The macula is extremely vulnerable to trauma. Acute trauma originates from three general categories of injury: blunt, remote, and photic. In all these types of trauma, minor injury may yield little or no permanent damage. The more severe cases of macular edema and tissue disorganization, however, can result in macular holes and scarring, which command the clinician's attention. Careful observation of the signs and symptoms involved in the natural history of macular trauma is needed.
Liability claims involving eye care for pediatric patients may constitute as much as 20% of claims against optometrists, with the most common sources of litigation being failure to detect tumors affecting the visual system, improper diagnosis and management of binocular vision disorders, and injuries from shattered spectacle lenses. Claims for pediatric patients tend to allege large damages, partially because of the significant effect exerted by lifelong vision impairment or loss of vision.
A general overview of age-related macular degeneration, including its definition, classification, and epidemiology, is followed by specifically described clinical findings of this disorder. Included are the differential diagnosis, histopathology, prevalence, risk factors, and natural history of each individual form. Also presented are the issues of optometric management, including clinical recognition of choroidal neovascularization, timely referral for retinal consultation and angiography, preventive therapies, current and emerging trends in the medical and surgical treatment, and appropriate follow-up.
Choroidal neovascularization (CNV) is an important clinical finding that is associated with many ocular conditions, including inflammatory, infectious, degenerative, hereditary, and congenital disorders, ocular tumors, trauma, and a few miscellaneous disorders. The growth of new choroidal vessels beneath the retinal pigment epithelium is associated with specific clinical signs. The clinical recognition of CNV plays a key role in the prognosis and management of these disorders. The clinical presentation of each disorder associated with CNV is reviewed in this paper, with comments on the location and the frequency of CNV occurrence.
Multiple sclerosis is a demyelinating disease of the central nervous system that commonly presents with ocular manifestations. These ocular manifestations include vision loss and optomotor deficit. Treatment modalities should include treatment of the systemic disease as well as the ocular disease. New treatment protocol suggests that the best way to treat optic neuritis is with IV methylprednisolone, unless there is some serious contraindication for the patient. The use of interferon and cyclosporin as well as other anti-inflammatory agents may be useful in the future.
The visual system and its processing of sensory information can be affected in a variety of ways that may be either normal or associated with numerous disorders and diseases. Visual images produced by the intrinsic components of the eyes are often normal and are known as entoptic phenomena. In contrast, the visual system may be disrupted by various disorders and pathologic processes, which can result in metamorphopsia, transient loss of vision, and positive scotomas. Such disruptions can be secondary to retinal and optic nerve disease, migraines associated with visual auras, and cerebrovascular and neurologic diseases; they can also be side effects of certain drugs. In addition, the visual system may process incoming sensory information in such a way that what is seen is perceived incorrectly, i.e. illusion; or the visual system may produce images of things not really there, i.e. hallucination. Various types of visual phenomena, disturbances, and hallucinations are discussed. The numerous visual presentations need to be differentiated so that appropriate treatment, management, and patient education can be rendered.
As the incidence of human immunodeficiency virus (HIV) infection increases throughout the world, there becomes a greater probability that the primary care clinician will be confronted by AIDS-related complications. Neuro-ophthalmic problems, including optic neuropathies, motility disturbances, and visual field defects, are an important and common part of the AIDS spectrum. However diverse and challenging to the clinician, they may be the initial presentation of HIV infection. While opportunistic infections and neoplasms comprise the major source of neuro-ophthalmic problems, HIV itself may also be included. This paper is a review of the common causes of AIDS-related neuro-ophthalmic disorders and their clinical manifestations.
For most people, walking is an automatic, unconscious activity, characteristic of each individual. Patterns of gait can be reflective of a person's body structure, occupation, and personality, as well as health status. Most parents who watch an infant beginning to walk realize that locomotion is a highly complex, learned process. Years of training and practice are necessary for the sensory-motor system to become adept at automatically generating the motor commands necessary to permit walking without conscious effort. The characteristic adult pattern of walking does not emerge until up to 7 to 9 years of age, after the neuromusculoskeletal systems have undergone constant modification and development of improved neural controls. Important information pertinent to the patient's health status can be obtained by observing his or her manner of walking. This article will review abnormal gait patterns due to nervous system dysfunction. To help understand abnormal gaits, a brief review of the underlying components of walking is necessary.
Leber's hereditary optic neuropathy (LHON) is a distinct form of optic atrophy with a unique pattern of inheritance. The clinical reports of this disorder remain consistent with the original classic description made by Theodor Leber in 1871. Recent advances in the field of molecular genetics, however, have yielded insights into the etiological determinants underlying the clinical expression of LHON. Disease presentation, both ophthalmoscopically and clinically, are reviewed. Classic and atypical presentations are discussed with genetic testing as the definitive diagnostic measurement. Clinical and histopathological findings have led to the investigation of promising preclinical indicators of LHON symptomatology. Evidence of a multifactorial etiology has implicated a broad spectrum of potential intervention protocols. Teaming of the clinician and laboratory geneticist to identify those at risk is critical, not only for future clinical protocols, but to allow for immediate intervention when an effective therapy becomes available.
Diplopia is a symptom that may be the result of paralytic strabismus. The causes of paralytic strabismus are deficiencies of cranial nerves III, IV, or VI. When encountering neurogenic diplopia, the clinician must determine which ocular motor nerve is involved. The clinician must then decide whether the disturbance is in the nerve nucleus, its fascicles, along the course of the nerve in the subarachnoid space, in the cavernous sinus, or at its termination within the orbit. With proper diagnosis, identification, and localization, appropriate management may be undertaken.
A comprehensive case history is vital in the diagnosis and management of neuro-ophthalmic disease. This history is developed throughout an examination, and it is expanded whenever follow-up evaluations occur. Major objectives for developing a neuro-ophthalmic case history include having the patient reveal any clues suggesting that organic lesions exist, and subsequently exploring for characteristic ocular and nonocular symptoms that might prove helpful in localizing such lesions. The history is considered when selecting diagnostic procedures for the workup of neuro-ophthalmic patients, and it is especially vital in the decision as to which management options to pursue.
Intracranial hypertension is not a definitive diagnosis, but rather a syndrome that may result from a number of neurologic and systemic disorders. Intracranial hypertension refers to prolonged elevation of intracranial pressure, generally above 200 mm H2O. This condition may be recognized by the various clinical signs and symptoms that are manifest in most patients, including headache, papilledema, transient visual obscurations, diplopia, ocular motor disorders, tinnitus, nausea, vomiting, and mental irregularities, as well as dysfunctions of the circulatory and respiratory systems. Thorough medical testing as well as a comprehensive ocular evaluation is indicated in these cases. Intracranial hypertension most commonly results from mass lesions, tension hydrocephalus, and pseudotumor cerebri. Other causes include disorders of venous outflow, such as dural sinus thromboses or arteriovenous malformations, and various encephalopathies. Management for intracranial hypertension may involve medical treatment, drug therapy, or surgical intervention. Typically, diuretics are used initially. Corticosteroids may be used as well, although they are not the first choice for treatment. Cerebrospinal fluid shunting procedures may be necessary if medical treatment fails. Optic nerve sheath decompression may also be attempted when chronic papilledema threatens visual function. It is important that the primary care optometrist recognize the manifestations of intracranial hypertension in order to make necessary referrals for management of the underlying etiologies.
The introduction of laser photocoagulation for the treatment of macular disease has enabled many patients to retain visual acuity and retard additional deterioration of vision. Treatable maculopathy can occur as the result of choroidal neovascular development, idiopathic central serous choroidopathy, and retinal vascular disease. Variations in the treatment of these maculopathies include type of laser used, spot size, duration of treatment, burn pattern, and intensity of the burn. The cause of the maculopathy determines the type of laser photocoagulation that is most appropriate. While some forms of treatment leave characteristic scars, others leave hardly a trace. Use of fluorescein angiography, and in some cases indocyanine green angiography, is essential in the determination of the appropriate laser treatment modality.
Macular hole is a common cause of vision loss in older persons. Macular hole is formed by an actual hole through the neurosensory retina in the foveola area. The neurosensory retina adjacent to the hole is typically detached, which results in decreased central vision. Macular hole can be bilateral. Vitreous interactions with the posterior retinal surface are thought to be the essential cause of idiopathic macular hole formation. Until recently, no treatment was available for macular hole. Various surgical procedures are now being performed to repair macular hole and restore the neurosensory retina to its normal anatomical position. This paper presents the clinical characteristics of macular hole, reviews its incidence and its pathogenesis, and discusses the benefits and risks of surgical intervention in idiopathic macular hole formation.
Ophthalmic fluorescein angiography is an important clinical procedure used to investigate and document the status of the retinal and choroidal vascular systems. Administered intravenously and followed by rapid-sequence serial photographs, the fluorescein dye produces an angiographic display that is used to visualize and document retinal blood flow dynamics while recording the integrity of the inner blood-retinal barriers and the fine details of the retinal pigment epithelium. It is an important diagnostic and research tool, and has the added advantage of serving to illustrate the manner in which the retina and choroid respond to disease. More visual resolution is possible with this diagnostic procedure than with others, and it is a valuable adjunct to stereoscopic fundus biomicroscopy and binocular indirect ophthalmoscopy. The procedure has further utility in determining the suitability for laser photocoagulation surgery in macular and retinal vascular disease states. Ophthalmic angiography is also applicable the anterior segment, where it is employed as a research tool in the evaluation of conjunctival, episcleral, corneal, and especially iris blood vessels. Anterior segment use of fluorescein angiography has yet to become a prevalent clinical tool; rather, it currently has more extensive application through research, in developing a better understanding of the nature of anterior segment disorders.
Choroidal neovascularization is an important disease process that can result in severe vision loss in the affected eye. It has been a challenge for ophthalmic physicians to manage this complicated disease, especially when the neovascularization is subfoveal. Our increased understanding of macular disorders has allowed the development of advanced instrumentation and techniques in the treatment and management of choroidal neovascularization. As a treatment alternative to laser therapy, skilled vitreoretinal surgeons today have the technical ability to partially restore and maintain central visual function by surgically removing subfoveal choroidal neovascular membranes. Management of this condition may consist of monitoring the neovascularization, performing laser therapy, or surgically removing the choroidal neovascularization. This paper is limited to the surgical management of this disorder.
Idiopathic central serous chorioretinopathy is a very commonly seen disease process involving atypical RPE cells allowing the development of a neuroepithelial retinal detachment. Typically, this disease is self-contained and resolves spontaneously; however, on occasion, one must intervene by treating the area of atypical RPE with laser photocoagulation. Patients with ICSC should be monitored closely for any signs of choroidal neovascular membrane.
Epiretinal membranes are a common finding in older patients but are rare in young patients. Although they may be associated with other ocular conditions, most epiretinal membranes occur in the absence of ocular pathology. Patient symptoms range from asymptomatic to complaints of severe vision loss and metamorphopsia. Epiretinal membranes are commonly classified according to their density and contractile characteristics. In this review, cellophane maculopathy refers to thin, glistening membrane, surface wrinkling maculopathy is characterized by fine, superficial retinal folds and macular pucker is associated with a dense, grayish-white membrane causing a characteristic pattern of severe retinal distortion. With sufficient visual disturbance, epiretinal membranes may be treated by pars plana posterior vitrectomy and epiretinal membrane peeling.
Cystoid macular edema (CME) may develop in association with a wide variety of ocular conditions. It is the result of cystic accumulation of extracellular intraretinal fluid in the outer plexiform and inner nuclear layers of the retina, as a result of breakdown of the blood-retinal barrier. It is most common following intraocular surgery, and in patients with venous occlusive disease, diabetic retinopathy, and posterior segment inflammatory conditions. A variety of approaches to the treatment of CME have been attempted, with a variable degree of success. These options have included topical and oral steroids, nonsteroidal anti-inflammatory agents, and laser photocoagulation treatment. The exact cause of CME and the effective treatment of this condition have remained elusive.
