Eye movement disorders Grant T. Liu, MD, Nicholas J. Volpe, MD, and Steven L. Galetta, MD Division of Neuro-ophthalmology, Hospital of the University of Pennsylvania and Children’s Hospital of Philadelphia, Scheie Eye Institute, Philadelphia, Pennsylvania, USA The ophthalmic, neurologic, and neuro-ophthalmic literature over the past year have included a wide variety of interesting case reports, patient series, and reviews involving eye movement abnormalities, This review highlights some of the more important articles and how they contribute to our understanding, diagnosis, and treatment of these disorders. A few topics will receive particular emphasis. In patients with sixth nerve palsies, botulinum toxin injection of the ipsilateral medial rectus muscle has been advocated. Recent results suggest that this treatment has no beneficial effect in acute sixth nerve palsies, but it may have a role in chronic cases. Two groups of authors, each supplying retrobulbar botulinum toxin injection for patients with acquired nystagmus and debilitating oscillopsia, obtained mixed results. One group of patients was moderately satisfied, whereas in the other group, no patients elected to repeat the treatment because of side effects such as ptosis, diplopia, or discomfort from keratitis, Finally, skew deviation is becoming a more recognized cause of vertical double vision from a central or peripheral basis. Articles published recently showed that cyclodeviation may be seen in skew deviation, and that binocular cyclotorsion distinguishes this motility abnormality from a fourth nerve palsy, which exhibits monocular excyclotorsion. Current Opinion in Ophthalmology 1995, 6;VI:27-33 Ocular motor palsies Vasculopathic palsies In a case-control study, Jacobson et al. (1*) identi- fied diahetes, left ventricular hypertrophy, and elevated hematocrit as risk factors for ischemic (vasculopathic) third, fourth, and sixth nerve palsies. The authors believed that the left ventricular hypertophy repre sented end organ clamage due to hypertension, which oddly was not found to be an independent risk fae- tor. Elevated hematocrit may have reflected high blood viscosity. Based on these results, Jacobson ef al. [14] recommended random glucose and hematocrit deter- minations, an electrocardiogram, and blood pressure measurements in patients older than 50 years of age with new isolated ocular motor palsies without known diabetes or systemic hypertension, Third nerve palsies ‘Two articles provided new information regarding the topographical arrangement of the oculomotor fascicles in the midbrain, Ksiazek et al, (2*] reported two patients ‘with pupillary mydriasis and inferior ane medial rec~ due to lesions affecting the oculomotor fas- authors also reviewed previous articles that described partial oculomotor palsies due to fascicular lesions. Their patients, and the findings in other re ported cases, support the notion that fibers innervat- ing the pupil and inferior and medial rectus muscle Ii medially within the fascicle. Gauntt et al. [3} describe a 54-year-old man with a monocular elevator paresis € 10 an angioma compressing the fascicle laterally Their article emphasized two major points: 1) that the superior rectus and inferior oblique fibers probably lie in the lateral and caudal portion of the oculomotor fas- Cicle, and that 2) the combination of ipsilateral levator, superior rectus, and inferior oblique weakness might Suggest a fascicular lesion, Pratt ef al. [4] added to the growing literature of oculo- ‘motor nuclear complex lesions detected with modem neuroimaging. Their 60-year-old dialvetic patient devel ‘oped an isolated nuclear oculomotor palsy, characte ized by left adduction and depressor deficits in addition to bilateral ptosis and elevation weakness. On mag. Abbreviations INO--internucear ophthalmoplegia: MRI-—-magnetic resonance imaging, © 1995 Rapid Science Publishers ISBN 1-85922-735-X ISSN 1040-8738 a728 Neuro-ophthalmology netic resonance imaging (MRD, a small hemorthage in the left midbrain, just ventral to the aqueduct in the region of the left oculomotor nuclear complex, was detected. Bengel and Huffman {5] reported a simi- lar 73-year-old man with an oculomotor nuclear com- plex syndrome also associated with a small midbrain hemorrhage as documented by computerized tomog- raphy. His deficit was accompanied by an ipsilateral in- ternuclear ophthalmoplegia due to involvement of the ‘medial longitudinal fasciculus just caudal to the ocu- Jomotor nucleus. The authors cautioned that the vestihulo-ocular reflex is normal in supranuclear up- ‘gaze disturbances, but abnormal in nuclear and in- franuclear third nerve palsies. Other causes of third nerve palsies were described. Arroyo and Horton (6) reported a 31-year-old patient with fower-extremity weakness and a painful, pupil-in- volving third nerve palsy due to chronic inflammatory ‘demyelinating polyneuropathy. Kaye-Wilson et al. [7] reported the case of a 23-year-old woman with an ocu- Jomotor neurinoma who initially developed mild my- riasis in the right eye, followed 1 year later by ip- silateral adduction, elevation, and depressor deficits and ptosis. The unenhanced MRI was normal, but the contrast study demonstrated enhancement of the third nerve just proximal to the right cavernous sinus. Via a subtemporal approach, the third nerve was removed from its origin in the interpeduncular fossa to distally within the cavernous sinus, and histologically the le- sion was found to be a neurinoma. Fourth nerve palsies ‘The most common cause of bilateral founh nerve palsies is closed Inead trauma, Astie and Miller {8} de- scribed the unique ease of @ 24-year-old man with br Jateral Muctuating fourth nerve palsies due to a cerebel- lar astrocytoma, Initially the fourth nerve palsies were his only symptoms, hut several months later headaches prompted neuroimaging, A midline cerebellar mass ex- tended superior into the area of the anterior medullary vellum, where the fourth nerves decussate dorsally in the brain stem, Sixth nerve pal Sturzenegger's [9%] case of a 17-year-old boy with a th nerve palsy due to brain stem demyelination high- lights the influence of MRI in the management of these ‘cases. The patient's MRI disclosed a high-signal lesion at the right pontomedullary junction along with sev- eral periventricular lesions consistent with demyelina- tion, The author emphasizes that in all large series analyzing sixth nerve palsies, “undetermined causes” made up the largest group, but most patients were seen prior to the advent of modern neuroimaging, Per- haps in the future more young patients with acquired sixth nerve palsies will be found to have demyelinating lesions on MRI, rather than given an “undetermined” etiology. This case also illustrates that “isolated” sixth nerve palsies can result from pontine lesions despite the proximity of the sixth nerve fascicle to the seventh nerve and corticospinal tracts for instance, Spontaneous intracranial hypotension and leukemia were the cause of sixth nerve palsies in two sep: arate articles, Individuals with spontaneous intracra- nial hypotension typically have postural headache, mild meningeal signs, and diffuse meningeal enhance- ment on MRI. The neurological examination is oth- erwise normal. Berit et al. [10], however, described two patients with bilateral sixth nerve palsies associ- ated with spontaneous intracranial hypotension, pre- sumably due to spontaneous cerebrospinal fluid leaks. Averbuch-Heller et al. [11] described a 43-year-old pa- tient whose initial presentation of acute Iymphoblas- tic leukemia was a spontaneously remitting sixth nerve palsy. An MRI demonstrated bone marrow replacement by an “enhancing material” which extended to the left cerebello-pontine angle and left cavernous sinus ‘Two articles discussed interesting associations between sixth nerve palsies and pupillary abnormalities. A ‘woman with a sphenoid wing meningioma had ipsa eral optic nerve compression, an inferior division third nerve palsy, loss of corneal sensation, and a mild ab- duction deficit (12). The pupil was large, had no reac- tion to light, but constricted during abduction. Miosis during abduction, described only twice before in cases of trauma, was presumed to be duc to aberrant misci- rection of sixth nerve fibers into the pupillary portion of the inferior division of the third nerve at the orhital apex. Myles and Maxner [13] reported a patient with a sixth nerve palsy, sensory loss in the maxillary di- Vision of the trigeminal nerve, and ipsilateral Homer's syndrome. Adenoid cystic carcinoma of the maxillary sinus had been removed 4 months previously, and the patent had received radiation, The sixth nerve palsy and Horner's syndrome localized the process t0 the ‘cavernous sinus, and MRI demonstrated tumor inva- sion of that structure, Botulinum toxin injection treatment of sixth nerve palsies In patients with acute sixth nerve palsies, botulinum neurotoxin A injection into the antagonist medial rec- tus muscle (chemodenervation) has been advocated ‘The neurotoxin causes muscle paralysis by preventing, the telease of acetylcholine at presynaptic nerve ter minals. Chemodenervation might prevent medial rec- tus contracture and facilitate restoration of normal oc- ular alignment during the recovery period. A prospec- tive, randomized trial by Lee et af, {14*] found that 20 ‘of 25 (60%) untreated patients with acute sixth nerve palsies recovered, compared with 19 of 22 (8686) in- jected patients. Seventy-two percent of their patients had presumed microvascular sixth nerve palsies and would have been expected to recover spontaneouslyanyway. The authors concluded that botulinum injec tions had no heneficial effect in the patients they stud- ied, Mild chronic sixth nerve palsies that do not improve may be amenable to medial rectus recession and lat- eral rectus resection. More severe chronic cases may require medial rectus recession (or chemodenervation) and vertical rectus muscle wanspositions. In rare in- stances vertical transpositions can cause anterior seg- ment ischemia or vertical misalignment, so Repka ef al. (25+) investigated the use of medial rectus injec- tions of botulinum neurotoxin A alone in these pa- tients. Seven of 22 patients (3296) enjoyed restoration of single binocular vision in primary position; some of these patients required multiple injections. The au- thors believed that hotulinum injections were helpful in some patients, but this treatment "compared less favor- ably" with transposition surgery combined with medial rectus chemodenervation, Thus, botulinum injections may be a reasonable pri- mary therapy of chronic sixth nerve palsies [16], and surgery reserved for those who fail. The authors of two letters, written in response to Repka ef al’s art cle [15*), made additional helpful suggestions. Gold stein (171 commented that Repka et al. (154) patients with severe abduction deficits, possibly with secondary contracture, tended to fail hotulinum therapy. There- fore, patients with no abduction or with a positive forced duction test might benefit from medical rectus recession in addition to transposition surgery. Laby and Rosenbaum (18) also suggested that patients with no remaining sixth nerve function had litle chance of re- covering with botulinum injections alone, so saccadic velocities should he measured, Supranuclear disorders In 1936, Drs. Frank Ford and Frank Walsh, reported a 47-year-old man with dementia, visual loss, supranu- clear ophthalmoplegia, and myoclonic ocular and fa ial jerks [19]. Their pathologic diagnosis was “epi- demic encephalitis.” Sixty years later, Knox et al (20°) reexamined the pathologic material and updated the diagnosis. Widespread encephalitis was present, and periodic acid-Schiff material was found in the eye brain, spinal cord, and pituitary. Electron microscopy demonstrated hacilli in the brain and eye, consistent ‘with the diagnosis of cerebral ocular Whipple's disease. Knox et al, [20°] published this interesting historical and pathological study in a tribute to Ford, a famous neu rologist, and Walsh, the father of American neuro-oph- thalmology. ‘Skew deviation is becoming increasingly recognized as 1 cause of vertical misalignment of the eyes. It results| from disruption of the prenuclear input to the ocu- lomotor and trochlear nuclei, owing to a disturbance Eye movement disorders Liu et a. in the brain stem, cerebellum, or peripheral vestibu- lar system, Safran’ et al. (21) treated five patients with vestibular neuritis, in each case characterized by ver: tigo and contralaterally directed nystagmus, and skew deviation. The hypottopic eye was ipsilateral to the vestibular neuritis in four of the five patients, and the motility pattern mimicked inferior oblique paresis in three. Galetta et al. (22*I, in a report of four patients with dorsolateral pontomedullary lesions and skew de viation, demonstrated that the cyclodeviation may oc- cur in this disorder. In three of their patients, the hy- potropic eye was excyclodeviated relative to the fellow eye (Fig. 1. The authors suggested that eyclodeviation| ‘may result from variable involvement of utricular, semi circular canal, and cerehello-ocular pathways, Cyclode- vintion is also a feature of fourth nerve palsies, but the results of their article imply its presence should not exclude skew deviation and an underlying posterior fossa process. Furthermore, documentation of binocu- lar conjugate cyclotorsion strongly suggests the diagno- sis of skew deviation, as a unilateral fourth nerve palsy should produce only ipsilateral monocular excyclotor- sion [231 ‘Two anicles discussed unusual causes of internuctear ophthalmoplegia (INO), an eye movement disorder characterized by an adduction deficit accompanied by abducting nystagmus of the other eye. INOS are usu ally attributable to disruption of the medical longitu dinal fasciculus, which contains sixth nerve interneu- rons ascending t0 innervate the contralateral medial rectus, Strauss ef al. [24] described two patients with INOs after head trauma, and each had a pontomes- encephalic hemorrhage, immediately anterior to the fourth ventricle, involving the medial longitudinal fas ciculus, Hughes et al. (25} reported a 57-year-old man ‘with bilateral INOs and a cervical radiculopathy due to biopsy-proven giant cell arteritis. They attributed the INOs to a vertebral artery emholus lodging in a per- forating branch of the basilar artery although an MRI failed to confirm the brain stem lesion. They believed that the radiculopathy was due to the involvement of one of the radicular arteries, which are branches of the vertebral arteries, Cavernous sinus Removal of cavernous sinus meningiomas is often not recommended because of the high incidence of sur- ically induced third, fourth, and sixth nerve palsies and trigeminal neuropathies. DeMonte et al. (26) re viewed their experience with aggressive removal of he- ‘niga meningiomas involving the cavernous sinus. After clinical or radiographic progression, 41 patients were operated on. Eighty percent had no change in cranial nerve function, 15% improved, and 6% worsened, Of the 12 patients followed up postoperatively for more than 5 years, only three had tumor regrowth. Based on these results DeMonte et al. [26] suggested aggressive resection of these lesions. However, this series’ mor 2930 Neuro-ophthalmology Fig. 1. A patient with cyclodeviation in skew deviation. The right eyes hypotropic and ex ‘yclodeviated. This combination of ocular sighs ‘Would be typical af aright medullary lesion bidity and mortality rate, which the authors found “ac~ ceptable,” actually paints a less sanguine picture. Three patients died perioperatively, two others had ipsilat- tral middle cerebral artery infarction in their dominant hemisphere, and another developed corneal ulceration and blindness Agarwal et al [271 weated a patient with acute bilat eral ophthalmoplegia due to bilateral cavernous sinus metastases from prostatic adenocarcinoma. The patient ‘was reated with radiation therapy, with some improve ‘meat in right eye motility. Ds. J Lawtom Smith, in his accompanying editorial comment, suggested adjune- tive use of chlorotrianisene, known as TACE, for this patient and other individuals with metastatic prostate carcinoma involving the orbit or cranium. Orbit Three articles described unusual orbital processes causing, among other problems, abnormal ocular ‘motility: Fan et al (28) studied seven patients with car cinoid tumor metastatic to the eye and orbit, These t= ‘mors originate in the chromaffin cells of the gastroin- testinal and bronchial tract. Three of the patients had orbital metastases and presented with limitation of eye movements; two patients also had proptosis. All three died within 2 years despite chemotherapy or radiation, Gillies et at [29] reported the findings of a unique family containing several individuals with dominantly inherited congenital fibrosis of the vertically acting extraocular muscles. Most had some ptosis, but all hhad superficial keratopathy. Computerized tomogra- phy showed hypoplasia of the superior recti and some {imes other muscles, intracranial ventricular asymmetry in three of five patients studied, and eye globe defor ities in two patients. Zimmerman et al. [30] described six patients with or bital infarction syndrome after intracranial aneurysm surgery. In all patients, proptosis, ophthalmoplegia, and blindness occurred immediately postoperatively Retinal edema, retinal arterial narrowing, and pale op- tic disc swelling were seen. The authors ascribed the limitation of motility with proptosis to mechanical re- striction, ischemia of the extraocular muscles and their nerve supply, or a combination of both. The causes ‘were multifactorial, but Zimmerman et al. [30] believed. that the common feature was lowering of ophthalmic artery perfusion pressure due to orbital venous outflow obstruction combined with increased intraocular andl orbital pressure, Ocular myasthenia gra Two highly recommended reviews (31°*,32¢4| on this subject were published recently. Weinherg et al. [31*] covered all aspects of this disorder including histor cal hackground, pathophysiology, immunogenetics, di- agnostic testing, treatment options, and drug-induced myasthenic syndromes. Theit comprehensive summary contains approximately 700 references. Schmic (328) emphasized the various eyelid ancl eye movement ab- normalities seen in myasthenia gravis, In this unique review, he lists common as well as uncommon signs, such as bilateral ptosis, lc twitch, “plus-minus lid” syn drome, pseudo one-and-a-half syndrome, and hypo- metric saccades, for instance, He includes the differ- ential diagnosis for each sign, eg, brain stem stroke fr chronic external ophthalmoplegia, then lists cop ous references for each myasthenic sign and its pseu- domyasthenic imitator,Eye movement disorders Liu etal Diplopia after cataract surgery Double vision after cataract surgery is @ vexing prob- lem and can be due to preexisting ocular misalignment, sensory deviations, or surgical trauma to the extracc” Ular muscles or orbital soft tissues, Hunter ef al. [33] described four patients with another possibility: infe- rior oblique muscle injury resulting from local anes- thesia, Three of their patients had delayed-onset hy- pertrophia with fundus extorsion in the eye operated on, owing to inferior oblique muscle overaction sec- ondary (© presumed contracture, Anesthetic myotoxi city may have been the cause in these patients. The ‘other patient had @ hypotropia with intorsion, consis- tent with inferior oblique paresis, perhaps due to direct trauma or toxicity to the nerve. Munoz [34] treated two patients with inferior rectus overaction afier cataract susgery. She surmised myotoxicity of the anesthetic agent (peribulbar bupivacaine and lidocaine) was the cctiology in her cases as well Nystagmus Spasmus nutans is characterized by asymmetric, fine, pendular, nystagmus accompanied by head bobbing and head tt It occurs in young children, and its etiok ogy is unknown. Gotloh ea, [35] described a girl with congenital stationary night Dlindness who exhiited clinical features similar {© spasmus nutans. Two sin Jar patients had been reponed previously [3]. Flectro- oculography in Gottlob’s (35) patient, demonstrating pendular, intermittent, out-of-phase, and asymmetric Oscillations, also mimicked that of spasmus nutans. Be- cause a spasmus nutans-like syndrome also can be seen in patients with chiasmal and optic nenve gliomas, Gottlob et al [351 speculated that the abnormality for spasmus nutans was in the anterior visual pathway. ‘This report highlights the need for excluding retinal and central nervous system disorders in patients with spasmus nutans, Botulinum and drug treatment of nystagmus Retrobulbar injection of botulinum neurotoxin, caus- ing extraocular muscle paralysis, is a proposed method of reducing oscillopsia and improving the visual func- tion in patients with acquired nystagmus, Repka ef al 7*1 prospectively studied this treatment in six patients with nystagmus from multiple sclerosis or brain stem hemorrhage. Each patient had subjective and objec- ive improvement in visual function after each injec- in. The effect was transient and usually lasted only 8 weeks, necessitating repeated injections. Two pa- tients developed transient prosis, but ocular misalign- ‘ment occurred in all patients, three of whom com- pluined of diplopia. Patient satisfaction was moder- ate. Tomsak et al. [38+] reponed their results in three Additional patients, Acquired pendilar nystagmus was aholished or diminished in all three. However, he- ‘cause of side effects including external ophthalmople- gia, ptosis, diplopia, and filamentary keratitis, no pa- tients elected to repeat the procedure. Tate 1. Danton a ven Hecive" ened Disorders Dug | clonazepam Scopsamine oii Valprcate Acie genta nsagrus Seesaw mtn Eten icon Saperar cine myeiyron | Carbamazeire Siccicocitions Conatepan Leigh ef al. [39%] reviewed the physiology of various types of nystagmus and saccadie oscillations and their pharmacologic, optical, and surgical treatment options. ‘The authors gave particular attention to drug treat- ments. Table 1 lists eye movement disorders and medi cations that may treat them. In most instances, dug ef- ficacy was demonstrated in single case repons or small series. Leigh ef al. [39% cautioned that few drugs have undergone the scrutiny of a double-blind tial, They also reviewed prism strategies, optical stabilization de- vices, the Anderson-Kestenbaum procedure, and ho- tulinum injections. The role of botulinum in ‘the treat- ment of nystagnmys, the authors wrote, had “yet to be demonstrated.” References and recommended reading Papers of panicular interest, published within the annual pesiod of review, have beer highlighted as: 2 Of speci nites! OOF outstanding interest 1. Jacobson DM, MeCanna "7D, Layde PM: Risk factors for is: + chemie ocular motor nerve palsies. Arch Ophbuimed 1994 1123961-566. Diabetes, left ventricular hypensophy, and elevated hematocrit were denied as risk factors. Catains guidelines for evaluating patients ‘wih presumed vasculopatie ocular motor pales. 2. Kslazek SM, Stamovita TL, Rosen CE, Burde HM, Pans F ‘= Fascicular arrangement in’partal oculomotor paresis. Am J Ophibabnol 1998, 1187-103, 3132 Neuro-ophthalmology ‘Two patents with a “medial fascicular syndome.* The authors peo- vide un excelleal review of previously tepored fascicular pases wth a diagram ofa proposed topographical arrangement ofthe third perve see. 43. Gaunt CD, Kashi S, Nagata. Monocular elevation paresis fend by an_oculomotor fscicular impairment.) Neuro ‘pbibaimol 1995. 111-14 4, Prat DV, Orengo-Nania S, Horowitz BL, Oram O: Magnetic resonance imaging findings in a patient with nuclear ocu omotor palsy. Arch Opbibalmo! 1995, 113:141-142 5. Bengel D, Huffmann G: Oculomotor nuclear complex sym drome as'2 single sign of midbrain haemorrhage. Newo “opbihaimolegy 894, 14279-282 6 Amoyo JG, Horton JC: Acute, painful, pupilsparing third ‘nerve palsy in chronic inflammatory demyelinating poiynew fopathy. Neurology 1995, 45846-847. 7. Kaye-Wikon 1G, Gitnon R, Hell JE, Steers ATW, Callen JF Gculomotor nerve nearinoma. Netro-opbibalalgy 1h, sv 8. Astle WE Miler S): Bibterat fuctuating trochler nerve Palsy secondary to cerebellar astrocytoma. Cun J Opbtsal- mol 1998, 2934-38, 9. Sturzenegger M: Isolated sixthnerve palsy a5 the present + ing sign oF multiple sclerosis. eur apbualmoley 1954, Hast ‘with modern neuro-imaging, more bola sixth nerve pases have been associated with pontine lesions 10. Bert P, Berg-Dammer E, Kuehne D: Abducens nerve palsy ‘in spontaneous inteacraniltypotension, ‘Neurology 1991, 1382 11, Avetbuct-4ellr fli, Hen-ue T: Transient sath-nerve palsy a the frst preseniaton of acute leukaemia {Letter J Neurol Newrasurg Poebiatr 1994, 57:50, 12, Wilhelm H, Wihelm 1B, Mikleaberger Primary aberrant regeneration of abdicens neve fibers into pupillary paths Aeuroephibalmology 1994, 1485-89. 13, Myles WM, Maner CE: Localiang value of concurrent sixth nerve paresis and posiganglonie Homer’ syndrome. Ga J (Ophinaimnl 1994, 2939-42 14, Lee J, Huis S, Cohen J. Cooper K, MacEwen C, Jones SS Results of a prospective eandomiaed teal of botulinum toxin therapy i acute unilateral sixth nerve pals. J Palate Ophinaionlsirabismus 1995, 31:283-236, Botulinum toxin treatment of acute sixth nerve pases bid never undergone the seutiny ofa prospective randomize tri unt this Joup feponed curly result at the 1991 tntermatonal Onhopsc Congress in Nuremberg, Germany. This ance repons the Tuner revolts of thee sty which compared 47 patients with ace xh nerve plies, 22 of whom recewed inkctions 15, Reps MX, lam GC, Morison NA: The efficacy of botuinam © neurotoxin Yor the treatment of complete and partially recovered chronic sixth nerve palsy. J Pear Opbihalmal ‘Sirabsts 19, 31:79-83, “The result of an analysis of patents with chronic sth neve palsies who received hetulium injection imo the antagonist medial rec ts muscle. Cootains an excellent dscussion regaing the passble ‘mectianism of botlinu in dis sting, 16, Miglan AW: The effcacy of botulinum neurotoxin A for the treatment of complete 4nd parily recovered chronic sath neve palsy [Discussion Pediatr Opbibalnl Strabinus 1993, 31384 17, Goldstein JH Theatment of chronic sith nerve palsy (Le ter) J Pediatr Ophibatmol Strabismus 1998, 32:7 18, Laby DM, Rosenbaum AL: Treatment of chronic sixth nerve palsy [Leterl.J Padiatr Opbihaliol Stabs 1994, isos, 19. Ford FR, Walsh Fk: Clinical observations ypon the impor tance of the vestbubar reflexes in ocular movement. Bt Jobns Hopkins Hosp 1936, 5880-88. 20. Knox PL, Green WR, Troncoso JC, Yarley JH, Hsv J, Zee + DS: Cerebral ocular Whipple's disease: A'G2-year oyssey {rom death to diagnosis. Neurology 1995, 45:617-625 Atbute to Drs. Frank Ford and Frank Walsh, and updates the clin ‘cal and pathologe diggnosis of patient these 9 distinguished physicians reported in 193, Reads lke a novel aswell asa cinco Pathologie repo. 21, Safran AB, Viber D, Issoua D, Hauser: skew deviation af ter vestibular neuntis. €m J Opbubaimo! 1994, 118238-245, 22, Galea SL. Liu GT, Raps EC. Solomon D, Wolpe NJ: Cy = clodeviation in shew deviation. am J Ophthalmol 1994, 18509514 Four patents are reported, three of whom had eyclodeviation in as sociation with skew deviation. skew deviation is becoming increas ingly recognized as 2 cause of vertical double vision, and this acle ‘emphasizes that relative excycorotation can occu in tis disorder. Reviews possible ental and penpheral mechanisms. 25, rand T, Dietesch Mt: Vestibular syndromes in the role plane: Topographic diagnosis from brainstem to eorex. 4 Neurol 1994, 36:357-337 24 Suauss C, Ganslandt 0, Huk W), Jonas JB: Isolated uni later internuclear ophthalmoplegia following head injury Findings in magnetic resonance fmaging. Nevropatol cay 1995, 1515-19. 25, Hughes TAT, Wiles CM, Houshan M: Cervical radiculopathy nd biltral internuclear ophthalmoplegia cause by tempo- Fab arentis, J Neurol Newresurg Pct? 194, 57.764-755. 26, DeMonte F, Smith 11K ALMefiy O: Outcome of aagressive removal of cavernous sinus meningiomas. J Netrasurg 154, 1245-251. 27. Agarwal Shatma K, Gupta BK, Dutta NR, Kumae S, Gael RD: Acute biteral ophthalmoplegia secondary to metastatic prostatic carcinoma. J Neuro-oplubalmel 1995, 155-47 28. Fan J, Buettner H, Banley GB, Bolling JP: Clinical fea tures and treatment of seven patents with carcinoid tumor metastatic to the eye and omit. Am) Opbihalma! 1995, Hg2it-218, 29. Gilles WE, Hams A), Brooks AMV, livers MR, Welle WB: ‘Congenital ross of the veriealy acting exirocular mus ‘les: Ophrhamoly 1995, 102-612, 30. Zimmerman CF, Van Patten PD, Golnik KC, Kopitik TA, “Anand Rt Orbital infarction syndrome after sunsery for in- Tracrnial aneurysms. Opbtbatnolagy 1995, 10259159, Si, Weinbeng DA, lesser RL, Vollmer Th, Ocular myasthenia: A s+) protean sore. Sir Ophibalonol 1994, 39:169-200 An outstanding review containing anything and everyting one ‘Would want to know about thi diirder Cover the hisial back round, pathophysiology. immunogenetics, dlagprosic testing, and {weatment of ocular myasineni Over 70 references ace used. 32. Schmid D: Signs in ocular myasthenia and pseudomyasthe- ‘nia: Diflerenal diagnostic cetera. A cincal review. Neuro ‘phtalmology 1995, 15:21-58 ‘Ocular myasthenia cin mimic any evel abnormality oF pupi-spar ing eye movement disorder, whether supeaniclear, «sow ace ‘ides, ntemuclesr ophthalmoplegia, or infanuctear (sth o fourth ferve pals) al the various mody abnormalities are hularied, feferenced, and discussed in deta. 33. Hunter DG, tam GC, Guyton DL: Inferior oblique muscle Injury fom loca! anesthesta for cataract stgery. OPPtha- soley’ 1995, 102:501-50. 2A. Munoz Me Inferior eeetus muscle overaction after cataract fextction. AnrJ Opbrbalnol 1994, 118.646635. Gotlob 1, Wizov $5, Reinecke RD: Quantitative eye and thead movement recordings of retinal disease. mimicking spasmus nutans, Am J Opbibaimol 1995, 1193374376. 36. Lambert Si, Newman Nj Retinal disease masquerading as spasmus nutans, Nevirolay 1993, 43:1607-1009. 37. Repka MK, Suvino 1), Reincke RD: Treatment of acquired nystagmus with botulinum neurocoxin A. Arch Opbibalniod 1994, 112:1320-1324, enon of sx patients, Eye movement recordings included. Overall patient safacton was moder. 38 Tomsk RL Remer BF: Averbuch-Heller L, Chandran M, Leigh ty: Gnsaistctory treatment of acquired aystaginus ‘with reirobulbar injection of botulinum toxin. am J Oph: atmo 1995, 1199-98, Results in tree patient, in whom the botulinum successfully re- ‘duced or abolished nystigmus. Eye movement recordings included, Eye movement disorders Liu et al However, the patients were disatsfied because of sde effects and eclined further tesiments 39. Leigh RI, Averbuch Heller, Tomsak RL, Hemlery BE, Yani ss SS, DellOsw LF Treatment of abnormal eye move: ‘ments that impale Vsion: Strategies based on current con- epts of physiology and. pharmacology. Arm Neurol 1994, 36:129-144 A readable discussion ofthe pathophysiology of nystagmus and sac: cade oscillations and a review ofthe pharmacolog, optical, and sungeal treatments ofthese disorders. Wellreferenced afte Grint TL, MP, Division of Neuro-ophitalmology. Deparment of Neurology, Hospi of de Universiy of Pennsylvania, 3400 Spruce Sweet, Pladeiphi, PA 19104, USA, 33