Labyrinthine exercises in the treatment of diseases characterized by vertigo: their physiologic basis and methodology.
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Vertical nystagmus provoked by simultaneous bilateral caloric stimulation has been known since 1907 (Bàràny). However, if a controlled and calibrated injection os water at 44 degrees C or 30 degrees C for 30 seconds at a flow rate of 250 ml/minute is given in normal subjects, this stimulus is insufficient to provoke a response, whilst in subjects with a central vestibular disorder there appear upward vertical movements with hot stimulation and downward movements with cold stimulation. The degree of this response is proportional to the degree of horizontal nystagmic responses to classical unilateral caloric tests. The authors feel that vertical nystagmic responses to simultaneous bilateral caloric stimulation reflect a loss of control of the vestibular reflex activity of the superior semicircular canals.
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Experiments were conducted to quantify the effect of a vestibular stimulation of known magnitude on a constant optokinetic nystagmus (OKN). Ten normal human subjects were tested with varying magnitudes of vestibular stimuli that were superimposed on a constant 30 degrees optokinetic stimulus. The gain of the vestibular system in the dark was 0.42 +/- 0.11, and the gain in the light during superimposition testing was 0.12 +/- 0.02. From these results, predictions were made that the degree of vestibular imbalance necessary to produce an asymmetric OKN would generate a spontaneous nystagmus in the dark, which would be equivalent to 20 to 30 degrees. Data from a large group of patients were used for corroboration of the results.
Recent evidence from experiments in animals suggests a rationale for more effective pharmacologic and physical therapy in patients with vertigo. In particular, one must consider the possible effects of medications on the adaptive processes that naturally mediate recovery from vestibular lesions. The challenge now is for clinicians to devise medication and exercise regimens for patients with vestibular disturbances and critically (and quantitatively) evaluate their effects.
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Fifty-two consecutive temporal bones of infants who died neonatally, or in utero of natural causes, were studied. Complete autopsies were performed. Twenty-eight infants had a variety of pulmonary disorders which resulted in severe respiratory distress prior to their death. Of these, the majority had bleeding intracranially and into the inner ear. There were five major pathways of central nervous system and subarachnoid hemorrhage involvement of the inner ear: 1) the modiolus, 2) cochlear aqueduct, 3) retrograde via the cochlear vein, 4) episodes of spontaneous bleeding into various compartments of the inner ear, and 4) hemorrhage via the otic capsule. The remaining 24 infants died of other natural causes. Two had CNS bleeding with no extension to the inner ear. We propose that there is a syndrome which consists of 1) neonatal respiratory distress, 2) intracranial hemorrhage, and 3) bleeding into the inner ear--an extension of a subarachnoid or subependymal matrix bleeding diathesis.
The vessels emerging from one side of the basilar artery are supplied exclusively by the homolateral vertebral artery. Since blood flow is laminar through the vertebrobasilar system, mixing between two sides does not normally occur. Based on this fact, an experimental model for research on cochlear hypoxia is proposed and described. The animal's own blood flow in the vertebral artery is completely replaced by a stream of poorly oxygenated blood injected retrogradely through the ipsilateral axillary artery. In this way, the territory supplied by the vessels emerging from this side of the basilar artery, including the ear, is rendered hypoxic. The changes in the cochlear action potentials induced by the reduced oxygen supply are recorded by a chronically implanted electrode and analyzed.
The dynamic stability of the head in pitch during normal upright posture has been studied in normal subjects and patients with neurological disease affecting neck muscle tone by examining angular head acceleration responses to unpredictable linear motion of the trunk in the direction of surge. Within the frequency range of natural head movements the transfer function between head and trunk for both normal subjects and patients approximated a second-order linear differential equation involving inertia and coefficients of viscosity and elasticity. The degree of neck rigidity was determined by the damping ratio (viscosity:elasticity), which averaged .35 for normal subjects and ranged from 0.6 to 0.96 for patients with rigid syndromes. A patient with absent labyrinthine function and a "floppy" head had a damping ratio 0.18. The technique gives a numerical measurement of neck rigidity, which could be of value in characterising severity of disorder and response to therapy.
Head movement-dependent oscillopsia (HMDO) with peripheral vestibular, brainstem and cerebellar lesions is reviewed. The differentiation of this kind of oscillopsia is based mainly on clinical grounds. HMDO with bilateral abolition of caloric responses, and in the absence of disease of the central nervous system, is due to bilateral vestibular disease. HMDO in patients with internuclear ophthalmoplegia and other brainstem signs is probably due to a lesion of VOR pathways in or near the medial longitudinal fasciculus. The occurrence of HMDO with ataxia of gait and cerebellar eye movement disorders (rebound nystagmus, flutter-like oscillations), in the absence of brainstem lesions (medial longitudinal fasciculus), is clinical evidence for HMDO due to a cerebellar lesion. An attempt is made to associate the different kinds of oscillopsia with current knowledge of the vestibulo-ocular reflexes.
Local placement of chloroform in either the external or the middle ear has been previously reported to induce a chemical labyrinthectomy. In order to examine the value of this effect as a research tool, we injected chloroform into the middle ears of guinea pigs and rats. Cochlear damage was assessed by electrocochleography (ECochG) and auditory brainstem response (ABR) audiometry. Both species developed complete deafness within a few hours after instillation of the chloroform. The deafness was permanent in the guinea pigs, whereas there was a partial recovery of auditory function in the rats. The survival rate of the auditory nerve fibers was estimated by measuring the ABR evoked by electrical stimulation via the scala tympani (EABR). A normal EABR recruitment pattern suggested that the main chloroform effect was located peripheral to the afferent axons. In conclusion, chloroform must be considered a severely ototoxic agent when applied locally.
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HLA typing of ten patients with well documented Cogan's syndrome failed to support previous reports of an increased incidence of HLA-B17. Although HLA-A9 (Aw24), Bw35, and Cw4 appeared increased in frequency among patients, the small number of cases precluded attaching importance to the significance of these increased frequencies.
In this study, H-reflex testing was used to identify possible static vestibular influences on soleus alpha motoneuron excitability in man in relation to different body tilts. Ten normal adult volunteers and one labyrinthine-defective patient were tested in an experimental situation designed to minimize all afferent inputs except the vestibular ones. Each subject was fixed to a rigid platform inclinable from the horizontal (0 degree) to the vertical (90 degrees) position and vice versa. On each subject, 10 consecutive H reflexes were recorded for each of the following positions: 0 degree, 15 degrees, 30 degrees, 45 degrees, 60 degrees, 75 degrees, 90 degrees and 90 degrees, 75 degrees, 60 degrees, 45 degrees, 30 degrees, 15 degrees, 0 degree. In all normal subjects, we observed a significant increase in amplitude of the H reflex as the body was tilted from horizontal to vertical, and a significant decrease when the body was returned to the original position. These progressive changes in spinal motoneuron excitability were linearly related to the tilt angles. By contrast, no significant change in H-reflex amplitude was observed in the labyrinthine-defective patient. These results would seem to indicate that the vestibular system exerts some influences on antigravity muscles in static tilts and that these influences are behaviorally adequate to provide for the postural stability.