A variety of abnormal ocular oscillations consequent to brain stem and cerebellar dysfunction are described. The brain stem eye signs include: see-saw nystagmus, convergence-retraction nystagmus, down-beat nystagmus, ocular myoclonus, ocular bobbing, and superior oblique myokymia. The "cerebellar system" eye signs discussed are five varieties of nystagmus, square wave and macro square wave jerks, macro saccadic oscillations, ocular dysmetria and flutter, and opsoclonus.

Brain Diseases↗

PubMedDate not supplied

Alexander's law: a model and resulting study.

Recently we developed an analog model to simulate Alexander's law in nystagmus secondary to dysfunction of a semicircular canal. Alexander's law is based on the observation that the amplitude of the nystagmus grows with increasing gaze in the direction of the fast phase and diminishes with gaze in the opposite direction. To investigate the assumptions made in the model, we conducted quantitative experimental studies on the effect of gaze on caloric-induced nystagmus in human subjects. A weak stimulus (water at 26.5 degrees C and 240 ml/min) was administered for several minutes which caused the development of jerk nystagmus. Both the average slow phase velocity and frequency reached a steady state at about three minutes after the start of irrigation and remained stable until the flow of water was stopped. To investigate the effect of gaze, each subject was asked to hold gaze at various positions from center, to the right, to the left, and to repeat the cycle. Results indicated that the slow phase velocity of the nystagmus was greatest in the direction of the fast phase and decreased approximately linearly with gaze in the other direction in accordance with Alexander's law. Frequency was not a function of gaze. We speculate as to the biological advantages of the brainstem neural circuitry responsible for Alexander's law.

Adolescent↗

PubMedDate not supplied

Progressive supranuclear palsy: a brief personalized history.

Progressive supranuclear palsy (PSP) was originally described in 1964. Although some contended it was merely a variant of Parkinson's disease, a specific electron microscopic finding of straight, rather than twisted, filaments in the neurofibrillary tangles established PSP as a distinct entity. The almost pathognomonic early clinical finding of paralysis of downward gaze is due to lesions involving the lateral portions of the rostral interstitial nucleus of the medial longitudinal fasciculus. Recent neurochemical studies have identified both a decrease in central dopamine and acetylcholine. The etiology of PSP is unknown, and the therapy is generally ineffective.

Dementia↗