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  1. 1. Oculomotor Functional Improvement in Scoliotic Children With 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 function Summary Coritcal deficits1 , as well as vestibulo-cerebellar2 , and brainstem abnormalities3,4,5 have long been identified as a co-morbidity to Idiopathic Scoliosis (ISc). Both vestibular and oculomotor deficits have been identified in the scoliosis population.6 Video Electronystamography (ENG) sub-testing of oculomotor function allows for the assessment of subtle abnormalities in brainstem and cerebellar systems, even when gross neurological testing is negative.7 Three case studies are presented here, all which were diagnosed with ISc. Various ENG subtests were performed to assess oculomotor function both in and out of a truncal scoliosis brace. Three brace types were studied, the Wilmington, the SpineCor, and the Progressive O & P. It is well accepted that truncal bracing causes changes in spinal posture. The resultant activation of muscle spindle and joint mechanoreceptors causes ipsilateral afferent stimulation of cerebellar pathways. Our study has shown a correlation linking truncal bracing and improved oculomotor function in a scoliosis population. Introduction The role of the cerebellum in both smooth pursuits and saccadic function has been studied 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 center of saccade size. Other studies reported saccadic dysmetria as a common feature of degenerative cerebellar disease10 Cerebellar damage disrupts saccades in humans11 and monkeys.12 Anatomical andrecording studies to date indicate that there are two parts of the cerebellar nuclei that participate in saccades: the caudal fastigial nucleus (CFN), also ,
  2. 2. called the fastigial oculomotor region, and the ventrolateral corner of the posterior interpositus nucleus (VPIN).13 Smooth pursuit abnormalities associated with cerebellar deficits were first identified by Westheimer and Blair in 197314 and Zee et al. in 198115 In 1989, O'Beirne J, and Goldberg et al. reported findings of smooth pursuit dysfunction in seven subjects with either idiopathic or congenital scoliosis.16 Human subjects with pathology of the cerebellum showed defects in the generation of pursuit eye movements17,18,19 Based on the anatomic projections to the cerebellum from areas within the pons that are concerned with pursuit,20,21,22 and the effects of focal lesions within the cerebellum of monkeys, two specific regions of the cerebellar cortex have been implicated in the control of pursuit:the cerebellar flocculus, paraflocculus,23 and the dorsal and posterior cerebellar vermis including lobules VI, VII24 , as well as the uvula.25 Furthermore, lesions within the portion of the fastigial nucleus that receives projections from Purkinje cells of the dorsal vermis, the so-called fastigial oculomotor region (FOR), also affect pursuit.26 Recently, the ventrolateral portion of the posterior interposed nucleus27 and the lateral cerebellar hemispheres28 have also been implicated in pursuit. It is apparent that many areas of the cerebellum contribute to smooth pursuits, saccades and optokinetic pursuits. Our study was not designed to unravel the precise contributions of the cerebellum to oculomotor function, but rather to show that truncal bracing causes improvement in global cerebellar function. This was objectively measured through the use of ENG testing. Of course it has also been well studied that lesions of the cerebellum such as Arnold Chiari Malformation, as well as cranio-cervical junction abnormalities as seen with syrinx, are involved in ISc. Materials and Methods Study Design- Three (3) Pediatric Case Studies of patients with Scoliosis were tested for oculomotor function utilizing Video Electronystagmography (ENG). The Studies were performed with the subjects both “in” and “out”, of their scoliosis brace. The following tests were completed; Saccade testing (Speed/Latency/Accuracy) was recorded and measured for a random stimulus in all participants, and a Fixed stimulus recording was made in two (2) of the participants, Optokinetic gain at 30 degrees per second (d/s), and
  3. 3. Sinusoidal Smooth pursuit gain at 0.1 hertz (hz), 0.2hz, and 0.4hz were recorded and measured. Objectives- The purpose of this study is to better understand the central neurological affects of truncal bracing on brainstem and cerebellar function as objectified by oculomotor testing. Methods- The patients were evaluated utilizing Micromedical Video Electronystagmography (ENG); with infrared video capture and pupillary tracking Spectrum 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 a computer controlled stimulus light bar. Testing was performed in a random order with regards to braced vs. non-braced. Data Acquisition and analysis The reliability of oculomotor testing was found to be good in studies performed both by Ettinger 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 Danlos syndrome, and a Superior Oblique Palsy of the left eye. Initial Fixed saccade testing was performed out of the brace for this patient. The waveforms were recorded and analyzed (Figure 1). Left sided saccade speed showed slowing, and hypometric in regards to accuracy. The findings were consistently reproduced over multiple attempts. The patient was immediately re-testing with her customized Progressive O &P truncal brace fastened. The waveforms and results (Figure 2) revealed normometric results in speed, accuracy and latency of saccades. Random Saccade testing was also performed for Participant 1. The “out of brace” results (Figure 3) revealed slowing of saccades bilaterally, hypometria on left sided saccades, and bilateral increases in latency. “In brace” results (Figure 4) were recorded to show normometric findings in bilateral speed, accuracy and latency of saccades. Optokinetic waveforms are presented in (Figures 5 and 6). Gain calculation on left sided pursuits improved from 0.58 to 0.88 when tested “out” then “in” the truncal brace ; right sided pursuits improved from 0.88 to 1.03 when tested “out then “in” the truncal brace.
  4. 4. Sinsoidal Smooth Pursuit testing was done first “out” of the brace. The findings revealed hypometric gain calculations of 0.68, 0.62, and 0.61 at 0.1hz, 0.2hz, and 0.4hz respectively. Testing “in” the truncal brace revealed normometric results in gain at all frequencies (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 showed hypometric 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 and 0.73 on left and right pursuits respectively. Random saccade testing “out” of the truncal brace was performed initially. Testing revealed slowing of all saccade attempts. “In” truncal brace testing revealed normometric 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 revealed normometric 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 diminished pursuit abilities bilaterally. A gain calculation was unavailable due to the saccadic intrusuions and gaze difficulties. “In” truncal brace testing revealed a dramatic change in gaze and pursuit abilities. The gain was calculated as 0.76 and 0.42 right and left respectively. All other measures were normal during both “out” and “in” brace testing. Raw data results revealed a significant improvement in all measures of Saccade performance, (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. Discussion Truncal bracing of scoliotic patients causes changes in spinal postures, and immediate changes in oculomotor function in the cases studied. These findings indicate abnormal spinal curvatures associated with Idiopathic scoliosis are linked with deficits of oculomotor function, and can be reversed with truncal brace correction. Further research in this area may give objective evidence that the success of bracing in scoliosis is due to a central neurological rehabilitation achieved through spinal postural support and correction. Further study is required to determine if improvements of oculomotor function can be associated with changes is abnormal curvatures of the spine found in Idiopathic scoliosis.
  5. 5. Further study is also required on somatic stimulations effect on oculomotor function is necessary. If a correlation is made between improved ocular control and a reduction of spinal curvatures, further study may identify oculomotor rehabilitation techniques that are valuable in scoliosis rehabilitation. Specific somatic stimulations have been shown to cause improvements in oculomotor function. Chiropractic adjustments, as well as unilateral upper limb girdle stimulation, have both been shown to improve abnormal eye movements29,30 Figure 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. 6. Results of Participant 1 on random saccade testing in the brace Figure 5 Optokinetic responses Out of brace Left / Right Figure 6 Optokinetic responses In Brace Left / Right Figure 7. Sinusoidal smooth pursuit results (out of brace)
  7. 7. Gain Asymmetry Phase Figure 8. Sinusoidal Smooth pursuits results (In brace) Gain Asymmetry Phase Figure 10- Participant 2 Out of Brace Optokinetic pursuits Participant 2 In Brace Optokinetic pursuits Figure 11 Participant 2 out of brace saccade results
  8. 8. Participant 2 In brace saccade results Figure 12 Participant 2 Smooth pursuits in brace Participant 2 Smooth Purusits Out of brace Figure 13- Participant 3 Optokinetic pursuits
  9. 9. Figure 14- Participant 3 Optokinetic pursuit waveforms Left “Out of brace” Right “Out of brace” Left “In brace” Right “In brace Reference (1)Equilibrial dysfunction in scoliosis--cause or effect? J Spinal Disord 1989 Sep;2(3):184-9 O'Beirne 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. (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 O'Beirne 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 pursuit eye 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 flocculus and 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. 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. Brain Res. 110: 1-14, 1996 (26)Ohtsuka, K., Sato, H., and Noda, H. Saccadic burst neurons in the fastigial nucleus are not 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 the ventrolateral 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 shoulder girdle elevators. .
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