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Research Review By Dr. Ceara Higgins©


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Date Posted:

October 2015

Study Title:

Idiopathic scoliosis and the vestibular system


Hawasli AH, Hullar TE, Dorward IG

Author's Affiliations:

Departments of Neurosurgery, Otolaryngology & Orthopaedic Surgery, Washington University School of Medicine, USA.

Publication Information:

European Spine Journal 2015; 24: 227-233.

Background Information:

1-3% of children between 10 and 16 years of age are affected by adolescent idiopathic scoliosis (AIS), a condition that can range from being benign and symptom-free, to presenting with back pain, pulmonary restriction, reduced mobility and potentially significant disfigurement (4). AIS is thought to be a multifactorial condition, resulting from some combination of genetic, biochemical, nutritional, and biomechanical factors, all of which are influenced by neurologic and neuromuscular factors (8). In the continued search for a definitive cause, recent evidence has suggested that sensory dysfunction; in particular vestibular dysfunction, may be a contributing factor to developing AIS.

The vestibular system in each ear consists of three semicircular canals and two otolith organs (the utricle and saccule). These semicircular canals are fluid-filled tubes containing sensitive hair cells which are affected by inertial forces during movement. Movement of the hair cells directly affects the rate at which the primary vestibular afferent neurons projecting into the brainstem fire. The otolith organs sense linear acceleration of the head in the forms of both translation and tilt. Asymmetric inputs between the vestibular systems in both ears are compared by the central nervous system (CNS) to determine the direction and amount of rotational and linear acceleration the individual is undergoing. The CNS also incorporates information from the visual system as well as somatic inputs (joint receptors, muscle tendon organs etc.) to achieve balance and smooth vision and movement.

The vestibulo-ocular reflex (VOR) uses this information to move our eyes according to sensory input, keeping them pointing in the same direction independently to head movement. This allows a visual image to stay stable on the retina. In addition, the vestibulocollic reflex (VCR) stabilizes your head on your body by altering tension in the cervical musculature in order to resist passive head movements. These reflexes work in conjunction with other afferents (including proprioceptive inputs) to allow us to move smoothly and view our world normally.

In order to examine the vestibular system, the output of each of these reflexes can be measured via exposure to a stimulus that induces a vestibular asymmetry. For example, rotational chair testing, where a patient’s eyes are measured while sitting in a chair and turning slowly in the dark. The speed of the head is compared to the speed of the eyes moving to compensate for head motion. The resultant ratio between eye and head velocity depends on the particular stimulus conditions, but when decreased can indicate vestibular weakness.

Perceived verticality, head yaw/position and other balance-related functions can be profoundly affected by the vestibular system, leading to a neurogenic shift in the trunk or torsional effects on the spine. It has been theorized that that this sort of muscle asymmetry may be enough to induce a scoliotic change on its own (3).

The authors of this paper discussed putative mechanisms for adolescent idiopathic scoliosis (AIS) by reviewing the current evidence supporting the role of the vestibular system in the development of this condition.


Scoliosis & Vestibular Responsiveness:

Patients with AIS have been shown to have a significantly higher prevalence of both spontaneous and positional nystagmus (13), increased sensitivity to caloric testing on the ipsilateral side to their curve and increased postural sway with caloric testing (14). EDITOR’S NOTE: Caloric testing is a test of the vestibulo-ocular reflex that involves irrigating cold or warm water or air into the external auditory canal. As well, studies have shown that individuals with AIS have significantly altered perception of subjective visual vertical placement (1), significant abnormalities in off-vertical axis rotation (20), loss of strategies to control head yaw (11), and, in those with Cobb angles greater than 15 degrees, altered visuo-oculomotor function in saccadic latency and velocity testing (10).

A number of studies have shown alterations in posturography and postural sway under both static and dynamic conditions (5) to different degrees with various types of scoliosis. Scoliotic patients have also been shown to have increased body sway and poorer balance control when experiencing visual or proprioceptive challenges (6), and impairments in cognitive integration of vestibular signals (18).

Scoliosis & Vestibular Anatomy:

Functional deficits such as those discussed above show evidence of anatomic correlates. Individuals with AIS have been shown to have 5% shorter distances between the centre of the lateral and superior semicircular canals, 6% smaller posterior canals (17), and 9% longer and 2% thinner vestibular canals (21). In addition, abnormal direct connections between the lateral and posterior vertebral canals have been found in 55% of patients with scoliosis. The same connections were found in only 15% of non-scoliotic patients (12). Patients with AIS also demonstrated differences in the thickness of the cerebral cortex in areas involved in vestibular functions (19).

Although the data suggests an association between vestibular dysfunction and scoliosis, it is unclear which of the two might be the causative factor. As well, in order to suggest that scoliosis could be the cause of vestibular dysfunction, the vestibular system would have to receive input from the spine to indicate the presence of the spinal deformity. This feedback system has not been well described to date. Vestibular abnormalities shown in stabilometry and electronystagmography have not been able to predict progression in scoliosis (15), and there have been several other genetic, congenital, and neuromuscular disorders associated with AIS. All of this suggests that AIS may remain a multifactorial disease spectrum.

A variety of animal models have been used in an attempt to clarify the issue of causation. When otolith receptor lesions were induced in guinea pigs, it was found to induce scoliotic curvatures with rotation of the thoracic vertebrae toward the contralateral side (2). When, the lesion was applied to the semicircular canals, head rotation was observed. When unilateral vestibular lesioning was created in tadpoles during a critical window in their development it was found that the frogs would develop scoliosis in the coronal and sagittal planes and along the rotatory axis (9). Finally, pinealectomy in chickens or bipedal rats has been shown to create scoliosis (7). These studies, when taken together, suggest that vestibular dysfunction may play a role in the development of scoliosis – albeit in animal models. Our ability to extrapolate these findings to human cases remains limited at this time.

Clinical Application & Conclusions:

A significant amount of level III-IV clinical evidence exists to support the association between AIS and vestibular system dysfunction. More limited evidence exists to suggest a causative role for the vestibular system in the development of AIS – most (all?) of which is animal research.

Further research is needed to determine the exact causal relationship between vestibular function and the development of AIS, as well as whether vestibular rehabilitation might mitigate some of the noted vestibular abnormalities, or the extent or progression of AIS.

Study Methods:

The authors conducted a PubMed search of the English literature for key words including ‘adolescent idiopathic scoliosis’, ‘AIS’, ‘vestibular’, ‘vestibular system’, and ‘labyrinth’. These results were confirmed through the Google Scholar Search Engine. 18 articles were ultimately included – all were unique papers published in English that evaluated interactions between AIS and the vestibular system.

Study Strengths / Weaknesses:

    The authors should be commended for completing one of the first literature summaries in this area.
  • The authors’ use of only PubMed & Google Scholar in conjunction with the exclusion of non-English papers may have resulted in overlooking some pertinent articles.
  • Clinical data showing the association between vestibular abnormalities and scoliosis provide level III-IV evidence only.
  • A limited number of case-controlled studies were available
  • There were very few studies that could contribute the notion of causation

Additional References:

  1. Cakrt O, Slaby K, Viktorinova L, et al. Subjective visual vertical in patients with idiopathic scoliosis. J Vestib Res 2011; 21: 161-165.
  2. De Waele C, Graf W, Josset P, et al. A radiological analysis of the postural syndromes following hemilabyrintectomy and selective canal and otolith lesions in the guinea pig. Exp Brain Res 1989; 77: 166-182.
  3. Deguchi M, Kawakami N, Kanemura T. Correction of experimental scoliosis by rib resection in the transverse plane. J Spinal Disord 1997; 10: 197-203.
  4. Fong DY, Lee CF, Cheung KM, et al. A meta-analysis of the clinical effectiveness of school scoliosis screening. Spine 2010; 35: 1061-1071.
  5. Gruber AH, Busa MA, Gorton IGE, et al. Time-to-contact and muscle entropy identify differences in postural control in adolescent idiopathic scoliosis. Gait Posture 2011; 34: 13-18.
  6. Haumont T, Gauchard GC, Lascombes P, et al. Postural instability in early-stage idiopathic scoliosis in adolescent girls. Spine 2011; 36: E847-E854.
  7. Kanemura T, Kawakami N, Deguchi M, et al. Natural course of experimental scoliosis in pinealectomized chickens. Spine 1997; 22: 1563-1567.
  8. Kouwenhoven JW, Castelein RM. The pathogenesis of adolescent idiopathic scoliosis: review of the literature. Spine 2008; 33: 2898-2908.
  9. Lambert FM, Malinvaud D,Glaunes J, et al. Vestibular asymmetry as the cause of idiopathic scoliosis: a possible answer from Xwnopus. J Neurosci 2009; 29: 12477-12487.
  10. Lion ML, Haumont T, Gauchard GC, et al. Visuo-oculomotor deficiency at early-stage idiopathic scoliosis in adolescent girls. Spine 2013; 38: 238-244.
  11. Mallau S, Bollini G, Jouve JCA. Locomotor skills and balance strategies in adolescent idiopathic scoliosis. Spine 2007; 32: E14-E22.
  12. Rousie D, Deroubaix J, Joly O, et al. Abnormal connection between lateral and posterior semicircular canal revealed by new modeling process. Ann N Y Acad Sci 2009; 1164: 435-457.
  13. Sahlstrand T, Petruson B. A study of labyrinthine function in patients with adolescent idiopathic scoliosis. An electo-nystagmohraphic study. Acta Orthop Scand 1979; 50: 759-769.
  14. Sahlstrand T, PetrusonB, Ortengren R. Vestibulospinal reflex activity in patients with adolescent idiopathic scoliosis. Postural effects during caloric labyrinthine stimulation recorded by stabilometry. Acta Orthop Scand 1979; 50: 275-281.
  15. Sahlstrend T, Lidstrom J. Equilibrium factors as predictors of the prognosis in adolescent idiopathic scoliosis. Clin Orthop Relat Res 1980; 152: 232-236.
  16. Shi L, Wang D, Chu WC, et al. Automatic MRI segmentation and morphoanatomy analysis of the vestibular system in adolescent idiopathic scoliosis. Neuroimage 2011; 54(Suppl 1): S180-S188.
  17. Simoneau M, Lamothe V, Hutin E, et al. Evidence for cognitive vestibular integration impairment in idiopathic scoliosis patients. BMC Neurosci 2009; 10: 102.
  18. Wang D, Shi L, Chu WC, et al. Abnormal cerebral cortical thinning pattern in adolescent girls with idiopathic scoliosis. Neuroimage 2012; 59: 935-942.
  19. Weiner-Vacher S, Mazda K. Assymmetric otolith vestibilo-ocular responses in children with idiopathic scoliosis. J Pediatr 1998; 132: 1028-1032.
  20. Zeng W, Lui LM, Shi L, et al. Shape analysis of vestibular systems in adolescent idiopathic scoliosis using geodesic spectra. Med Image Comput Comput Assist Interv 2010; 13: 538-546.

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