Caudal Prefrontal Cortex

The caudal prefrontal (PF) cortex supports the visual search for objects such as foods both through eye movements and covert attention, and its connections explain how it can do this. The caudal PF cortex, which includes the frontal eye field, has connections with both the dorsal and ventral visual streams. The direction of eye movements depends on its connections with the superior colliculus and oculomotor nuclei. Covert attention depends on enhanced sensory responses that are mediated through top-down interactions with posterior sensory areas. Along with the granular parts of the orbital PF cortex, the caudal PF cortex evolved in early primates. Together, these two new areas led to improvements in searching for and evaluating objects that are hidden in a cluttered environment.

Recruitment orders underlying binocular coordination of eye position and velocity in the larval zebrafish hindbrain

BackgroundThe oculomotor integrator (OI) in the vertebrate hindbrain transforms eye velocity input into persistent position coding output, which plays a crucial role in retinal image stability. For a mechanistic understanding of the integrator function and eye position control, knowledge about the tuning of the OI and other oculomotor nuclei is needed. Zebrafish are increasingly used to study integrator function and sensorimotor circuits, yet the precise neuronal tuning to motor variables remains uncharacterized.ResultsHere, we recorded cellular calcium signals while evoking monocular and binocular optokinetic eye movements at different slow-phase eye velocities. Our analysis reveals the anatomical distributions of motoneurons and internuclear neurons in the nucleus abducens as well as those of oculomotor neurons in caudally adjacent hindbrain volumes. Each neuron is tuned to eye position and/or velocity to variable extents and is only activated after surpassing particular eye position and velocity thresholds. While the abducens (rhombomeres 5/6) mainly codes for eye position, in rhombomeres 7/8 a velocity-to-position coding gradient exists along the rostro-caudal axis, which likely corresponds to the velocity and position storage mechanisms. Position encoding neurons are recruited at eye position thresholds distributed across the behavioral dynamic range, while velocity encoding neurons have more centered firing thresholds for velocity. In the abducens, neurons coding exclusively for one eye intermingle with neurons coding for both eyes. Many of these binocular neurons are preferentially active during conjugate eye movements, which represents a functional diversification in the final common motor pathway.ConclusionsWe localized and functionally characterized the repertoire of oculomotor neurons in the zebrafish hindbrain. Our findings provide evidence for a mixed but task-specific binocular code and suggest that generation of persistent activity is organized along the rostro-caudal axis in the hindbrain.

Neural mechanisms of oculomotor abnormalities in the infantile strabismus syndrome

Infantile strabismus is characterized by numerous visual and oculomotor abnormalities. Recently nonhuman primate models of infantile strabismus have been established, with characteristics that closely match those observed in human patients. This has made it possible to study the neural basis for visual and oculomotor symptoms in infantile strabismus. In this review, we consider the available evidence for neural abnormalities in structures related to oculomotor pathways ranging from visual cortex to oculomotor nuclei. These studies provide compelling evidence that a disturbance of binocular vision during a sensitive period early in life, whatever the cause, results in a cascade of abnormalities through numerous brain areas involved in visual functions and eye movements.

The Extraocular Muscles and Diplopia

deals with action and innervation of the extraocular muscles. In their intact state, the extraocular muscles and the cranial nerves that innervate them are responsible for every movement of the eyes signaled by the cortex. Diplopia, or double vision, is the commonest subjective complaint associated with a lesion affecting the extraocular muscles, their neuromuscular junctions, the oculomotor nuclei or nerve, or pathways in the brainstem that maintain alignment of the eyes. The diplopia history focuses on distinguishing monocular from binocular diplopia and the diplopia examination pays attention to head position, ocular alignment, and the range of eye movements during monocular and binocular viewing as keys to diagnosis. Diplopia with full eye movements is fully discussed. Four illustrative cases are presented: episodic diplopia due to ocular myasthenia gravis; a case of esotropia (paresis of the lateral rectus with inward deviation of the eye) due to an abducens nerve palsy; a case of exotropia (paresis of the medial rectus with outward deviation of the eye) due to a fascicular oculomotor nerve palsy; and a case of hypertropia (vertical misalignment of the eyes due to paresis of the superior oblique muscle vs. skew deviation) caused by a post-traumatic trochlear nerve palsy.

Alterations of Eye Movement Control in Neurodegenerative Movement Disorders

The evolution of the fovea centralis, the most central part of the retina and the area of the highest visual accuracy, requires humans to shift their gaze rapidly (saccades) to bring some object of interest within the visual field onto the fovea. In addition, humans are equipped with the ability to rotate the eye ball continuously in a highly predicting manner (smooth pursuit) to hold a moving target steadily upon the retina. The functional deficits in neurodegenerative movement disorders (e.g., Parkinsonian syndromes) involve the basal ganglia that are critical in all aspects of movement control. Moreover, neocortical structures, the cerebellum, and the midbrain may become affected by the pathological process. A broad spectrum of eye movement alterations may result, comprising smooth pursuit disturbance (e.g., interrupting saccades), saccadic dysfunction (e.g., hypometric saccades), and abnormal attempted fixation (e.g., pathological nystagmus and square wave jerks). On clinical grounds, videooculography is a sensitive noninvasivein vivotechnique to classify oculomotion function alterations. Eye movements are a valuable window into the integrity of central nervous system structures and their changes in defined neurodegenerative conditions, that is, the oculomotor nuclei in the brainstem together with their directly activating supranuclear centers and the basal ganglia as well as cortical areas of higher cognitive control of attention.

Cranial Nerves 3, 4, 6, 12

Chapter 12 discusses cranial nerves 3, 4, 6, 12 and their anatomy, as well as extraocular movements, extraocular muscles (recti muscles and oblique muscles) and oculomotor nuclei.

Outcome of Neonates with Hyperbilirubinemia

Hyperbilirubinemia or jaundice refers to excessive levels of bilirubin in the serum of newborn infants. It is of interest to developmentalists, since serum bilirubin can cross the blood–brain barrier and, in high levels, may cause brain damage, particularly in the globus pallidus, substantia nigra reticulata, subthalamic nucleus, brainstem auditory structures (vestibular and cochlear), oculomotor nuclei, the hippocampus, and the cerebellum. Very high levels of bilirubin can cause the classic acute and chronic bilirubin encephalopathies. Controversy exists as to whether lower levels cause minor neurological, cognitive, or behavioral deficits. Hyperbilirubinemia develops in neonates primarily due to their physiologic immaturity, although other conditions and factors may play a role. Bilirubin is a yellow pigment that results from the breakdown of hemoglobin from red blood cells. In routine clinical practice, bilirubin is measured as total serum bilirubin (TSB). Many healthy full-term infants develop a mild degree of jaundice usually termed “physiologic” jaundice or jaundice not attributable to pathologic factors or disease. The number and rate of breakdown of red cells is higher in the newborn and leads to an increased release of bilirubin to the circulation. The newborn’s liver has reduced capacity to take up bilirubin due to immaturity. Additionally, loss of water in combination with reduced intake of fluid prior to establishment of breast feeding may make the infant jaundiced because of dehydration (Stevenson et al. 2004). Although most neonatal jaundice is physiologic, Table 33.2 lists some of the more common ‘‘pathologic’’ mechanisms causing jaundice in newborns (Stevenson et al. 2004). In actuality, all healthy, full-term infants develop some level of neonatal hyperbilirubinemia as a consequence of physiological immaturity in metabolizing bilirubin, mild dehydration, and/or factors in the breast milk (if they are breast-feeding) (Davidson 1941; Maisels et al. 1986). Clinical jaundice is visible at serum bilirubin levels of approximately 5–7 mg/dL, and approximately 50% (Palmer and Mujsce 2001) of all normal newborns appear jaundiced during the first week of life.