Abstract
Purpose :
Directional sensitivities to nasal vs temporal and superior vs inferior motion are set prenatally by Starburst retinal ganglion cells which express specific cocaine and amphetamine regulated transcripts (CART). The directional specificity of this circuit is set by the neuronal connectivity between the dendritic branches of amacrine and ganglion cells whose axons project to downstream pre-motor neurons. We postulated that prenatal exposure to cocaine and methamphetamine would perturb the neuronal circuitry underlying gaze holding and conjugate eye movements.
Methods :
Eight children (mean age 3.4y) with documented prenatal and/or perinatal exposure to cocaine /methadone and/or amphetamine were studied. All had normal or nearly normal visual acuities and examinations of the anterior and posterior segments were normal. Each child had assessments of gaze holding, vertical saccades and vertical optokinetic nystagmus (OKN) quantified by binocular video-oculography (VOG).
Results :
Six of 8 subjects had gaze holding instabilities; 4 had asymmetric, horizontal, pendular nystagmus and 2 had conjugate horizontal jerk nystagmus. Average gains for saccades to point targets stepped upward 5deg, 10deg and 20 deg were 1.0±0.55, 0.82±0.48 and 0.8 ± 0.36, respectively. Average gains for saccades stepped downward 5deg, 10deg and 20 deg were 0.57±0.22, 0.73± 0.22, and 0.87±0.36, respectively. Average OKN gains for horizontally-oriented gratings drifted at velocities of 15, 30 and 45deg/s were respectively 1.03±0.44, 0.69±0.35 and 0.84±0.22 in the upward direction and 0.38±0.18, 0.69±0.35 and 0.54±0.22 in the downward direction.
Conclusions :
Our data show that infants with prenatal exposure to cocaine, amphetamines or methadone were likely to exhibit gaze-holding instabilities. All subjects generated vertical saccades and vertical OKN across velocities with similar gains in the upward and downward direction except for target steps of 5 deg and velocities of 15deg/s. We hypothesize that prenatal exposure to these drugs may lead to dysregulation of the CART resulting in the failure of DSGC to connect with the appropriate downstream neurons. The resulting failure to organize target neurons into precise neural circuits may account for the gaze-holding instabilities.
This is an abstract that was submitted for the 2017 ARVO Annual Meeting, held in Baltimore, MD, May 7-11, 2017.