Labyrinth

LABYRINTH (labyrinthus), a bony and membranous formation contained in the pyramid of the temporal bone and forming the inner ear (anatomy, physiology-see Inner ear; inflammatory diseases of the labyrinth-see Labyrinthitides).-Among non-inflammatory diseases of the labyrinth, the following are distinguished: 1) injuries to the labyrinth, 2) degenerative-atrophic-dystrophic lesions of the labyrinth, 3) neurovegetative lesions in the labyrinth, 4) lesions of the labyrinth in tumors of the posterior cranial fossa.- Injury to the labyrinth can occur in two ways-direct and indirect. Direct injury is usually caused by the penetration of sharp objects through the windows (such as: a needle during paracentesis, the end of a pin when cleaning the external auditory canal) and gunshot wounds. Symptoms: dizziness, spontaneous nystagmus, sharp reduction in hearing, and sometimes leakage of cerebrospinal fluid. Only in rare cases do gunshot injuries with loss of function of the entire inner ear not lead to a fatal outcome. The location of the bullet is determined by X-ray examination. Treatment initially consists of complete rest; however, if later a traumatic serofibrinous or purulent labyrinthitis develops with a tendency to spread beyond the inner ear, there is an absolute indication for labyrinthotomy. In the presence of a bullet in the middle ear with complete loss of function of the inner ear, removal of the bullet by radical mastoidectomy is recommended. Indirect injury to the labyrinth usually occurs in the following ways: 1) a blow to the head or concussion of the entire body (fall, bruise, collapses), 2) a sharp change in air pressure in the external auditory canal (a blow to the ear), 3) a single exposure to loud sounds, 4) constant exposure to strong sound stimuli (professional noise). In the vast majority of cases, injury to the labyrinth is accompanied by commotio cerebri, so that along with objective and subjective changes in the labyrinth, similar changes may also be observed in the psyche and nervous system. Deafness, as well as sharply reduced (sometimes increased) excitability of the vestibular system in the presence of dizziness, are often caused by the aforementioned factors. The consequences of labyrinthine injury may prove particularly fatal for the patient if, prior to the injury, purulent otitis had been noted. In such cases, complete deafness or labyrinthogenic meningitis with a fatal outcome is often observed. In the injuries noted, various patho-anatomical changes may be observed, ranging from microscopic hemorrhages (commotio labyrinthi) to ruptures, i.e., fractures of the labyrinthine capsule, which is most commonly observed in fractures of the base of the skull. In most cases, these fractures are localized in the area of the pyramid [see separate table (255-256), fig. 5]. In cases of commotio labyrinthi where only temporary functional impairment is observed (rapidly passing dizziness, spontaneous nystagmus, noise in the ears, reduced hearing, hypesthesia, or sometimes hyperesthesia of hearing), the basis is paralysis of the vasomotor apparatus of the labyrinth. As a result, passive hyperemia occurs in the labyrinth. In severe concussions, extravasates up to hemorrhages are also observed. In such cases, clinical manifestations are more pronounced and persistent: noise in the ears, reduced hearing become permanent, while dizziness may disappear over time, labyrinthine reactions to caloric and rotational stimuli may vary in intensity.- Treatment. In cases not complicated by an inflammatory-purulent process requiring surgical intervention (see Skull), complete rest is necessary. Subcutaneous preparations of strychnine, pilocarpine, internally-iodine. In the presence of symptoms from the nervous system-general strengthening treatment, hydrotherapy. The prognosis for the return of lost function is uncertain. The clinical equivalent of the degenerative-atrophic process in the labyrinth is the so-called labyrinthine deafness, which occurs either with or without a vestibular syndrome. Symptoms: with normal eardrums, hearing gradually decreases, sometimes reaching complete deafness, with shortened bone conduction as well as air conduction for high tones, and lateralization of sound to the healthy ear, and often changes in the functions of the semicircular canals (vestibular syndrome-dizziness, reduction or absence of reaction to caloric and rotational stimuli). Patho-histologically, a primary degenerative process is observed in the area of the sensory epithelium in the Corti organ (auditory spots and ampullary crests) with a complete absence of inflammatory phenomena. The causes of these phenomena are definitely unknown. Recent investigations by Wittmaack indicate that the genesis of this process is due to a qualitative disturbance of labyrinthine fluid (reduced alkalinity). Reduced alkalinity of labyrinthine fluid is observed in a number of chronic constitutional diseases (nephritis, diabetes, lymphomatosis, tertiary syphilis, congenital syphilis, cachexia of various etiologies), in which increased acidity of the blood with symptoms of labyrinthine deafness has been established. Similar disturbances in the secretory activity of the labyrinthine epithelium can be caused by the presence of toxins due to metabolic disorders and endocrine organs. The prognosis for functional recovery is unfavorable. Treatment is exclusively causal. Almost identical clinical manifestations are observed in lesions of the inner ear caused by new formations in the posterior cranial fossa (tumors of the cerebellopontine angle, resp. tumor nervi acustici). To the manifestations noted from the cochlear apparatus are added vestibular nuclear symptoms, which are caused not only by lesions of the labyrinth but also of the medulla oblongata and pons. They manifest as large-amplitude nystagmus and spontaneous past-pointing. The main differential point for degenerative atrophic processes in the labyrinth is the complete absence of both general symptoms of nervous system lesions and otoneurological symptoms (spontaneous large-amplitude nystagmus, spontaneous past-pointing), characteristic of processes in the posterior cranial fossa. Due to the extreme branching of the n. acustici in the central nervous system, even a slight disease of the brain with a certain localization should affect the function of this nerve. Indeed, in organic nervous and mental diseases, symptoms caused mainly by lesions of the n. vestibularis are observed. In some cases, vestibular syndromes predominate over others to such an extent that the entire clinical picture of the disease is colored by them. These cases must be considered as vestibular neuroses. N. vestibularis (labyrinthine nerve) in the inner ear is connected with the sympathetic nervous system through the cervical sympathetic ganglion, and therefore, considering the important role played by the autonomic nervous system in the pathogenesis of neuroses and in the process of vascular innervation, it becomes understandable how changes in this area can affect the function not only of the auditory nerve located in the inner ear but also throughout its course in the brain. That is why the entire vestibular symptom complex observed in neuroses should be considered as a consequence of lability of the autonomic, especially vasomotor, system, which is caused by circulatory and innervation disorders in the area of the labyrinth. These disorders manifest themselves both from the n. cochlearis (cochlear nerve) and the labyrinthine nerve, either as irritative phenomena or as loss of function. Thus, noise in the ears, hearing impairment, painful auditory sensations, dizziness, disturbance of equilibrium, spontaneous nystagmus, pathological reactions to nystagmus, spontaneous and atypical experimental past-pointing are observed. All these phenomena were designated by older authors and continue to be without reason called the symptom complex of Ménière (it would be correct to call them the vestibular symptom complex). From this group of diseases, several forms with a well-defined clinical picture can be distinguished, namely: angioneurosis of the eighth nerve (octavopathia angioneurotica). Symptoms: noise in the ear, sudden weakening of hearing, pallor of the face, nausea, sometimes vomiting, dizziness. These phenomena quickly pass with the appearance of normal facial color. To this same category of angioneuroses belongs another form-the type of Lermoyez; begins with noise in the ears, a sensation of a plug in one or both ears, whispered speech is perceived as sharply shortened, tuning fork C₁₂₈ through air is barely audible; Weber's symptom in both the healthy and diseased ear. Such a state of varying intensity can last from several minutes to 10-12 hours, until suddenly dizziness appears (a heavy sensation described by patients as "nausea," inability to look at light, sometimes a sensation of movement with the bed, sometimes nystagmus toward the diseased side and pulling pains in the neck and diseased ear), lasting several hours, after which hearing returns almost to normal.

Since after vertigo hearing appears, Lermoye gave this type of vertigo the name 'le vertige, qui fait entendre' (vertigo that causes hearing). Finally, one must observe vestibular attacks in the complete absence of cochlear pathological phenomena. In such cases, a sharply expressed enophthalmus is noted. Unlike the type just noted, another form is observed with similar symptoms, but where after the vertigo appears, hearing does not recover, but gradually, with the increasing frequency of vertigo attacks, hearing and labyrinthine function fade away. These are the cases that were described by Meniere at the time. The following patho-anatomical and physiological changes may underlie the above-mentioned symptom complexes. Considering the presence of lesions of the sympathetic nervous system and the endocrine system in these diseases, it must be assumed that they can cause a change in the chemical composition of the endolymphatic fluid in the inner ear. As a result, a whole range of processes may occur, starting from edema with an increase in intralabyrinthine pressure of an intermittent nature up to the formation of atrophic-degenerative changes. In the presence of changes in the nucl. triangularis, a similar symptom complex is obtained, but most often without phenomena of disturbance from the side of the cochlear apparatus. The changes may be caused not only by the above-mentioned circumstances, but also by exogenous and endogenous intoxication (nephritis, diabetes, gout, leukemia, encephalitis, arteriosclerosis, tbc, worms, botulism). Thus, this circumstance must be taken into account in the differential diagnosis of vestibular neuroses. Vegetative vasomotor disorders of the ear in general constitute partial phenomena of the general vascular neurosis. Often the phenomena of the general vascular neurosis are weakly expressed, and the entire picture of the disease is colored by labyrinthine symptoms. Thus, the diagnosis of vegetative neurosis is often made on the basis of an analysis of labyrinthine symptoms. Subjective noises in the ear in neurotics - a frequent symptom. Neuroses are observed where exclusively ear noises are noted. No less a frequent symptom in neurotics is intermittently occurring vertigo, but not in the form of an attack with the above-mentioned violent phenomena, but in the form of unsteadiness when standing with eyes closed and trembling of the eyelids with a tendency to fall backward, sensation of rotation of objects, loss of balance when fixing moving objects (visual vertigo), sensation of a receding support of one's own body ('tactile vertigo'). Thus, at the basis of the concept of 'vertigo' there is a deceptive sensation regarding the relationship between the personality and surrounding space. Ultimately it is caused by direct or indirect irritation of the vestibular system. In neurotics, this latter method (deep breaths) especially succeeds in causing vertigo and even spontaneous nystagmus. Caloric examination of labyrinthine function in such cases notes a motley picture, starting from sharply increased excitability, ending with almost complete suppression. Sometimes normal excitability is noted. Treatment. Since we are dealing with a lesion of the autonomic nervous system, it must be assumed that along with other phenomena, spasm or dilation of blood vessels may sometimes occur. Thus, therapy should be carried out in two directions: 1) depending on the clarified etiology, therefore causal, and 2) symptomatic, i.e., along the line of action on the autonomic nervous system and increased intralabyrinthine pressure (Adrenalin, 10% Calc. chlorati orally, Alenil 5-10 cm³ intravenously, atropin 0.0005 pro dosi, Sol. Natrii rhodanati 1.5 : 200.0, hot water bottles on the legs, laxative, Luminal, Salyrgan intravenously, endocrine preparations). In addition - action on the general neurosis by the application of physical and psychotherapeutic procedures.