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Show ]. Clin. Neuro-ophth.lInwl. 2:5-11, 1082. Periodic Alternating Nystagmus Clearing after Vitrectomy SHELLEY ANN CROSS, MD. 1. LAWTON SMITH, MD. EDWARD W. D. NORTON, MD. Abstract Periodic alternating nystagmus t) may be related to vestibulocerebellar system disease, 2) may occur with loss of vision, and 3) may be congenital in origin. We report the case of a patient with acquired periodic alternating nystagmus in whom the nystagmus followed bilateral vitreous hemorrhages. Upbeating nystagmus was interposed between the right beating and left beating phases. Bilateral vitrectomy resulted in the prompi disappearance of the nystagmus. The importance of visual function in relation to periodic alternating nystagmus and associated motility disturbances is emphasized. Introduction We recently saw a patient with periodic alternating nystagmus with three remarkable features: 1) the nystagmus followed a subarachnoid hemorrhage complicated by bilateral vitreous hemorrhages (Terson's syndrome); 2) upbeating nystagmus was interposed between the right beating and left beating phases; and 3) restoration of visual function by bilateral vitrectomies resulted in the prompt disappearance of the nystagmus. Case Report A 54-year-old Puerto Rican man was referred to the Bascom Palmer Eye Institute because of severely reduced vision in both eyes. Aside from mild hypertension and headaches since childhood, he was well until May 1981, when he experienced a severe headache followed by abrupt loss of consciousness. When first examined, several hours after the event, he was awake, oriented, and amnestic for recent events. He complained of blurred vision. The blood pressure was 140/90. There was nuchal rigidity, but no evidence of Irauma. The From the Bascom Palmer Eye Institute, OepJrtment of Uphthalmology, University of Miami School of Medicine, Mi,'mi, Florida. March 1982 deep tendon reflexes were brisk on the right, <lnd both loes were downgoing. Eye examination revealed a m<lrked loss of visual field in both eyes. The eyes were convergent, and bilateral sixth nerve palsies were suspected. A lumbar puncture yielded bloody fluid, and a CT scan confirmed the presence of subarachnoid blood and located its area of highest concentration in the right sylvian fissure. The patient was treated with Inderal (propranolol) for hypertension. He was neurologically stable, but remained blind. Neuro-ophthalmological examination was performed on September 8, 1981, 4 months after the subarachnoid hemorrhage. The visual acuity was light perception with projection in both eye~. The pupils reacted 2+ to light. The versions were nearlv full, with 1-2 mm of sclera visible in the abducting eye on lateral gaze in each direction. Convergence was intact. The eyes exhibited periodic alternating nystagmus with upbeating interposed between the right beating and left beating phases. The eves would beat rightward for about 00 seconds, then upward for 10-15 seconds, and then leftward for about 90 seconds. Then they would either repeat the cycle beginning by beating rightward, or thev would again beat upward for 5-10 seconds befor~ restarting the cycle. No downbeating or oblique movements were seen. On slitlamp examinatil.ln, mild posterior subcapsular lens changes were seen. Both fundi were obscured bv dense vitreous hemorrhages. The remainder' of the ex.1Olin.ltil.ln yielded only slight hyperreflexia in the right side and bilaterally downgoing toes. A CT sc<1o done with and without cl.1Otrast enhancement demonstrated bint bklod densitv in the globes bilaterally. In addition, in the .lnteril.lr p.lrt of the right sylvi.ln fissure, a sn1l.11.1th-w.lI1ed enhancing structure m,'sl n'l1sistent with .In aneurysm was seen. There W.1S no SUb.H.Khnl.lid blood, hydroceph.llus, ,Ir evidence of inbrctil.1O (Figs. 1 .1Ild 2). Orbital echography documented the vitreous blood. Electroretinogr.lphy, visual-evoked potentials, and blue field entoscopy were normal. Laser interferometer testing showed that the patient could see red light, but was unable to discern grid patterns with either eye. 5 Periodir AIll'rn,lting NVst,lglllllS Figure 1. UncnhJnced computed tomogrJphlC ,cJn. I'\ot(' right middle f"55J Ic",'n (whltc JrrowhcJds). Figure 2. [nh,lJ1red rOlllpuled tonH>gr,lphir ,r,ln. N"te IllJrl..cd enhJncemcnt of lesion seen in fig. I (white .HflIWhc.ld,). Journal of Clinical Neuro-ophthalmology The patient underwent a vitrectomy in the right eye by Dr. G. Blankenship on September II, 1081. On the first postoper.ltive day, the right eye vision was 20/400. The periodic .lltern.lting nystagmus had changed rem.ubbly. With the right eye fixing, the nystagmus W.1S not clinic.llly evident. With the left eye fixing. the nyst.lgmus W.1S unch.1I1ged in pattern, but its amplitude W.1S much reduced. A vitrectomy in the left eye W.1S performed September l-l, 1081. The immedi.lte postoper.1tive .lCuity in the left eye \V.1S 20/-l00. On September IB, lOBI, the right eye visil1l1 \V.1S 20/100-2, .1I1d the nyst.lgmus \V.1S nl) Il)nger visible. Electronyst.1gn1l)graphy d,)ne in the light ren)rded no nyst.lgmus while thdt done in the d.Hk. recorded very low .lmplitude nystagmus of the same periodic .llterndting pdttern a~ had previ,)usly been noted. Selective bibter.ll c.Hotid and vertebral .Hteriogrdphy demonstrdted a large saccular aneurysm at the bifurcdtion of the right middle cerebrdl artery (Figs. 3 and -l). The aneurysm was clipped uneventfully via a right frontotemporal craniotomy by Dr. L. Page on September 21, 1981. Postoperatively, the vision in each eye was 20/100. No nystagmus was present. The neurological examination was otherwise unchanged. Discussion Definition Periodic alternating nystagmus is a form of central nystagmus consisting of horizontal or horizon- Cross, Smith, Norton t.11-rotary jerk-type nyst,lgmus which undergoes cyclic changes in amplitude .lI1d direction Each cycle bsts for 60- 180 seconds, .1 nd between the right be.lting and left beating phd<,es, the eyes ch.H.lCteristically rem.1in nlOtionles<, for 5-15 seconds. This quiet period rarely may be repldced by d period of downbedting nyst.1gmus.' Reldted motility disturbances, including rebound nystdgmus" and dlternating periodic devidtion of the eyes,:l"1 C.1I1 be seen in pdtients with periodic dlternating nyst.lgmUS. In .lddition, the patients show incre. 1sed sensitivity to c.lloric stimulation, and this incn>.lsed sensitivity can preceed the development of periodic alternating nystagmus'" The pdtients mayor may not have symptoms of oscillopsia, blurred vision, unsteadiness, or vertigo. Relation to Vision and Fixation The relationship of periodic alternating nyst.lgmus to visual acuity and fixation is of interest. Reported cases of congenit.ll periodic alternating nystagmus have augmentation of the amplitude of their eye movements with fixation." A number of cases of acquired periodic alternating nystagmus, however, have been diagnosed following sudden loss of vision. Davis and Smith" reported the case of a 70-year-old man who suffered bilateral vitreous hemorrhages. Examination of the patient after the involvement of the second eye showed periodic alternating nystdgmus with cy~les of 90-120 seconds. During the oscillations, the patient experi- March 1982 Figure 3. Right cdrotid MtcriogrJm (IJtN.11 vil'w) r('v('JIs IJrg(' right middl£' '·N('br.11 .ulery bifurcation Jnl'urysm (blJck MWW). 7 ['erindic Altl'rn.lting Nyst.lgmus Figure 4. Right carotid arteriogram (anteroposterior view) shows right middle cerebral artery bifurcation aneurysm (white arrow). enced a vertiginous sensation and an illusion of movement which correlated with the direction of the rapid phase. Pastpointing was demonstrable and was much attenuated during the quiet periods. Cold calories caused interruption and reversal of the nystagmus. Neurological examination was otherwise normal. Another of Davis and Smith's patients had periodic alternating nystagmus associated with syphilitic optic atrophy. In addition to amaurosis, he had deafness and a syphilitic amyotrophic lateral sclerosis-like syndrome with fasciculations and wasting in the shoulders, arms and legs, and upgoing toes. Related to those cases in which there is onset of periodic alternating nystagmus concomitant with loss of vision are those seen with eye closure, and those seen in darkness only. Toglia;' reported periodic alternating nystagmus present only with the eyes closed. The patient was a 71-year-old man with a chief complaint of poor balance, mostly upon rapid changes of body posture. He had a long history of tinnitus, progressive sensorineural hearing loss, hypertension, and gIJucoma. The vision '.")' '.O/:,nn in [,,,th ('yes. Neurological examination showed that the patient was unable to keep his balance, especially on position change. No nystagmus was visible. Electronystagmography recorded, with the eyes closed, the characteristic pattern of periodic alternating nystagmus. There was no recordable spontaneous nystagmus with the eyes open. Ten months later, when the symptoms had subsided, the periodic alternating nystagmus could be elicited only after rotatory tests had been performed. Rudge and leech~ discussed the case of an 18-year-old woman who had either encephalitis or an episode of demyelinating disease. She had inconstant horizontal nystagmus in the light, and periodic alternating deviation of the eyes and periodic alternating nystagmus in the dark. These cases, in which periodic alternating nystagmus is seen with visual loss, in darkness, or with eye closure, prompt the speculation that loss of vision elicits an otherwise suppressed motility pattern. This was probably the case in our patient, in whom loss of vision was associated with the development of periodic alternating nystagmus, and restoration of vision with its prompt disappearance. Journal of Clinical Neuro-ophthalmology TABLE L Etiologies of Periodic Alternatin~ Nysta~mus L OVl'rrid;ng [videl1l'e l,f Ve~tibtll,,-n'rl'bl'll.H \)i~l'.,,,· Anllltd Chi"r; tvpe I 1ll.1Ifl'nll,ltillll~ Ar~H:hllllid cyst l'\ln\pres~in~ ,:en-hellulH .lnd Illl'dull.l CCfebdl.H d('gl~n('r.'ti\.ln Sl'(lllH.i.lrv ill .,I,:\,h\,I .. lIl11pli"",lh'd by Oitliltin (phl~nVhlin) int""il-.,tlllll Friedre;,-h'~ ,It,"i,' C.'rebell.H ,·v~t Chrl)I1IC ,-,litis nwdi.l \'t.... rtebrob.lsil.H bdlclnil dlsl'",,"' [n,q,h.,hti~ Svphlh~ [1t....nlvclin.lttl1f, dl~l·.ISl· Br.lln stem .1stn'l.-yh'n,.1 Tunll'lr llt th,,· (l'rpUS \',llklSUfll T\lnlh.11ll., (It the fll1llf \)t t\lurth \'l'ntridc B."d.H ~k"ll fr,Ktllre Hvpl'''' bIrth IIll1lrV _. LllS~ \)t \'bh..11l .1S the DlHTlIIl.lnt Abnl1rm.,lity 5<'vcre ,·i5U.l1 1\."lS5 3, Cl",genlt~1 \ \ith""t JS~l'''~ted d,'felts ..\S~l'(IJted with Jlblnism Pathology Periodic alternating nystagmus has been reported with lesions of the pontomedullary region and the cerebellum of various etiologies. These include Arnold Chiari Type 1 malformations,~' ~ arachnoid cyst compressing the cerebellum and medulla, III cerebellar degeneration secondary to alcohol complicated by Dilantin (phenytoin) intoxication, II Friedereich's Ataxia, I~ cerebellar cyst," chronic otitis media,ti vertebrobasilar ischemic disease," encephalitis,';'" syphilis,"'" demyelinating disease, L '; brain stem astrocytoma,1:1 tumor of the corpus callosum:; toruloma of the floor of the fourth ventricle, I~ basilar skull fracture," and hypoxic birth injury.~ It may rarely be congenital in origin/' '•. ti and has been reported in a 40-year-old albino man with diaphanous irides and albinotic fundi." (Table 1), There have been several pathologically studied cases of periodic alternating nystagmus. Keane l reported the case of a 54-year-old woman who succumbed to severe demyelinating disease of the brainstem. Multiple bilateral shallow areas of demyelination were scattered along the floor of the fourth ventricle and involved portions of all the vestibular nuclei. Those lesions involving the vestibular nuclei were proposed as causative, but the wide distribution of the findings prevented the drawing of definite conclusions. Karp and Rorke l :! reported the history of an ll-year-old girl with periodic alternating nystagmus. The patient had a left frontal astrocytoma which had been treated with radiation and vincristine. Eleven months after March 1982 ('rt '<'''. Smith, orton tn'dtment she presented with periodic <llternating nystdgmus. The patient died soon after. At autopsy, the tumor had seedC'd the basal meninges, the ependym<l, .lnd the subarachnoid space .Hound the spin.ll ('('rd, The tumor involved, unilaterally, the vestibular nuclC'i at multiple levC'ls, and numC'rous .He.1S of the pons .lnd medulla. Towle and Rom.lOul's C.ISC'11I was one of an .Hachnoid cyst caudal tt' thC' cerebellum, displacing that structure upw.Hd, .lnd compressing the medulla. Susac and Henry'" reported the pathological findings in a p.ltient with neurosyphilis and periodic .llternating nyst.lgmus. ThC' clinical findings had previously been rC'ported by Davis and Smith (case I)" The patient had optic neu ritis and optic atrophy, chronic leptomeningitis with vasculitis of the cerebral vessels, involvement of the fasciculus gracilis consistent with tabes, and mild gliosis of the inferior olives and the vestibular nuclei. Because the pathology in each of these cases is widespread, no definite conclusions can be drawn as to any anatomical defect necessary for the generation of periodic alternating nystagmus, The cerebellum, the pontomedullary junction, and the vestibular nuclei, however, have been consistently implicated. Mechanism -Related Eye Movements The importance of the vestibulocerebellar system in the generation of periodic alternating nystagmus is emphasized in studies attempting to elucidate its mechanism, Meinenberg and Hoyt~ made oculographic recordings during nystagmusfree intervals in a patient with acquired periodic alternating nystagmus. They showed hypermetric refixation sJccades and saccadic pursuit movements, indicating cerebellar-type oculomotor disturbances. Dilantin (phenytoin), which affects cerebellar function, evoked periodic alternating nystagmus in a patient with alcohol-related cerebellar degeneration, during a period of dilantin intoxication." (This is not to exclude Dilantin from consideration as a drug potentially useful ft)r the tre.ltment of this nyst.lgmus, .1S will be discussed I.lter.) Cerebellar pathology is the principle .lbn"rm.1Iity found in cases of rebound nystagmus. It; <In eye movement pattern .1ssociated with periodic alternating nystagmus, II and prob<lblv sometimes confusC'd with it. I'. ThC' assl)ciatilln l)f peri,)dic .lltertl.1ting nyst.1gmus with downbl'.ll nvst.lglllus h.1S been well-d,)cumented, I and suggests p<lth"I,'gv .It the cervicomedulldry junctillll, The upbe<lt cllmpllnent of our patient's peril,dic <lltC'rtlating nvst.1gmus is a previously undescribed fe.lture. Upbe.,ting nystagmus has been demllnstr.1ted in lesions damaging upward pursuit pathways, namely lesions at the level of the inferior o;ives, the nucleus prepositus hypoglossi, and the cerebellar vermis." Nystagmus which combines periodic alternating 9 nyst.lgmus with bl)th upbeating .lnd dllwnbl'ating nYst.lgmus W.lS described by S.lUnders. IM This ".lltern.lting windmill nyst,lglnUs" nccurred in an elderly Wlm1.ln blind fn)m acquired lIphthalmoIl) gic dise.!Se. The versilH1S were nnrmal. The eyes nhlved tlHl)ugh ,1 cycle nf jerk nystagmus beating in turn .1long e,lch .1xis nf g.lze in .l clockwise direclilH1, ,md then, .1fter .1 3000 cycle was completed, in.1 cnunterclockwise direction, ag,lin beating .1ltmg e.lCh .1xis nf g.1Ze. DelrOsso, in his analysis l,f the case, I" described windmill nystagmus as ~)eri,)dic alternating nystagmus with a superimposrd .llternating vertical nystagmus, with the prril) ds out of ph.lse. Our C.lse of periodic alternating nystagmus, with upbe.lting between the right beating and left beating ph.lses, is, c1inic.llly, a "missing link" between prriodic .lltern.lting nystagmus, periodic alternating nystagmus with downbeating, and windmill nystagmus. Its occurrence reinforces the idea that the mechanisms which generate alternation of direction of nystagmus both vertically and horizontally must be closely linked anatomically and physiologically. Although our patient's loss of vision brought out his nystagmus, we can only speculate as to the underlying lesion responsible for it. Hypertension could have caused lacunes, but there was no history suggesting that these had occurred. After the hemorrhage and the period of depressed consciousness, the patient was awake and was intact neurologically except for the convergence of his eyes and the hyperreflexia on the right. The convergence could have been due to increased intracranial pressure, bilateral nuclear sixth nerve palsies, or (misinterpreted) convergence nystagmus. One would not have expected the patient to have had such an intact mental status after rapid herniation. Central sixth nerve palsies without demonstrable lower pontine or upper medullary signs are also unlikely. Midbrain transient ischemia secondary to blood in the third and fourth ventricles, increased intr.lcr.lnial pressure, and the force of blood from right to left are more likely causal. Movement of the left peduncle against the tentorium could h.lve c.lUsed the brisk reflexes on the right. AlternJtively, there may have been some unrelated preexisting lesil>n in the brainstem or cerebellum, l)r simply increased sensitivity of the vl'stibul.u systl'm such th.1t loss of vision unmaskl'd .In exagger.1tl'd norm.ll nl'ur.ll rhythm Treatment Although thl' mech.mism l)f pNiodic .lltern.1ting ny"t.1gmu" i... not known, its .lssoci.ltion with vestibul. u hypcrn'''rl'llslvl'nl'<'s,'-' urbe.lting nyst.1grnu", dllwllhe.lllllg nv"t.lgmus, I rrbound nyst.lg"" 1".' .11lL! ."'('rn.JI"l .. ~ !'('ril,dic devi.1ti,)n of the ryrs" suggests failure of an oculomotor inhibitory system originating in the rostral brain stem. and the cerebellum. Elicitation of periodic alternatmg nystagmus in a case of Dilantin (phenytoin) intoxication in a patient with underlying cerebellar degeneration II underlines again the importance of the cerebellum and its connections in the pathogenesis of this disorder. Elimination of the nystagmus by restoration of vision (as in our patient), partial suppression by fixation/ and elicitation by eye c1osure~ all suggest the importance of visual input. The fact that congenital periodic alternating nystagmus is augmented by fixation~ implies that the mechanism of its production is different from that of the acquired form. These features of periodic alternating nystagmus suggest treatment possibilities. The motor pattern of periodic alternating nystagmus may be produced under conditions of unstable or imbalanced neuronal activity via either reciprocally inhibitory neurons exhibiting postinhibitory rebound,14 or via oscillator neurons.~ Dilantin (phenytoin), Tegretol (carbamazepine). and other neuroleptics might have beneficial effects by altering such relationships. Davis and Smith~ treated one of their patients, a 49-year-old man with "attacks" of periodic alternating nystagmus associated with dysarthria and truncal cerebellar signs, with Dilantin. The drug decreased the cycle length and increased the quiet period. Tegretol (carbamazepine). Antivert (meclizine HCl). and Vasodilan (isoxuprine HCll were ineffective. Treatment of the nystagmus might also be achieved by influencing the reflex arc at the level of the sensory neuron, or bv influencing the level of excitation of neurons in the brain stem. Halmagvi I~ treated two patients with longstanding acquired periodic alternating nystagmus, and one patient with congenital periodic alternating nystagmus, with Lioresal (baclofenl. 30 mg/day. In the cases of acquired nystagmus, baclofen abolished the prim.lry position movements, and both patients were left with rebound nystagmus. The pattern of nyst.1gmus in the congenital form was not altered by this medication. The authors speculated that the principle action of baclofen was inhibition of the release of glutamate, although GABA-mimetic action in the afferent limb of the reflex arc is also a possibility. Depakene (valproate), a drug that elev. ltes cerebellar GABA, was not effective. Bodo~tI tre.lted .l patient with congenital periodic alternating nystagmus with intravenous chlorpromazine .md barbiturates. Both drugs were successful in .lbolishing the nystagmus for brief periods of time. In .lddition, the chlorpromazine abolished caloric responses. Improvement in visual acuity may dampen or abolish acquired periodic alternating nystagmus. Our patient had successful treatment of his nystagmus by vitrectomy. Journal of Clinical Neuro-ophthalmology Conclusions Patients with periodic alternating nystagmus comprise a heterogeneous group. One of three features may dominate their clinic,11 presentation: 1) The nyst,lgmus m,ly occur with overriding evidence of vestibulocerebellar system dise,lse. 2) The nystagmus may occur, ,1S it did in our p,ltil'nt, with loss of vision. In this group, br,linstem ,1I1d cerebellar abnormalities underlie the development of the nystagmus, but these fe,ltures .He subtle, or even not clinically detl'ct,lble. 3) The nyst,lgmus may be congenit,ll. In the first gwup, ,1ttention tc) the intrinsic central nervous system dise,lse is ,1 primary consideration, ,md its tre,ltment may ,1lso modify the nystagmus. In the second gwup, attention to visual acuity may be spectacularly beneficial. Congenital periodic alternating nystagmus, like other forms of congenital nystagmus, has characteristics different from those of acquired forms with respect to behavior with fixation and response to drugs. There has been no reported successful therapeutic modification of this form of nystagmus. The possibility of successful treatment of periodic alternating nystagmus, particularly in patients presenting with visual loss as the main feature of their illness, should be emphasized. In addition, patients with clear evidence of vestibulocerebellar system disease may also benefit from attention to their visual function, since fixation may dampen or suppress acquired periodic alternating nystagmus even in these instances. References 1. Keane, J,R.: Periodic alternating nystagmus with downward beating nystagmus. Arch. Neurol. 30: 399-402, 1974. 2. Baloh, R.W., Honrubia, Y., and Konrad, H.K.: Periodic alternating nystagmus. Brain 99: 11-26, 1976. 3. Walsh, F.B., and Hoyt, W.F.: Clinical Neuro-ophtha/ mology, Vol. 1 (3rd ed.). Williams & Wilkins, Baltimore, 1969, p. 236. 4. Goldberg, R.T., Gonzalez, C, Breinin, G.M., and Reuben, R.N.: Periodic alternating gaze deviation with dissociation of head movement. Arch. Ophtha/ mol. 73: 324-330, 1965. 5. Kornhuber, H.H.: Der periodisch alternierende (nystagmus alternanas) und die Enthemmung des visti- March 1982 Cross, Smith, Norton bul,!ren systems. Arch. Ohrcn-Ndsen-Kehlkopfheilkd. 174: 182-209, 1959. b. Ddvis, D.C., dnd Smith, J.L.: Periodic alternating nystdgmus. A report of eight Cdses. Am. f. Ophthd/mol. 72: 757-7b2, 1971. 7. Togli'l, I.U.: Periodic ,lltern.lting nystagmus. Arch. Oto/.lryngo/. 88: 148-151, 1968. 8. Rudge, 1'., ,md Leech, J.: Andlysis of d case of periodic ,lltl'rndting nystdgmus. /. Nf'uro/. Neurosurg. Psychi,ltry 39: 314-319, 1976. 9. Meinenberg, a., and Hoyt, W.F.: Ocular motor control disorder during the neutrdl phase of periodic alterndting nystagmus. r. Neuro/. 223: 309-312, 1980. 10. Towle, P.A., dnd Romdnul, F.: Periodic dlternating nystdgmus: First pdthologicdlly studied case. Neurology 20: 408, 1970. II. Campbell, W.W.: Periodic nystdgmus in phenytoin intoxication. Arch. Neuro/. 37: 178-180, 1980 12. Gormdn, W.F., and Brock, S.: Periodic alternating nystagmus in Friedreich's Ataxia. Am. f. Ophthalmol. 33: 860-864, 1950. 13. Karp, JS, and Rorke, L.B.: Periodic alternating nystagmus. Arch. Neurol. 32: 422-423, 1975. 14. Halmagyi, G.M., Rudge, P., Gresty, M.A., Leigh, R.J., and Zee, os: Treatment of periodic alternating nystagmus. Ann. Neurol. 8: 609-611, 1980. IS. Susac, J.O., and Henry, J.M.: Periodic alternating nystagmus: Clinicopathological correlation. In Neuro-ophtha/mology less Symposium of the University of Miami and the Bascom Palmer Eye Institute, Vol. 8, J.S. Glaser, J.L. Smith, Eds. CY. Mosby, St. Louis, 1975, pp. 284-292. 16. Hood, J.D., Kayan, A., et al.: Rebound nystagmus. Brain 96: 507-526, 1973. 17. Gilman, N., and Baloh, R.W.: Primary position upbeat nystagmus. Neurology 27: 294-298, 1977. 18. Saunders, M.D.: Alternating windmill nystagmus. In Neuro-ophtha/mology Symposium of the University of Miami and the Bascom Palmer Eye Institute, Vol. 7, J.L. Smith, JS Glaser, Eds. CY. Mosby, St. Louis, 1973, pp. 133-136. 19. Perkel, D.H., and Maloney, B.: Motor pattern production in reciprocally inhibitory neurons exhibiting postinhibitory rebound. Science 185: 181-183, 1974. 20. Bodo, G.: Approach to the generation centre of nystagmus alternans by means of drug tests. Acta. Otolaryngol 53: 328-332, 19b I. Write for reprints to: J LawtlJn Smith, M.D., Bascom Palmer Eye Institute, P.O. Box Olb880, Miami, Florida 33101. 11 |
