Journal of Neuro-Ophthalmology, September 1999, Volume 19, Issue 3

Neuro-Ophthalmology of the Pregeniculate Afferent Visual System

Journal of Neitro- Ophlhahnology I9( j): 207- 216, 1999. 0 1999 Lippincoll Williams & Wilkins, Inc., Philadelphia Neuro- Ophthalmology of the Pregeniculate Afferent Visual System: Part II: June- December 1998 Laura J. Balcer and Steven L. Galetta The pregeniculate afferent visual system was the focus of many interesting reviews, reports, and investigations during the second half of the year 1998. This semiannual review includes the months of June through December 1998. The following table of contents has been provided for ease of reference to the topics presented: 1) EVALUATION OF THE AFFERENT VISUAL SYSTEM a) MR Imaging b) Visual Field Testing c) The Pulfrich Phenomenon 2) NEURO- OPHTHALMOLOGY AND THE RETINA a) Cancer- Associated Retinopathy ( CAR) b) Tamoxifen Retinopathy c) Creutzfeldt- Jacob Disease d) HIV- Associatcd Visual Loss e) Vascular Disease and the Retina 3) THE OPTIC NERVE a) Anterior Ischemic Optic Neuropathy b) Giant Cell Arteritis c) Optic Neuritis d) Infectious, Inflammatory, and Post- Surgical Optic Neuropathies e) Meningiomas and Other Neoplasms f) Idiopathic Intracranial Hypertension g) Leber's Hereditary Optic Neuropathy 4) THE OPTIC CHIASM AND BEYOND a) Pituitary Adenomas b) See- Saw Nystagmus c) Band Optic Atrophy d) Scllar Arachnoid Cysts e) Traumatic Lateral Geniculate Hemorrhage Manuscript received May 5, 1999; accepted July 6, 1999. This work was supported in part by grant EY00351- 01 from the National Eye Institute, Belhesda, Maryland ( Dr. Balcer). From the Division of Neuro- Ophthalmology, Departments of Neu­rology and Ophthalmology, Hospital of the University of Pennsylvania, Scheie Eye Institute, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, USA. Address correspondence to Dr. Steven L. Galetta, Department of Neurology, 3 East Gates, 3400 Spruce Street, Philadelphia, PA 19104. EVALUATION OF THE AFFERENT VISUAL SYSTEM MR Imaging Differentiating normal- tension glaucoma from optic nerve or chiasmal compression as a cause for optic disc cupping is one of the most important diagnostic dilem­mas faced by neuro- ophthalmologists. The question of who needs neuroimaging for a cupped optic disc was addressed in a recent study by Greenfield el al. ( 1). They compared the clinical and neuroradiologic findings for two groups of patients who had undergone magnetic resonance imaging ( MRI) or computerized tomography ( CT) scanning to evaluate optic disc cupping. Group 1 consisted of 29 patients ( 52 eyes) with normal intraocu­lar pressures and normal neuroimaging ( normal tension glaucoma group); group 2 included 28 patients ( 44 eyes) with known compressive lesions of the anterior visual pathway ( nonglaucomatous cupping group). Factors sig­nificantly associated with nonglaucomatous cupping in­cluded younger age ( mean 50.3 years for compressive lesions vs. 68.7 years for glaucoma, p = 0.0001), worse visual acuity at presentation ( 47.7% of eyes better than 20/ 50 for compressive lesion vs. 76.9% for glaucoma, /; = 0.002), temporal or diffuse thinning of the neuroreti-nal rim { p = 0.0001), pallor out of proportion to cupping ( 45.5% of eyes in compressive group vs. 9.6% of those with glaucoma, p = 0.0001), and visual field defects with respect for the vertical meridian ( 21/ 44 eyes vs. 9/ 52 eyes,/; = 0.003). Age < 50 years ( 93% specific) and disc pallor in excess of cupping ( 90% specific) were found to have the highest specificities for nonglaucoma­tous cupping. Although all of the patients in this study had received neuroimaging to exclude or confirm the presence of a compressive lesion, the presence of certain clinical characteristics may provide helpful clues to the existence of nonglaucomatous cupping. Visual Field Testing Computerized and noncomputerized perimetry may be useful for the detection of functional visual field defects. However, in patients with nonphysiologic visual loss, computerized perimetry may reveal abnormalities other than the typical spiral or tubular defects. Assi and Brazier ( 2) reported two patients in whom a monocular temporal 208 L. J. BALCER AND STEVEN L. GALETTA hemianopia was the predominant defect. Both patients had normal MR and CT imaging of the brain and orbits; electroretinograms and visual evoked responses were also normal. Binocular Goldmann perimetry was useful in both cases, demonstrating constriction ipsilateral to the monocular defect despite the patient having both eyes open for testing. However, both authors emphasized the importance of considering organic disease since true field abnormalities may be masked by nonphysiologic perimetric findings. Patterns of " hysterical hemianopia" were also the topic of an extensive review by Keane of 454 patients with " pseudoneurologic" signs ( 3). In these patients, whose evaluations spanned a 25- year period, most func­tional visual field defects were readily documented using confrontation techniques. Monocular temporal defects, which persisted on binocular testing, were the most com­mon pattern of functional hemianopia ( 58%), followed by monocular blindness ( 20%). Keane ( 3) stressed that despite advances in the use of computerized perimetry, confrontation techniques, particularly using double si­multaneous finger counting, continue to be helpful for documenting functional visual field defects. The Pulfrich Phenomenon The Pulfrich phenomenon, a sensitive sign of unilat­eral optic neuropathy, may correlate with difficulties in performing certain visual tasks, such as judging distances while driving. The development of a simple yet highly predictive bedside test for the Pulfrich phenomenon was recently undertaken by Mojon et al. ( 4). They examined 18 patients with unilateral optic neuritis, 2 normal vol­unteers with optic neuropathy simulated by neutral den­sity filters, and 90 normal control subjects using the " swinging pen test." As the name suggests, this new test involves the manual oscillation of a black pen in front of a white background ( a lab coat) by the examiner at a fixed distance from the patient ( Fig. 1). The mechanical pendulum test, a standardized method of detecting the Pulfrich phenomenon, was also performed for all partici­pants in the study. Results of the swinging pen test were compared to those of the mechanical pendulum test with respect to the magnitude of perceived oscillation ( the degree of perceived elliptical rotation of the pen or pen­dulum). For the two normal volunteers with simulated optic nerve disease ( neutral density filters), high corre­lations ( r = 0.92- 0.96) were found between the magni­tudes of simulated oscillation using the swinging pen versus mechanical pendulum test. These magnitudes also correlated well among 18 patients with optic neuritis ( rs = 0.90), demonstrating that the swinging pen test can be useful in detecting degrees of disease severity. Since none of the 90 normal control subjects perceived a Pul­frich phenomenon using the swinging pen test or the mechanical pendulum test, the positive predictive value of the new swinging pen test was 100% among the pa­tients with optic neuritis. This new test, which also dem­onstrates excellent interobserver reliability, provides a simple, familiar, and potentially useful adjunctive method for detecting optic neuropathies. FIG. 1. The swinging pen test. The examiner holds the thumb of one hand in the region of the epigastrium pointing toward the head. A black pen is held with the other hand directly above the thumb and oscillated in a plane perpendicular to the viewer. The observer looks at the thumb and describes how the pen oscil­lates. Normal subjects report the oscillation to be in one plane. If an elliptical movement is perceived, the thumb can be moved toward the patient to determine the size of the illusion. Reprinted with permission from: Mojon DS, Rosier KM, Oetliker H. A bed­side test to determine motion stereopsis using the Pulfrich phe­nomenon. Ophthalmology 1998; 105: 1337- 44. NEURO- OPHTHALMOLOGY AND THE RETINA Cancer- Associated Retinopathies Whitcup and colleagues ( 5) presented the first known case of a patient with retinopathy and serum antibodies to a 23- kd antigen ( recoverin) in whom an associated malignancy has not been found. As emphasized in an accompanying editorial by Keltner and Thirkill ( 6), the case description by Whitcup et al. ( 5) adds to our knowl­edge of immune- mediated retinopathies. In addition to comments regarding the mechanisms of cancer-associated retinopathies ( CAR), Keltner and Thirkill ( 6) also provided a useful summary of recommendations for evaluation, serologic diagnosis, and treatment of CAR, stressing that our understanding of this condition is con­tinuously evolving. Tamoxifen Retinopathy Treatments for systemic malignancies may also be as­sociated with retinal dysfunction, as indicated in a recent report by Lee ( 7) of a patient with tamoxifen retinopathy. This 64- year- old woman developed painless visual loss in both eyes 5 years after surgical resection, local radio­therapy, and initiation of daily tamoxifen therapy for breast cancer. Visual acuities at presentation were 20/ 15 in the right eye and 20/ 60 in the left. Funduscopic ex- J Neum- Oplulmlmol, Vol. 19. No. 3, 1999 PREGENICULATE AFFERENT VISUAL SYSTEM 209 amination revealed crystalline deposits in the macula of each eye, as were well demonstrated by color photo­graphs. As emphasized by the authors ( 7), tamoxifen therapy may be associated with numerous ocular find­ings in addition to crystalline retinopathy, including cor­neal opacity and decreased visual acuity. Creutzfeldt- Jakob Disease Visual signs and symptoms occur frequently in the setting of Creutzfeldt- Jakob disease ( CJD), and may of­ten be presenting features of this disorder. Because Creutzfeldt- Jakob ( CJD) disease is a disorder character­ized by pathologic changes within gray matter, DeSeze and colleagues ( 8) investigated the possibility of retinal dysfunction in patients with suspected CJD. The predic­tive value of noninvasive visual electrophysiologic test­ing, including eletroretinography ( ERG) and visual-evoked potentials ( VEP), was examined in 41 consecu­tive patients. Twenty- four patients had definite ( pathologically proven) or probable ( meet published laboratory/ clinical criteria) CJD, while 17 were diag­nosed with other neurologic disorders ( control patients). Fundus examinations were normal in all patients. ERG, performed in 19 of the 24 patients with CJD, demon­strated significant reduction in the amplitude of the B1 wave in patients with CJD compared with controls ( j? < 0.0005). Impairment of the Bl wave, with relative spar­ing of the A wave, correlated closely with pathologic findings demonstrated in the retinas of these patients, which included spongioform changes in the outer plexi-form and ganglion cell layers. The amplitude of the flash VEP was significantly increased in the CJD group ( p < 0.0005), although there were no differences in VEP la­tencies. These findings are consistent with early dysfunc­tion of inner retinal layers in patients with CJD; however, caution in the interpretation of a reduced Bl wave on ERG is also warranted since this finding may occur in the setting of other neurodegenerative diseases. HIV- Associated Visual Loss HIV optic neuropathy has been implicated as a cause of visual loss in some patients with human immunode­ficiency virus ( HIV). However, a recent report of a pa­tient by Donahue ( 9) emphasizes that this diagnosis must be made with caution if an ERG has not been performed. A 35- year- old man had progressive visual loss in both eyes 12 years after diagnosis with HIV. Examination revealed reduced visual acuities ( 20/ 50- 20/ 60), abnor­mal color vision, constricted visual fields, attenuated retinal vessels, and bilateral optic disc pallor. Despite the absence of detectable virus in the patient's serum, his visual loss progressed during the next 6 months. An ERG demonstrated severe attenuation of rod and cone func­tion, with reduction of the 30- Hz flicker and B- wave responses. The authors ( 9) appropriately indicate that CAR may be included in the differential diagnosis for this patient, and that the markedly abnormal ERG in this case was the key factor in excluding HIV optic neurop­athy as the sole cause of visual loss. Vascular Disease and the Retina Episodic monocular visual loss may result from em­boli, vasospasm, vasculitis, and, more rarely, arteriove­nous malformations ( AVMs) of the retina. Hardy and O'Day ( 10) presented a patient who developed a central retinal vein occlusion and visual loss in association with a retinal AVM. At the age of 20 years, she had first noted intermittent blurred vision in the right eye. A retinal AVM arising from the right optic disc was noted; cere­bral angiography demonstrated no evidence of orbital or intracranial abnormalities. Episodic severe visual loss, worse at higher altitudes, developed when the patient was 36 years of age; the fundus examination at that time was unchanged. Seven years later, however, persistent visual loss developed and a central retinal vein occlusion was noted. Using fluorescein angiography, the blood supply to the AVM was found to be reduced, and neo­vascularization later developed. The transient episodes of visual loss described by this patient before the retinal vein occlusion represent uncommon manifestations of retinal AVMs, and are most likely to represent ischemia secondary to " steal" phenomena. Several potential mechanisms for venous occlusions in the setting of this rare entity were implicated, including venous stasis and compression with reduced outflow at the level of the central retinal vein. In patients with retinal emboli, the aortic arch may represent an underrecognized source. Atheromatous plaques in the aortic arch may be demonstrated by transesophageal echocardiography, as indicated in two recent case reports by Romano et al. ( 11). Both patients, aged 91 and 67 years, had retinal emboli, the most likely source of which could not be identified by carotid ultra­sound, MR angiography, or transthoracic echocardiogra­phy. When transesophageal echocardiography was per­formed, calcified plaques in the aortic arch and ascend­ing aorta were recognized in both patients. The authors ( 11) suggest that, although the optimal treatment for aor­tic arch embolic disease has not been defined, transe­sophageal echocardiography in selected patients may help identify this underemphasized cause of retinal em­boli. Retinal and other neuro- ophthalmologic manifesta­tions of internal carotid artery dissection were reviewed by Biousse and colleagues ( 12). They evaluated 146 con­secutive patients ( 29 retrospectively, 117 prospectively) who had extracranial internal carotid artery dissection from 1972 to 1997. Ophthalmologic signs and symptoms were frequent in this series. The most common manifes­tation was a painful Horner's syndrome ( present in 65/ 146, 44%), which was isolated in nearly 50% of cases. Transient monocular visual loss and " scintillations" were also common ( 41/ 146, 28%), and were often induced by looking at a bright light. Permanent visual loss caused by ischemic optic neuropathy occurred in four patients. Given the subsequent occurrence of hemispheric stroke in nearly one third of patients in this series who had neuro- ophthalmologic findings, the importance of recog­nizing internal carotid artery dissection, particularly in J Neiiro- Ophllmlmol, Vol. 19, No. .1. 1999 210 L. J. BALCER AND STEVEN L. GALETTA the setting of a painful Horner's syndrome, was empha­sized. THE OPTIC NERVE Anterior Ischemic Optic Neuropathy Nonarleritic anterior ischemic optic neuropathy ( NAION) is a disorder for which an embolic etiology has been rarely implicated or documented. Whether patients with recent NAION may have higher frequency of ipsi-lateral emboli in intracranial vessels by transcranial Doppler ( TCD) monitoring was investigated by Kosmor-sky et al. ( 13). Such an association, according to the authors ( 13), may provide evidence for a possible em­bolic mechanism in some patients. TCD was performed on 11 patients with recent (< 121 days prior) NAION and 10 age- matched controls. Both ( right and left) middle cerebral arteries were monitored for 30 minutes, and the frequency of microemboli in these arteries was recorded. During the TCD monitoring, no microemboli were de­tected among any of the 1 1 patients with recent NAION. One control patient, who had a remote history of NAION but also had a prosthetic heart valve, had evidence of emboli ( frequency 12/ hour). Thus, a recent history of NAION within 4 months before presentation did not ap­pear to be associated with an increased frequency of TCD- detectable microemboli in the middle cerebral ar­teries. Anatomic factors, such as the " disc at risk," are likely contributors to the causation of NAION. Although NAION has been shown to occur most frequently in patients with cupless optic discs, Parsa et al. ( 14) re­cently described a patient with sequential ( 6 years be­tween events) NAION who had generous physiologic optic cups ( 0.5 cup- to- disc ratio). This 61- year- old man developed typical findings of pallid disc edema and in­ferior altitudinal field defects during both attacks of NAION. This " exception to the rule" places emphasis on the fact that, despite a strong association with the " disc at risk," NAION occurs in the absence of this important anatomic risk factor. Macular edema may also be a feature of NAION. Tomsak and Zakov ( 15) examined a series of 12 patients with this finding to determine the visual outcome and fluorescein angiography characteristics. All patients ( 13 eyes) demonstrated neuro- ophthalmologic findings con­sistent with NAION, including visual acuity loss, field defects, and disc edema. During an average follow- up period of 5.3 months, improvement in visual acuity oc­curred in 11/ 13 eyes ( 85%), with a mean improvement of 2.3 Snellen lines ( range of improvement up to 9 lines). Although this study examined a small number of pa­tients, this report suggests that patients with NAION and macular edema may have a higher probability of visual recovery. As the authors ( 15) point out, this recovery is likely caused by the resolution of the macular edema. Furthermore, the macular edema associated with NAION was often subtle in this group, suggesting that its pres­ence may often be undcrrecognized in the acute setting. Giant Cell Arteritis A common and formidable cause for anterior ischemic optic neuropathy ( AION), giant cell arteritis ( GCA), is a disorder for which the clinical course and microscopic pathology suggest the possibility of an infectious etiol­ogy. Nordborg and colleagues ( 16) hypothesized that va­ricella zoster virus ( VZV) may be involved in the patho­genesis of GCA, given its tendency to reactivate and to occur in elderly persons. Temporal artery biopsy speci­mens were obtained from 10 patients with GCA ( all women, mean age 76.6 years). Using polymerase chain reaction ( PCR) techniques and immunohistochemical analysis, no evidence of VZV was identified in any of the specimens. These findings indicate that VZV is not an immediate causal agent of GCA. Visual loss and neurologic dysfunction related to pos­tural changes may occur in GCA. Diego and Margo ( 17) recently reported two patients with biopsy- proven GCA, both of whom described bilateral transient visual loss after bending over or arising from a supine position. The first patient was a 72- year- old man who reported several 2- to 15- minute episodes of painless visual loss ( total darkness) in both eyes associated with changes in posi­tion. No signs of carotid disease or ocular abnormalities, such as disc swelling, were discovered on examination; the patient's visual loss was thus attributed to low flow in the vertebrobasilar circulation. The second patient, also 72 years of age, had bilateral arteritic AION. On the second day of her hospitalization for intravenous steroid therapy, she experienced a 15- minute episode of com­plete visual loss in both eyes after bending over. The cause in this patient was thought to be insufficiency in the vertebral or ocular circulations. While both patients in this report had other symptoms suggestive of GCA, including headache, jaw claudication, and scalp tender­ness, postural vision loss may be an important cause of visual dysfunction in GCA. Many unusual nonvisual manifestations may also ac­company GCA. One such sign is scalp necrosis. In a report of two patients, Dudenhoefer et al. ( 18) empha­sized that this valuable sign may be overlooked. Both of their patients had scalp necrosis, characterized by alope­cia, crusting, vesicles, edema, and erythema in the dis­tribution of the superficial temporal arteries. In one pa­tient, the visual loss was preceded by scalp necrosis, while in the other, the skin findings were key to estab­lishing the GCA diagnosis. Vernet's syndrome, characterized by simultaneous unilateral involvement of cranial nerves IX, X, and XI, is another rare manifestation of GCA. Gout et al. ( 19) re­cently described a 73- year- old man who was hospitalized for the sudden onset of dysphagia and dysphonia. He had also developed temporal headache. Examination re­vealed paralysis of the right palatine velum, right vocal cord paralysis, and weakness of the right sternocleido­mastoid. The sedimentation rate was 130 mm/ hour. CT and MRI scans of the brain and skull base were normal. Temporal artery biopsy was consistent with GCA. Ver­net's syndrome, rare in the setting of GCA, is thought to be caused by arteritic involvement of external carotid ./ Nnim- Oplilliuliiml, Vol. 19. No. J, 1999 PREGENICULATE AFFERENT VISUAL SYSTEM 211 artery branches, including the ascending pharyngeal ar­tery. In the patient presented by Gout et al. ( 18), the ascending pharyngeal artery was narrowed on cerebral angiography. The sudden onset of the patient's symp­toms and their rapid resolution after steroid therapy also provided evidence for an arteritic etiology. Optic Neuritis Important 5- year results from the Optic Neuritis Treat­ment Trial ( ONTT) were reported in late 1998. Cole and colleagues ( 20) reassessed the predictive value of cere­brospinal fluid ( CSF) ohgoclonal banding for the devel­opment of clinically definite multiple sclerosis ( CDMS) within 5 years after monosymptomatic optic neuritis. Among the 457 patients who participated in the ONTT, 76 underwent lumbar puncture and brain MRI within 24 hours of enrollment. The baseline demographic charac­teristics of this subgroup were similar to those of the entire ONTT cohort, with a mean age of 33 years. During the 5- year follow- up period, 22/ 76 patients ( 29%) devel­oped CDMS. Among the 38 patients who had ohgoclonal bands in the CSF at the time of the initial attack of optic neuritis, CDMS developed in 16 ( positive predictive value = 42%), whereas only 6/ 38 patients ( 16%; nega­tive predictive value 84%) without oligoclonal bands de­veloped CDMS. The presence of CSF oligoclonal bands was thus associated with the development of CDMS in this group of patients ( odds ratio = 3.88; 95% CI 1.18, 13.86; p = 0.02). However, when the results of the initial brain MRI were also considered, the predictive value of CSF oligoclonal banding was most apparent in the group with no brain lesions on MRI ( 39 patients). CDMS developed in 3/ 11 patients ( 27%) with normal MRI and positive oligoclonal banding, whereas 1 patient of 28 ( 4%) with normal MRI and no oligoclonal bands developed CDMS ( p = 0.06). No such differences were found among those with abnormal MRI scans ( one or more brain lesions). As Cole et al. ( 20) emphasized, CSF oligoclonal banding is a potentially useful predictor of CDMS at 5 years after monosymptomatic optic neuritis. Oligoclonal bands were most helpful in predicting CDMS among those patients for whom the initial brain MRI was normal. Brain MRI therefore continues to be the most powerful predictor of CDMS in patients with monosymptomatic optic neuritis. Cerebrospinal fluid oligoclonal bands are typically ab­sent in patients with Devic's neuromyelitis optica, a dis­order characterized by demyelination of the optic nerves and spinal cord without brain involvement. Because the outcomes of patients with this disease are often poor, Mandler et al. ( 21) performed an observational pilot trial of steroids and azathioprine treatment in seven patients with newly diagnosed Devic's neuromyelitis optica. All patients were women, ranging in age from 31 to 73 years. Brain MRI scans were normal in all, with the exception of optic nerve involvement. CSF oligoclonal bands were absent in all seven patients. After baseline laboratory testing, all patients were given high- dose intravenous methylprednisolone ( 500 mg twice daily) for 5 days, fol­lowed by oral prednisone at 1 mg/ kg per day for 2 months. This was followed by a slow taper to a mainte­nance dose of 10 mg/ day. Three weeks after the start of steroid therapy, oral azathioprine was begun at a dose of 2 mg/ kg per day, with the goal of a maintenance dose of 75 to 100 mg per day. Expanded Disability Status Scale ( EDSS) scores demonstrated significant improvement from baseline ( mean score 8.2- severe disability) at 6 months ( mean 6.6, p < 0.001), 12 months ( mean 5.0, /; < 0.0001), and 18 months ( mean 4.0, p < 0.0001). The mean EDSS score at 18 months ( 4.0, range 3.0- 6.0) in­dicated that, by that time, most patients could ambulate without assistance. This pilot trial, although observa­tional, provides preliminary evidence that prednisone and azathioprine therapy may provide safe and effective treatment for patients with newly diagnosed Devic's neu­romyelitis optica. However, larger randomized trials are needed to address this question and to further evaluate the prevalence of side- effects. Infectious, Inflammatory, and Postsurgical Optic Neuropathies Unusual presentations of infectious and inflammatory optic neuropathies continue to be reported in the neuro-ophthalmologic literature. Mansour ( 22) recently de­scribed a 29- year- old patient with the rare finding of an optic disc tubercle. The patient had blurred vision in both eyes of several weeks' duration. Examination revealed granulomatous iritis and bilateral optic disc edema. The left optic disc, however, was severely swollen, with a large nodular evaluation at the nasal border. A nodule was likewise present on chest radiography, and the pu­rified protein derivative ( PPD) test was positive for tu­berculosis. The patient's visual symptoms resolved with antituberculous therapy ( isoniazid, ethambutol, rifampin), although the peripapillary granuloma in the left eye persisted. Mansour ( 22) emphasized the uncom­mon nature of disc edema and optic disc tubercles as presenting features of tuberculosis, and stressed that tu­berculosis must always be included on the list of poten­tial causes for infiltrative optic neuropathy. An unusual case of hypertrophic cranial pachymenin­gitis and optic neuropathy caused by Pseudomonas aeruginosa was described by Girkin et al. ( 23). A 60- year- old man developed multiple progressive cranial neuropathies manifested by hoarseness, dysphagia, de­creased hearing, facial weakness, and diplopia. The ini­tial lumbar puncture and MRI were unrevealing. Six months later, he had ptosis, ophthalmoparesis, and loss of vision in the right eye to no light perception. Diffuse dural thickening and enhancement were noted on MRI, particularly at the right sphenoid ridge, clivus, petrous apex, and cavernous sinus. Subfrontal biopsy revealed thickening of the dura with granulomatous inflammation and intracellular gram negative bacteria. Cultures grew P. aeruginosa. The patient was treated with tobramycin and ceftazidime with marked improvement of the cranial neuropathies. This report and comprehensive review by Girkin et al. ( 23) serves as a reminder of the many po­tential causes of cranial and optic neuropathies. In the case of hypertrophic cranial pachymeningitis, a search .1 Neiim- Oplilhalmol, Vol. 19. No. J, 1999 212 L. ./. BALCER AND STEVEN L. GALETTA for an underlying infectious cause must be undertaken so that appropriate therapy may be initiated. Forman and Rosenbaum ( 24) presented the clinical, biopsy, and autopsy findings for a patient who had iso­lated optic neuropathy as the presenting feature of lym-phatoid granulomatosis. This 41- year- old woman was seen initially for a 1- week history of visual loss and pain on eye movement. Examination revealed a visual acuity of 20/ 100 in the affected left eye; color vision loss, an afferent pupillary defect, and optic disc edema were noted. The visual loss progressed to no light perception in the left eye. A lung biopsy, performed to evaluate progressive dyspnea and pulmonary infiltrates, was con­sistent with lymphatoid granulomatosis, demonstrating atypical lymphoid cells that were immunopositive for T- cell markers. After the patient's death as a result of respiratory failure, a cross section of the optic nerve re­vealed infiltration by atypical lymphocytes with pleo­morphic nuclei, again immunopositive for T- cell mark­ers. This unusual neuro- ophthalmologic presentation of lymphatoid granulomatosis was initially consistent with typical idiopathic optic neuritis. In such patients, the con­tinued progression of visual loss or other atypical char­acteristics should prompt investigation for systemic dis­orders that may cause inflammatory optic neuropathies. A more benign form of optic disc edema, which may occur after trabeculectomy, was discussed by Kawasaki and Purvin ( 25) in a report of two patients. The first patient, a 24- year- old woman, was found to have asymp­tomatic optic disc edema 2 weeks after trabeculectomy for glaucoma. The edema persisted for 4 months despite intraocular pressures that were no lower than 7 to 14 mmHg. She reported a 10- month history of headache and pulsatile tinnitus; her medical history was remarkable for obesity. Examination revealed unilateral optic disc edema and enlargement of the blind spot on visual field testing. MRI was normal and CSF opening pressure was 250 mm water. The disc edema resolved with observa­tion and weight loss. The second patient, a 51- year- old moderately overweight woman ( 207 pounds), developed similar unilateral optic disc edema with blind spot en­largement. Her CSF opening pressures were likewise mildly elevated at 195 to 210 mm water, and, retrospec­tively, she had been experiencing transient visual obscu­rations. The authors ( 25) propose that relative decreases in intraocular pressure to the low- normal range in these patients, along with high- normal intracranial pressures, may have precipitated the development of optic disc edema. Because the development of optic disc edema after trabeculectomy likely depends on the relative dif­ference in intracranial versus intraocular pressure, severe ocular hypotony may not be required for disc edema to manifest in patients with mildly elevated intracranial pressure. Meningiomas and Other Neoplasms Anterior visual pathway meningiomas account for as many as 10% of all primary orbital tumors, as recently emphasized by Stafford et al. ( 26). They reviewed the records of 581 consecutive patients at the Mayo Clinic, Rochester, NY, who underwent resection for primary meningiomas from 1978 to 1988. Their search revealed 43 patients with anterior visual pathway meningiomas, involving the intraorbital or intracranial portions of the optic nerve. Records were reviewed for completeness of surgical resection ( gross total vs. subtotal), evidence of radiographic recurrence, treatment after recurrence, his­topathologic features, and demographic characteristics. The group of 43 patients with resected anterior visual pathway meningiomas was compared to those who had undergone resection for nonanterior visual pathway me­ningiomas ( 528 patients) to determine whether certain factors may be associated with tumor recurrence. The anterior visual pathway group was significantly younger at diagnosis, with a median age of 47 years ( vs. 58 years in the nonanterior visual pathway group, p = 0.001). As may have been expected based on tumor location, a sig­nificantly greater proportion of the anterior visual path­way group had subtotal resections ( 60% vs. 17%, p = 0.001). Recurrence- free survival in the anterior visual pathway group was significantly less than in the nonan­terior visual pathway group ( p < 0.001, Kaplan- Meier method); the relative risk of recurrence in the anterior visual pathway group was 3.4 ( 95% CI 2.1- 5.3) over a median follow- up of 8.3 years. At 5 years, recurrence-free survival in the anterior visual pathway group was 62% ( 95% CI 49- 70%) vs. 85% to 90% in the nonan­terior visual pathway group. As the authors ( 26) point out, the lower recurrence- free survival in the anterior visual pathway group is likely related to factors other than subtotal resection alone, such as tumor site within the anterior visual pathway, male sex, age younger than 40 years, and increased numbers of mitotic figures ( mul­tivariate analysis). Although surgical resection remains the treatment modality in patients with symptomatic me­ningiomas of the anterior visual pathway, radiation therapy is recommended in the setting of optic nerve sheath or cavernous sinus involvement ( 26), for which the potential morbidity of surgical resection is great. POEMS syndrome ( polyneuropathy [ P], organome­galy [ O], endocrinopathy | E], monoclonal gammopathy [ M], and skin changes [ S]) may be associated with optic disc swelling. Wong and colleagues ( 27) presented a 25- year- old woman who developed episodic horizontal dip­lopia, metamorphopsia, and positive visual phenomena. Initial examination revealed visual acuities of 20/ 25 in both eyes and a left abduction deficit. Two months later, she was noted to have bilateral optic disc swelling and blind spot enlargement. Brain CT and spinal fluid open­ing pressure were normal. The patient was later found to have osteolytic bone lesions secondary to multiple my­eloma. She died from multiorgan failure and hepatic ve­nous blockage after an autologous bone marrow trans­plant. This patient met criteria for POEMS syndrome, with a progressive demyelimating polyneuropathy, hepa­tomegaly, hypothyroidism, monoclonal gammopathy, and skin hyperpigmentation. Unusual features in this pa­tient, as pointed out by the authors ( 27), included young age, female sex ( older males are most typically affected), and the presence of osteolytic ( rather than osteosclerotic) J Neuw- Ophthulmol, Vol. 19, No. 3. 1999 PREGENICULATE AFFERENT VISUAL SYSTEM 213 bone lesions. Neuro- ophthalmologists should be alerted to this unusual cause of optic disc swelling, which may be related to cytokine- mediated changes in vascular per­meability at the optic nerve head. Another uncommon cause of visual dysfunction that must be considered in the setting of bilateral, unex­plained visual loss is paraneoplastic optic neuropathy. Luiz et al. ( 28) described one such patient whose under­lying malignancy was small cell carcinoma of the lung. This 59- year- old woman developed acute, painless, bi­lateral visual loss accompanied by headaches and diffi­culty walking. Visual acuities were 20/ 30 in the right eye and 20/ 40 in the left; examination was notable for keratic precipitates, vitreous cells, severely constricted visual fields, and bilateral optic disc edema. Horizontal jerk nystagmus, dysarthria, and ataxia were also present. MRI of the brain was normal; however, CT scans of the chest demonstrated mediastinal, paratracheal, and hilar ade­nopathy. Lumbar puncture revealed a lymphocytic pleo-cytosis ( 122 WBC) and elevated protein ( 111 mg/ dl). Small cell lung carcinoma was demonstrated by medias-tinoscopic biopsy because no masses were detected in the lungs. Serum autoantibodies were demonstrated against a 60 kd protein, which is present in optic nerve, cerebral cortex, and cerebellum. Anti- Hu, anti- Yo, anti- Ri, and CAR antibodies were negative. ERG was normal, although a focal ERG was not performed. A diagnosis of paraneoplastic optic neuropathy and cerebellar syndrome was made. The visual loss and ataxia improved with corticosteroid treatment and chemotherapy. Idiopathic Intracranial Hypertension The pathophysiologic mechanisms that underlie the development of idopathic intracranial hypertension ( IIH) remain unknown. Leker and Steiner ( 29) found a high prevalence of anticardiolipin antibodies in a group of 14 patients with IIH. These patients were evaluated in Je­rusalem, Israel, from 1989 to 1995. All patients in the analysis had normal MRI, normal MR venography or conventional angiography, and CSF opening pressures above 250 mm water. Five additional patients with IIH had been excluded because of inadequate neuroimaging or minor abnormalities, such as an empty sella. The mean age in the group of 14 patients with IIH was 25.9 years ( range 13- 42); 12 patients ( 86%) were female. An­ticardiolipin antibodies were detected in the serum of 6/ 14 patients ( 43%) on at least two occasions. A high prevalence of anticardiolipin antibodies was found in this small group of patients with IIH. The direct implications of this finding in the pathogenesis of IIH remain unclear. Although the authors ( 29) suggest screening for anticar­diolipin antibody in patients with IIH, they are also cor­rect in emphasizing the need for future studies in which larger groups of consecutive patients are examined. Minocycline and other tetracycline antibiotics have also been implicated in the etiology of IIH. Although neither causation or definite association have been dem­onstrated in large case- control studies, reports describing the development of IIH after the initiation of minocy­cline treatment have continued to emerge. Chiu et al. ( 30) reviewed the records of 12 patients with IIH who had been treated recently with minocycline for refractory acne vulgaris. These patients, from five neuro- ophthal-mic referral centers, had a median age of 26.5 years ( range 13- 40); 33% were obese. Symptoms of IIH had developed within 2 months of the start of minocycline treatment in 9/ 12 patients ( 75%). The authors ( 30) state, based on the findings of this observational study, that minocycline is a cause or precipitating factor in the de­velopment of IIH. However, we agree that efforts to examine this potential association must continue in the form of large, multicenter studies of risk factors for IIH. A history of minocycline use should be sought in all patients with a new diagnosis of IIH. Magnetic resonance imaging is an important tool in the diagnostic evaluation of IIH. Brodsky and Vaphiades ( 31) investigated whether the presence of certain find­ings of MRI could provide evidence for elevated intra­cranial pressure in patients with suspected IIH. They re­viewed MR images of the brain and orbits for 20 patients with IIH and 20 age- matched controls. The following findings were detected in a higher proportion of patients with IIH versus controls: 1) flattening of the posterior sclera ( 80% IIH vs. 5% controls), 2) empty sella ( 70% vs. 5%), 3) distension of the perioptic subarachnoid space ( 45% vs. 5%), 4) enhancement of the prelaminar optic nerve ( 50% vs. 0%), 5) vertical tortuosity of the orbital optic nerve ( 40% vs. 5%), and 6) intraocular pro­trusion of the prelaminar optic nerve ( 30% vs. 5%). These findings are demonstrated in Figure 2; all were 95% to 100% specific for increased intracranial pressure in association with IIH. Each of the 20 patients with IIH had at least one radiographic sign present. These MRI findings, especially flattening of the posterior sclera and empty sella, may be useful in supporting the diagnosis of IIH. Obesity and weight gain are known risk factors for IIH. Johnson and colleagues ( 32) investigated whether weight loss, in conjunction with acetazolamide therapy, could be associated with a more rapid resolution of pap­illedema in patients with IIH. They reviewed the records of 48 consecutive patients with IIH; 15 met criteria for this study, including initial neuro- ophthalmologic exami­nation within 10 days of diagnosis, initial treatment with acetazolamide and weight loss only, a single lumbar puncture performed at diagnosis, stereoscopic optic disc photographs obtained at diagnosis and during follow- up, and weight measurements obtained at initial examination and throughout the 24- week follow- up period. The mean weight at initial examination for the 15 patients was 110.5 kg, with a mean body mass index of 40.7 kg/ m2. Using the Frisen classification, it was determined that 11 patients ( 73.3%) had improvement of papilledema during follow- up, with complete resolution over a median pe­riod of 8.5 weeks in 10 patients ( 66.7%). The degree of weight loss observed in patients whose papilledema re­solved by one Frisen grade was 3.3%, while a 6.6%; weight loss was seen in those who had improvement by three Frisen grades ( corresponding to complete resolu­tion of marked papilledema). Of the four patients who J Neuro- Ophlhulmol, Vol. 19, No. .1, 1999 214 E. J. BALCER AND STEVEN E. GAEETTA FIG. 2. A- F. Neuroimaging findings observed in 20 patients with idiopathic intracranial hypertension ( IIH). A: T1- weighted axial magnetic resonance ( MR) image with fat suppression demonstrating bilateral flattening of the posterior sclera ( arrows). B: T1- weighted axial MR image with fat suppression showing prelaminar enhancement of the left optic nerve head ( upper arrow). C: Enhanced T1- weighted MR image demonstrating bilateral perioptic cerebrospinal fluid space distension ( lower arrows). D: T2- weighted axial MR image showing intraocular protrusion of swollen optic discs ( arrows). E: T1- weighted axial MR image demonstrating vertical tortuosity of the right orbital optic nerve with " smear sign" ( lower arrow). F: T1- weighted sagittal MR image showing empty sella ( arrows) with compressed adjacent pituitary gland ( posteriorly). Reprinted with permission from: Brodsky MC, Vaphiades M. Magnetic resonance imaging in pseudotumor cerebri. Ophthalmology 1998; 105: 1686- 93. took acetazolamide but did not experience weight loss during follow- up, none had improvement of papillede­ma. Percent weight loss was significantly correlated with papilledema grade change ( rs = 0.73, p = 0.002). In addition to improvement of papilledema in 11/ 15 pa­tients, 13 patients had stabilization or improvement of visual acuity to 20/ 20 or better during follow- up. Larger investigations, incorporating papilledema and other indi­cators of visual outcome and natural history data, will be needed to confirm these findings. Until then, weight loss remains a valuable treatment modality for IIH. Leber's Hereditary Optic Neuropathy In response to the observation of other investigators that the pupillary light reflex may remain intact in pa­tients with Leber's hereditary optic neuropathy ( LHON), ./ Neiiw- Ophlhtilinol, Vol. 19, No. J, 199V PREGEN1CULATE AFFERENT VISUAL SYSTEM 2/ 5 Jacobson et al. ( 33) retrospectively examined a cohort of patients with LHON and monocular visual loss to evalu­ate this issue. The neuro- ophthalmologic examination records of 10 patients with LHON and monocular visual loss were reviewed. All patients had undergone pupillary examinations with quantification of the afferent pupillary defect ( APD) using neutral density filters. For each pa­tient, the magnitude of the APD was compared with the magnitude of the APD that would have been predicted based on the degree of visual loss documented by auto­mated ( eight patients) or Goldmann ( two patients) pe­rimetry. APDs were detected in all patients, ranging in magnitude from 0.3 to 1.8 log units ( median 0.9 log units). The median predicted APD magnitude was 0.9 log units, and there was no significant difference in mag­nitude between the measured and predicted APDs ( p = 0.13). Therefore, contrary to prior observations, this study did not demonstrate that pupillary light reactions are relatively spared in patients with LHON. THE OPTIC CHIASM AND BEYOND Pituitary Adenomas Pituitary adenomas, common tumors in adult patients, occur infrequently in children. The clinical characteris­tics of 10 pediatric patients with pituitary adenomas were recently reviewed by Lee et al. ( 34). These children, aged 2 to 16 years ( median 4 years), were seen at two neuro-ophthalmic referral centers from 1989 to 1996. Visual loss was present in five patients ( 50%) at diagnosis, with visual acuities ranging from 20/ 20 to 20/ 200 in the better eyes, and 20/ 100 to light perception in the worse eyes. Temporal and bitemporal field defects were present in four of five patients with visual loss. Three patients ex­perienced visual improvement after surgery. Of the five children with visual loss, four were adolescents ranging in age from 12 to 15 years. The two youngest children in the group, aged 2 and 7 years, did not have visual loss but had accelerated growth and precocious puberty. Lee and colleagues ( 34) noted that the pediatric patients included in this study seemed to have severe visual loss, perhaps more severe than that initially seen in adult patients. Further studies, with direct comparisons between adult and pediatric patient populations with pituitary adeno­mas, are necessary to confirm this observation. See- Saw Nystagmus See- saw nystagmus may be a presenting feature of tumors and other mass lesions in the parasellar region. Dell'Osso and Daroff ( 35) recently described " Two Ad­ditional Scenarios for See- Saw Nystagmus": aehiasma and hemichiasma. Aehiasma, a congenital absence of the optic chiasm, precludes the development of binocular vision. As reported by the authors ( 35), aehiasma has been associated with see- saw nystagmus not only in ca­nine models, but also in humans ( four individuals have been identified to date). Such patients demonstrate ab­normalities on visual evoked potential testing and MRI. Although hemichiasma, or uniocular failure of retinal fiber decussation, has not yet been described in humans, the authors ( 35) suggest considering aehiasma and hemi­chiasma in infants and young children with see- saw nys­tagmus. Band Optic Atrophy Band, or " bow- tie," optic atrophy is most commonly associated with lesions of the contralateral optic tract. A variable degree of temporal disc pallor is also noted in the eye ipsilateral to the optic tract lesion. Band optic atrophy may also be present unilaterally in the setting of congenital abnormalities, as demonstrated in a report by Turbin et al. ( 36). They presented an II- year- old boy who had findings of band optic atrophy in the left eye and an ipsilateral dense temporal hemianopic defect. The right eye funduscopic examination and visual field were normal, with a visual acuity of 20/ 20. The left eye visual acuity was reduced to 20/ 200, attributed in part to stra­bismic amblyopia ( the patient had a large angle eomitant esotropia for at least 3 years before examination). An MRI scan of the brain revealed atrophy of the left optic nerve from the globe to the chiasm and an area of left cortical gray matter heterotopia. No evidence of an optic tract lesion was noted. The authors ( 36) suggest that the unilateral band optic atrophy that occurred in this unique patient may relate to neuronal migration abnormalities similar to those responsible for the ipsilateral cortical heterotopia. However, band atrophy may result from any anterior visual pathway lesion associated with a temporal hemianopic defect. Sellar Arachnoid Cysts Arachnoid cysts arising in the parasellar region may be confused with cysts of the pituitary, and may repre­sent a rare cause of visual loss secondary to optic chiasm or tract involvement. Chun et al. ( 37) presented two such patients. The first was a 33- year- old woman who had diplopia and painless, progressive visual loss in 1987. Decompression of a suprasellar arachnoid cyst produced improvement in her vision. Nine years later, her vision again worsened, and an incongruous left homonymous hemianopsia was noted. MRI revealed a suprasellar arachnoid cyst compressing the right optic tract and chi­asm. Fenestration of the cyst and placement of an Om-maya shunt resulted in visual improvement. The second patient, a 64- year- old man with a history of headaches, was found to have a bitemporal hemianopsia on a routine ophthalmologic examination. Upward displacement of the optic chiasm by a sellar arachnoid cyst was demon­strated by the initial MRI scan. However, repeat MRI, performed after the visual field defects had been ob­served to spontaneously resolve, showed resolution of the mass effect, likely secondary to spontaneous decom­pression. The authors ( 37) point out that the most typical neuro- ophthalmologic finding in patients with suprasel­lar arachnoid cysts is bitemporal hemianopsia. This un­usual entity should be added to the list of possible etiol­ogies for compressive lesions involving the optic chiasm and, even more uncommonly, the optic tracts. Traumatic Lateral Geniculate Hemorrhage " Why Fighting Makes You See Black Holes Instead of Stars" was the topic of a report by Kosmorsky and Lan- .1 Neuro- Ophlluilmol, Vol. 19, No. J. 1999 216 L. J. BALCER AND STEVEN L. GALETTA cione ( 38) of a boxer who developed a traumatic lateral geniculate hemorrhage. One month after a knockdown by his opponent, this 19- year- old was evaluated for vi­sual loss in his left hemifield. 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