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Preview — Retinopathy of Prematurity by John T. Flynn Editor ,. William Tasman Editor. Mackenzie Freeman Foreword. Retinopathy of Prematurity presents a review of the current knowledge of this disease, which tragically renders many premature infants blind. First, the volume covers the natural history, classification and histopathology of ROP, followed by examination techniques, recommendations for follow-up and therapy and finally a panel discussion providing answers to frequent questi Retinopathy of Prematurity presents a review of the current knowledge of this disease, which tragically renders many premature infants blind.
First, the volume covers the natural history, classification and histopathology of ROP, followed by examination techniques, recommendations for follow-up and therapy and finally a panel discussion providing answers to frequent questions and areas of legal concern. Get A Copy. Paperback , pages. In that regard, we shall tentatively take into account the most relevant present knowledge about the organization of the brain and its development. This knowledge will come from both biology and medicine.
Some knowledge from anatomy, physiology, as well as genetics and molecular biology, will be thus considered. Tychsen has stated already that it is the brain that must be repaired if ophthalmologists want to treat strabismus Tychsen, We evidently agree with that idea but much still remains to be done prior to the complete treatment of strabismus.
To treat consequences of strabismus on visual perception is already relatively effective, with conventional treatments including optical treatment with glasses, monocular occlusion, and alignment of the eyes through surgery. Newly developed strategies such as binocular training and transcranial magnetic stimulations TMS could improve in the future the efficacy of conventional strabismus treatment since it has been shown that such strategies permit the recovery of visual acuity and binocular vision in amblyopia, even at adulthood after alignment of the eyes ; e.
Furthermore, considering strabismus at source and dealing in particular with its central origins is currently far from effective. The same applies to loss of binocular vision with a central origin. However, as a general rule in medicine, it is always better to treat pathology at source provided its origin and pathophysiology are precisely defined rather than dealing with its dilatory consequences. Our article aims at assisting in this regard by treating the question of the origins of strabismus, even if practical therapeutical consequences will not be immediate.
From the eyes to the brain, the visual system and the oculomotor system are both formed of complex neural networks which link numerous structures. Interactions exist between these structures within each system separately, as well as between both systems. Thus, all of these structures must function perfectly and in synchrony to ensure a normal visual function, i. In the visual system, as illustrated in Figure 2 , the retino-geniculo-cortical pathway is the main sensory route that links the retina to V1: most ganglion cells of the retina project to the dorsal lateral geniculate nucleus dLGN via the optic nerves and the optic tracts.
Geniculate cells then project to V1 through the optic radiations. Other afferents may interconnect both hemispheres through the CC. Any abnormality within one of these structures alters vision e. Some fibers from the optic tracts also project to extra-geniculate structures which are themselves implicated in vision, such as the Superior Colliculus SC. This structure, among other functions, is also responsible for a precise ballistic of the eye movements and for visual attention Krauzlis et al.
Figure 2. Potential origins of strabismus. In periphery, one may notice, for example, abnormal vision or abnormal development of the extraocular muscles. Centrally, strabismus may, for example, result from an abnormal activity in the brainstem, the Medial Reticular Formation MRF , the Pontine Reticular Formation PRF , the thalamus, the cerebellum or the superior colliculus. At the cortical level, visual, parietal or frontal cortex may also not function properly.
Altogether, this indicates that origins of strabismus may be numerous. One may emphasize that those with a central origin likely dominate. The oculomotor system must also function perfectly to provide eye movements and alignment of the eyes with optimal characteristics. This begins with the six EOMs and their pulleys, which allow movements of the eyes: the external and internal rectus, the superior and inferior rectus, as well as the inferior and superior obliques.
The motor activity of these muscles is controlled directly by the IIIrd common oculomotor , IVth trochlear , and the VIth abducens cranial nerves. During these eyes movements, some receptors in the EOMs including their tendons are also activated, sending sensory messages related directly to eye movements all around the brain, including within V1 and the frontal cortex Buisseret and Maffei, for visual cortex; cf. Buisseret, for review through the ophthalmic branch of the Vth trigeminal cranial nerve e. Such proprioceptive information is relayed in different sub-cortical structures located in the brainstem, and also in the cerebellum and the vestibular nuclei, finally reaching the parietal and the frontal cortex e.
Our hypothesis here is that strabismus can be caused by an insult at every level of both the visual and the oculomotor systems. Below we shall thus describe different possible origins of strabismus at different levels of each system. Notice that many other possible origins might be proposed. As a first step, abnormalities at the level of the EOMs, whether genetic in origin or not, will be discussed as potential origins of strabismus.
The potential role of the oculomotor muscles themselves in this process will also be discussed, as well as their sensory afferents or motor efferents. Abnormal weakness of extraocular or oculomotor muscles may occur for various reasons. First, it may be due to muscular dystrophies or other genetic myopathies. In that case, the muscles themselves are affected, which can cause strabismus Shieh, The most common forms of muscular dystrophies include Duchenne muscular dystrophy, Becker muscular dystrophy, facio-scapulo-humeral muscular dystrophy and Steinert myotonic dystrophy.
Variable phenotypes of strabismus and abnormalities of ocular movements are often associated with such muscular dystrophies.
Second, it may be the transmission of neurotransmitters at the level of the neuromuscular junction that is affected in myasthenia which may lead to variable and intermittent forms of strabismus. Moreover, EOMs, being the most fatigue-resistant muscles of the body, can therefore be less or lately affected by a muscular dysfunction.
The understanding of eye movements have been deeply modified by Demer's work, which described the role of the pulleys in the kinematics of EOMs e. Abnormal position or function of those pulleys may lead to strabismus. This affects patients with congenital restrictive ophthalmoplegia Engle, ; Graeber et al.get link
CFEOM is a misnomer for various incomitant strabismus which were described in several families, indicating a possible hereditary trait. Indeed, genetics have proven that CFEOM result from mutations in genes that are implicated in the growth of oculomotor nerves.
In the absence of normal innervation, a variable atrophy of the muscles may occur. CFEOM 1 results from KIF21A mutations and is characterized by a quasi total absence of movement of the eyes, the primary position being hypotropic with elevation being impossible, whereas the horizontal position can be either esotropic or exotropic. The heterozygous mutation of the gene is sufficient to cause the disease which results in a dominant inheritance. KIF21A is located on chromosome 12 and is responsible for the production of a developmental kinesin.
Kinesins are molecular motors that interact with and transport cargo along the microtubules of axons. In CFEOM 1, abnormal development of the superior branch of the IIIrd nerve particularly affects the function of the superior rectus muscle and the levator palpebrae superioris muscle.
PHOX2A is a paired-linked transcription factor gene and its expression is restricted to differentiating neurons in the central and peripheral nervous systems. In CFEOM 3, similar to CFEOM 1, it is only the development of the IIIrd nerve that is affected, although in a more severe way since all of its branches are affected in this situation and not only those branches which innervate the superior rectus muscle and the levator palpebrae superioris muscle. The gene responsible for the disease is located at 16qter.
The primum movens of these latter syndromes is an absence of development of the VIth nerve, either unilaterally or bilaterally. Variable forms of abnormal innervation of the lateral rectus muscle by branches of the IIIrd nerve have also been observed, resulting either in esotropia or exotropia. Again, it is an abnormal development of a nerve that underlies the pathogenesis of this condition, with genes located at 8q13 and at 2q Duane Radial Ray Syndrome DRRS is a particular form of Duane Syndrome in which the ocular movement abnormality is associated with bone abnormalities in the hand, such as an absence or a malformation of the thumb which can look like a finger.
Again, it is a mutation in a transcription factor gene SALL4, located at 20q13, which causes the disease by altering the normal neural development.
Such phenotype combines a total impossibility of horizontal gaze movements, along with a scoliosis that occurs during the first decade of life. ROBO3 is a developmental gene and is expressed in the hindbrain of the human fetus. Human ROBO3 is similar to roundabout genes that are responsible for axon guidance in other species such as mice, zebrafish or drosophile.
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In zebrafish, and in drosophile, the loss of function of ROBO3 results in aberrant midline crossing by axons Seeger et al. In BSAS, which is a recessive condition, a bilateral Duane trait is associated with other cranial nerve dysfunctions, such as deafness due to a bilateral absence of the cochlea and misdevelopment of the VIIIth vestibulo-cochlear nerve. In ABDS, horizontal gaze restriction is associated with central deafness and mental retardation.
In CCDDs, the insult can cause ocular movement disorders but other conditions without strabismus can occur, such as isolated congenital ptosis which can result from a mutation in a gene located at 1pp As a general rule, genetics of CCDDs teach us that an abnormal development in general and an abnormal early routing of neurons in particular, may cause strabismus.
In CCDDs, the insult occurs at the frontier between peripheral and central locations. It is the same when considering the cranial nerves that emerge from the brainstem and lead toward abnormal EOMs. The model of the CCDDs therefore emphasizes that an abnormal neural network can cause strabismus. Similar to CCDDs, it is a neural disorder although the cause is often acquired and not innate. The nerve palsy causes an atrophy of the innervated muscle. Acute palsy of the IIIrd nerve is an emergency since it can be caused by a direct compression of the nerve by a cavernous sinus thrombophlebitis, or by an aneurysm of the posterior communicant artery.
A palsy of the IVth nerve is either congenital or acquired.
Retinopathy of Prematurity: A Clinician's Guide
When acquired, it is a peripheral cause that is the primum movens. It may however result from a direct insult after a severe cranial traumatism. A palsy of the VIth nerve may finally result from a direct compression of the nerve's fine and fragile branches.
This can arise from a hypertrophic brainstem due to intracranial hypertension. It may also result from numerous other central causes such as tumors, infections, etc. In all cases however, this will induce strabismus. The outflow theory supports the idea that it is an efferent copy of the oculomotor signal from the motor centers that gives information about the position of the eyes to the brain Von Helmholtz, By contrast, the inflow theory claims that it is the proprioceptive signals from eye muscle receptors that give such information Sherrington, More recent experiments support one theory or the other.
Thus, authors now consider that both theories are right and that efferent copy co-exists with extraocular proprioception.