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Several skeletal muscles are composed of multiple neuromuscular compartments that can be controlled individually by corresponding motor neuron pools.1–3 The transversus abdominis is composed of distinct regions that contract differentially.3 Similarly, the human cricothyroid muscle has three bellies with distinct functions innervated by separate motor nerve branches.3 The triceps brachii is composed of multiple fascicles that may be considered as distinct muscles with completely independent motoneuron subnucleus innervation.4 There exist more extraocular muscle (EOM) fibers and motor neurons than apparently required by conventionally recognized mechanisms of ocular motility.5,6 Could this be because individual EOMs are compartmentalized to implement multiple functions? One such example is the active pulley hypothesis that proposes that orbital layers of EOMs insert in connective tissue rings, called pulleys, through which pass the global layer fibers that in turn insert on the sclera to rotate the eye. Consequently, during EOM contraction, shifts in pulley positions influence EOM pulling directions.7–10 This laminar aspect of compartmentalization is evident in all oculorotary EOMs. Peng et al.11 traced the intramuscular arborization of the abducens nerve (CN6) within the lateral rectus (LR) muscles of two macaque monkeys and two humans, demonstrating that CN6 bifurcates externally to the EOM into two major trunks whose arborizations remain segregated into superior versus inferior zones throughout the EOM's length. Based on this finding, Peng et al.11 proposed that selective neural control of the two LR zones could execute significant torsional and vertical actions that are not classically recognized. This neuroanatomical finding of Peng et al.11 is consistent with the LR's dual-headed origin in the deep orbit.12,13 Some aspects of the LR are unique among EOMs, however, so that compartmentalization of LR innervation might be a developmental artifact rather than neural control strategy. Older studies of EOM embryology claimed that the LR originates from two different myotomes.14,15 More recent studies in birds demonstrate that the LR arises from somitomeres 4 and 5,16,17 and that CN6 arises from both rhombomeres 5 and 6.16 Separation of CN6 into two parallel nerve trunks is not rare. Indeed, 8–15% of CN6 in humans are split in this way.18–21 The LR can also exhibit longitudinal splitting, most prominently in congenital disorders of cranial nerve development such as processes involving the EOM or cranial nerve development such as congenital fibrosis of the extraocular muscles type 1,22 congenital oculomotor palsy,23 congenital trochlear palsy,23 and Duane syndrome.24–26 The possibility of selective activation of compartments requires topographical projection of motor nerves within segregated EOM regions. If selective control of rectus EOM compartments is a general neural strategy, evidence of compartmentalization should be evident in the intramuscular innervation of other rectus EOMs besides the LR. This study aimed at confirming, in additional specimens, Peng et al.'s report of compartmentalized LR innervation11 and extending study by tridimensional reconstruction of nerve arborizations, to the inferior (IR), medial (MR), and superior rectus (SR) muscles of humans and monkeys.

PURPOSE. Cerebral palsy (CP) is a permanent, nonprogressive disorder of movement and posture due to a lesion of the fetal or infant brain. The goal was to determine whether children with different severities of CP, as defined using the Gross Motor Function Classification System (GMFCS), had different degrees or types of visual dysfunction. METHODS. An observational, cross-sectional‐design study was conducted by using neurologic and masked ophthalmic measurements on a representative cohort of 50 children with CP. Mean age was 5.6 years (range, 2‐19.5 years); mean gestational age was 31 weeks. RESULTS. The likelihood of debilitating visual deficits was greater in children with higher GMFCS scores, independent of gestational age. Children with level 5 disease (most severe) were at greatest risk for high myopia, absence of binocular fusion, dyskinetic strabismus, severe gaze dysfunction, and optic neuropathy or cerebral visual impairment (CVI). These deficits were rare or absent in children with the mildest disease, level 1. When categorized by anatomic or physiologic CP subtype, diplegic and spastic children were more often hyperopic and esotropic, but had the highest prevalence of fusion and stereopsis. In contrast, children with quadriplegic and mixed CP (dyskinetic, athetoid, hypotonic, and ataxic) more often had high myopia, CVI, dyskinetic strabismus, and gaze dysfunction. CONCLUSIONS. Visual deficits differ in children who have mild versus severe CP. Children with GMFCS level 1 to 2 have sensorimotor deficits resembling those of neurologically normal children with strabismus and amblyopia; children at level 3 to 5 have more severe deficits, not observed in neurologically normal children. (Invest Ophthalmol Vis Sci. 2008;49: 572‐580) DOI:10.1167/iovs.07-0525