amino acid sequence including N-terminal for CBP-15 obtained from the guinea pig cochlea coincided with that of β-type parvalbumin, i.e.oncomodulin (OM), which had never been identified in the inner ear tissue of any other species. CBP-15 was also found in the organ of Corti of the mice studied. Monoclonal and polyclonal antibodies to rat OM cross-reacted with CBP-15s in the guinea pigs, rats, and mice. Furthermore, this cross-reaction was strongly observed in the outer hair cells in the organ of Corti of the guinea pigs. Several authors reported that OM was able to stimulate a phosphodiesterase and to accelerate DNA synthesis in calcium-deprived rat liver at a tenfold lower concentration than calmodulin. These present results strongly suggest that OM plays an important role in the calcium regulation within the outer hair cells of the cochlea.
In order to determine the incidence of cholesteatoma in Japan, an epidemiological study was conducted in Miyagi Prefecture which is located in northern part of Japan, of approximately 2, 300, 000 population. The study was performed by questionnaires sent to all the otologists in the area as to the surgically proven cholesteatoma during the two years period between January 1993 and December 1994. One hundred and ninty cases (199ears) underwent surgery for cholesteatoma at hospitals in Miyagi Prefecture. The age of 190 cases (116 male and 74 female) ranged from 2 to 70years, with an average of 37years. The types of cholesteatoma were as follows: pars flaccida type was found in 138ears (69%), pars tensa type in 32 ears (16%), congenital type in 10 ears (5%). There were 3 additional cases which were sent to hospitals outside the Miyagi Prefecture. Including these cases the annual incidence of cholesteatoma was calculated as 4.2 cases per 100, 000 persons per year.
Bone conduction thresholds sometimes elevate in inflammation diseases of the middle ear, especially chronic otitis media (COM) and cholesteatoma. In the present syudy, we examined the preoperative bone conduction thresholds of 175 ears of COMs and cholesteatomas. The preoperative ears examined were devided into three groups according to the operation methods; myringoplasty or tympanoplasty type I with COM (group I), tympanoplasty type III-EIV with ossicular reconstruction or tympanoplasty and mastoidectomy with COM (group II) and tympanoplasty with cholesteatoma (group III). We found that the preoperative bone conduction thresholds did not show siginificant difference among three groups. Furthermore, no siginificant difference was found among three groups about the rate of mean bone conduction threshold worse than 30dB. These results suggested that recently, COMs and cholesteatomas operated received sufficient preoperative treatments for the middle ear inflammation.
Canal down tympanoplasty for middle ear cholesteatoma with mastoid obliteration was performed in 787 ears at Tokai University Hospital between April 1975 and April 1992. These ears were followed up more than five ears, and recurrent cholesteatoma occured in twelve ears (1.5%). Among them we experienced four cases had normal aeration in the tympanic cavity and the epitympanum. In these cases, the cholesteatoma matrix invaded into the mastoid from the posterior shallow wall of the external ear canal. These findings suggested that the mastoid cholesteatoma was caused by the negative pressure in the mastoid and the bony blockage of the aditus because of the mastoid obliteration technique in the initial operation, not by the residual cholesteatoma.
Hearing acuity at higher frequency ranges was investigated by using a tinnitus audiometer. Based on our previous report for normal subjects, we evaluated the effectiveness of the evaluation at higher frequency regions by using a tinnitus audiometer for pathological ears. First, we detected hearing impairment at the higher frequency in those whose hearing thresholds were within normal limits by evaluating the conventional frequency regions. Secondly, it was proved useful in detecting hearing impairment earlier in those who received drug administration such as Cis-platinum. Thirdly, it was useful to divide the type of hearing impairment in downsloping or dip when we detected the hearing impairment at 8kHz. Finally, it is useful to detect the aging effect on hearing. It is our result that the high frequency audiometry above conventional frequency ranges is useful in some pathological ears.
15 patients with dizziness who had already undergone antihypertensive therapy, were administered drugs to improve cardiovascular circulation. Particular diseases were not demonstrated by audiometry, vestibular function tests and magnetic resonance imaging. Dizziness of 14 patients disappeared within four weeks after initiation of treatment for cerebrovascular circulatory disorders. At once low frequency hearing loss improved or tended to improve binaurally. Clincal findings of these patients are summaried below. 1) Dizziness was transient and recurrent, and rotatory or floating sensation was accompanied. 2) Cochlear symptoms, if present, were not related to dizziness. 3) Transient nystagmus was occasionally observed. 4) Directional preponderance was occasionally seen in caloric testing. 5) Bilateral low frequency hearing problem was found.