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Biomedical subjects

P J Ranalli

Publications and source records attributed to P J Ranalli.

11 recordsLinked to original sources
PubMed1993

Oblique misdirection and slowing of vertical saccades after unilateral lesions of the pontine tegmentum.

Three patients with unilateral lesions of the pontine tegmentum, identified by CT and MRI, had abnormal vertical saccades and slowed ipsilateral horizontal saccades. Attempted vertical saccades were misdirected obliquely, away from the side of the lesion, and their vertical components were prolonged. Oblique saccades had curved trajectories and prolonged durations of their vertical components. Unilateral damage to excitatory burst neurons and pause cells in the medial part of the caudal paramedian pontine reticular formation may cause these abnormal vertical and oblique saccades. Misdirection and slowing of vertical saccades can accompany the paralysis or slowing of ipsilateral horizontal saccades caused by pontine damage.

Electrooculography↗
PubMed1991

Vertical vestibulo-ocular reflex control after supranuclear midbrain damage.

The vertical vestibulo-ocular reflex (VOR) and its visual enhancement and cancellation were measured in patients with focal midbrain lesions that caused paralysis of upward, or upward and downward saccades. VOR gain was reduced in darkness during active vertical head pitch at frequencies from 0.25 to 2 Hz. Visual enhancement of the reflex by fixating a stationary target was subnormal upward and downward. Cancellation of the VOR was defective in both vertical directions during eye-head tracking. The VOR showed abnormal phase lead of the eyes in darkness, indicating that pretectal midbrain damage impairs the integration of eye velocity commands.

Brain Injuries↗
PubMed1988

Vertical vestibulo-ocular reflex, smooth pursuit and eye-head tracking dysfunction in internuclear ophthalmoplegia.

Vertical smooth eye movements were quantified by magnetic search coil oculography in 7 patients with internuclear ophthalmoplegia (INO), 4 bilateral and 3 unilateral, and compared with age-matched normal subjects. The upward and downward vestibulo-ocular reflex (VOR) had reduced gain and abnormal phase lag in both unilateral and bilateral INO during active head motion at frequencies from 0.25 to 2 Hz. The phase lag was attributed to disruption of vestibular eye velocity signals and relative preservation of eye position signals. Fixation of a stationary target enhanced smooth eye movement gain during vertical head motion but it remained subnormal. Vertical smooth pursuit gain was mildly reduced. All patients had normal gaze (eye plus head) gain when tracking with both the head and eyes despite defective cancellation of the vertical VOR; they employed high amplitude head tracking to compensate for the uncancelled VOR. Cancellation was more impaired than smooth pursuit. Dissociation between cancellation and ocular pursuit was also demonstrated by a model of VOR cancellation that uses measured pursuit gain with the head immobile to predict gaze gain of eye-head tracking. The model predicted eye-head tracking gain in normal subjects but not in patients with INO. The results indicate that the medial longitudinal fasciculi or neighbouring tegmental tracts convey bidirectional signals for vertical pursuit, cancellation, and vestibular smooth eye movements in man, and that smooth pursuit and cancellation of the VOR can be dissociated in INO.

Adult↗
PubMed1988

Palsy of upward and downward saccadic, pursuit, and vestibular movements with a unilateral midbrain lesion: pathophysiologic correlations.

Upward and downward gaze palsy was measured by a magnetic search coil technique and correlated with neuropathologic findings in a patient with a unilateral midbrain infarct. Oculography demonstrated (1) saccadic palsy above primary position and slow, limited vertical saccades below; (2) low-gain, restricted vertical pursuit; and (3) low-gain, abnormal phase lead, and restricted range of the vertical vestibulo-ocular reflex (VOR). Bidirectional palsy of vertical saccades is attributed to unilateral loss of burst cells in the rostral interstitial nucleus of the medial longitudinal fasciculus (riMLF) and interruption of burst cell fibers from the opposite riMLF. Pathways mediating vertical pursuit and integration of the vertical VOR also traversed the infarct, which included the interstitial nucleus of Cajal.

Brain↗
PubMed1987

Comparison of smooth pursuit and combined eye-head tracking in human subjects with deficient labyrinthine function.

The effects of deficient labyrinthine function on smooth visual tracking with the eyes and head were investigated in ten patients with bilateral peripheral vestibular disease. Ten normal subjects served as controls. In the patients active, combined eye-head tracking (EHT) was significantly better than smooth pursuit (SP) with the eyes alone with a target frequency of 1.0 Hz. Normal subjects pursued equally well with SP and with active EHT. The gain of compensatory eye movements during active head rotation in darkness was also measured. Compensatory eye movements in labyrinthine-deficient patients (attributable to residual vestibulo-ocular reflex (VOR), cervico-ocular reflex (COR) and pre-programmed eye movements) were always less than in normal subjects. These data were used to examine current hypotheses that postulate central cancellation of the VOR (or compensatory eye movements) during EHT. A model that proposes summation of an internal smooth pursuit command and VOR/compensatory eye movements accounted for the findings in normal subjects and labyrinthine-deficient patients. In seven labyrinthine-deficient patients and nine normal subjects, passive EHT was measured during en bloc rotation while they viewed a head-fixed target. With a target frequency of 1.0 Hz, both subjects and patients showed significantly better tracking during passive EHT than during SP. Normal subjects also showed superior tracking during passive EHT compared with active EHT. These findings support the notion that during passive EHT, parametric gain changes contribute to modulation of the VOR.

Adult↗
PubMed1987

Amyloid angiopathy in Alzheimer's disease.

Thirty cases of Alzheimer's disease and 30 age-matched controls were studied to determine the incidence of cerebral amyloid angiopathy and its relationship to age, neuritic plaque formation, and amyloid plaque content. Cerebral amyloid angiopathy (CAA) was present in 86% of AD cases and 40% of age-matched controls. Its frequent occurrence in AD is not merely a reflection of the advancing age of this group: it was seen only in the presence of neuritic plaques, regardless of age, and represents an integral component of AD. Neuritic plaques however, did occur in the absence of CAA in 17% of all cases. The amount of vascular and plaque amyloid tended to be of comparable severity in many cases, but significant discrepancies were observed, with preferential deposition of amyloid in either plaque or vessel. Our results suggest that neuritic plaque formation and amyloid deposition are linked genetically or etiologically, but independently expressed, without a cause-and-effect relationship.

Adult↗
PubMed1986

Contrapulsion of saccades and ipsilateral ataxia: a unilateral disorder of the rostral cerebellum.

Contralateral pulsion of saccades and ipsilateral limb ataxia were manifestations of unilateral damage to the rostral cerebellum studied in a patient with occlusion of one superior cerebellar artery. The saccadic disorder consisted of three elements: horizontal saccades away from the lesion during attempted vertical saccades, resulting in oblique trajectories; hypermetria of contralateral saccades; and hypometria of ipsilateral saccades. Magnetic search coil oculography showed that durations of the horizontal components of oblique contrapulsive saccades were lengthened toward the durations of the vertical components. Lengthening of horizontal vectors indicated temporal coupling of the orthogonal components, as occurs in normal oblique saccades. The bias of saccades arose proximal to brainstem loci that decompose commands for oblique saccades into their horizontal and vertical vectors. Contrapulsion of saccades may be explained by imbalanced cerebellar outflow.

Adolescent↗