PubMed HealthSearch

Biomedical subjects

R B Daroff

Publications and source records attributed to R B Daroff.

At least 19 recordsLinked to original sources

Latent, manifest latent, and congenital nystagmus.

Manifest latent nystagmus (MLN) was identified in 31 patients by accurate eye movement records. All the patients had horizontal tropias, and the nystagmus fast phases were always in the direction of viewing eye. The slow phases of MLN are decreasing-velocity exponentials while those of the jerk form of congenital nystagmus (CN) are increasing velocity exponentials. Several subjects who were believed to have latent nystagmus (LN) on clinical examination had small amplitude nystagmus evident by eye movement recording with both eyes open: these were actually cases of MLN. Many patients with MLN are misdiagnosed as having CN. An explanation for MLN and LN is provided based on confusion of egocentric directions between monocular and binocular viewing conditions.

Adolescent

A model of Alexander's law of vestibular nystagmus.

The observation that the amplitude of vestibular nystagmus grows as gaze is increased in the direction of the nystagmus fast phase and diminished with gaze in the opposite direction is known as "Alexander's law". We have developed an analog computer model to simulate Alexander's law in nystagmus secondary to dysfunction of a semicircular canal. The model utilizes relevant brainstem anatomy and physiology and includes gaze modulation of vestibular signals and push-pull integration to create eye position commands. When simulating normally functioning semicircular canals, the model produced no nystagmus. When simulating total impairment of the canal on one side with gaze directed maximally in the opposite direction, the model produced a large amplitude nystagmus with linear slow phases directed toward the affected side. As gaze was changed from far contralateral to ipsilateral, the nystagmus gradually diminished to zero. When simulating partial impairment of one canal, the nystagmus was smaller in amplitude and absent in ipsilateral gaze.

Brain Stem

Saccades in extremes of lateral gaze.

Saccades (between targets at 30 degrees and 40 degrees) were recorded with DC electro-oculography in 10 normal subjects. Velocity-amplitude relationships were examined on the basis of abduction vs. adduction and centering vs. eccentric movement. In these small peripheral saccades the former pairing showed no consistent differences in peak velocity, whereas centering saccades were consistently faster than both eccentric movements and those made around primary position.

Adult

Saccadic velocity characteristics: intrinsic variability and fatigue.

Saccadic eye movements exhibit a characteristic peak velocity vs. amplitude relationship. As with all quantifications of biological function, there exists and associated intra- and intersubject variability of this relationship. This paper documents this variability and demonstrates both the absence of a predictable short-term "muscle fatigue" effect and the presence of a generalized "mental fatigue" (i.e. tiredness) effect.

Adolescent

Saccadic system plasticity in humans.

A subject with a medial rectus paresis secondary to a partial third nerve palsy was forced to use the affected eye for six days while the good eye was constantly patched. Saccadic eye movements were carefully measured each day; the grain increased, with a time constant of 0.85 day. The patch was then switched to the paretic eye and the gain decreased, with a time constant of 0.85 day. The patch was then switched to the paretic eye and the gain decreased, with a time constant of 1.54 days. This demonstrated central nervous system plasticity of the pulse and step of neural activity responsible for the generation of saccades in the adult human. In addition to gain changes, postsaccadic drift velocity and saccadic velocity/amplitude relationship alterations during the patching are reported. A major conclusion that can be drawn from analysis fo these data is that the gain changing is accomplished by pulse width changes rather than pulse height (firing frequency), which was not markedly altered.

Eye Movements

End-point nystagmus.

Infrared oculography was performed during sustained lateral gaze in 12 normal subjects to investigate end-point nystagmus while fixating a target light. Five failed to develop nystagmus despite deviation up to 40 degrees from 4 to 5 min. Six subjects developed nystagmus immediately or shortly after reaching the deviated position. In one, the nystagmus (0.5 degrees to 1 degree and 1.0 Hz) began with only a 20 degree deviation. In another subject, "fatigue" nystagmus developed after 1 min at 30 degrees, and at 35 degrees nystagmus began within 2 sec. One subject developed only fatigue nystagmus, which began after more than 4 min of sustained deviation. In all instances the slow phase had primarily a linear, rather than exponential, waveform.

Adult

"Inverse latent" macro square-wave jerks and macro saccadic oscillations.

A patient recovering from an acute encephalopathy demonstrated several ocular motor disturbances reflecting cerebellar and brainstem dysfunction. Two of these, macro square-wave jerks and macro saccadic oscillations, have never been reported in the same patient. The macro square-wave jerks disappeared with monocular viewing, a previously undescribed "inverse latent" characteristic.

Adult

The ocular motor defects in progressive supranuclear palsy.

The results of quantitative infrared horizontal eye movement recordings in 8 patients with progressive supranuclear palsy are presented. Some of the patients had total paralysis of vertical movements, but none had completely lost the ability to perform horizontal eye movements. All patients had a defect in ocular fixation previously undescribed in this condition: the universal presence of square-wave jerks. Analysis of refixation saccades demonstrated hypometria, slow velocity/amplitude relationships, and profound prolongation of duration. The pursuit abnormality, characterized clinically by "cogwheel" eye movements, represented the inability to match eye velocity to target velocity. The ratio of peak eye velocity to peak target velocity (pursuit gain) was 0.2 to 0.5. Defects in the vestibuloocular reflex included inability to increase the gain of the reflex (ratio of peak eye velocity to head velocity) during viewing of a visible, stationary target and failure to suppress the reflex when viewing a target rotating with the head.

Aged

Vertigo.

Vertigo reflects dysfunction in the vestibular system. Any disease state which changes the firing frequency of a vestibular end-organ and which produces unequal neural input to the brainstem causes vertigo. Caloric stimulation mimics acute end-organ dysfunction and helps establish the diagnosis.

Caloric Tests

Braking saccade--a new fast eye movement.

A new type of fast eye movement (FEM) is described whose main function is to stop a runaway slow eye movement (SEM). It conforms to the velocity-amplitude relationship characteristic of other types of saccades. The identification of this FEM is the result of examination of the many waveforms manifested by subjects with congenital nystagmus. It is a common, repeatable phenomenon present in all subjects with any of six different types of nystagmus waveform. The fact that braking saccades reset SEM to zero velocity, whereas no other type of saccade interacts with SEM, indicates a developmental mechanism in such subjects.

Eye