Chapters authored
Nystagmus By Ivana Mravicic, Selma Lukacevic, Maja Bohac, Maja Pauk-Gulic and Vlade Glavota
Nystagmus is an involuntary rhythmical movement of the eyes. The cause of nystagmus is a disruption in the afferent, central or efferent parts of the eye movement system. If it happens in the first few months of life during the sensitive period of visual development, it is most often a case of infantile nystagmus. On the other hand, the majority of nystagmus in adult age is caused by some neurological disorder, and it is usually called acquired nystagmus. The important role of an ophthalmologist is to recognize the origin of nystagmus. Acquired forms are usually caused by some neurological disorders and do not belong in our field of treatment. However, most of the nystagmus types in a child’s age require ophthalmological treatment. When we have a child with nystagmus, we have to enable the development of the visual system and help fixation and fovealization by the dampening of nystagmus. If the reason of nystagmus is of ocular origin, we have to treat the underlying disease. Optical treatment by glasses, contact lenses or magnifying devices is usually reasonable. In some cases when the patient has abnormal head posture, it is possible to treat nystagmus by surgery. Some medications are used in several types of nystagmus as well as some new developing treatments.
Part of the book: Eye Motility
Treatment of Paralytic Eye Motility Disorders By Ivana Mravicic, Alma Biscevic, Melisa Ahmedbegović Pjano, Ivona Petrovska, Anja Shumejko and Nina Ziga
Paralytic strabismus is caused by paresis or paralysis of one or more extraocular muscles that are innervated by cranial nerve lll, IV and Vl. They are characterized by squinting angle that depends on the direction of the gaze and the fixating eye. Typically, the angle is greater in the field of affected muscle, and when the patient is fixing with the affected eye. While younger children in some cases can suppress double vision, older children and adults with acquired paralytic strabismus usually have diplopia, which they try to avoid by compensatory head posture. Some types of paralytic strabismus can be congenital but it is important to diagnose acquired paralytic strabismus that can be caused by some neurological or systemic disorders and requires further investigation. Treatment of the paralytic strabismus is challenging, and despite the multiple surgeries, results can be disappointing.
Part of the book: Treatment of Eye Motility Disorders
Thyroid-Associated Orbitopathy and Ocular Motility Disorders By Ivana Mravicic, Ivana Gabric, Selma Lukacevic,
Emma Grace Oreskovic and Anja Shumejko
Thyroid-associated orbitopathy is an autoimmune inflammatory disorder of the orbit associated with autoimmune thyroid disease. Autoimmune-mediated inflammation leads to the expansion of retrobulbar adipose tissue and extraocular muscles. This initiates a vicious cycle of progressive morphologic and functional orbital changes. Patients experience a variety of symptoms. Eyelid retraction, globe proptosis, erythema, and edema of periorbital soft tissues affect patients' appearance. Diplopia is a result of extraocular muscle changes. Corneal and optic nerve involvement represent vision-threatening complications. Reliance solely on clinical assessment is insufficient in differentiating between active inflammatory disease and inactive fibrotic stages. Imaging methods – ultrasound, computed tomography, and magnetic resonance imaging – are used in the assessment of the disease. Nowadays, optical coherence tomography has shown promise in evaluating disease activity in thyroid-associated orbitopathy by assessing choroidal parameters alongside retinal nerve fiber layer thickness, which may precede clinical signs of compressive optic neuropathy. Treatment modalities vary according to the phase of the disease. Corticosteroid therapy remains the first-line treatment for moderate-to-severe active disease. Teprotumumab (Tepezza), a monoclonal antibody targeting the insulin-like growth factor-1 receptor, has demonstrated superior clinical outcomes in reducing proptosis, diplopia, and disease activity, even in patients with long-standing disease. Botulinum toxin is used in the active phase of the disease to improve diplopia and abnormal head position. Surgical procedures represent the treatment of choice after the disease has entered the inactive phase, for patients with residual proptosis, diplopia, and strabismus, or for the improvement of eyelid malposition and function.
Part of the book: Ocular Motility and Systemic Disorders [Working title]
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