Susan Faye Dent, MD

• Instructor in the Department of Medicine
• Member of the Duke Cancer Institute

https://medicine.duke.edu/faculty/susan-faye-dent-md

The nature and extent of the deviations of the eyes in relation to each other may be assessed subjectively with the red glass or Maddox rod and confirmed objectively by the alternate-cover test acne y clima frio polar order 30gm elimite free shipping. The latter test with prisms can provide quantifiable measurements that help to localize the underacting muscles and allow careful follow-up acne x soap generic elimite 30gm without prescription. For a patient with a complaint referable to cranial nerve dysfunction skin care steps generic elimite 30gm with amex, the problem must be approached in an orderly acne tretinoin cream 005 generic elimite 30 gm visa, logical acne extractions order elimite online, and acne yellow crust order elimite from india, above all, anatomic manner. Localization of the lesion helps to determine the differential diagnosis and subsequent management. Associated symptoms are of extreme importance in the evaluation of the third, fourth, and sixth cranial nerves. The patient must be asked about headache or localized pain of the orbit, globe, or periorbital region; a red or protruding eye; visual involvement; facial or body numbness or weakness; hearing loss; tinnitus; self-audible bruits; loss of smell or taste; or any previous episodes of neurologic or ophthalmic dysfunction. During visual assessment, binocularity of the diplopia is verified by monocular occlusion. Associated abnormalities of visual acuity, color vision, or visual fields may be important localizing features. They can result from lesions anywhere along the anatomic pathway from the nucleus to the muscle. The pupil is usually involved (either miotic, because of presumed aberrant regeneration, or dilated), but pupillary sparing has been noted in some cases. However, when the lesion can be localized to a specific site along the course of the nerve (by either the accompanying signs or the particular nature of the palsy), a more limited and manageable differential diagnosis emerges (Table 296. Lesions involving the oculomotor nucleus have a particular constellation of clinical signs reflecting the unique anatomy described earlier. Although a unilateral, stereotactically placed experimental lesion could conceivably result in bilateral ptosis, contralateral superior rectus dysfunction, and abnormalities of the remaining muscles ipsilaterally, the clinical picture is more likely that of a complete ipsilateral oculomotor nerve palsy with additional contralateral ptosis and superior rectus dysfunction. Motility photographs (a) show poor elevation of the right eye in both adduction and abduction. A 78-year-old man had sudden onset of lethargy, left hemiparesis, bilateral ptosis, and ophthalmoplegia. Examination was notable for bilateral complete ptosis and no ocular motility except normal abduction of both eyes. The patient was a 70-year-old woman with sudden onset of a right oculomotor nerve palsy and left hemiparesis. The subarachnoid space is the most likely site of injury in cases of isolated oculomotor palsies. Involvement may be partial or complete, although most commonly there is progression to total involvement over time. Because of the dorsal and peripheral location of the pupillary fibers, a dilated pupil may be the first sign of a compressive lesion in the subarachnoid space. Almost without exception, there is pain (although sometimes modest) and eventually other evidence of oculomotor nerve involvement. Other locations of aneurysmal dilatation that have been shown to cause third-nerve palsies include the top of the basilar artery and the junction of the basilar and superior cerebellar arteries. Although bifurcation of the nerve into its two divisions typically occurs in the anterior cavernous sinus,90,91 there is evidence that a functional bifurcation occurs more proximally along the course of the oculomotor nerve, probably within the brain stem,40,41,46,92 making localization of a divisional paresis problematic. To identify clinically a cavernous sinus location of an oculomotor nerve palsy, one must note the company it keeps. The patient, a 34-year-old woman, had severe deficits, including a right third-nerve palsy, a left hemiparesis, and a left homonymous hemianopia. The pupil may be small or midsized and poorly reactive because of concurrent oculosympathetic involvement. Causes include trauma, neoplasms, mucoceles, vascular malformations, and inflammation. The patient was an otherwise quite healthy 85year-old woman who presented with headache, diplopia, and ptosis and was found to have a right pupil-involved oculomotor nerve palsy. The patient was a 42-year-old woman who had left ptosis and both horizontal and vertical diplopia for 3 weeks. True pupillary sparing implies that each of the extraocular muscles innervated by the oculomotor nerve is involved to some extent, but the pupil remains of normal size and reactivity. The cause of most isolated pupil-sparing third-nerve palsies is believed to be microvascular ischemia, frequently associated with diabetes mellitus or other vascular risk factors. In some cases, the spasms can be brought on by voluntary efforts in the direction of paretic muscles. The cause is unknown, but most authors speculate some element of aberrant regeneration after nerve or nuclear damage, similar to proposed mechanisms of ocular neuromytonia (see further ahead). Most of these patients have a history of radiation therapy to either the parenchymal or the peripheral course of the ocular motor nerves. A pseudo-Graefe sign is shown in a patient with a right cavernous sinus aneurysm and aberrant regeneration of branches of the third nerve. A 30-year-old man had sudden onset of diplopia, incoordination, and poor tandem gait and was noted to have a partial oculomotor nerve palsy in the right eye involving primarily the inferior rectus. The approach to the patient with an isolated third-nerve palsy differs among clinicians, and some of the issues remain controversial. If no cause for the third nerve palsy is found, one must proceed in this setting to vascular imaging. The contralateral carotid circulation should also be evaluated, because ~20% of patients have more than one aneurysm. There is some controversy about the application of this rule to children younger than 10 years, in whom aneurysms are extremely rare. Minimal work-up for the known diabetic patient would consist of a measurement of systemic blood pressure, serum glucose, erythrocyte sedimentation rate and C-reactive protein. If there is no history of diabetes, a glucose tolerance test or a serum hemoglobin A1c level should be obtained. These patients must be observed closely for the next week for evidence of pupillary involvement. Compressive or traumatic oculomotor nerve palsies may take longer to improve, and incomplete recovery with or without synkinesis is more likely. Despite rare reports of continued improvement in third-nerve palsies years after onset,153 once the deficit has stabilized (usually within 6 months after injury), further recovery is unlikely. The chronic oculomotor palsy, especially in younger age groups, requires serial neuroimaging over the years, especially as the sensitivity of the techniques improves. Various surgical procedures have been used to provide binocular fusion in at least primary position after third-nerve palsy and to correct vision-limiting or cosmetically annoying upper lid ptosis. However, complete oculomotor nerve palsies rarely allow a completely satisfactory surgical result. The role of botulinum toxin injection in the management of acute or chronic third-nerve paresis has not been adequately investigated. The two intorters of each eye are the superior oblique and superior rectus muscles. If the superior oblique is paretic, the superior rectus, on attempted intorsion, further elevates the eye, because this is its primary function. Thus, the vertical deviation worsens when the head is tilted in such a way that intorsion is necessary. Other causes of vertical strabismus, such as paralysis of more than one vertical muscle, dissociated vertical divergence, previous muscle surgery, contracture of the vertical rectus muscles, myasthenia gravis, thyroid ophthalmopathy, and skew deviation, may result in a positive three-step test and cause errors in diagnosis. Patients typically compensate for a superior oblique palsy by tilting the head to the opposite side. Another clue to trochlear nerve paresis in the observant patient is a torsional component of the vertical diplopia: the two vertically separated images are not parallel but rather approach each other as if to meet in the direction of the involved eye. The patient was a 62-year-old man with insulindependent diabetes mellitus and new-onset diplopia and complete left ptosis. Examination 2 weeks after symptom onset (a) showed resolution of the ptosis, but nearly complete deficits of adduction, elevation and depression of the left eye, and equal and reactive pupils. In the acquired forms, such as those seen with rheumatoid arthritis and other connective tissue abnormalities, pain and tenderness of the superomedial orbit may be prominent. Idiopathic trochleitis typically presents as isolated orbital pain with superior medial orbital tenderness, but in the susceptible person it may trigger chronic migraine. When an etiology is known, the most common cause is trauma, although the exact locus of involvement remains unclear. As with oculomotor nerve palsies of similar cause, it is unknown where an ischemic lesion occurs along the course of the fourth nerve. This could be caused by weakness of elevators of the right eye or depressors of the left eye. Neoplastic, inflammatory, and infiltrative causes are essentially the same as those discussed earlier in relation to oculomotor nerve abnormalities in the same location. Neoplastic, inflammatory, ischemic, and traumatic processes within the orbit may affect the trochlear nerve, the superior oblique muscle, or the trochlear tendon or its sheath. Fine vertical or intorsional monocular movements are best viewed at the slit lamp and can sometimes be induced by directing the patient to look in the primary direction of action of the superior oblique muscle. Successful medical therapy has been achieved with carbamazepine, low-dose propranolol, gabapentin, and even topical b-blockers. The main differential diagnosis of isolated trochlear nerve paresis includes skew deviation, ocular myopathies, and myasthenia gravis. Thyroid ophthalmopathy is rarely restricted to a single muscle, and orbital myositis affecting only the superior oblique is typically quite painful. Disorders of the neuromuscular junction can mimic any single ocular muscle paralysis. For the patient with evidence of a decompensated congenital trochlear nerve palsy. Successive old photographs of a patient with a congenital left fourth-nerve palsy. Note the overaction of the left inferior oblique at age 6 months (a) and the right head tilt at age 7 years (b), 16 years (c), and 40 years (d). Further evaluation can probably be avoided as long as careful observation shows nonprogression and the absence of associated signs. The majority of acquired trochlear nerve palsies of traumatic, microvascular, or undetermined etiology improve over time, usually within 6 months. In the interim, monocular occlusion or vertical prisms may help the patient symptomatically. Various surgical procedures have been proposed involving the paretic muscle, its antagonist, or the contralateral yoke muscle. Although the abducens nerve may appear to be a simple arrangement of one nerve supplying a single ipsilateral extraocular muscle, the unique organization of its nucleus and the surrounding brain stem structures provides for a rich assortment of congenital and acquired clinical syndromes. An examination of the patient with suspected sixth-nerve palsy must include a close inspection of the function of the other cranial nerves of pontine origin and of the motility of the contralateral eye. A 52-year-old woman had sudden onset of dizziness, poor balance, and vertical binocular diplopia and was found to have right superior oblique weakness. A 61-year-old man presented with pain and vertical diplopia for 1 week and was found to have a subtle left fourth-nerve palsy. Etiologies are heterogeneous, including maldevelopment, intrauterine insults such as infections or hypoxia, and trauma. The patient, a 29-year-old man, first presented with diplopia in upgaze and right upper lid ptosis. A petroclival mass was partially resected, and postoperatively he noted diplopia on downgaze as well. Examination 9 years later revealed mild limitation of adduction and substantial limitation of depression in adduction of the right eye (a), consistent with partial right third- and fourth-nerve palsies. The likely cause of this syndrome is an anomaly of innervation involving the third and sixth nerves. The most common reported pathology is a congenital absence of abducens neurons with innervation of the lateral rectus muscle by branches of the oculomotor nerve. Retraction of the globe with consequent narrowing of the palpebral fissure in some cases reflects co-contraction of the lateral and medial rectus muscles on attempted adduction. Furthermore, the proximity of the facial nerve fascicle as it loops around the abducens nucleus frequently results in a peripheral facial palsy as part of the clinical picture. The structures affected are the abducens fascicles or nucleus, the facial nerve fascicles, the nucleus of the tractus solitarius, the spinal tract of the trigeminal nerve, the central tegmental tract, and the cochlear nuclei, respectively. The former is a combination of sixth-nerve palsy and contralateral hemiplegia secondary to involvement of the abducens fascicles as they course through the ipsilateral pyramidal tract. The patient was a 54-year-old woman who had binocular vertical diplopia for 4 weeks. Examination revealed full-appearing ductions and versions, but crosscover and Maddox rod testing revealed a right hypertropia that increased with left gaze, downgaze, and right head tilt, diagnostic of weakness of the right superior oblique muscle. There was no abduction of the left eye on attempted gaze to the left (right panel). With gaze to the right (left panel), the left globe retracted, and there was consequent palpebral fissure narrowing. Meningeal processes, including infectious, inflammatory, and neoplastic etiologies, may present with abduction deficits. The patient was a 40-year-old man, human immunodeficiency virus positive, with newonset fever and diplopia. Examination revealed a complete right horizontal gaze palsy and a right peripheral facial palsy, exquisitely localizing the lesion to the right sixth-nerve nucleus. The patient was a 40-year-old woman with her third episode of brain stem dysfunction secondary to brain stem hemorrhage. Examination revealed a right horizontal gaze palsy, right internuclear ophthalmoplegia, rotary nystagmus, right peripheral facial palsy, palatal myoclonus, decreased hearing in the right ear, and left hemiparesis and hemisensory loss. The patient was a 6-year-old girl who had progressive horizontal binocular diplopia for 2 months.

In addition skin care in your 20s purchase elimite 30gm on-line, corneal skin care pregnancy generic 30 gm elimite with amex, episcleral skin care questionnaire buy discount elimite 30 gm line, and scleral diseases are common and may lead to significant morbidity acne 8dpo buy elimite 30gm online. Primary care providers need to be aware of these ocular disorders so as to facilitate routine eye care for their patients and to provide appropriate referrals to the ophthalmologist as soon as ocular morbidity is suspected acne diet generic 30 gm elimite with visa. However skin care 0-1 years purchase generic elimite on-line, it has become clear that no single marker has adequate specificity or sensitivity to form the basis for clinical decisions. Greiner A, Plischke H, Kellner H, Gruber R: Association of anti-cyclic citrullinated peptide antibodies, anti-citrullin antibodies, and IgM and IgA rheumatoid factors with serological parameters of disease activity in rheumatoid arthritis. Mielke H, Daniel W, Deicher H, et al: the importance of skin wall immune deposits in the course of systemic and articular features of rheumatoid arthritis. Fujita M, Igarashi T, Kurai T, et al: Correlation between dry eye and rheumatoid arthritis activity. Iwase-Okada K, Nagatsu T, Fujita K, et al: Serum collagenase-like peptidase activity in rheumatoid arthritis and systemic lupus erythematosus. Konishi T, Saida T, Nishitani H: Orbital apex syndrome caused by rheumatoid nodules. Roquer J, Herraiz J, Maymo J, et al: MillerFisher syndrome during treatment with salts in a patient with rheumatoid arthritis. The revised 11 diagnostic criteria proposed by the American Rheumatism Association are widely accepted (Table 324. At the time of presentation, only one organ system may be involved, with or without the presence of autoantibodies. It should be noted, however, that there is a general consensus that these current criteria overrepresent cutaneous lupus, may not capture early lupus, and do not capture some patients with lupus nephritis and neurologic lupus. Most patients have periods of quiescence interrupted by exacerbations rather than a relentless and progressive disease. Cardiopulmonary involvement includes pleuritis, pleural effusion, pericarditis, myocarditis, vegetative endocarditis, and coronary artery disease. Gastrointestinal disease is often difficult to diagnose because of nonspecific signs and symptoms but may lead to intestinal perforation and death. In addition to pregnancy, the use of sulfonamides and contraceptives has been associated with exacerbations of the disease. Pregnancy in lupus is complicated by a high rate of spontaneous abortions and stillbirths as well as flare-ups of the disease. Congenital lupus includes discoid lupus and congenital heart block and is caused by maternal antibodies that cross the placenta. The most commonly implicated drugs in descending order of importance include procainamide, hydralazine, isoniazid, chlorpromazine, penicillamine, practolol, methyldopa, and oral contraceptives. Signs and symptoms are usually reversible and rarely persist after the inciting drug is discontinued. Skin findings include the typical malar butterfly rash, discoid lesions, a nonspecific erythematous maculopapular rash, and cutaneous vasculitic lesions. Renal disease is the primary cause of death, and prognosis is dependent on the histopathologic changes. Renal biopsy is sometimes needed to verify the severity of involvement before beginning immunosuppressive therapy. Discoid Rash Raised, erythematous patches with adherent keratotic scaling and follicular plugging 3. Photosensitivity Rash by history or physician observation caused by unusual reaction to sunlight 4. Serositis Pleuritis: by history or if rub or effusion is present Pericarditis: electrocardiographic changes, rub or pericardial effusion 7. Neurologic Disorder Seizures or psychosis in the absence of metabolic disease or offending drugs 9. Updating the American College of Rheumatology Revised Criteria for the classification of systemic lupus erythematosus. Diagnosis is made if four or more criteria are present, serially or simultaneously, during any interval of observation. Dermatologic changes are particularly responsive to hydroxychloroquine (200 to 800 mg/day). Life-threatening and severely disabling disease requires high-dose systemic corticosteroids that are slowly tapered. The gold standard for inducing remission in lupus nephritis is the combination of cyclophosphamide and glucocorticoids. The amount, size, charge, complement-fixing capacity, and antigen content of the immune complexes and the amount and nature of the autoantibodies undoubtedly govern which organs are affected and how severe the process is. The best evidence today suggests that a dysfunction in immunoregulation in an individual genetically predisposed develops after an environmental trigger (drug, microbe), with consequent perturbation of regulatory T-cell function, resulting in inappropriate autoantibody production by B cells. Clotting within blood vessels may be initiated by lupus anticoagulants; this is discussed later. Reluctance on the part of some rheumatologists to believe that this phenomenon occurs sometimes results in delayed diagnosis and permanent disability because of such delay. But even then it is critical that ophthalmologists and rheumatologists alike understand that the onset of two ocular manifestations, in particular, has profound systemic importance. Note the erythematous, raised, scaly dermatitis with madarosis and thick, erythematous lid margins. Histopathologic studies reveal that the epithelium is mildly hyperkeratotic with focal intracellular edema leading to liquefactive degeneration of the basal layer. Dilated dermal vessels and abundant cellular infiltrates, primarily of lymphocytes, in a perivascular and periappendageal distribution are typical. Additional small, discrete spots may also be seen alone or in areas of retinal edema and infarction. Although many patients have hypertension, these findings are probably distinct from those in hypertensive retinopathy. Patients with the previously described retinal findings constitute the majority of patients with lupus retinopathy. Severe visual loss is not usually seen in this group of patients, whose retinopathy improves with treatment of their systemic disease. Superficial punctate keratitis and recurrent epithelial erosions have been reported in patients with discoid lupus erythematosus. The classic hallmark of discoid lupus is discrete, raised, scaly lesions of the skin. A correct diagnosis is 4432 Systemic Lupus Erythematosus manifests as branch retinal vein occlusion, central retinal vein occlusion, central retinal artery occlusion, or a combination of these. This heterogeneous group of antibodies react with negatively charged phospholipids on platelet membranes, clotting factors, and vascular endothelial cells (see Table 324. They are related to anticardiolipin antibodies, which can be detected as a false-positive Venereal Disease Research Laboratory result. The presence of lupus anticoagulants, another group of antiphospholipid antibodies, is demonstrated by an elevated partial thromboplastin time that is not corrected by the addition of normal plasma. Confirmatory evidence is obtained by tissue thromboplastin inhibition and platelet neutralization tests. Endothelial swelling has also been reported and may be a predisposing factor in thrombus formation. Note the vasculitis with arteriolar occlusion, with two retinal infarcts, seen as cotton wool spots. The visual prognosis is much worse: more than 50% of the affected eyes have visual acuity of 20/200 or worse. Laser photocoagulation for proliferative retinopathy, using criteria from studies on diabetes and branch retinal vein occlusions, is thought to be beneficial. Control of systemic disease in three of these patients resulted in improvement of their serous detachments. Pathologic findings include demyelination and axonal necrosis or a combination of the two. Cases of optic neuritis47 and ischemic optic neuropathy34 associated with lupus anticoagulants have been reported. A mistaken diagnosis of multiple sclerosis is frequently made in these cases of lupus neuropathy because of similar clinical presentations in typically young women. Similarly, oculomotor disturbances are rarely thought to be caused by lesions outside the midbrain. Various ophthalmic manifestations are possible, and these are listed in Table 324. The ocular inflammatory lesion may precede extraocular manifestations of disease reaction by several months. Such patients must therefore be monitored with care for the emergence of extraocular evidence of potentially lethal problems. Orbital myositis manifesting with proptosis and pain with external ocular movements has also been described. Ocular manifestations have been described in drug-induced lupus caused by hydralazine. Updating the American College of Rheumatology Revised Criteria for the Classification of Systemic Lupus Erythematosus. Petri M, Magder L: Classification criteria for systemic lupus erythematosus: a review. Bootsma H, Spronk P, Derksen R, et al: Prevention of relapses in systemic lupus erythematosus. Takeuchi T, Tsuzaka T, Abe T, et al: T cell abnormalities in systemic lupus erythematosus. Halmay O, Ludwig K: Bilateral bandshaped deep keratitis and iridocyclitis in systemic lupus erythematosus. Kremer I, Gilad E, Cohen S, Ben Sira I: Combined arterial and venous retinal occlusion as a presenting sign of systemic lupus erythematosus. Matsuo T, Nakayama T, Koyama T, Matsuo N: Multifocal pigment epithelial damages with serous retinal detachment in systemic lupus erythematosus. Gharbiya M, Bozzoni-Pantaleoni F, Augello F, Balacco-Gabrieli C: Indocyanine green angiographic findings in systemic lupus erythematosus choroidopathy. Galindo-Rodriguez G, Avina-Zubieta A, Pizarro S, et al: Cyclophosphamide pulse therapy in optic neuritis due to systemic lupus erythematosus: an open trial. Davalos A, Matias-Guiu J, Codina A: Painful ophthalmoplegia in systemic lupus erythematosus. Jackson G, Miller M, Littlejohn G, et al: Bilateral internuclear ophthalmoplegia in systemic lupus erythematosus. It is typically a disease of individuals over the age of 50 years; women are affected at least twice as often as men. Jennings reported the first case of blindness associated with the disease and also documented an increased erythrocyte sedimentation rate. In 1934 Horton et al wrote, "A name cannot be given to this condition until more cases have been observed and the condition is dignified by nomenclature. The concern with giant cell arteritis is that giant cells are not necessary for the diagnosis and are seen in approximately half of positive temporal artery biopsies. Severe and permanent loss of vision, often in both eyes, can occur as a result of ischemic optic neuropathy and central retinal artery occlusion. The first patient was a 64 year old woman with "soreness of the scalp, painful nodules along the temporal arteries, anorexia, weight loss, and headaches. As is true of all healthcare studies, international differences may be related to differences in standards of care and healthcare delivery systems. The disease affects all races, but occurs most commonly in the Caucasian population. The highest incidence rates have been reported from Scandinavia and Minnesota, the population of which is predominantly of similar descent. It is a systemic vasculitis that affects medium- and large-sized arteries with defined internal and external elastic lamina. A 68 year old man presented complaining of brief episodes of purple vision for 3 weeks. External examination revealed enlarged, nodular, painful temporal arteries that were pulseless. A primary role for the elastic lamina is suggested by the disintegration of the inner elastic lamina of affected arteries and the concentration of the inflammatory reaction around it. The theory is further supported by the observation that susceptibility of the individual arteries of the head and neck correlates with the amount of elastic tissue in the media and adventitia. An immune reaction in the wall of the artery precipitates a cascade that results in structural changes, intimal hyperplasia, and luminal occlusion. Microbial infection has been implicated as the trigger, but evidence is not conclusive. Cellular immunity plays a vital role in the pathology, but humoral immunity is also involved. The process is dependent on T cells found in the the vasa vasorum in the adventitia and that produce interferon-g, which attracts monocytes/macrophages. Experimental data support the concept that the disease is initiated in the most outer layer of the arterial wall, the adventitia. T cells and macrophages infiltrate into all wall layers and acquire different effector functions dependent on cues in their immediate microenvironment. The end result is myofibroblastic proliferation, luminal stenosis, and tissue ischemia. Key Features Systemic symptoms often precede ophthalmic symptoms by several weeks and include headache; scalp tenderness; jaw claudication; and constitutional symptoms such as myalgias, anorexia, weight loss, fever, malaise, and depression. Patients with scalp tenderness may complain of pain on combing or washing the hair. The offending artery may be enlarged, nodular, erythematous, and nonpulsatile, but scalp tenderness may not be localized to the course of the superficial temporal artery.

This becomes less likely as the degree of refractive error becomes larger and the age of the child becomes more advanced acne zones on face cheap 30 gm elimite fast delivery. Very high degrees of hyperopia are not normal in newborns acne einstein buy generic elimite 30gm line, and the presence of high hyperopia (greater than 5 D) often portends a lack of normal ocular growth acne active buy cheapest elimite. The cornea and lens may flatten normally acne hat cheap elimite 30gm free shipping, but the axial length often lags behind skin care khobar elimite 30gm without a prescription, causing permanent high hyperopia which may even increase for a few years before stabilizing acne los angeles 30gm elimite visa. Such eyes are predisposed to angle-closure glaucoma later in life as the aging lens begins to enlarge. Risk of angle closure glaucoma, choroidal effusion, and other complications of intraocular surgery are increased in these eyes. In general, eyes with hyperopia of greater than 5 D have little chance of emmetropization and will likely need some type of optical correction lifelong. Some newborns have been reported to be myopic shortly after birth, only to emmetropize within the first year or two. Some children with moderate to high myopia will experience a decrease in magnitude of myopia, though rarely resolution, over the first years of life. In most cases, however, childhood or juvenile myopia represents a failure of emmetropization which progresses throughout adolescence and early adulthood. Parents and children should be counseled about the natural history to avoid feeling that something wrong was done if the myopia progresses. There may be myopic changes in the fundus, such as tessellation and myopic crescent, and there is an increased risk of lattice degeneration and retinal holes and detachment. The axial length is longer than the norm, while other components are usually within the normal range. It may be isolated, but is often associated with other syndromes or systemic disorders. Physiologic and intermediate myopia may be preceded by unusually low hyperopia in early childhood. One study found that the best predictor of myopia development was having less than +0. Young children may not be able to describe visual changes well and may complain instead of headache or trouble reading, or may exhibit signs such as squinting the eyelids to create a pinhole effect, or frequent blinking. This type of myopia usually progresses throughout adolescence and the 20s, stabilizing in the 20s and 30s. Pathologic myopia often begins with myopia of high degree in infancy or early childhood. It is usually progressive and, in some studies, carries a 50% lifetime risk of legal blindness. The hyperopic eye is usually shorter in length than normal, or may have a normal axial length but a very flat cornea or lens. The result is that images are focused behind the retina, rather than crisply on it. The bad news is that the accommodative effort, if extreme, may cause asthenopia and esotropia. The amount of hyperopia which can be easily compensated for, and which will not be detected on routine manifest refraction, is termed latent hyperopia. The amount of hyperopia detected on manifest refraction is termed manifest hyperopia. The full amount of hyperopic refractive error in children can only be detected by cycloplegic refraction, which paralyzes accommodation and therefore measures both latent and manifest hyperopia (see section on Measurement of Refractive Errors in Children). Children can usually accommodate 14 D at 8 years of age or less; accommodative ability decreases by 1 D every 4 years, reaching 11 D at age 20 years. By 40 years of age the accommodative capacity is ~6 D, and it decreases more rapidly after this. Even this seemingly physiologically programmed loss of accommodation, however, is subject to environmental modification. Presbyopia has been reported to start at a later age in persons living further from the equator, suggesting a role for ultraviolet light exposure. Average age of presbyopia has been reported to be 47 years in England, but 39 years in Puerto Rico. Irregular astigmatism is more rare, and cannot be corrected with a simple cylindrical lens because there are many different meridians. Anisometropia in children less than 9 years may also result in amblyopia, a form of cortical vision loss in which the brain disconnects with the eye having the greater refractive error. If both eyes are hyperopic, but of differing degrees, accommodation is used to try to clear the image. Since accommodation is a bilateral phenomenon with the eyes only able to accommodate differentially ~0. Each eye receives a clear image of objects at its far point, the location short of infinity at which the myopic eye is focused. If the two eyes are not widely disparate in refraction, amblyopia often does not develop. If one eye is myopic and the other hyperopic, whether or not amblyopia develops and how symptomatic the patient is depends on the degree of refractive error. People who have one mildly myopic eye and one mildly hyperopic may become monofixators, using the hyperopic eye for distance and myopic eye for near. In general it takes less hyperopia than myopia to create amblyopia (see also the section on Management of Refractive Errors in Children). In myopia, images are focused anterior to the retina, either because the cornea and lens refract too much for a given axial length, or because the axial length is too long for a normally refracting anterior optical system. Accommodation moves images more anteriorly, so efforts to focus only create more blur. Narrowing or squinting the eyelids creates a pinhole effect that transiently improves acuity. There are actually several different types of myopia that have been described, based on anatomic differences. Cornea, lens, and axial length are all essentially within normal limits, but the combination causes a small myopia. It is inconvenient to have the child use drops at home before the examination, and since overdose of atropine has many side effects, including anticholinergic effects, constipation, and even death in young children, cyclopentolate is the more practical, and almost equivalent, choice in a typical practice. Cyclomydril, a dilute mixture of phyenylephrine, tropicamide, and cyclopentolate, may be used in babies less than 6 months old, one drop each eye given 5 min apart three times. Cyclopentolate is also associated with possible side effects, including hallucinations, seizures, and anticholinergic effects. These usually resolve spontaneously, but may require observation in the emergency room, and rarely, an antidote. Cycloplegic medications bind to pigment, so children with darkly pigmented irides may need higher concentration or more doses to achieve the same cycloplegia as children with less pigmentation. Repeating the dose once only, then waiting additional time, is safer than multiple repeat doses. At the peak of cycloplegia, the child is brought, with the parent, into a darkened room. Having the child fixate a distant target may be the best way to eliminate any accommodation, but can cause errors in reading astigmatism axis. If the child is well cyclopleged, accommodation should not be an issue regardless of where the child fixates. Therefore many practitioners prefer to make the room as dark as possible to give the child only one possible target to fixate: the retinoscope light. If the child has either latent or manifest strabismus, it is important to cover one eye while retinoscoping the other to avoid having the child switch fixation, creating an off-axis reading. They may be frightened of it, but more commonly, they squirm and turn their head and eyes while sitting behind it, making it difficult for the examiner to tell whether the child is really fixating centrally. For most young children, the most accurate measurements will be obtained using loose lenses with the retinoscope. This method theoretically allows the child an unobstructed view to a target at the end of the room for fixation. However, it does not prevent off-axis measurement or allow monitoring of the eye that is fixating in children with tropias or phorias. An alternate method which insures that the child is fixating on axis, even when strabismus is present, is for the examiner to hold the retinoscope over the right eye with the right hand, holding the trial lens with the left hand, to retinoscope each eye. This indicated that the growth of the eye and emmetropization are not just preprogrammed anatomically, but require active visual input to proceed normally. It has been shown that even if the optic nerve is cut, lid suture myopia will occur. This points to local factors in the retina as being involved, factors triggered by light and form. Atropine has been noted to retard experimental myopia, again even when the optic nerve is severed. Thus a complex system of chemical mediators and receptors is involved in both normal and disordered axial elongation. Animals raised in darkness from birth often remain hyperopic, whereas animals raised in the light but with lids sutured, that is, with vision but not form vision, become myopic. Because of their large accommodative capacity, noncycloplegic retinoscopy and/or manifest refraction in children often measures refractive error combined with accommodative reserve, resulting in the prescription of incorrect lenses. Noncycloplegic refraction in children tends to result in undercorrection of hyperopia and astigmatism, and overcorrection of myopia. In addition, even very bright cooperative children may not be able to adequately participate in manifest refraction, requiring an objective measurement by retinoscopy. In general, a cycloplegic refraction should be performed as part of the initial ophthalmologic examination on every child 9 years of age or less. Even if the problem which prompted referral seems unrelated, cycloplegic refraction and dilated fundus may detect common problems such as amblyopia or amblyogenic factors that cannot be picked up in any other way. Because of the rapid changes in anatomy during this stage, children followed for chronic problems should have cycloplegic refraction at least once a year. Even teenagers and adults less than 45 years of age may be over- or undercorrected with manifest refraction alone due to uncontrolled accommodation. Therefore, cycloplegic refraction on all patients at initial visit (which may be delayed if presenting for trauma, iritis, etc), then at least yearly for children less than 9 years, and on a case-bycase basis for all others depending on diagnosis, signs, and symptoms is recommended. Alternatively, an adhesive patch may be placed over the eye that is not being examined if the child will allow it; however, this often causes fear and can make one lose the opportunity for a good retinoscopy. In children already wearing spectacles or contact lenses, especially if the prescription is of high power, an overrefraction may be done. After cycloplegia the current lenses are worn, and any additional prescription found is added to the known prescription they are wearing. This technique eliminates the error introduced by vertex distance with high prescriptions. If additional cylinder at an axis different from the original is found, confirmation with loose lenses alone is recommended. When possible, a subjective refinement should be performed, but this is rarely useful in children less than 7or 8 years old, and is almost never useful at the first visit if amblyopia is present. After dilation and retinoscopy if the child is cooperative a subjective refinement can be attempted, and repeated on subsequent visits under noncycloplegic conditions. Most of the time young children must be prescribed spectacles based on retinoscopy alone. Some children, for example those with developmental delay, may be unable to cooperate with a complete eye examination and may require examination under anesthesia. Cycloplegic retinoscopy can be performed under anesthesia, but because the child cannot fixate on a target, significant errors in cylinder axis are possible. Children break their glasses frequently, and parents may not remember whether this has happened since the last visit. The accuracy of dispensed lenses is not always ideal, and children often cannot or do not complain if their vision is less than clear in a new pair of glasses. Although refractive errors rarely cause asthenopia or headache, treatment of mild refractive issues may sometimes be recommended to rule this out as a cause. When the lens is removed, either because of a congenital cataract, trauma, or surgery for retinal detachment, macular vision will not develop and nystagmus will result. Some infants have very large refractive errors in the aphakic range even without aphakia. Nanophthalmic eyes, eyes that had severe retinopathy of prematurity, eyes with pathologic myopia due to Stickler syndrome or other connective tissue disorders, may have hyperopia or myopia of such large degree that optical correction is mandatory within the first 3 months of life. In general, if hyperopia or myopia is greater than 10 D, prompt correction should be considered in the neonatal period to prevent irreversible amblyopia. Hyperopia may rapidly improve in neonates; very high myopia above 10 D is unlikely to improve much. However for a newborn, whose main visual stimulus is a face close to its own, and food close to its mouth, even fairly high amounts of myopia permit normal visual development. In aphakia, there is no zone of clear vision and no lens to accommodate, so the resultant amblyopia is profound.

Cheap 30 gm elimite mastercard. Radical Skincare Youth Infusion Serum 1 oz. on QVC.

Paraneoplastic disorders can affect the retina acne keloidalis nuchae pictures purchase elimite 30 gm free shipping, optic nerve skin care database generic elimite 30gm overnight delivery, or a combination of the two acne free generic elimite 30gm without a prescription. In a report of 16 patients with paraneoplastic retinopathy and optic neuritis acne quick fix cheap elimite 30gm mastercard, 15 had accompanying neurologic deficits including ataxia acne location generic 30 gm elimite otc, peripheral neuropathy skin care routine for acne discount 30 gm elimite amex, and movement disorders. Tumors associated with paraneoplastic optic neuropathy include small cell lung carcinoma, thymoma, and thyroid carcinoma. One review of the literature120 reported that the presenting symptom was bilateral optic neuritis in 36% of patients, unilateral optic neuritis in 40%, transverse myelitis in 13%, and simultaneous optic neuritis and transverse myelitis in 11%. The visual deficit was almost always bilateral (91%) and usually severe, with unilateral or bilateral blindness in 58%. Incomplete neurological improvement is common and there may be up to 16% mortality in the acute stages. Progressive vision loss can occur acutely, subacutely, or in a slowly progressive fashion and generally requires corticosteroid treatment. Some authors have described a steroid-dependent optic neuropathy associated with laboratory features suggestive of a collagen vascular disorder. Dietary deficiency is the common denominator, and thiamine therapy, B12, and folate improves vision in the early phase of the neuropathy, in spite of continuing abuse of alcohol or tobacco. These patients are well nourished, nonintoxicated, and nonreactive on serologic tests for syphilis, yet no form of therapy affords relief, and there is no spontaneous recovery. The male predominance ranges from 80% to 90% in most white pedigrees to ~ 60% in families from Japan. Symptoms include painless subacute bilateral visual loss and central or cecocentral scotoma. Most commonly, impaired visual acuity occurs in one eye only, and sequential visual loss develops in the contralateral eye weeks or months later. Unlike adults, it is not unusual for severe disk edema or peripapillary hemorrhages to be present. In most patients, visual loss remains profound and permanent, although spontaneous improvement of some degree has been reported. During the acute stage, circumpapillary telangiectatic microangiopathy is present, with hyperemia of the disc, swelling of the peripapillary nerve fiber layer, vascular tortuosity, and absence of leakage from the disk or vessels at fluorescein angiography. Unlike adults, children with anterior optic neuritis tend to relapse with a rapid corticosteroid taper. The major positive component, P100, is preceded and followed by smaller negative peaks, N75 and N145. The response is reproducible and sensitive to conduction defects in the visual pathways. The P100 amplitude is correlated with visual acuity, whereas the P100 latency is not. A latency of over 118 ms or an interocular difference of more than 9 ms may signify optic nerve dysfunction. While approximately one-third of adults have unilateral disk edema, between 50% and 75% of children have bilateral vision loss and swelling of the optic nerves. Normal individuals can voluntarily alter the P100 amplitude and latency by defocusing their eyes or looking away from the pattern stimulus. The Diagnosis of Multiple Sclerosis Depends upon Dissemination in Time (Attacks Separated by at Least One Month) and Space. The reasons for this are that (1) the disorder has protean manifestations since any white matter tract of the 3880 Optic Neuritis nervous system can be affected and (2) no laboratory test can diagnose the disease unequivocally. The diagnosis is therefore based upon a combination of the clinical presentation and the laboratory evaluation. The common presenting symptoms seen by ophthalmologists include optic neuritis, internuclear ophthalmoplegia (unilateral or bilateral), and nystagmus. Uncommon presentations involve homonymous visual field loss, gaze palsies; and isolated ocular motor palsies. It used to be assumed that a diagnosis of multiple sclerosis cannot be made after an episode of isolated optic neuritis. Cases identified post mortem without apparent symptoms and signs during life have been documented, the so-called subclinical form. A more severe form, characterized by moderate disability, allows most patients to continue a productive life. About one-third of patients have a severe form and may become confined to a wheelchair or bedridden. Therefore, oral prednisone alone should not be used to treat acute optic neuritis and probably not other multiple sclerosis attacks. The beneficial effect was greatest in the group with abnormal brain magnetic resonance images and lasted for ~2 years. Less than 1% of patients have a white blood cell count greater than 25/mm3, and all these are usually mononuclear cells. When the protein is fractionated, the immunoglobulin electrophoretic pattern of the gamma-globulin level is often elevated. The presence of oligoclonal bands in the gammaglobulin region is more specific than either the total protein or the IgG level. The presence of myelin basic protein was initially thought to be a specific marker of multiple sclerosis; although it may be an antigenic stimulus in multiple sclerosis, it is found in other disorders that destroy myelin. The National Multiple Sclerosis Society is an excellent source for current information. For example, taking a hot bath or shower, exercising, or even smoking a cigarette can induce enough elevation in temperature in the region of the optic nerve to cause blurring of vision. Visual function may improve if the patient keeps body temperature low by staying in a cool or cold environment. The reason for this is that neural transmission is more efficient at cold temperatures. Patients may complain of visual distortions as objects approach them, such as misperceived veering of oncoming tennis balls, owing to delayed conduction through one optic nerve. These patients can be fitted with a neutral-density contact lens over the unaffected eye to alleviate this type of distortion. Some patients with the optic neuropathy of multiple sclerosis see better in dim light than in bright light. When ophthalmologists diagnose optic neuritis, they usually face a dilemma as to how to inform the patient of the diagnosis and its implications. Most ophthalmologists do not have the background, knowledge, or experience to educate their patients fully about this disease. Optic Neuritis Study Group: the clinical profile of acute optic neuritis: experience of the optic neuritis treatment trial. Optic Neuritis Study Group: the five-year risk of multiple sclerosis after optic neuritis. Optic Neuritis Study Group: High- and lowrisk profiles for the development of multiple sclerosis within 10 years after optic neuritis. Optic Neuritis Study Group: Visual function more than 10 years after optic neuritis: experience of the optic neuritis treatment trial. Kinnunen E: the incidence of optic neuritis and its prognosis for multiple sclerosis. A neuro-ophthalmological investigation by means of visually evoked response, Farnsworth-Munsell 100 Hue test and Ishihara test and their diagnostic value. Ulrich J, Groebke-Lorenz W: the optic nerve in multiple sclerosis: a morphological study with retrospective clinicopathological correlations. Colombati S, Borri P, Tosti G, et al: Two cases of papillitis in patients with early syphilis. Katz B: the dyschromatopsia of optic neuritis: a descriptive analysis of data from the optic neuritis treatment trial. Travis D, Thompson P: Spatiotemporal contrast sensitivity and colour vision in multiple sclerosis. Pulfrich C: Die Stereoskopie im Dienste der isochromen und heterochromen Photometrie. Rushton D: Use of the Pulfrich pendulum for detecting abnormal delay in the visual pathway in multiple sclerosis. Marshall D: Ocular manifestations of multiple sclerosis and relationship to retrobulbar neuritis. Riikonen R, Donner M, Erkkila H: Optic neuritis in children and its relationship to multiple sclerosis: a clinical study of 21 children. Riikonen R, Ketonen L, Sipponen J: Magnetic resonance imaging, evoked responses and cerebrospinal fluid findings in a follow-up study of children with optic neuritis. Atilla H, Tekeli O, Ornek K, et al: Pattern electroretinography and visual evoked potentials in optic nerve diseases. Hoeppner T, Lolas R: Visual evoked responses and visual symptoms in multiple sclerosis. Bobak P, Bodis-Wollner I, Harnois C, et al: Pattern electroretinograms and visual evoked potentials in glaucoma and multiple sclerosis. Sandberg-Wolheim M, Bynke H, Cronqvist S, et al: A long-term prospective study of optic neuritis: evaluation of risk factors. Comi G, Filippi M, Barkhof F, et al: Effect of early interferon treatment on conversion to definite multiple sclerosis: a randomised study. Other etiologies for optic disk swelling in this age group include inflammation, infiltration or metastasis, and compression. On this basis, ischemic optic neuropathies are usually categorized as nonarteritic or arteritic. The immediate retrolaminar segment of the optic nerve is supplied by recurrent pial arterioles of the peripapillary circulation and pial capillaries of the central retinal artery running in the fibrous supportive septa of the nerve. The orbital and intracanalicular segments of the optic nerve are supplied by penetrating capillaries of the peripheral pial plexus of the ophthalmic artery and, to some extent, by the intra-axial central retinal artery circulation. In contrast, Hayreh has concluded that impaired perfusion pressure in a watershed zone within the distribution of the posterior ciliary artery circulation of the optic disk predisposes the optic disk to infarction. A precise understanding of the events that lead to the visual impairment is lacking, in part because of the inability to obtain sufficient histopathological material at the time of acute vision loss. Several mechanisms leading to ischemia have been hypothesized, often at odds with one another. As a result of these differing opinions, there is no consensus about the cause of idiopathic ischemic optic neuropathy. Two limited surveys calculated the age-adjusted annual incidences in the white population 50 years and older to be 2. Schematic representation of blood supply of (a) the optic nerve and (b) optic nerve head. Significant eye or brow discomfort or headache is uncommon, occurring in ~10% of cases, whereas in optic neuritis, orbital ache or pain on eye movement is a prominent symptom. The type of visual-field defect is most commonly arcuate or altitudinal, usually inferior, but central scotomas also can be present. The loss of vision is typically maximal at onset or shortly thereafter, but progressive loss of visual field and visual acuity for several days to several weeks after initial onset also can occur. The proportion of the optic disk that is swollen can vary from a small sector to involvement of the entire disk and can progress after initial onset. One hypothesis is that this is due to a subthreshold level of optic nerve ischemia, enough to cause the Ischemic Optic Neuropathies axonal swelling, but not yet sufficient to result in visual impairment let alone irreversible damage to the optic nerve. A retrospective diagnosis of optic atrophy from a prior episode of idiopathic ischemic optic neuropathy can often be made when a small optic disk is observed in the affected and contralateral eyes and when results of other investigations of possible causes of optic atrophy are normal. After ischemic infarction of one disk, there is a known risk of second-eye involvement. Treatments that have been proposed include hyperbaric oxygen,20 levodopa or carbidopa,21 aspirin,22 transvitreal optic neurotomy,23 and vitrectomy. Whereas visual function worsened spontaneously in 12% of 125 control eyes, vision worsened in 24% of 119 eyes subjected to decompressive surgery. Attention is given to eliminating other potential treatable optic neuropathies in the differential diagnosis, such as optic neuritis or a compressive optic neuropathy, and identifying any potential modifiable vascular risk factors that may have a bearing on the risk of future involvement of the fellow eye. Some of these settings include: following general surgical procedures, after cataract surgery, following hemorrhagic shock, after administration of certain medications, and in association with optic disk drusen. It is important to emphasize that the mechanism by which optic nerve ischemia occurs in these situations is not firmly established, although hypotension, anemia, hypoxia, and alteration of autoregulation of optic nerve arterial perfusion have all been cited as contributing factors. There is no consensus regarding the aggressiveness with which blood pressure or hematocrit should be maintained under general anesthesia in patients undergoing these types of surgery. In some situations, the arterial circulation to the optic nerve becomes vulnerable after elevation of the intraocular pressure in the postoperative period33 possibly due to retained viscoelastic in the anterior chamber. Vision loss after cataract surgery can occur within hours, days, or in some cases, in a delayed fashion after several weeks. The mechanism by which ischemic optic neuropathy occurs in this situation, remains speculative. Paradoxically, the ischemic optic neuropathy may supervene after the anemia and hypotension have been corrected. Amiodarone is one of the most effective medications used for the treatment of ventricular and supraventricular arrythmias. Hyperemia of the conjunctival and episcleral vessels, mild to moderate corneal edema, lowered intraocular pressure, anterior chamber cellular reaction, iris rubeosis, and rapidly progressive cataract may be observed if anterior segment ischemia occurs.

Lesions in the central nervous system can be intraparenchymal or extraaxial acne girl discount elimite 30 gm fast delivery, the majority of the extraaxial lesions occurring in the posterior fossa acne cure trusted elimite 30gm. Cavernous hemangiomas are the most common vascular malformation of the orbit and are more common than their intracranial counterpart acne zap generic 30gm elimite visa. Because of their slow flow acne jeans order elimite 30 gm visa, cavernous hemangiomas are rarely evident by angiography stop acne generic 30gm elimite mastercard. The pathology of the lesions is the same regardless of location acne paper discount 30gm elimite mastercard, consisting of small, dilated spaces filled with blood and divided by fibrous tissue. In the retina, the lesions may be contained within or above the substance of the disk and retina. Congenital syndromes such as congenital diffuse hemangiomatosis204 and blue rubber bleb nevus syndrome205 may result in multiple cavernous lesions. The majority of intraparenchymal cavernous hemangiomas are supratentorial and located in the cortical and subcortical regions. Angiomas of the pregeniculate visual pathway produce acute and progressive vision loss in one or both eyes. Extraaxial lesions produce symptoms via hemorrhage, elevated intracranial pressure, or a mass effect. Symptoms include ptosis, anisocoria, hemifacial spasm, oculomotor nerve pareses, and proptosis. The nidus of vessels forming the malformation is usually in the proximity of a dural sinus and may produce narrowing or obstruction of the sinus. The clinical presentation of these lesions may result from either hemorrhage or venous congestion caused by obstruction or arterialization. Many patients with symptoms (such as a bruit) are diagnosed only if the clinician suspects a shunt and investigates the patient adequately. Such symptoms generally occur when there is Neurovascular Neuro-ophthalmology diffuse venous hypertension rather than a single large draining vein. These pulsatile noises are often not reported by patients and result from shunting of blood into the sigmoid or lateral sinus. Patients with cortical venous drainage are at high risk for hemorrhage and typically require treatment. Cyanoacrylate or polyvinyl alcohol is used to occlude the vessels and is delivered via superselective catheterization. Transvenous delivery of embolic material or detachable balloons through the jugular vein may be used to induce thrombosis of the affected sinus. Clinical signs may not improve initially because of the presence of thrombosis in the affected venous sinuses. Radiation has been used to treat extensive lesions not amenable to embolization or surgery. Posterior fossa dural arteriovenous malformations Patients may present with focal or diffuse signs as a result of cerebral infarction or intracranial hemorrhage. Those in the area of the transverse sigmoid sinus and the cavernous sinus region are least likely to present with hemorrhage or progressive neurologic deficits. In the former, meningeal branches of the cavernous carotid artery are typically involved in the development of the shunt. The two arteries most commonly involved are the meningohypophyseal trunk and the artery of the inferior cavernous sinus. In the cavernous region, branches of the dorsal meningeal artery may anastomose with other branches of the external carotid artery: the internal maxillary artery, the ascending pharyngeal artery, and the occipital artery. The middle meningeal artery arises from the internal maxillary artery and supplies the dura in the region of the foramen ovale and foramen spinosum. In this area, there may be anastomoses with branches from the artery of the inferior cavernous sinus. It is unclear whether these were congenital or acquired lesions, but the latter appear most likely. The location of the lesions typically determines the nature of the focal neurologic deficit. The pathogenetic mechanisms of supratentorial lesions are protean: hemorrhage, venous hypertension, and vascular steal. Neurologic dysfunction may result from intracerebral, subdural, or subarachnoid hemorrhage. Dementia may result from diffuse cerebral venous hypertension or from lesions involving the temporal lobe. Certain angiographic patterns may correlate with more aggressive clinical behavior. These include leptomeningeal drainage, cortical venous drainage, variceal or aneurysmal venous dilatation, and galenic venous drainage. These malformations tend to have bilateral arterial contributions, high flow, and venous outflow stenosis. Angiography must be performed in a superselective fashion if therapy is planned and all feeder vessels must be identified. Course and Treatment Many patients have a benign course, with some malformations spontaneously thrombosing. Patients without cortical drainage and with minimal symptoms can usually be followed without therapy. In one case, a patient was reported to develop posterior ischemic optic neuropathy presumably on the basis of arterial steal. Orbital congestion can worsen (sometimes paradoxically with treatment) as a result of thrombosis of the orbital veins and subsequent increased orbital venous stasis. Large choroidal effusions may result in rotation of the ciliary body and anterior movement of the lensiris diaphragm, producing angle-closure glaucoma or anterior displacement of a posterior chamber lens. Eye movement abnormalities result from congestion and ischemia of the extraocular muscles or cranial nerve palsies. Midperipheral blot hemorrhages are present along the lower temporal arcade (open arrows). After treatment, the prognosis for recovery of eye movement abnormalities, whether myopathic or neuropathic, is good. Patients may rarely develop seizures, infarcts, or hemorrhages as a result of abnormal pial drainage into the cerebral hemispheres. Such problems are more frequently seen in association with bilateral fistulas and significant cavernous sinus thrombosis. Diagnosis is dependent on neuroimaging and angiography, and treatment is typically by transarterial embolization. Additional diagnostic studies helpful in the evaluation of these lesions include pneumotonometry, orbital echography, and color Doppler imaging. Thrombosis of the cavernous sinus and superior ophthalmic vein usually appears as high signal intensity on T1-weighted images. Additional studies may be indicated to rule out an anterior draining pial arteriovenous malformation. Fortunately, between 20% and 80% of these lesions close spontaneously, often after angiography or air travel. Sixty of 66 patients were treated successfully by embolization, which in some patients had to be performed on more than one occasion. Despite the associated anterior segment changes, cataract surgery can be performed successfully in patients with dural fistuals. Ideally, this is accomplished through the external carotid artery (when all feeders originate from that circulation), but a transvenous or internal carotid approach is sometimes necessary. Transorbital canalization of the superior ophthalmic vein and fistula embolization has been used successfully. Ocular symptoms generally begin to improve within days of treatment with intraocular pressure control;250 cranial nerve palsies require longer. The cavernous sinus (large arrow) fills immediately after injection of contrast agent into the ipsilateral external carotid artery. Middle meningeal artery (small arrow) and internal maxillary artery (curved arrow) are also visualized. Demonstration of ophthalmoscopically occult emboli and post-embolic endothelial damage after attacks of amaurosis fugax. Michelson J, Friedlander M: Angiography of retinal and choroidal vascular disease. Frisen L: Quadruple sectoranopia and sectorial optic atrophy: a syndrome of the distal anterior choroidal artery. Horowitz M, Jovin T, Levy E, Anderson W: Emergent basilar artery and bilateral posterior cerebral artery angioplasty, urokinase thrombolysis, and stenting for acute basilar artery occlusion secondary to diagnostic cardiac catheterization: case presentation. Keller E, Pangalu A, Fandino J, et al: Decompressive craniectomy in severe cerebral venous and dural sinus thrombosis. Kusaka K, Shimamura I, Ohashi Y, Ota S: Long term survival of patient with invasive aspergillosis involving orbit, paranasal sinus, and central nervous system. Stehbens W: the pathology of intracranial arterial aneurysms and their complications. LeBlanc F, Charette E, Dobelle A: Neurological complications of aortic coarctation. Hijdra A, Vermeulen M, van Gijn J, van Crevel H: Rerupture of intracranial aneurysms: a clinicoanatomic study. Kuzniecky R, Melmed C, Schipper H: Carotid-ophthalmic aneurysm: an uncommon cause of acute monocular blindness. Leivo S, Hernesniemi J, Luukkonen M, Vapalahti M: Early surgery improves the cure of aneurysm-induced oculomotor palsy. Berenstein A, Ransohoff J, Kupersmith M, et al: Transvascular treatment of giant aneurysms of the cavernous carotid and vertebral arteries. Hojer-Pedersen E, Haase J: Giant anterior communicating artery aneurysm with bitemporal hemianopsia: case report. Zingale A, Chiaramonte I, Consoli V, Albanese V: Distal posterior inferior cerebellar artery saccular and giant aneurysms: report of two new cases and a comprehensive review of the surgicallytreated cases. Isamat F, Ferrer E, Twose J: Direct intracavernous obliteration of high-flow carotid-cavernous fistulas. Miyachi S, Negoro M, Handa T, Sugita K: Contribution of meningeal arteries to cerebral arteriovenous malformations. Yokoyama K, Asano Y, Murakawa T, et al: Familial occurrence of arteriovenous malformation of the brain. Clinical and radiologic features in 26 cases with comments on differentiation from migraine. Bajandas F, Aptman M, Stevens S: the sylvian aqueduct syndrome as a sign of thalamic vascular malformations. Fournier D, Terbrugge K, Rodesch G, Lasjaunias P: Revascularization of brain arteriovenous malformations after embolization with bucrylate. Steiner L, Lindquist C, Cail W, et al: Microsurgery and radiosurgery in brain arteriovenous malformations. Yamamoto M, Jimbo M, Kobayashi M, et al: Long-term results of radiosurgery for arteriovenous malformation: neurodiagnostic imaging and histological studies of angiographically confirmed nidus obliteration. Colombo F, Pozza F, Chierego G, et al: Linear accelerator radiosurgery of cerebral arteriovenous malformations: an update. Lyness R, Williams R: Intramuscular haemangioma arising in the lateral rectus 149. Costa E, Silva I, Symon L: Cavernous hemangioma of the optic canal: report of two cases. Kawai K, Fukui M, Tanaka A, et al: Extracerebral cavernous hemangioma of the middle fossa. Acciarri N, Padovani R, Giulioni M, et al: Intracranial and orbital cavernous angiomas: a review of 74 surgical cases. Yamasaki T, Handa H, Yamashita J, et al: Intracranial and orbital cavernous angiomas. Lasjaunias P, Chiu M, ter Brugge K, et al: Neurological manifestations of intracranial dural arteriovenous malformations. Bitoh S, Hasegawa H, Fujiwara M, Nakao K: Irradiation of spontaneous carotidcavernous fistulas. Kurul S, Cakmakci H, Kovanlikaya A, Dirik E: the benign course of carotid-cavernous fistula in a child. Kirsch M, Henkes H, Liebig T, et al: Endovascular management of dural carotid-cavernous sinus fistulas in 141 patients. The importance of the typical limbal vascular loops for the diagnosis, the recognition of glaucoma and the uses of conservative therapy in this condition. Brunette I, Boghen D: Central retinal vein occlusion complicating spontaneous carotid-cavernous fistula. A new noninvasive technique to diagnose and monitor carotid cavernous sinus fistulas. Indications and techniques for primary embolization via the superior ophthalmic vein. Ishijima K, Kashiwagi K, Nakano K, et al: Ocular manifestations and prognosis of secondary glaucoma in patients with carotid-cavernous fistula. Both afferent and efferent visual features occur with migraine, including positive and negative visual phenomena, visual-field defects, pupillary abnormalities, ptosis, and diplopia. Trigeminal autonomic cephalgias are characterized by firstdivision trigeminal pain and autonomic features (Horner syndrome, conjunctival injection, eyelid edema, lacrimation, congestion, and rhinorrhea). Ocular migraine produces transient monocular visual loss or positive visual phenomena.