Clinical/Scientific Notes Women and men are equally disabled by Charcot–Marie–Tooth disease type 1A Table 2 Neuropathy Impairment Score (NIS) comparison Emily R. Swan, BS; Darren R. Fuerst, PhD; and Michael E. Shy, MD Previously pregnant women Proposed usage of progesterone modulation to treat Charcot– Marie–Tooth disease type 1A (CMT1A)1 has raised questions as to whether endogenous progesterone alters the clinical phenotype of affected women. We evaluated 44 previously pregnant women with CMT1A (average age 50 ⫾ 11), using the Charcot–Marie– Tooth Neuropathy Score (CMTNS)2 and compared them with 15 women who had never been pregnant (average age 36 ⫾ 11) and 47 men with CMT1A (average age 48 ⫾ 14). Statistical analysis was by analysis of variance and analysis of covariance. CMTNS similar for men and women and not affected by pregnancy. There was no difference (F[1, 89] ⫽ 0.24, NS) in CMTNS between women who had been pregnant (15.5 ⫾ 5.2) and men (14.9 ⫾ 5.2). A CMTNS of 15 indicates moderate disability in which patients can easily function independently although they may require ambulation aids.2 The mean CMTNS for women who had never been pregnant was 11.2 ⫾ 5.6 compared with 15.5 ⫾ 5.2 for woman who had been pregnant (F[1, 61] ⫽ 8.86, p ⬍ 0.01). However, the nonpregnant group was younger (age 32 ⫾ 12.7) than the previously pregnant group (age 49 ⫾ 11.3; F[1, 61 ⫽ 30.21], p ⬍ 0.001) and CMTNS increased with age in both groups (r ⫽ 0.287 for nonpregnant and r ⫽ 0.523 for previously pregnant group). We therefore recalculated the test for previously pregnant vs never pregnant women with age as a covariate. The resulting equation confirmed a difference for age (F[1, 60] ⫽ 8.39, p ⬍ 0.01) but not pregnancy status (F[1, 60] ⫽ 0.83, NS). Finally we compared the CMTNS between all men and all women, independent of pregnancy status. For women, the average CMTNS was 14.2 ⫾ 5.6), and for men it was 14.9 ⫾ 5.22 (F[1, 108] ⫽ 0.52, NS). The average age of women was 44.4 and of men was 48. These results suggest that there is no difference in disease severity between women who have been pregnant and those who have not, between women who have been pregnant and men, or between men and women with CMT1A. CMTNS for women who indicated a worsening of symptoms during pregnancy. Twenty-three of the 44 women who had been pregnant (52%) indicated they had noticed worsening of their symptoms during pregnancy, whereas 21 (48%) indicated no change. For women reporting a change, the most common complaints were increased weakness (n ⫽ 11), alterations in balance (n ⫽ 9), and alterations in sensation (n ⫽ 9); individual patients may have noticed more than one change. Thirteen of the women who felt they had worsened during pregnancy perceived a temporary worsening; nine reported a permanent change, and one woman was not certain. Women who noted a temporary change indicated it took an average of 2.5 months for their symptoms to return to normal after giving birth. For women who indicated a change in their symptoms, the average CMTNS was 16.0 ⫾ 4.69; for women who did not report a change in their symptoms, the average was 14.9 ⫾ 5.81. For women who believed there was a permanent change in their neuropathy, the mean CMTNS was 15.3 ⫾ 5.5; for those who had Never pregnant women Age bracket, y Av. (SD) NIS n Age bracket, y Av. (SD) NIS n 21–30 31–40 41–50 51–60 76.5 (6.4) 62.4 (13.1) 59.2 (16.5) 67.0 (23.8) 2 5 15 15 21–30 31–40 41–50 51–60 46.4 (8.3) 65.5 (11.7) 63.0 (18.4) 53.0 (24.0) 5 6 2 2 experienced a temporary exacerbation, it was 16.5 ⫾ 4.3 (table 1). None of these differences was significant. To quantitate changes in symptoms between women who perceived or did not perceive changes during pregnancy, we utilized the CMT Symptom Score (CMTSS), which comprises the first three components of the CMTNS. The mean CMTSS for women who reported no worsening of symptoms was 3.04 ⫾ 2.10 compared with 3.43 ⫾ 2.06 for those who had noted an exacerbation (maximum score ⫽ 12).3 These differences were not significant. Neuropathy Impairment Score not increased by pregnancy or in women. We next correlated pregnancy and gender with the Neuropathy Impairment Score (NIS), a quantitative neurologic exam.4 The average NIS for men was 68.5 ⫾ 21.0 (maximum score 288), whereas for women it was 61.1 ⫾ 18.9. The average NIS for women who had been pregnant was 64.4 ⫾ 18.9, whereas for never pregnant women it was 57.1 ⫾ 14.6. We compared the average NIS of women and pregnancy status by age, and with the exception of women age 21 to 30, in which there were only two previously pregnant women to evaluate, and ages 51 to 60, in which there were only two never pregnant women to evaluate, the differences were not significant (table 2). We found no relationship between gender or pregnancy in patients with CMT1A analyzed by timed 25-foot walk, nerve conduction velocities, compound muscle activation potential amplitudes, and hand function questionnaire (not shown). Conclusion. These data suggest that gender, pregnancy, or plasma progesterone levels do not significantly contribute to the severity of neuropathy in women with CMT1A. We speculate that the lack of clinical fluctuations is because endogenous circulating progesterone is 97% protein bound5 and is unlikely to have access to myelinated peripheral nerves. From the Department of Neurology (E.R.S., D.R.F., M.E.S.) and Center for Molecular Medicine and Genetics (M.E.S.), Wayne State University, Detroit, MI. Supported by grants from National Institute of Neurological Disorders and Stroke (R01NS43168-01A1) and the Muscular Dystrophy Association. Disclosure: The authors report no conflicts of interest. Received August 15, 2006. Accepted in final form November 15, 2006. Address correspondence and reprint requests to Dr. M.E. Shy, Department of Neurology, Wayne State University, 421 E. Canfield, Detroit, MI 48201; e-mail: m.shy@wayne.edu Table 1 Charcot–Marie–Tooth Neuropathy Score (CMTNS) comparison Previously pregnant women Copyright © 2007 by AAN Enterprises, Inc. References Never pregnant women Age bracket, y Av. (SD) CMTNS n Age bracket, y Av. (SD) CMTNS 21–30 18.0 (0.0) 2 21–30 7.1 (3.6) 5 31–40 11.6 (4.5) 5 31–40 13.2 (4.6) 6 41–50 13.1 (3.2) 15 41–50 12.5 (9.2) 2 51–60 18.0 (6.2) 15 51–60 17.5 (3.5) 2 n 1. Sereda MW, Meyer Zu Horste G, Suter U, Uzma M, Nave KA. Therapeutic administration of progesterone antagonist in a model of CharcotMarie-Tooth disease (CMT-1A). Nat Med 2003;12:1533–1537. 2. Shy ME, Blake J, Krajewski K, et al. Reliability and validity of the CMT neuropathy score as a measure of disability. Neurology 2005;64:1209–1214. 3. Shy ME, Siskind C, Swan ER, et al. CMT1X phenotypes represent loss of GJB1 gene function. Neurology 2007;68:849 – 855. 4. Dyck PJ, Litchy WJ, Lehman KA, Hokanson JL, Low PA, O’Brien PC. Variables influencing neuropathic endpoints: the Rochester Diabetic Neuropathy Study of Healthy Subjects. Neurology 1995;45:1115–1121. 5. Mahesh VB, Brann DW, Hendry LB. Diverse modes of action of progesterone and its metabolites. J Steroid Biochem Mol Biol 1996;56:209–219. March 13, 2007 NEUROLOGY 68 873 VIDEO Ocular lateropulsion from a brainstem stroke can compensate for hemianopia Lea Pollak, MD; Olga Zeleni, MD; Yitzhak Kimigiar, MD; and José Martin Rabey, MD Ocular lateropulsion is common in lateral medullary infarcts.1,2 It is assumed to be due to damage to fibers that project from the contralateral inferior olivary nucleus via the inferior cerebellar peduncle to the Purkinje cells in the cerebellar cortex.3 Disinhibition of the Purkinje cells leads to decreased activity of the ipsilateral fastigial nucleus in the vermis. The fastigial nucleus projects, via the uncinate fasciculus in the superior cerebellar peduncle, upon the medial and superior vestibular nuclei and the paramedian pontine reticular formation of the contralateral side and accelerates contralateral saccades. Its inhibition results in a motor bias of horizontal eye movements toward the side of the lesion.3,4 The eyes tend to move conjugately to the side of the infarct while there is no limitation in ductions or versions, as opposed to gaze palsy. The ocular drift can be seen as a continuous tendency of the eyes to look ipsilaterally during primary gaze or—in its mild form— can be observed as gaze deviation followed by a corrective movement to the midline when the eyes are opened following lid closure. On saccade testing, the patient performs hypermetric saccades to the side of the stroke and hypometric saccades contralaterally.2 We describe a patient with an old right homonymous hemianopia due to a left temporo-occipital stroke who reported improved vision after a left lateral medullary infarction that caused left ocular lateropulsion. Case report. A 49-year-old man was admitted because of sudden onset of vertigo, dysphagia, vertical diplopia, and loss of coordination in the left limbs. His medical history comprised noninsulin-dependent diabetes mellitus. Two years previously he had a left temporo-occipital infarct with a congruous right homonymous hemianopia (figure). On examination his eyes deviated to the left (see video at www.neurology.org). The range of eye movements was full, and Additional material related to this article can be found on the Neurology Web site. Go to www.neurology.org and scroll down the Table of Contents for the March 13 issue to find the title link for this article. the doll’s eye maneuver overrode the deviation. There was a mild skew deviation with the right eye hypertropic. A horizontal nystagmus to the right on primary and right gaze, which changed its direction to the left on left gaze, was seen. His visual acuity was 6/6 in both eyes. Visual field testing confirmed a right homonymous hemianopia (figure). The pupils were normal in size, and the pupillary reactions to light were preserved. His speech was dysarthric, and a left palate weakness was found. The finger–nose and heel– knee tests were severely dysmetric on the left. The patient was unable to walk owing to body lateropulsion to the left. Sensation to pinprick was decreased over the left face and the right limbs. There was no tactile inattention. Brain MRI revealed a recent ischemic lesion in the left dorsolateral medulla oblongata and a chronic left occipitotemporal mediocaudal infarct (figure). Doppler flow studies of the carotid and vertebral arteries, EKG, and transthoracic echocardiogram were normal. Blood tests, including coagulation properties, were within normal limits, except for increased fasting glucose levels. Vertical diplopia and skew deviation resolved during the first week following the stroke. At that time, the patient reported that his vision had improved and became better than before hospitalization. Since the previous stroke, his vision was blurred, he used to bump into objects on the right, and he had difficulty reading. He now reported seeing more clearly, being better able to observe moving objects, and being able to read more fluently. He bisected randomly scattered horizontal lines at a point placed to the right of the midline. The improvement in vision lasted for the next 2 weeks of follow-up, in parallel with the persisting ocular lateropulsion. The patient was then transferred to another hospital for rehabilitation. Discussion. Ocular search of a patient with hemianopia would be expected to occur toward the blind hemifield in order to bring the objects onto the retina of the healthy side. The principal question in this case is why eye deviation toward the “wrong” hemifield would improve vision. A patient with left hemianopia without neglect was reported who became able to identify objects in the hemianopic field when looking to the right.5 Several possibilities were proposed as the assumed mechanism of this gaze-dependent visual improvement. First, gazing in the direction opposite the blind hemifield could enhance an alternative visual system, possibly by activation of the superior colliculus–pulvinar system and the uncrossed retinogeniculate fibers. Second, the direction of gaze opposite the hemianopic side may have corrected a visual defect that was due to dysfunction of cells that function upon hemispheric rather than retinotopic coordinates. Once both halves of the retina were Figure. The left side of the figure shows the chart of the visual fields indicating a congruent right homonymous hemianopsia. On the right side of the figure is the axial T2-weighted MRI showing a large chronic left occipitotemporal stroke (A) and the fluid-attenuated inversion recovery MRI showing an increased signal in the left dorsal lateral medulla, compatible with a recent ischemic stroke (B). 874 NEUROLOGY 68 March 13, 2007 brought into the healthy hemispheric field, vision improved or normalized. Finally, the possibility of changes in the modalityspecific attention, a special type of attention that is not necessarily spatially distributed, was raised. Changes in this subtype of attention on lateral gazing may therefore help in overcoming visual field deficit as a compensatory mechanism.5 We would like to comment upon the tendency of our patient to bisect a horizontal line ipsilaterally to the side of hemianopia, that is, contralaterally to the side of occipital lesion. Patients with complete hemianopia can see only the line on the side of the normal hemifield and would thus be expected to bisect the line ipsilaterally to the brain lesion. However, this is true only in patients with hemianopia and hemispatial neglect, whereas patients with pure hemianopia, as in our case, show a tendency to bisect the line contralaterally to the side of the lesion, toward the hemianopic visual field.6,7 This is explained by a change in attentional distribution when a patient with hemianopia tends to search for the end of the line in the direction of the blind hemispace as an adaptive mechanism.7,8 However, this adaptation may occur on cost of accuracy in perception, as the erroneous bisection shows. The onset of ocular lateropulsion in the direction opposite to the direction of adaptation would therefore possibly temper this attentional redistribution and lead to a greater ease in accurately perceiving the visual world. Neck–proprioceptive and caloric–vestibular stimulation have been shown to improve visual neglect.9 It seems possible that even though our patient had no neglect, the acute onset of vestibular imbalance due to infarction of the left vestibular nucleus could have contributed to the reset of his attentional distribution and to the pronounced left ocular lateropulsion as well. The skew deviation resolved earlier than the ocular lateropulsion. This might be due to differences in the neural substrates underlying skew deviation and ocular lateropulsion. Whereas skew deviation in lateral medullary infarcts is related to damage to the otolith pathways at the level of the medial vestibular nucleus, ocular lateropulsion is the result of involvement of the olivocerebellar fibers in the inferior cerebellar peduncle, as described above. A different impact of the ischemia on these two, although VIDEO Fixed dystonia unresponsive to pallidal stimulation improved by motor cortex stimulation L.M. Romito, MD; A. Franzini, MD; D. Perani, MD; F. Carella, MD; C. Marras, MD; L. Capus, MD; V. Garibotto, MD; G. Broggi, MD; and A. Albanese, MD Fixed dystonia is a rare condition in which immobile dystonic postures do not return to a neutral position at rest. It is typically focal or segmental and painful in about 50% of cases.1 Corticectomy, plexotomy, and peripheral denervation are often tried, but prognosis is poor.1 We describe a patient with primary fixed dystonia unresponsive to pallidal stimulation who improved markedly with unilateral motor cortex stimulation. Case report. A right-handed woman with no remarkable personal or family history developed severely painful elevation of the left shoulder in 1990 at age 31. Left anterior scalene myotomy in 1994 was unsuccessful. By 1998 she had progressed to severe segmental dystonia, with fixed elevation and anterorotation of the left shoulder, abduction of the upper limb, severe trunk involvement, and fixed kyphoscoliosis (figure, A; video 1 [on www. neurology.org]). Gestes antagonistes and overflow dystonia were not present. Attempts to stand or walk were thwarted by unbearable pain in the affected shoulder and arm, whereas at rest there was little pain. Benzodiazepine, baclofen, and trihexyphenidyl produced no benefit. DYT1 and DYT5 gene mutations were absent. Nothing indicated somatoform or psychogenic disorder. Additional material related to this article can be found on the Neurology Web site. Go to www.neurology.org and scroll down the Table of Contents for the March 13 issue to find the title link for this article. anatomically proximate, neural structures might explain the different speed of recovery. Despite the fact that the mechanism responsible for improvement of vision is unknown, it seems that ocular lateropulsion can occasionally be of benefit to patients such as in the reported case of a patient with hemianopia. However, as ocular lateropulsion following stroke is of transient duration, this benefit may last only for several weeks. From the Department of Neurology, Assaf Harofeh Medical Center, Zrifin, and Sackler Faculty of Medicine, University of Tel Aviv, Israel. Disclosure: The authors report no conflicts of interest. Received July 5, 2006. Accepted in final form November 20, 2006. Address correspondence and reprint requests to Dr. L. Pollak, Kibutz Galuyot 4, 74012 Nes Ziona, Israel; e-mail: lea.pollak@gmail.com Copyright © 2007 by AAN Enterprises, Inc. References 1. Waespe W, Wichmann W. Oculomotor disturbances during visualvestibular interaction in Wallenberg’s lateral medullary syndrome. Brain 1990;113:821–846. 2. Baloh RW, Yee RD, Honrubia V. Eye movements in patients with Wallenberg’s syndrome. Ann NY Acad Sci 1981;374:600–613. 3. Noda H, Sugita S, Ikeda Y. Afferent and efferent connections of the oculomotor region of the fastigial nucleus in the macaque monkey. J Comp Neurol 1990;302:330–348. 4. Ranalli PJ, Sharpe JA. Contrapulsion of saccades and ipsilateral ataxia: a unilateral disorder of the rostral cerebellum. Ann Neurol 1986;20:311– 316. 5. Nadeau SE, Heilman KM. Gaze-dependent hemianopia without hemispatial neglect. Neurology 1991;41:1244–1250. 6. Meienberg O, Zangemeister WH, Rosenberg M, Hoyt WF, Stark L. Saccadic eye movement strategies in patients with homonymous heminaopia. Ann Neurol 1981;9:537–544. 7. Barton JJS, Black SE. Line bisection in hemianopia. J Neurol Neurosurg Psychiatry 1998;64:660–662. 8. Barrett AM, Peterlin BL, Heilman KM. Ipsilateral neglect versus hemianopic compensation. Neurology 2003;61:120–123. 9. Heilman KM, Valenstein E. Mechanisms underlying hemispatial neglect. Ann Neurol 1979;5:166–170. Brain MRI was normal. Under deep sedation, left shoulder and arm posture became almost normal, and the continuous electromyographic (EMG) activity of the left trapezius and pectoralis major disappeared. Repeated botulinum toxin (Dysport) injections to the left superior trapezius (up to 500 U), levator scapulae (up to 75 U), and pectoralis major (up to 300 U) did not relieve pain or dystonia. At age 44, internal global pallidus (GPi) stimulators were implanted bilaterally, but no improvement in dystonia or pain occurred over 12 months. A four-plate Medtronic Resume electrode array was placed epidurally over the right primary motor cortex parallel to the central sulcus2 (figure, C) under local anesthesia and MRI control; the GPi electrodes and subclavian generators were left in place. The right generator was connected to the plate, and the left was switched off. Stimulation started the day after implant (3.8 V, 60 Hz, 60 microseconds, contacts ⫺0 ⫹1 ⫺2) and remained unchanged thereafter. Gradual recovery became evident at 4 months, and by 6 months the pain and dystonic postures of the shoulder and trunk had almost resolved, although the fist remained clenched (figure, B; video 2). This marked improvement persisted at 22 months. Two resting [18F]fluorodeoxyglucose ([18F]FDG) PET scans were performed (6 months before and 6 months after cortical implant), using a multiring tomograph. The patient’s parametric images of [18F]FDG distribution were compared with those in 21 healthy subjects using voxel based SPM99 procedures (Wellcome Department of Cognitive Neurology, London, UK). Differences were considered significant at p ⬍ 0.001. PET during GPi stimulation showed significantly increased glucose consumption in the sensorimotor cortex (more extensive on the left) and supplementary motor cortex and anterior cingulate gyrus bilaterally. PET under cortical stimulation showed significant hypometabolism in the cerebellum, more pronounced on the right, and no increase in cortical metabolism (figure, D). March 13, 2007 NEUROLOGY 68 875 Figure. (A) Clinical appearance of fixed dystonia before surgical treatments. Note severe fixed segmental dystonia, with elevation and anterorotation of left shoulder, upper limb hyperabduction, and severe kyphoscoliosis. (B) After 6 months of continuous right motor cortex stimulation, the axial and left limb proximal dystonia had improved, without improvement of the left hand. (C) MRI after motor cortex implant shows artifact indicating approximate position of electrode (arrow). (D) Voxel-based statistical parametric mapping analysis (p ⬍ 0.001). Statistical maps superimposed on standard anatomic template show bilateral cerebellar hypometabolism (blue) under continuous chronic cortical stimulation. Discussion. Mechanisms of fixed dystonia have not been elucidated but may differ from those of primary torsion dystonia.1 Our patient did not improve with GPi stimulation, which is often effective in primary and nonprimary dystonia,3 suggesting that the modulation of data flow within the GPi during stimulation was insufficient to improve the fixed dystonia symptoms. The improved movements and fixed dystonia during cortical stimulation were not due to reduced pain because before cortical implant, fixed posturing at rest persisted, although there was little pain. A PubMed search uncovered no reports of fixed dystonia treated by epidural cortical stimulation, but found a report that strokerelated hand dystonia and pain improved with epidural cortical stimulation.2 It remains unclear why motor cortex stimulation is effective in these conditions. Low-frequency motor cortical stimulation is thought to activate neurons within the cortex,4 which results in modulation of the corticopontocerebellar and the corticopallidothalamocortical loops. The significant bilateral reduction of cerebellar glucose metabolism during cortical stimulation (figure, D) suggests a modulating effect on cerebellar function. Interestingly, selective elimination of cerebellar output improves dystonia in experimental animals.5 Alternatively, modified cerebellar outflow to the motor cortices may have caused plastic reorganization of the cortical representation of movements, to produce the improved motor function. Both basal ganglia and cerebellum— key structures in motor control—may be involved in the various manifestations of dystonia.6,7 The current case suggests that motor cortex stimulation may be a useful treatment option for fixed dystonia. From the Fondazione I.R.C.C.S. Istituto Neurologico “Carlo Besta” (L.M.R., A.F., F.C., C.M., G.B., A.A.), Università Vita e Salute San Raffaele, IRCCS 876 NEUROLOGY 68 March 13, 2007 San Raffaele, IBFM-CNR (D.P., V.G.), and Università Cattolica del Sacro Cuore (A.A.), Milano, and Università di Trieste, Ospedali Riuniti, Trieste (L.C.), Italy. Supported by the Italian Ministry of Universities and Research (grant PRIN 2004062394). Disclosure: The authors report no conflicts of interest. Received June 5, 2006. Accepted in final form November 22, 2006. Address correspondence and reprint requests to Dr. A. Albanese, Istituto Nazionale Neurologico Carlo Besta, Via G. Celoria, 11 20133 Milano, Italy; e-mail: alberto.albanese@unicatt.it Copyright © 2007 by AAN Enterprises, Inc. References 1. Schrag A, Trimble M, Quinn N, Bhatia K. The syndrome of fixed dystonia: an evaluation of 103 patients. Brain 2004;127:2360–2372. 2. Franzini A, Ferroli P, Dones I, Marras C, Broggi G. Chronic motor cortex stimulation for movement disorders: a promising perspective. Neurol Res 2003;25:123–126. 3. Vidailhet M, Vercueil L, Houeto JL, et al. Bilateral deep-brain stimulation of the globus pallidus in primary generalized dystonia. N Engl J Med 2005;352:459–467. 4. Tsubokawa T, Katayama Y, Yamamoto T, Hirayama T, Koyama S. Treatment of thalamic pain by chronic motor cortex stimulation. Pac Clin Electrophysiol 1991;14:131–134. 5. LeDoux MS, Lorden JF, Ervin JM. Cerebellectomy eliminates the motor syndrome of the genetically dystonic rat. Exp Neurol 1993;120:302–310. 6. Raike RS, Jinnah HA, Hess EJ. Animal models of generalized dystonia. NeuroRx 2005;2:504–512. 7. Vitek JL. Pathophysiology of dystonia: a neuronal model. Mov Disord 2002;17(suppl 3):S49–S62. Ocular lateropulsion from a brainstem stroke can compensate for hemianopia Lea Pollak, Olga Zeleni, Yitzhak Kimigiar, et al. Neurology 2007;68;874-875 DOI 10.1212/01.wnl.0000256817.73598.e8 This information is current as of March 12, 2007 Updated Information & Services including high resolution figures, can be found at: http://www.neurology.org/content/68/11/874.full.html Supplementary Material Supplementary material can be found at: http://www.neurology.org/content/suppl/2007/03/04/68.11.874.DC1.ht ml References This article cites 9 articles, 4 of which you can access for free at: http://www.neurology.org/content/68/11/874.full.html##ref-list-1 Citations This article has been cited by 1 HighWire-hosted articles: http://www.neurology.org/content/68/11/874.full.html##otherarticles Subspecialty Collections This article, along with others on similar topics, appears in the following collection(s): All Neuro-ophthalmology http://www.neurology.org//cgi/collection/all_neuroophthalmology Ocular motility http://www.neurology.org//cgi/collection/ocular_motility Oscillopsia http://www.neurology.org//cgi/collection/oscillopsia Visual fields http://www.neurology.org//cgi/collection/visual_fields Permissions & Licensing Information about reproducing this article in parts (figures,tables) or in its entirety can be found online at: http://www.neurology.org/misc/about.xhtml#permissions Reprints Information about ordering reprints can be found online: http://www.neurology.org/misc/addir.xhtml#reprintsus Neurology ® is the official journal of the American Academy of Neurology. 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