Common neuro-ophthalmic pitfalls case-based teaching pdf

Gonioscopy revealed angle recession in the left eye, presumed due to his past history of eye injury. He was treated with topical medications to lower the IOP in his left eye, and subsequent serial examinations showed that his visual field defect was stable.

Discussion: The optic disc has a limited repertoire of expression. Acquired excavation of the optic nerve head, or disc cupping, is traditionally divided into glaucomatous and non-glaucomatous forms. The large majority of cases of disc cupping are glaucomatous in origin. Glaucomatous optic nerve damage has a characteristic appearance. The disease has a predilection for the arcuate fibers, which produces progressive loss of the neural rim starting at the superior and inferior poles of the optic disc, and causes vertical elongation of the cup.

If both eyes are equally affected, this early stage of the disease may be difficult to recognize. Another helpful finding is the presence of a single splinter hemorrhage on the disc margin, termed a Drance hemorrhage Figure 1. While similar hemorrhages are seen in a variety of conditions that cause disc edema, in the absence of disc swelling this finding is strongly suggestive of glaucoma. Focal damage to the nerve fiber layer, appearing as a notch in the neural rim, is also characteristic of glaucomatous optic neuropathy and sometimes follows a Drance hemorrhage Figure 1.

Uncommonly, causes of optic nerve damage other than glaucoma produce optic disc excavation. These mechanisms include compression, disc infarction due to giant cell arteritis, trauma and radiation necrosis. The fundus feature that is most helpful for distinguishing glaucomatous from non-glaucomatous cupping is the status of the remaining neural rim.

In glaucomatous discs, the rim generally maintains a more normal hue. Even in advanced cases of glaucoma in which nerve fiber loss is severe, the degree of disc excavation is disproportionately greater than the severity of rim pallor Figure 1. In contrast, rim pallor is a prominent feature of non-glaucomatous cupping. Other fundus features may also be helpful in making this distinction. Focal thinning of the temporal retinal rim is more characteristic of nonglaucomatous damage, whereas diffuse obliteration of the neural rim and peri-papillary atrophy usually reflect glaucomatous change.

In addition to optic disc appearance, measures of optic nerve function are also important. In keeping with the predilection for superior and inferior nerve fiber bundles, field defects in glaucoma are typically arcuate, particularly affecting the superior field. Central vision is spared until late in the course of the disease. In contrast, compressive causes of acquired disc excavation are often associated with visual field loss that respects the vertical meridian.

The clinical challenge in cases such as the above is to distinguish optic disc excavation from disc atrophy. Despite advances in optic disc imaging techniques such as ocular coherence tomography OCT , careful fundus examination is usually the key to making this diagnosis.

Diagnosis: Glaucomatous optic neuropathy Tip: Glaucoma should be included in the differential diagnosis for any patient with unexplained optic neuropathy. Painful mydriasis Case: A year-old librarian periodically noted a dull pain around her right eye when she worked nights in the archives section. At times, along with Chapter 1: Ocular disease or neurologic disease?

A B C Figure 1. A Greater loss of nerve fiber layer in the right eye results in asymmetric cupping. B Peri-papillary pigment disturbance and a characteristic Drance splinter hemorrhage at the inferotemporal disc margin. C Focal excavation of the neural rim inferiorly arrow.

A Despite severe cupping due to glaucoma, the remaining neural rim retains a nearly normal color. B Following optic nerve trauma, this disc shows cupping and severe pallor of the remaining neural rim.

Her symptoms always resolved by the following morning so she did not seek medical advice until one evening when her dull pain rapidly escalated to a severe right-sided headache. She felt weak and nauseated and could not see well. There was mild anisocoria in room light right pupil 4. Eye movements were full and there was no ptosis.

Before any further examination could be performed, she became bradycardic and hypotensive and vomited. Acute third nerve palsy due to ruptured posterior communicating artery pCOM aneurysm was suspected, and she was sent for immediate brain MRI and magnetic resonance angiography MRA.

These imaging studies, however, were normal. What clues suggest an alternative diagnosis? The first clue is the unilateral pupillary unreactivity in the absence of other neurologic deficits.

When the pupil is dysfunctional due to a pCOM aneurysm, it is virtually always associated with other elements of a third nerve palsy NP. In the setting of transtentorial herniation, a dilated pupil is occasionally the earliest sign of third nerve compression, but in such cases there is also alteration of consciousness and, in most cases, other focal neurologic deficits.

The presence of an isolated, non-reactive pupil in an awake patient should be considered an indication of ocular rather than intracranial disease. This symptom is not due to the pupillary unresponsiveness but indicates, in addition, an aberration of the ocular media. In this patient, the most likely cause is corneal edema secondary to acute angle closure glaucoma.

After her negative neuro-imaging, an ophthalmic consultant confirmed an elevated intraocular pressure of 55 mmHg in the right eye and closure of the angle.

Examination also revealed mild conjunctival injection and corneal haze Figure 1. The patient was treated with acetazolamide, timolol and pilocarpine followed by anterior chamber paracentesis, which brought dramatic relief of pain. She subsequently underwent bilateral peripheral laser iridotomies and has had no further attacks of pain. Discussion: Angle closure glaucoma can be categorized as primary due to a structurally narrow angle or secondary due to inflammation, trauma, ischemia or other ocular disorders.

In secondary glaucoma the examination typically shows evidence of the condition that produced the changes in the drainage system. In contrast, in patients with primary angle closure the examination between episodes may be entirely normal and thus the diagnosis may be more challenging. The clinical manifestations of angle closure glaucoma are variable with some patients hardly symptomatic and others nearly prostrate with pain.

Many patients have repeated self-limited episodes of subacute angle closure before a full attack. Such prodromal attacks generally consist of unilateral face or head pain accompanied by blurred vision and halos around lights, typically lasting 30—60 minutes. Pain is usually localized around the eye but may extend to the maxillary region and mimic dental pathology. In occasional patients, headache rather than eye pain is the presenting symptom.

Because there is often conjunctival injection during an attack, these painful episodes may be mistaken for cluster headache or other hemi-cranial headache syndromes.

It is important that neurologists keep the possibility of angle closure attacks in the differential diagnosis for these patients and consider ophthalmic referral to evaluate this possibility in selected patients. Factors that may precipitate an attack in predisposed individuals include prone position, a dark or dim light environment, prolonged near-work, stress, sneezing, pharmacologic mydriasis and certain anesthetic agents.

Patients with a high degree of hyperopia are particularly prone to such attacks. During an attack of angle closure, the IOP increases Chapter 1: Ocular disease or neurologic disease? Slit-lamp photograph shows mild conjunctival hyperemia, corneal haze and forward bowing of the iris consistent with acute angle closure glaucoma.

Photograph courtesy of Dr. Emilie Ravinet. The pupil is midsize and fixed. In subacute cases, the angle reopens spontaneously and symptoms and signs resolve. Between attacks the examination is usually normal although careful inspection will often reveal the narrow angle that predisposes to acute closure. The diagnosis is established by gonioscopy or ultrasound biomicroscopy.

Although assessment of intraocular pressure by digital examination is generally considered to be unreliable, this technique may be useful in cases with markedly elevated pressures when biomicroscopy is not immediately available. When the onset of pain is explosive and accompanied by a vasovagal reaction and vomiting, as was the case above, the clinical scenario mimics acute intracranial pathology.

The presence of a dilated pupil further adds to the impression of a cerebral aneurysm. It is important that neurologists keep the possibility of acute angle closure glaucoma in the differential diagnosis of painful isolated mydriasis and seek urgent ophthalmic referral in selected patients before proceeding with neurologic investigations.

Diagnosis: Acute angle closure glaucoma Tip: Acute angle closure glaucoma causes acute headache and an unreactive pupil. A history of blurred vision with halos in the eye with mydriasis suggests the diagnosis. Invisible retinal disease In most cases, retinal disease can be detected by a thorough dilated fundus examination.

Occasionally, however, such abnormalities are absent either due to the nature of the disease process, the timing of the examination or the expertise of the examiner. In 13 14 Chapter 1: Ocular disease or neurologic disease? The cases that follow are examples of such occult retinal disorders. Many macular disorders that at one time would have been considered occult are now readily identified with optical coherence tomography OCT.

Common examples in this category include central serous choroidopathy and cystoid macular edema. In some conditions in which the fundus examination and fluorescein angiographic findings may be normal, the pathology can be demonstrated with electrophysiology. The full-field electroretinogram ERG is abnormal in paraneoplastic retinopathies, retinitis pigmentosa and in vitamin A deficiency; however certain other disorders can be demonstrated only with multi-focal ERG.

Examples of the latter include outer retinal inflammatory diseases and some toxic maculopathies such as that induced by chloroquine. The importance of recognizing the symptoms and other clinical features that indicate a retinal disorder is in knowing when to employ these ancillary tests.

Twinkling scotoma Case: A year-old female graduate student sought medical attention because of a one-month history of scintillations. Specifically, she described a dark, oval-shaped spot temporal to fixation in her right eye, with continuous sparkling at its edge. She had noticed no change in the size or shape of the spot since onset and there was no associated head or eye pain. She was generally healthy and her only medication was oral contraceptives.

General eye examination was unrevealing and an MRI of the brain was also normal. She was started on topiramate for presumed migraine, but her twinkling scotoma persisted. Another atypical aspect of the history is the monocular nature of her scotoma. However, it should be noted that many patients with episodic visual disturbance involving one hemifield interpret their visual deficit as affecting just the eye with the temporal field defect.

In such cases it is helpful to ask the patient what they can and cannot see during the attack. Inability to see one half of an object such as a face or a clock is inconsistent with monocular loss and indicates instead a homonymous hemifield deficit. In the above case, the examiner verified that the visual disturbance was truly monocular. Subsequent neuro-ophthalmic examination demonstrated normal visual acuity, pupillary responses and fundus appearance. Goldmann perimetry showed marked enlargement of the physiologic blindspot in the right eye.

A multi-focal electroretinogram mfERG revealed decreased amplitude in the corresponding area of the right eye Figure 1. The patient was followed expectantly and over the next several years the blindspot in her right eye became smaller but the sparkling continued.

Ten years later, she still noted persistent scintillations in the involved area but found that they did not interfere with her daily activities. The peri-papillary retina in that eye had now developed a mottled, grayish appearance Figure 1. Discussion: Photopsias are a form of positive visual phenomenon that can arise anywhere along the afferent visual pathway. Several clinical features are helpful in localizing their origin.

Photopsias that are evoked by eye movement indicate a disorder in the anterior part of the visual system, usually due to vitreous traction, retinal detachment or optic neuritis. The last of these is typically associated with Chapter 1: Ocular disease or neurologic disease? A Goldmann perimetry shows enlargement of the physiologic blindspot in the right eye to nearly four times the normal-sized blindspot in the left eye.

In cases of spontaneous photopsias, the pattern of visual loss can suggest the correct localization, hence the utility of formal visual field testing in patients with this symptom. Occipital disorders are a frequent source of positive visual phenomena, including photopsias.

The three main diagnostic considerations in this location are migraine, transient ischemic attacks TIAs and occipital seizures. The previously enlarged blindspot had gradually diminished but she continued to experience photopsias in the right eye. A The peri-papillary retina in the right eye now has a grayish, moth-eaten appearance. B The left fundus is normal. Migraine visual aura usually consists of scintillations that are geometric and achromatic lasting 20 to 30 minutes see Chapter 11, Episodic scintillating scotoma.

Such TIAs last a few minutes and may be accompanied by other focal neurologic deficits. Occipital seizures may resemble migraine aura but are generally shorter in duration, lasting for 5 minutes or less, and often consist of colored circles rather than the achromatic zigzags of migraine. Occipital seizures may be accompanied by alteration of awareness and by automatisms such as frequent blinking or gaze deviation.

Regardless of the mechanism, the duration of positive visual phenomena emanating from the occipital cortex is finite. This is not the case for the outer retina. Any metabolic failure involving photoreceptors or retinal pigment epithelium cells can result in positive phenomena such as flashing lights, shimmers and sparkles, which can persist indefinitely.

This is because photoreceptors are normally in a depolarized state, becoming hyperpolarized in response to a light stimulus. Energy failure of any cause can result in an inability to maintain depolarization and thus the production of light flashes. Specific etiologies include retinitis pigmentosa, paraneoplastic retinopathies, toxic retinopathies and a spectrum of presumed inflammatory disorders of the outer retina.

The latter disorders are sometimes classified under the term acute zonal occult outer retinopathy AZOOR. The common feature in all of the AZOOR syndromes is a dense, sharply demarcated scotoma which appears acutely in any portion of the visual field with minimal or no fundus abnormalities. Individual descriptions of the photopsia include terms like light flashes, stars, strobe lights, sparkling, whirling, shimmering or flickering.

In acute idiopathic blindspot enlargement the fundamental feature is a dense, steeply margined scotoma centered around the physiologic blindspot, as in the above Chapter 1: Ocular disease or neurologic disease? Diagnosis: Acute idiopathic blindspot enlargement Tip: Continuous photopsias indicate a disorder of the outer retina. Sudden monocular visual loss with normal fundus Figure 1.

The peri-papillary retina is the target of inflammation, and the focal area of disturbed photoreceptor function is best demonstrated with multi-focal rather than full-field ERG. In the acute stage, the fundus is normal save for mild optic nerve swelling in some patients.

Multiple evanescent white dot syndrome MEWDS , a closely related syndrome, is characterized in its acute stage by small whitish lesions in the posterior pole Figure 1. The disorder usually affects healthy young women, and evaluation discloses no evidence of an underlying systemic disease. There is no established treatment but the natural history usually includes spontaneous improvement of the scotoma, although photopsias may persist.

As in the above case, prominent photopsias in patients with AIBSE may be mistaken for the visual disturbance of migraine. Because this disorder presents as acute onset of a monocular scotoma, it may also suggest a diagnosis of demyelinating optic neuritis. The absence of pain and the continuous nature of the scintillations are important distinguishing features.

Case: This year-old gentleman experienced sudden, painless visual loss in the left eye while watching television. At the onset of his visual loss he saw an arc of yellow lights briefly passing across the superior visual field in the left eye. He was generally healthy except for prostate cancer for which he was taking diethylstilbesterol. Based on the normal fundus appearance, he was thought to have a retrobulbar optic neuropathy, but an MRI of brain and orbits was completely normal.

What other mechanism of visual loss would you consider? Are there any historical features that are helpful here? A compressive or infiltrative optic nerve lesion should be in the differential, however the very abrupt onset of visual loss in this case would be unusual and his MRI was unrevealing. Acute painless monocular visual loss in a patient over the age of 50 years is most often ischemic in origin, and that should be the main consideration in this case.

The question is whether this ischemia affects the optic nerve or the retina. In the large majority of cases, ischemic optic neuropathy affects the most anterior portion of the nerve so that disc edema is seen acutely, termed anterior ischemic optic neuropathy AION.

In this patient, however, the disc was normal. Ischemia of the retrobulbar segment of the optic nerve, termed posterior ischemic optic neuropathy PION , is rare. A diagnosis of PION in any other setting should be suspect. In addition, the presence of photopsias heralding the onset of visual loss would be highly unusual in either form of ischemic optic neuropathy but sometimes accompanies a retinal ischemic event.

Retinal artery occlusion is therefore the leading diagnosis in this case. Why might a retinal stroke not have been apparent on examination?

Retinal whitening due to arterial occlusion may take up to 24 hours to develop. Ophthalmic examination three days later showed no change of visual acuity in the left eye.

There was a large central scotoma and small relative afferent pupillary defect RAPD. Dilated fundus examination now showed retinal whitening edema of the posterior pole with a macular cherry-red spot, confirming a diagnosis of CRAO Figure 1. Ancillary investigation revealed no embolic source, and testing for vasculitis and coagulation disorders was similarly unrevealing.

His CRAO was attributed to a hypercoaguable state secondary to treatment with diethystilbesterol. Discussion: Retinal artery occlusion typically produces acute, painless, monocular visual loss. Unlike individuals with ischemic optic neuropathy, who often note visual loss upon awakening, patients Figure 1. There is diffuse retinal whitening and a cherry-red spot in the macula, indicating central retinal artery occlusion.

In contrast, such episodes of preceding transient monocular visual loss are distinctly uncommon in patients with non-arteritic AION. The fundus appearance in retinal artery occlusion depends on the timing of the examination. In the hyperacute phase there may be obvious attenuation and segmentation of the blood column within retinal arteries, and the responsible embolus may be visible.

If the embolic material has moved on through the retinal circulation, however, and flow has already been restored, the retina may have a completely normal appearance. This phase may last up to 24 hours. As edema develops, areas of retinal whitening appear. This may take the form of cottonwool spots indicating small nerve fiber infarcts or of patchy or diffuse retinal whitening. The distribution of retinal edema varies depending on whether the central or a branch retinal artery was involved Figure 1.

In cases of central retinal artery Chapter 1: Ocular disease or neurologic disease? A There is a sharp demarcation between the area of acute retinal infarction, which appears white due to edema, and the normal adjacent retina. B Confluent cotton-wool spots represent focal infarcts of the nerve fiber layer. In the chronic phase, after retinal edema has resolved, differentiating between retinal and optic nerve ischemia may again be difficult.

Because of retrograde axonal degeneration, in the wake of a retinovascular event the optic disc will appear pale, either focally or diffusely. In this stage, electrophysiologic testing, usually with the mfERG, can be helpful for making this distinction.

Diagnosis: Hyperacute occlusion central retinal artery Tip: In a hyperacute retinal artery occlusion, the retina may have a normal appearance. Goldmann perimetry showed mild superior depression, and dilated fundus examination was normal Figure 1.

A fluorescein angiogram and ocular coherence tomography OCT were also unrevealing. Based on the negative ophthalmic work-up, a neurologic cause was suspected and the patient was referred for neurologic evaluation. An MRI showed a few white matter lesions consistent with small vessel disease but was otherwise normal.

This became so severe that he started using a nightlight and stopped driving after dark. He had no head or eye pain, focal neurologic deficits or systemic symptoms. His medical history Difficulty seeing at night nyctalopia strongly suggests retinal disease, specifically a disorder of photoreceptors preferentially involving the rods.

In this patient, a full-field electroretinogram ERG showed markedly reduced amplitudes on scotopic testing and mild reduction on photopic testing, confirming rod dysfunction Figure 1. A serum retinol 19 20 Chapter 1: Ocular disease or neurologic disease?

There is mild superior depression affecting central and mid-peripheral isopters in both eyes. The patient received a diagnosis of retinal dysfunction due to hypovitaminosis A related to prior gastric bypass surgery. He was treated with units of oral vitamin A per day, and over the next six weeks experienced progressive recovery of vision.

A repeat ERG showed an increase in the scotopic amplitudes bilaterally Figure 1. Discussion: Vitamin A is a fat-soluble vitamin that is absorbed across the small intestinal mucosa and transported to the liver, where it is stored in its esterified form retinol and available in protein-bound form to reach target tissues.

In the retina it is stored in the retinal pigment epithelial cells and converted to the aldehyde form retinal , which then combines with opsin to form rhodopsin. Vitamin A deficiency can result from inadequate nutritional intake common in underdeveloped countries , poor intestinal absorption, impaired liver storage capacity or inadequate enzymatic conversion of retinol to retinal a process that is dependent upon zinc as a co-factor.

Causes of malabsorption include intestinal bypass surgery, regional enteritis and cystic fibrosis. Liver disease may cause hypovitaminosis A by a variety of mechanisms: decreased production of retinol-binding protein, inadequate storage of retinol, malabsorption due to decreased bile salts and depletion of zinc stores.

Occasionally, deficiency is caused by the use of a synthetic vitamin A analog such as isotretinoin. Ophthalmic manifestations of vitamin A deficiency typically include dry eyes and retinopathy. The earliest symptom is usually nyctalopia due to the greater dependency of rods on rapid transport with retinal pigment epithelial RPE cells.

If the deficiency is not corrected, this is followed by visual field loss, photophobia and decreased acuity. Severe loss of visual acuity and color vision is unusual. Visual field testing may show central and paracentral defects that affect the superior field more than the inferior field.

Funduscopic examination is often normal, especially in early vitamin A deficiency, thus causing confusion with neurologic visual loss. With pro- longed deficiency, multiple yellowish-white dots may appear in the mid-peripheral retina, giving it a stippled appearance.

Fluorescein angiography may demonstrate numerous punctate RPE defects which correspond to these retinal lesions. These clinical abnormalities are present to varying degrees and are generally reversible within several months after vitamin repletion. Electrophysiologic tests such as dark adaptometry and full-field ERG are quite sensitive in this condition, revealing abnormal rod function even in the absence of visual symptoms.

Eventually there is elevation of the threshold and loss of waveform amplitude for both rods and cones, though rod function is more severely affected. The diagnosis should be suspected on clinical grounds and confirmed by testing the vitamin A level. Following treatment, the electrophysiologic abnormalities are faster to improve than the fundus abnormalities, and the final visual prognosis is generally good although in cases of prolonged depletion permanent damage may occur.

Diagnosis: Hypovitaminosis A Tip: Even in the absence of ophthalmoscopic abnormalities, a history of acquired, progressive nyctalopia should suggest a retinal disorder. He did not have eye pain but did have prominent photophobia and noted that his vision was much worse in bright light.

The visual field in the right eye showed a ring scotoma and was normal in the left eye. Dilated fundus examination and fluorescein angiography were normal. A retrobulbar optic neuropathy was suspected but an MRI of brain and orbits with gadolinium was normal.

He received a tentative diagnosis of posterior ischemic optic neuropathy. Two months later, similar though milder visual loss developed in the left eye 21 22 Chapter 1: Ocular disease or neurologic disease?

In the right eye there is a dense ring scotoma breaking out to the periphery. In the left eye there is an inferior arcuate scotoma that breaks out nasally. As before, the fundus appearance was normal. A full-field ERG was nearly unrecordable under both scotopic and photopic conditions, indicating severe dysfunction of both rods and cones. Serologic testing showed antibodies to recoverin, diagnostic of cancer-associated retinopathy CAR. A chest radiograph was normal but a chest computerized tomography CT scan revealed a small lesion which, on biopsy, proved to be a small cell lung carcinoma.

His primary tumor was treated with radiation and chemotherapy and he received a course of high-dose intravenous corticosteroids followed by rituximab. Vision stabilized but unfortunately showed minimal improvement. Discussion: Cancer-associated retinopathy CAR is a paraneoplastic syndrome in which antibodies directed toward a neoplasm also attack specific sites in the retina.

It is most commonly associated with small cell lung carcinoma but has been described with various other malignancies including non-small cell lung cancer, breast and gynecologic malignancies, prostate and bladder cancer. In half of patients with the syndrome, the presence of a malignancy is unsuspected at the onset of visual loss. The typical presentation consists of subacute, bilateral visual deterioration associated with photopsias and a variety of other entoptic phenomena including swirls, clouds, smoke and floaters.

Early in the disease, the fundus appearance is normal. Later, attenuated arterioles, mottling of the retinal pigment epithelium, disc pallor and vitreous cells may be seen.

The triad of photosensitivity, ring scotomas and attenuated retinal arterioles, particularly in an older patient, should suggest a diagnosis of CAR syndrome. The autoimmune mechanism of CAR has been established with the discovery of auto-antibodies directed toward retina-specific antigens. It presents current knowledge about seizures and epilepsy in a comprehensive, socially conscious, and clear manner. The editors have provided this information in a comprehensive,.

Common Pitfalls in Sleep Medicine. Focusing on disorders and presentations that are a frequent source of confusion, key diagnostic principles are illustrated clearly.

Questions to the reader move the narrative along logically, whilst highlighting specific aspects of clinical presentation that lead to the correct diagnosis. Videos of patients connect readers to the cases and demonstrate how to avoid diagnostic pitfalls.

An online version of the book can be accessed on Cambridge Core, via the code printed on the inside of the cover. Savitz Author , James Grotta Author. Woods Editor. Martins Editor , Charles S. Brennan Editor , Stephanie J. This book offers an overview on the most recent advances in global neuro-opthalmic care. Global variation in the incidence and prevalence of specific neuro-ophthalmic conditions results in geographic differences in differential diagnosis, evaluation, management, and treatment of specific disorders.

It covers a variety of disorders from optic neuritis, idiopathic intracranial hypertension to traumatic optic neuropathy. To understand the key differences in neuro-ophthalmic health care, this book has gathered recognized experts from around the world to describe and define these regional.

Each chapter provides a discussion of the diagnosis, key points to remember, and selected references for further reading. For this new edition, all cases and references have been updated and new cases have been added, including neuroretinitis, autosomal dominant optic atrophy, carotid-cavernous fistula,. Seasoned Elsevier authors Neil J. Friedman and Peter K. Kaiser help you get the best possible results in your exams with Case Reviews in Ophthalmology.

This medical reference's case-based approach gives you just the practice you need to assess, reinforce, and broaden your mastery of every essential concept in ophthalmology for clinical rounds, oral boards or recertification. Neuro-ophthalmology is a field of medicine that touches on every subspecialty in neurology, but has an undeserved reputation as a branch of knowledge that is difficult to learn and practice.

Many neurologists and ophthalmologists do not receive sufficient exposure to neuro-ophthalmology during their residencies, and are uncomfortable diagnosing and treating patients with neuro-ophthalmic problems. Authored by neuro-ophthalmologists whose careers span three generations in the field, Neuro-Ophthalmology helps clinicians evaluate and manage patients with neuro-ophthalmic problems. This "curb-side consult" approach is.

Author : Valerie A.