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Biomedical subjects

R B Daroff

Publications and source records attributed to R B Daroff.

At least 55 records · Page 3Linked to original sources

Absence of REM and altered NREM sleep in patients with spinocerebellar degeneration and slow saccades.

The pontine tegmentum contains the neurons responsible for generation of saccadic eye movements and certain phases of sleep. We studied two genetically unrelated patients with spinocerebellar degeneration and slow saccadic eye movements. Multiple all-night sleep studies in both patients disclosed absence of REM and stage 4 sleep with an extremely short stage 3 and long stage 2. Both patients had a sleep stage (X) not previously reported. These are the first awake and ambulatory humans in whom consistent absence of REM sleep has been demonstrated. Both behaved appropriately during wakefulness and showed no overt psychological abnormalities.

Adult↗

Internuclear ophthalmoplegia: recovery and plasticity.

We studied refixational eye movements of a patient during the gradual resolution of an internuclear ophthalmoplegia (secondary to head trauma) in an attempt to determine the relative contributions of both medial longitudinal fasciculus (MLF) recovery and secondary central plastic changes. Adduction-refixational eye movements in the affected eye consisted of an initial fast (saccadic) portion followed by a slow drift toward the new intended eye position. The fast and slow components of the movements reflected, respectively, the pulse and step increases in neural innervation. Shortly after the traumatic insult, the affected eye exhibited low adduction gain (pulse gain 0.34; step gain 0.37) and slow saccades with peak velocities of 55% and durations of 278%, normalized for achieved, rather than intended, amplitudes. Several months later the pulse and step gains, peak velocities, and durations of the saccades improved to 0.81, 0.92, 87%, and 145%, respectively. The increased gains and faster velocity were accomplished by increases in the firing frequency of the pulse and step, reflecting recovery of MLF axons, rather than saccadic system plasticity, which would have resulted in increased duration of the saccadic pulse.

Adolescent↗

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↗