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Biomedical subjects

R W Baloh

Publications and source records attributed to R W Baloh.

At least 181 records · Page 10Linked to original sources
PubMed1981

Arnold-Chiari malformation: improvement in eye movements after surgical treatment.

We studied abnormalities of eye movement in five patients with Arnold-Chiari malformation before and after suboccipital decompression. Before operation all patients complained of oscillopsia at rest and visual blurring of fixated targets during and immediately after their heads were in motion. Three patients had downbeat nystagmus, one patient had horizontal nystagmus in the primary position and on eccentric gaze and one patient had rotatory nystagmus on lateral gaze only. Smooth pursuit, optokinetic nystagmus and fixation suppression of vestibular nystagmus were markedly impaired. Within two months after operation nystagmus in the primary position had resolved in three patients, and four had complete to near-complete resolution of nystagmus in all gaze positions over subsequent months. Oscillopsia decreased concurrently. affording significant functional visual improvement. One patient had only slight functional improvement and continued to have prominent nystagmus seven years after operation. Smooth pursuit, optokinetic nystagmus and fixation suppression of vestibular nystagmus improved in all patients, but none had complete recovery at the higher velocities of stimulation. They still complained of visual blurring associated with head motion, probably due to the poor fixation suppression of vestibular nystagmus. Our findings suggest that abnormalities of eye movement in Arnold-Chiari malformation are due to compression of the herniating cerebellum against the caudal brain-stem and not a congenital aberrancy of oculomotor pathways. Nystagmus resolved more readily than pursuit or fixation suppression abnormalities, but most patients showed gradual improvement in all abnormalities four months after operation.

Adult↗
PubMed1981

Eye movements in patients with Wallenberg's syndrome.

We studied electro-oculographic and videotape recordings of eye movements in six patients with Wallenberg's syndrome. With fixation, all patients had a spontaneous rotatory nystagmus with the fast phase directed toward the intact side. With loss of fixation, the patients' eyes deviated tonically toward the side of the lesion. Voluntary and involuntary saccades had larger amplitude when directed toward the side of the lesion than away from it. The spontaneous nystagmus predictably interacted with all slow eye movements, producing asymmetric smooth-pursuit, optokinetic, and vestibular responses. In addition, smooth-pursuit and optokinetic responses were decreased significantly in both directions compared to normal subjects. Fixation suppression of vestibular nystagmus also was impaired in both directions. We concluded that two different types of oculomotor bias were present in these patients--a velocity bias and a position bias. The former resulted from damage to the caudal lateral vestibular nuclei, and the latter from interruption of cerebellopontine pathways.

Adult↗
PubMed1981

Downbeat nystagmus: a type of central vestibular nystagmus.

We used electrooculography to study horizontal and vertical eye movements in 17 patients with downbeat nystagmus (Chiari malformation, 9; multiple sclerosis, 2; olivopontocerebellar atrophy, 2; brainstem infarction, 2; and idiopathic nystagmus, 2). In all patients the velocity of slow components of the spontaneous nystagmus increased on lateral gaze, remained relatively unchanged with loss of fixation, and increased markedly after rapid positional changes in the sagittal plane. Horizontal and vertical smooth pursuit was impaired in all patients. Vertical pursuit recordings at multiple ramp velocities suggested superimposition of the spontaneous nystagmus on attempted pursuit rather than selective impairment of downward pursuit. Finally, all patients had impaired fixation suppression of vestibular nystagmus when they were rotated with a fixation point moving with their head. We conclude that downbeat nystagmus is a type of central vestibular nystagmus resulting from an imbalance in the central vertical vestibuloocular pathways.

Adolescent↗
PubMed1981

A study of congenital nystagmus: vestibular nystagmus.

The vestibulo-ocular response (VOR) to rotatory stimuli was studied by electro-oculography in 41 patients with congenital nystagmus. The pattern of the VOR and the gain of the slow component velocity (peak eye velocity/peak chair velocity) were normal in 55 per cent of the patients. In 10 per cent of patients an abnormal pattern of the VOR in which the eyes deviated tonically in the direction of the slow component of the VOR was found. In these patients a mild defect in the generation of vestibular fast components might be present since the slow component velocity (SCV) appeared to be normal, but the amplitude and frequency of fast components were decreased. Thirty-two per cent of patients demonstrated persistence of an intense nystagmus with eyes opened in the dark. However, summation of the smooth movement velocity of the nystagmus and the SCV of a probably normal VOR could be demonstrated. The VOR was basically normal in patients with congenital nystagmus with or without associated ocular lesions.

Electrooculography↗
PubMed1980

Effect of aging on eye tracking.

The visually controlled eye tracking systems (saccadic, smooth pursuit, and optokinetic) were compared in 25 young and middle-aged normal subjects (mean age, 42 years), 14 elderly patients with vertebrobasilar insufficiency (VBI) (mean age, 67 years) and 14 elderly normal subjects (mean age, 65 years). The young normal subjects were consistently superior to both elderly groups on all measurements, but there was no significant difference between the performance of patients with VBI and the elderly normal subjects. This study emphasizes the critical importance of taking age into consideration when evaluating saccades, smooth pursuit and optokinetic nystagmus.

Adult↗
PubMed1980

Ocular lateropulsion. A sign of lateral medullary disease.

Four patients with clinically localized lesions in the lateral medulla exhibited a tonic bias of their eyes toward the damaged side despite full extracular movements. Each reported that his eyes were being pulled toward the involved side. Although the tonic bias was most prominent when fixation was inhibited, it also occurred with fixation and interfered with saccadic and smooth-pursuit eye movements. Saccades were hypometric when directed against the bias, whereas they were hypermetric when directed toward the side of the lesion. Smooth pursuit toward the intact side was severely impaired, whereas pursuit in the direction of the bias was normal or near normal. Lateropulsion of the eyes seems to be a unique sign of disease in the lateral medullary region of the brainstem.

Adult↗
PubMed1980

Quantitative eye tracking tests in lead workers.

A microcomputer system for on-lone analysis of saccadic and smooth-pursuit tracking eye movements is described. Results from a longitudinal study of lead workers and matched controls reveal a consistent decrease in saccade accuracy in the lead workers compared to the controls. Saccade peak velocity and latency and smooth pursuit were not significantly different in the two groups. The abnormal saccade accuracy measurements may indicate a subclinical effect of increased lead absorption, but because of the large scatter in normal values, saccade accuracy measurements are not a reliable indicator of early lead toxicity in a single lead worker.

Environmental Exposure↗
PubMed1980

Optokinetic nystagmus and parietal lobe lesions.

In an attempt to define better the mechanism of impaired optokinetic nystagmus (OKN) caused by parietal lobe lesions, we recorded the eye movements of two patients. One had a slowly enlarging parietal glioma, and the other, an infarction involving the parietal and occipital lobes. In both patients, ipsilateral foveal pursuit and full-field pursuit of a surrounding optokinetic drum were impaired while voluntary and involuntary saccades (fast components) were normal. Foveal pursuit was impaired more than full-field pursuit, suggesting the existence of two separate pathways by which visual signals for OKN slow phases reach the oculomotor centers in the brainstem. We conclude that the ipsilateral slow phase OKN deficit seen in our patients resulted from damage to the foveal pursuit pathway that runs from the occipitoparietal association area to the ipsilateral brainstem horizontal gaze center.

Adult↗
PubMed1980

Identification of the location of vestibular lesions on the basis of vestibulo-ocular reflex measurements.

Quantitative analysis of electro-oculographic recordings of eye movement in response to precise visual and vestibular stimuli makes possible the differentiation of three categories of vestibular syndromes due to pathological changes in three different parts of the visual vestibulo-ocular reflex arc: (1) decreased vestibulo-ocular reflex gain (e.g., decrease in slow component velocity), but normal fast components and visual-vestibular interaction (labyrinth and eighth nerve); (2) normal slow component velocity but abnormal fast components to all stimuli (pontine or medullar reticular formation); and (3) normal slow component velocity to vestibulo-ocular stimulaton but abnormal visual-vestibular interaction as well as normal fast components (visual-motor pathways or cerebellum).

Cerebellar Diseases↗
PubMed1980

Study of congenital nystagmus: optokinetic nystagmus.

A severe defect of optokinetic nystagmus (OKN) was found in 46 patients with congenital nystagmus. Abnormal patterns of OKN, such as superimposition of pendular oscillations on the optokinetic slow component and inversion of OKN, were observed. Optokinetic gain (eye movement velocity/drum velocity) was decreased compared to that in normal subjects, and optokinetic after-nystagmus, or transient persistence of OKN after cessation of visual stimulation, was absent. These findings suggest that there is a defect in the subcortical optokinetic system in congenital nystagmus. Optokinetic responses did not clearly differentiate patients who had ocular lesions that impair vision, such as ocular albinism and opacities of the ocular media, from patients who did not have such lesions. Similar abnormal patterns of OKN were found in both groups of patients, although optokinetic gain tended to be lower in patients with ocular lesions than in those without lesions.

Electrooculography↗
PubMed1980

On-line analysis of eye movements using a digital computer.

We describe a microcomputer system for on-line analysis of eye movement recordings. Quantitative data from the patient and statistical comparison with normative data is available within seconds of test completion. Three types of eye movements are analyzed--voluntary saccades, smooth pursuit, and nystagmus. The first two are induced by a computer-controlled laser dot projected onto a screen and the third by a computer-controlled optokinetic drum, caloric infusion, and rotatory chair. The computer algorithm differentiates the eye position signal to yield an instantaneous eye velocity record. Saccades are identified based on their characteristic velocity profile. For pursuit and nystagmus. The first two are induced by a computer-controlled laser dot projected onto a screen and the third by a computer-controlled optokinetic drum, caloric infusion, and rotatory chair. The computer algorithm differentiates the eye position signal to yield an instaneous eye velocity record. Saccades are identified based on their characteristic velocity profile. For pursuit and nystagmus, the velocity record is modified by linearly interpolating across segments in which saccades occurred. The gain (output eye velocity/input eye velocity) is calculated after Fourier analysis of the data.

Computers↗
PubMed1980

Subclinical effects of chronic increased lead absorption--a prospective study. III. Neurologic findings at follow-up examination.

Neurologic examination, nerve conduction testing and electro-oculographic testing have been performed at a baseline examination and a follow-up examination in a group of lead workers with blood lead levels predominantly between 60 and 80 micrograms/dl and in a group of control workers. A statistically significant decreased saccade accuracy measurement in the lead workers compared to the controls was found at both examinations. No other simple test or pattern of findings differentiated between the lead workers and the controls, and the biological significance of the lower saccade accuracy is not clear. Nerve conduction measurements do not appear to be a satisfactory method of detecting subclinical neurologic effects of lead exposure.

Humans↗
PubMed1979

Modification of constant optokinetic nystagmus by vestibular stimuation.

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.

Adult↗
PubMed1979

Uniocular nystagmus in monocular visual loss.

Uniocular nystagmus was studied by electro-oculography in ten patients with monocular visual loss caused by ocular and optic nerve lesions. In these patients, visual loss was congenital or acquired in childhood or adult life. In all patients the oscillations were present in the primary position of gaze and were vertical, pendular, and of variable and low frequency (less than, or equal to, 1.0 HZ) and amplitude (usually less than 5 degrees). Refixation saccades, smooth pursuit, optokinetic nystagmus, and vestibuloocular responses to rotation in the horizontal and vertical planes were within normal limits. The irregularity, low frequency, and low amplitude of this form of nystagmus cause it to often be missed during casual clinical examination, but easily differentiate it from other causes of uniocular nystagmus.

Adolescent↗
PubMed1979

Benign paroxysmal positional nystagmus.

A characteristic nystagmus profile of benign paroxysmal positional nystagmus was determined from analyses of horizontal and vertical electro-oculographic recordings in 32 patients. The vertical component was upbeat in both eyes (fast phase toward the ground in the head-hanging position), whereas the horizontal component was dissociated with the ipsilateral eye beating away from the down ear and the contralateral eye beating toward the down ear. The amplitude of the vertical component was larger in the ipsilateral eye. This dissociated nystagmus profile is consistent with a burst of excitatory activity originating in the posterior canal of the ear that is undermost at the end of the positioning maneuver.

Adult↗
PubMed1979

The mechanism of benign paroxysmal positional nystagmus.

A characteristic nystagmus profile of benign paroxysmal positional nystagmus (BPPN) was determined from analyses of horizontal and vertical electro-oculographic recordings in 8 patients. The vertical component was upbeat in both eyes (fast phase toward the ground in the head-hanging position) while the horizontal component was dissociated with the ipsilateral eye beating away from the down ear and the contralateral eye beating toward the down ear. The amplitude of the vertical component was larger in the contralateral eye while that of the horizontal component was larger in the ipsilateral eye. This dissociated nystagmus profile is consistent with a burst of excitatory activity originating in the posterior canal of the ear that is undermost at the end of the positioning maneuver.

Electrooculography↗
PubMed1979

Visual-vestibular interaction and cerebellar atrophy.

The vestibular and optokinetic ocular control systems were studied in 10 patients with cerebellar atrophy and in 10 normal subjects using (1) constant velocity optokinetic stimulation, (2) sinusoidal rotation in the dark, and (3) sinusoidal rotation in the light with a surrounding fixed optokinetic drum. The gain (maximum slow component velocity/maximum head or drum velocity) of induced nystagmus was calculated from electro-oculographic recordings. Optokinetic nystagmus was abnormal in seven patients and the average optokinetic gain in the patients was significantly (p less than 0.01) less than that of the normal group. Three patients with "clinically pure" cerebellar atrophy had increased vestibular responses, and one patient with clinical signs of peripheral neuropathy had decreased responses, probably due to associated vestibular nerve disease. The average vestibulo-ocular reflex gain in patients did not differ significantly from controls (p greater than 0.05). Three patients had normal vestibular and optokinetic responses when tested independently, but had abnormal visual-vestibular interaction. These patients probably had selective disorders of the midline cerebellar pathways that mediate visual-vestibular interaction. By studying each system, both independently and during interaction, all patients were identified as abnormal, and a more precise anatomic localization of the atrophy was obtained.

Adolescent↗