Biomedical subjects

T C Hain

Publications and source records attributed to T C Hain.

At least 37 records · Page 2Linked to original sources

PubMed1996

Early diagnosis of Usher syndrome in infants and children.

The electroretinogram (ERG) is the only test currently available that has the potential to identify patients with Usher syndrome before onset of fundoscopic and visual abnormalities. The ERG is a noninvasive technique that can diagnose retinitis pigmentosa via measurement of corneal-retinal potentials. Forty-seven children with bilateral severe to profound sensorineural hearing loss were evaluated. Usher syndrome was diagnosed in five children, all of whom subsequently underwent cochlear implantation. We have found that accurate diagnosis of Usher syndrome in infants and young children is possible via ERG. Benefits of early diagnosis include timely counseling regarding genetic issues, educational and vocational placement, and cochlear implantation. For this reason we recommend that all newly identified children with bilateral severe to profound sensorineural hearing loss undergo ERG testing.

Child↗

PubMed1995

Antivertigo medications and drug-induced vertigo. A pharmacological review.

The approach to drug treatment of vertigo is almost exclusively symptomatic. There are 3 major goals for drug treatment of vertigo. The first one is to eliminate the hallucination of motion. Drugs with vestibular 'suppressant' properties are used for this purpose. The major vestibular suppressants are anticholinergic and antihistamine drugs. The second goal is to reduce the accompanying neurovegetative and psychoaffective signs (nausea, vomiting, anxiety). Antidopaminergics are used for this purpose. The third goal is to enhance the process of 'vestibular compensation' to allow the brain to find a new sensory equilibrium in spite of the vestibular lesion. Until now, the pharmacological manipulation of vestibular compensation has been assessed in animals but not in humans with vestibular lesions. Vestibular suppressant drugs delay rather than enhance compensation. A variety of other drugs is also used in the treatment of vertigo, including benzodiazepines, histaminergic agents, sympathomimetics and calcium antagonists. Their mechanism of action is poorly understood. The data base derived from clinical trials evaluating antivertigo medications is often questionable because of methodological limitations. This explains why habits of prescription are mainly empirical, and why striking differences can be noticed from one country to another. We can hope that new treatments may emerge from the present interest in receptor subclasses and neuromodulators of the vestibular system, and we must be ready to evaluate these potential new pharmacological agents with reliable clinical methods in humans.

Animals↗

PubMed1995

Cochlear implants in young children with Usher's syndrome.

Usher's syndrome (US) is an autosomal recessive disorder characterized by congenital sensorineural hearing loss and retinitis pigmentosa. The majority of affected individuals have severe to profound sensorineural hearing loss and are therefore potential cochlear implant candidates. A goal of our otology program has been early identification and implantation of children with US. At our center, early diagnosis of US has been achieved by comprehensive ophthalmologic evaluation including electroretinography. Four of our 19 pediatric cochlear implant recipients with congenital sensorineural hearing loss were identified with US and implanted prior to the onset of signs or symptoms of visual loss. All children have received measurable benefit from cochlear implantation. In light of the dual sensory deficits present in US, the need for early diagnosis and cochlear implantation is of special importance in this population.

Child↗

PubMed1994

Localizing value of optokinetic afternystagmus.

Previous reports have indicated that optokinetic afternystagmus (OKAN) becomes asymmetric after the occurrence of unilateral peripheral vestibular lesions, and suggested that OKAN may be used for localizing the side of the lesion. These studies did not take into account spontaneous nystagmus. We compared OKAN in 12 subjects with unilateral vestibular loss after resection of acoustic neuroma to OKAN in 30 normal subjects. After offsetting the data for spontaneous nystagmus, we calculated the initial amplitude, the time constant, and the slow-phase cumulative eye position (SCEP) parameters of OKAN. The directional asymmetry of parameters to rightward and leftward stimulation were also calculated. The mean SCEP, initial amplitude, and time constant parameters were reduced significantly in the patients, and each also showed a directional asymmetry, such that they were greater for stimulation toward the side of the lesion. The directional preponderance of the SCEP parameter had the highest sensitivity for the side of the lesion, being abnormally elevated in 58.3% of patients with unilateral loss. We conclude that OKAN might be useful in combination with other subtests of a battery, but that by itself OKAN is only moderately sensitive to unilateral peripheral vestibular loss.

Adult↗

PubMed1994

Modified liberatory maneuver: effective treatment for benign paroxysmal positional vertigo.

A modification of the liberatory maneuver was used to treat 25 patients with benign paroxysmal positional vertigo (BPPV). The modified liberatory maneuver relieved symptoms without recurrence in 11 (44%) patients. A partial response was noted in 6 (24%) patients, and there was no improvement in 8 (32%) patients. Follow-up ranged from 1 to 20 months (median 4.0 months). Patient age was not predictive of response to treatment. Duration of symptoms before treatment, however, was greater in nonresponders (median 15.5 months) than in complete (median 5.0 months) or partial (median 3.5 months) responders. The modified liberatory maneuver takes approximately 5 minutes to perform and provides effective treatment in two thirds of patients who suffer from BPPV.

Adult↗

PubMed1994

Characteristics of postural stability in patients with aminoglycoside toxicity.

Postural stability in patients with bilateral vestibular deficits from aminoglycoside toxicity was characterized by examining their ability to use different sensory cues to maintain balance and by recording their automatic postural responses to sudden translational and rotational (pitch) perturbations of the support surface. We found our patients had increased sway on sensory tests in which either visual or somatosensory cues were altered and were unable to maintain their balance when both visual and somatosensory cues were altered compared to age-matched normal subjects. The amount of vestibular loss, as inferred from the VOR Tc, accounted for a significant amount of A-P sway on test 4 in which somatosensory cues were altered. The frequency response of anterior-posterior sway in the BVL group suggests that they use more hip movements than do normal subjects to maintain postural stability. The responses of BVL patients to sudden translations of the support surface did not differ from those of normal subjects. More BVL patients lost their balance, however, on the initial trial of the toes-up rotational perturbation of the support surface than did normal subjects.

Adult↗

PubMed1992

Velocity storage in labyrinthine disorders.

We studied 13 patients with unilateral peripheral vestibular lesions following removal of acoustic neurinomas. The time constant of the VOR after surgery was 6.4 +/- 2.6 seconds (normal is 18.5 +/- 7.7 seconds). The time constant of OKAN after surgery was 7.2 +/- 1.8 seconds (normal is 11.3 +/- 3.2 seconds). The mean initial velocity of OKAN after surgery was 9.7 +/- 2.4 deg/second (normal is 11.7 +/- 5.9 deg/second). These data suggest that unilateral peripheral vestibular loss is associated with a complete loss of velocity storage for canal input but only a partial loss of velocity storage for visual input. These results can be accounted for by current mathematical models of the velocity storage mechanism.

Humans↗

PubMed1992

Slow cumulative eye position to quantify optokinetic afternystagmus.

In 30 normal subjects we computed the slow cumulative eye position (SCEP) of optokinetic afternystagmus (OKAN) that followed 60 seconds of full-field optokinetic stimulation at 60 degrees/s. The mean SCEP was 112.8 degrees +/- 65.0 degrees. The lower and upper fifth percentile limits for directional preponderance of the SCEP were -38.8% and 44.3%, respectively. The time constant, which we calculated by dividing the SCEP by the initial velocity, was 12.0 +/- 7.4 seconds. This value is nearly identical to the time constant obtained from semilogarithmic regression of the decay of OKAN slow-phase velocity versus time. We conclude that the SCEP is a good measure of OKAN and that it reflects the substantial amount of variability and directional asymmetry observed in the optokinetic responses of normal subjects.

Algorithms↗

PubMed1992

Clinical implications of otolith-ocular reflexes.

While difficult to test clinically, otolith-induced vestibular responses play an important role in both vestibulo-ocular and vestibulo-spinal reflexes, and are likely a source of symptoms in patients with vestibular disorders. Here we review basic aspects of otolith-induced vestibulo-ocular reflexes and consider some clinical implications of disordered otolith function. Emphasis is placed on ocular responses to translation and to tilt and the influence of gravity on vestibulo-ocular responses induced during head rotation.

Adaptation, Physiological↗

PubMed1991

Microsaccadic flutter.

Microsaccadic flutter is a rare symptomatic saccadic oscillation that has been reported only twice previously. Here we describe 5 patients with this disorder. The oscillation is horizontal, has a frequency of 15-30 Hz, an amplitude of 0.1-0.5 degrees, and cannot be seen with the unaided eye. It is usually not associated with any underlying neurological disorder. We hypothesize that microsaccadic flutter is due to malfunction of the brainstem omnipause neurons.

Abducens Nerve↗

PubMed1991

Abolition of optokinetic afternystagmus by aminoglycoside ototoxicity.

We studied optokinetic afternystagmus in eight subjects with loss of or impairment of vestibular function due to ototoxic antibiotics. We found that the initial amplitude, the time constant, and the slow-phase cumulative eye position of optokinetic afternystagmus were significantly reduced in the patients. Slow-phase cumulative eye position most reliably distinguished our patients' responses from those of a normal group.

Adult↗

PubMed1990

Static roll and the vestibulo-ocular reflex (VOR).

We measured the effect of static lateral tilt (roll) on the gain and time constant of the vestibulo-ocular reflex (VOR) in five normal subjects by recording both the horizontal and vertical components of eye velocity in space for rotation about an earth vertical axis with the head either upright or rolled to either side. The time constant of the VOR in the upright position was 19.6 +/- 3.2s (mean +/- standard deviation). The time constant of the horizontal component with respect to the head decreased to 15.7 +/- 4.0s for 30 degrees roll and to 12.7 +/- 2.7s for 60 degrees roll. The time constant of the vertical component with respect to the head was 11.0 +/- 1.4s for 30 degrees roll and 7.5 +/- 1.6s for 60 degrees roll. The gain of the horizontal VOR with respect to space did not vary significantly with roll angle but a small space-vertical component to the VOR appeared during all rotations when the head was rolled away from upright. This non-compensatory nystagmus built up to a maximum of 2-3 degrees/s at 17.0 +/- 4.7s after the onset of rotation and then decayed. These data suggest that static otolith input modulates the central storage of semicircular canal signals, and that head-horizontal and head-vertical components of the VOR can decay at different rates.

Adult↗

PubMed1990

Optokinetic nystagmus and afternystagmus in human beings: relationship to nonlinear processing of information about retinal slip.

In four normal human subjects we measured eye movements during full-field optokinetic stimulation (10-220 deg/s) and determined the relationship among retinal-slip velocity (drum velocity minus slow-phase eye velocity), the slow-phase velocity of optokinetic nystagmus (OKN) and the initial value of the slow-phase velocity of optokinetic afternystagmus (OKAN) measured in darkness. OKN and OKAN were maximum (63-84 and 11-19 deg/s, respectively) when retinal slip ranged from 30-100 deg/s. For higher values of retinal slip, OKN and OKAN fell (in 3 subjects) or reached a plateau (in the fourth). The amplitude of OKAN in human beings was much less than that reported in monkeys. The shape, however, of the curve relating retinal slip to the amplitude of OKAN was similar to that of monkeys. Furthermore, in both cases the curve resembles that obtained by plotting the results of experimental recordings of neural discharge in the nucleus of the optic tract as a function of retinal slip. These results imply that the processing of visual information for generation of OKAN is similar in monkeys and human beings but that the gain of the system is much less in human beings. We also found that fixation of a small target during optokinetic stimulation nearly completely prevented the development of OKAN while fixation of a small target for short periods after optokinetic stimulation did not alter the pattern of decay of OKAN. Thus, fixation may actively prevent the coupling of visual information into the velocity-storage mechanism.

Adult↗

PubMed1990

Ipsiversive eye deviation and epileptic nystagmus.

We studied an 11-year-old boy with focal seizures in the right temporo-occipital cortex. During the seizure, there was a 1- to 2-second period of ipsiversive (rightward) conjugate eye deviation, followed by 10 to 15 seconds of horizontal jerk nystagmus with slow phases that were directed to the right and appeared linear. The patient was conscious throughout the seizure. These findings fit the description of epileptic nystagmus. We postulate that the eye deviation and slow phases of the nystagmus in this patient were induced by epileptic activation of a cerebral smooth pursuit pathway originating from temporoccipital cortex.

Child↗

PubMed1990

Phoria adaptation in patients with cerebellar dysfunction.

The authors studied phoria adaptation to horizontal base-out prism in 17 patients with well-documented cerebellar lesions. There was no significant difference between mean adaptation measured in the patients and ten normal controls. Individually, normal adaptation was found in 12 patients. Abnormal adaptation was found in five patients, all but one of which had other neurologic lesions. These results suggest that phoria adaptation to base-out prism is not diminished by a cerebellar lesion unless it is accompanied by another nervous system lesion(s).

Adaptation, Ocular↗

PubMed1989

Central adaptation models of the vestibulo-ocular and optokinetic systems.

A theoretical analysis of two models of the vestibulo-ocular and optokinetic systems was performed. Each model contains a filter element in the vestibular periphery to account for peripheral adaptation, and a filter element in the central vestibulo-optokinetic circuit to account for central adaptation. Both models account for 1 adaptation, i.e. a response decay to a constant angular acceleration input, in both peripheral vestibular afferent and vestibulo-ocular reflex (VOR) responses and 2 the reversal phases of optokinetic after-nystagmus (OKAN) and the VOR and 3 oscillatory behavior such as periodic alternating nystagmus. The two models differ regarding the order of their VOR transfer function. Also, they predict different OKAN patterns following a prolonged optokinetic stimulus. These models have behavioral implications and suggest future experiments.

Adaptation, Physiological↗

PubMed1989

Optokinetic afternystagmus in humans: normal values of amplitude, time constant, and asymmetry.

It has been suggested that the appearance of directional asymmetry and/or a reduced time constant of optokinetic afternystagmus (OKAN) might be a clinical index of vestibular imbalance. However, we do not know the limits for OKAN parameters in normal humans. Accordingly, we studied OKAN in 30 normal subjects using a "sampling" method, in which a number of values of OKAN are obtained by turning out the lights periodically during optokinetic stimulation. We found that the initial velocity of OKAN has a large intrasubject variability. Accordingly, if precision is desired so as to obtain 95% confidence that the measured mean of the initial velocity of OKAN is within 25% of the true mean in an individual subject, at least eight measurements of the initial OKAN velocity must be taken. When 12 measurements are made, all subjects had a minimum value of 5 degrees/s initial OKAN, and there was little directional asymmetry (mean of -0.47 degree/s +/- 3.13 degrees/s). The intrasubject variability of the time constant of OKAN was similar to the variability of initial OKAN velocity. However, because it is not possible to obtain repeated measures of the time constant in a short period of time, the time constant of OKAN is less likely to be useful in clinical testing.

Adult↗

PubMed1989

Vergence.

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Convergence, Ocular↗