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  • 1. Oculomotor FunctionalImprovement in Scoliotic ChildrenWith Bracing.Marc J. Lamantia D.C., D.A.C.N.B., Gary Deutchman D.C., Charles Bagley M.D.Keywords: Scoliosis, Truncal bracing, Electronystagmography, oculomotor functionSummaryCoritcal deficits1, as well as vestibulo-cerebellar2, and brainstem abnormalities3,4,5 havelong been identified as a co-morbidity to Idiopathic Scoliosis (ISc).Both vestibular and oculomotor deficits have been identified in the scoliosis population.6Video Electronystamography (ENG) sub-testing of oculomotor function allows for theassessment of subtle abnormalities in brainstem and cerebellar systems, even when grossneurological testing is negative.7Three case studies are presented here, all which were diagnosed with ISc. Various ENGsubtests were performed to assess oculomotor function both in and out of a truncalscoliosis brace. Three brace types were studied, the Wilmington, the SpineCor, and theProgressive O & P.It is well accepted that truncal bracing causes changes in spinal posture. The resultantactivation of muscle spindle and joint mechanoreceptors causes ipsilateral afferentstimulation of cerebellar pathways. Our study has shown a correlation linking truncalbracing and improved oculomotor function in a scoliosis population.IntroductionThe role of the cerebellum in both smooth pursuits and saccadic function has beenstudied extensively.Studies done by Keller,8 Buttner and Straube9 implicate midline cerebellar structures,especially the oculomotor vermis and caudal fastigial nuclei (CFN), as the control centerof saccade size. Other studies reported saccadic dysmetria as a common feature ofdegenerative cerebellar disease10 Cerebellar damage disrupts saccades in humans11 andmonkeys.12 Anatomical and recording studies to date indicate that there are two parts ofthe cerebellar nuclei that participate in saccades: the caudal fastigial nucleus (CFN), also,
  • 2. called the fastigial oculomotor region, and the ventrolateral corner of the posteriorinterpositus nucleus (VPIN).13Smooth pursuit abnormalities associated with cerebellar deficits were first identified byWestheimer and Blair in 197314 and Zee et al. in 198115In 1989, OBeirne J, and Goldberg et al. reported findings of smooth pursuit dysfunctionin seven subjects with either idiopathic or congenital scoliosis.16Human subjects with pathology of the cerebellum showed defects in the generation ofpursuit eye movements17,18,19 Based on the anatomic projections to the cerebellum from areas within the pons that areconcerned with pursuit,20,21,22 and the effects of focal lesions within the cerebellum ofmonkeys, two specific regions of the cerebellar cortex have been implicated in the controlof pursuit: the cerebellar flocculus, paraflocculus,23 and the dorsal and posterior cerebellarvermis including lobules VI, VII24, as well as the uvula.25Furthermore, lesions within the portion of the fastigial nucleus that receives projectionsfrom Purkinje cells of the dorsal vermis, the so-called fastigial oculomotor region (FOR),also affect pursuit.26Recently, the ventrolateral portion of the posterior interposed nucleus27 and the lateralcerebellar hemispheres28 have also been implicated in pursuit.It is apparent that many areas of the cerebellum contribute to smooth pursuits, saccadesand optokinetic pursuits. Our study was not designed to unravel the precise contributionsof the cerebellum to oculomotor function, but rather to show that truncal bracing causesimprovement in global cerebellar function. This was objectively measured through theuse of ENG testing.Of course it has also been well studied that lesions of the cerebellum such as ArnoldChiari Malformation, as well as cranio-cervical junction abnormalities as seen withsyrinx, are involved in ISc.Materials and MethodsStudy Design- Three (3) Pediatric Case Studies of patients with Scoliosis were tested foroculomotor function utilizing Video Electronystagmography (ENG). The Studies wereperformed with the subjects both “in” and “out”, of their scoliosis brace. The followingtests were completed; Saccade testing (Speed/Latency/Accuracy) was recorded andmeasured for a random stimulus in all participants, and a Fixed stimulus recording wasmade in two (2) of the participants, Optokinetic gain at 30 degrees per second (d/s), and
  • 3. Sinusoidal Smooth pursuit gain at 0.1 hertz (hz), 0.2hz, and 0.4hz were recorded andmeasured.Objectives- The purpose of this study is to better understand the central neurologicalaffects of truncal bracing on brainstem and cerebellar function as objectified byoculomotor testing.Methods- The patients were evaluated utilizing Micromedical VideoElectronystagmography (ENG); with infrared video capture and pupillary trackingSpectrum Software. All recordings were taken of the left eye, with three (3) channels.Testing was performed with the patient in a seated position thirty nine (39) inches from acomputer controlled stimulus light bar. Testing was performed in a random order withregards to braced vs. non-braced.Data Acquisition and analysisThe reliability of oculomotor testing was found to be good in studies performed both byEttinger U, and Kumari V, et al. at the Institute of Psychiatry, University of London.Results-Participant 1; a 13 year old female, previously diagnosed with ISc, Ehler Danlossyndrome, and a Superior Oblique Palsy of the left eye.Initial Fixed saccade testing was performed out of the brace for this patient. Thewaveforms were recorded and analyzed (Figure 1). Left sided saccade speed showedslowing, and hypometric in regards to accuracy. The findings were consistentlyreproduced over multiple attempts.The patient was immediately re-testing with her customized Progressive O &P truncalbrace fastened. The waveforms and results (Figure 2) revealed normometric results inspeed, accuracy and latency of saccades. Random Saccade testing was also performedfor Participant 1. The “out of brace” results (Figure 3) revealed slowing of saccadesbilaterally, hypometria on left sided saccades, and bilateral increases in latency.“In brace” results (Figure 4) were recorded to show normometric findings in bilateralspeed, accuracy and latency of saccades.Optokinetic waveforms are presented in (Figures 5 and 6). Gain calculation on left sidedpursuits improved from 0.58 to 0.88 when tested “out” then “in” the truncal brace ; rightsided pursuits improved from 0.88 to 1.03 when tested “out then “in” the truncal brace.
  • 4. Sinsoidal Smooth Pursuit testing was done first “out” of the brace. The findings revealedhypometric gain calculations of 0.68, 0.62, and 0.61 at 0.1hz, 0.2hz, and 0.4hzrespectively. Testing “in” the truncal brace revealed normometric results in gain at allfrequencies (0.99, 0.96, and 1.01).Participant 2; an 11 year old female, fitted with the SpineCor brace.Optokinetic testing “out” of the truncal brace was performed first. Results showedhypometric gain calculations of 0.52 and 0.49 on left and right pursuits respectively.Subsequent “In” truncal brace results showed a improved gain calculations of 0.81 and0.73 on left and right pursuits respectively.Random saccade testing “out” of the truncal brace was performed initially. Testingrevealed slowing of all saccade attempts. “In” truncal brace testing revealednormometric speed on all saccade attempts.Sinusoidal Smooth Pursuit testing “out” of the truncal brace exposed a gain of 0.83, 0.83,and 0.77 at 0.1hz, 0.2.hz, 0.4hz respectively. “In” truncal brace testing revealednormometric gain calculations of 0.97, 0.96, and 0.94 respectively.Participant 3; a 13 year old female fitted with the Wilmington Brace.Optokinetic testing “out” of the truncal brace revealed gaze difficulties and diminishedpursuit abilities bilaterally. A gain calculation was unavailable due to the saccadicintrusuions and gaze difficulties. “In” truncal brace testing revealed a dramatic change ingaze and pursuit abilities. The gain was calculated as 0.76 and 0.42 right and leftrespectively. All other measures were normal during both “out” and “in” brace testing.Raw data results revealed a significant improvement in all measures of Saccadeperformance, (acc-8%-30%, lat-25% sp-100%>275 d/s), Sinusoidal gain increases(20%-40%) and optokinetic gain increases in performance (30%-60%) during the “In”truncal brace testing.DiscussionTruncal bracing of scoliotic patients causes changes in spinal postures, and immediatechanges in oculomotor function in the cases studied. These findings indicate abnormalspinal curvatures associated with Idiopathic scoliosis are linked with deficits ofoculomotor function, and can be reversed with truncal brace correction. Further researchin this area may give objective evidence that the success of bracing in scoliosis is due to acentral neurological rehabilitation achieved through spinal postural support andcorrection.Further study is required to determine if improvements of oculomotor function can beassociated with changes is abnormal curvatures of the spine found in Idiopathic scoliosis.
  • 5. Further study is also required on somatic stimulations effect on oculomotor function isnecessary.If a correlation is made between improved ocular control and a reduction of spinalcurvatures, further study may identify oculomotor rehabilitation techniques that arevaluable in scoliosis rehabilitation. Specific somatic stimulations have been shown tocause improvements in oculomotor function. Chiropractic adjustments, as well asunilateral upper limb girdle stimulation, have both been shown to improve abnormal eyemovements29,30Figure 1.Waveforms and results of Participant 1 Fixed Saccade testing (out of brace)Figure 2 Waveforms and results of Participant 1 Fixed Saccade testing (in the brace)Figure 3 - results of Participant 1 on random saccade testing out of the brace
  • 6. Results of Participant 1 on random saccade testing in the braceFigure 5 Optokinetic responses Out of brace Left / RightFigure 6 Optokinetic responses In Brace Left / RightFigure 7. Sinusoidal smooth pursuit results (out of brace)
  • 7. Gain Asymmetry PhaseFigure 8. Sinusoidal Smooth pursuits results (In brace) Gain Asymmetry PhaseFigure 10-Participant 2 Out of Brace Optokinetic pursuitsParticipant 2 In Brace Optokinetic pursuitsFigure 11Participant 2 out of brace saccade results
  • 8. Participant 2 In brace saccade resultsFigure 12Participant 2 Smooth pursuits in braceParticipant 2 Smooth Purusits Out of braceFigure 13- Participant 3 Optokinetic pursuits
  • 9. Figure 14- Participant 3 Optokinetic pursuit waveforms Left “Out of brace” Right “Out of brace” Left “In brace” Right “In braceReference (1)Equilibrial dysfunction in scoliosis--cause or effect? J Spinal Disord 1989 Sep;2(3):184-9 OBeirne J, Goldberg C, Dowling FE, Fogarty EE. (2)Arch Ital Biol. 2002 Jan;140(1):67-80 Vestibular mechanisms involved in idiopathic scoliosis. Manzoni D, Miele F. (3) An evaluation of brainstem function as a prognostication of early idiopathic scoliosis. J Pediatr Orthop 1982;2(5):521-8 Yamamoto H, Tani T, MacEwen GD, Herman (4)Clin Orthop. 1984 Apr;(184):50-7. Etiology of idiopathic scoliosis. Yamada K, Yamamoto H, Nakagawa Y, Tezuka A, Tamura T, Kawata S. Acta Orthop Scand. 1991 Oct;62(5):403-6 (5) Spinal cord and brain stem anomalies in scoliosis. MR screening of 26 cases. Samuelsson L, Lindell D, Kogler H. 6)Cerebellum. 2003;2(3):223-32. Roles of the cerebellum in pursuit-vestibular interactions. kushima K. 7) Scoliosis associated with congenital brain-stem abnormalities. A report of eight cases Int Orthop 1984;8(1):37-46 Dretakis EK (8)Keller EL. The cerebellum. In: Wurtz RH, Goldberg ME, editors. The neurobiology of saccadic eye movements. Amsterdam: Elsevier; 1989. p. 391–411 (9)Büttner, U., and Straube, A. The effect of cerebellar midline lesions on eye movements. Neuro- ophthalmol. 15: 75-82, 1995.
  • 10. (10) Kanayama R. Bronstein AM, Shello-Hoffman J. Rudge P. Husain M. Visualyy and memory guided saccades in a case of cerebellar saccadic dysmetria, J. Neurol Neurosurg Psychiartry 1994 : 57 : 1081-4 (11)Selhorst JB, Stark L, and Ochs AL. Disorders in cerebellar ocular control. II. Macrosaccadic oscillations:an oculographic, control system, and clinico-anatomical analysis. Brain 99: 509-522, 1976 (12)Ritchie L. Effects of cerebellar lesions on saccadic eye movements. J Neurophysiol 39: 1246- 1246, 1976 (13)Ohtsuka K, and Noda H. Direction-selective saccadic-burst neurons in the fastigial oculomotor region of the macaque. Exp Brain Res 81: 659-662, 1990 (14)Westheimer, G., and Blair, S. Oculomotor defects in cerebellectomized monkeys. Invest. Ophthalmol. 12: 618-621, 1973 (15)Zee DS, Yamazaki A, Buler PH, Gucer G. Effects of ablation of Flocculus and Paraflocculus on eye movements in primates 1981; 46; 878-99 (16)Equilibrial dysfunction in scoliosis--cause or effect? J Spinal Disord 1989 Sep;2(3):184-9 OBeirne J, Goldberg C, Dowling FE, Fogarty EE. (17)Büttner, U., Straube, A., and Spuler, A. Saccadic dysmetria and "intact" smooth pursuit eye movements after bilateral deep cerebellar nuclei lesions. J. Neurol. Neurosurg. Psychiatry 57: 832-834, 1994 (18)Lewis, R. F., and Zee, D. S. Ocular motor disorders associated with cerebellar lesions: pathophysiology and topical diagnosis. Rev. Neurol. (Paris) 149: 665-677, 1993 (19)Straube, A., Scheuerer, W., and Eggert, T. Unilateral cerebellar lesions affect initiation of ipsilateral smooth pursuit eye movements in humans. Ann. Neurol. 42: 891-898, 1997 (20)Glickstein, M., Gerrits, N., Kralj-hans, I., Mercier, B., Stein, J., and Voogd, J. Visual pontocerebellar projections in the macaque. J. Comp. Neurol. 349: 51-72, 1994 (21)Nagao, S., and Kitazawa, K. Differences of responsiveness to step-ramp smooth pursuiteye movements in the primate flocculus and ventral paraflocculus. Neurosci. Res. Suppl. 22: 316, 1998. (22)Yamada, J., and Noda, H. Afferent and efferent connections of the oculomotor cerebellar vermis in the macaque monkey. J. Comp. Neurol. 265: 224-241, 1987 (23)Zee, D. S., Yamazaki, A., Butler, P. H., and Gücer, G. Effects of ablation of the flocculusand paraflocculus on eye movements in primate. J. Neurophysiol. 46: 878-899, 1981 (24)Keller, E. L. Cerebellar involvement in smooth pursuit eye movement generation:flocculus and vermis. In: Physiological Aspects of Clinical Neuro-ophthalmology, edited by C.Kennard, and F. Rose. London: Chapman and Hall, 1988, p. 341-355.
  • 11. (25)Heinen, S. J., and Keller, E. L. The function of the cerebellar uvula in monkey during optokinetic and pursuit eye movements: single-unit responses and lesion effects. Exp. BrainRes. 110: 1-14, 1996 (26)Ohtsuka, K., Sato, H., and Noda, H. Saccadic burst neurons in the fastigial nucleus arenot involved in compensating orbital non-linearities. J. Neurophysiol. 71: 1976-1980, 1994 (27)Robinson, F. R., and Brettler, S. C. Smooth pursuit properties of neurons in theventrolateral posterior interpositus nucleus of the monkey cerebellum. Soc. Neurosci. Abstr. 24:1405, 1998. (28)Robinson, F. R., Straube, A., and Fuchs, A. F. Participation of caudal fastigial nucleus in smooth pursuit eye movements. II. Effects of muscimol inactivation. J. Neurophysiol. 78: 848-859, 1997 (29) Fujiwara K, Kunita K, Toyama H. Percept Mot Skills. 2003 Feb;96(1):173-84 Latency of saccadic eye movement during contraction of bilateral and unilateral shouldergirdle elevators..
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