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The Postural Control System

Introduction

Postural control is the ability of the central nervous system (CNS) to integrate sensory information from the visual, vestibular, and somatosensory systems and produce the motor output needed to maintain upright posture.[1][2][3] Concussion commonly disrupts one or more of these systems, which is why dizziness, balance impairment, and visual disturbance are common, persistent symptoms after concussion. This page reviews each system, its role in postural control, and its relationship with concussion.

Postural Control

Postural control has two components:[4]

  • Postural orientation: the active alignment of the trunk and head relative to gravity, the support surface, the visual environment, and internal references.
  • Postural equilibrium: the coordination of movement strategies to keep the centre of mass stable when balance is disturbed, whether by the person's own movement or by an external perturbation.

Clinical note: If one sensory system is impaired, the other two can compensate through sensory reweighting. This is where the brain adjusts how much it relies on each sensory input depending on which inputs are most reliable at the time. This happens automatically, but can be improved with rehabilitation. When more than one system is affected in combination with central nervous system involvement, postural control can be significantly compromised. This is associated with an increased risk of falls and injury.[1]

Vestibular System

The vestibular system manages balance, spatial orientation, and eye movement by detecting head motion and position. It helps orient the trunk to vertical by weighting available sensory cues, and contributes to controlling the body's centre of mass (COM) in static and dynamic positions. It also stabilises the head during changes in body position[5] [6][7] and helps to regulate blood pressure through the vestibulosympathetic reflex (VSyR). This is mediated by the otolith organs, alongside the baroreflexes. This reflex rapidly adjusts sympathetic outflow to the heart and blood vessels as a fast compensatory mechanism.[1] A poorly functioning VSyR is associated with decreased orthostatic tolerance (i.e. feeling lightheaded on standing).[1][8]

Vestibular System Anatomy

The vestibular apparatus has two main sensory structures: the semicircular canals, which detect rotation, and the otolith organs, which detect linear movement and head position.

Semicircular Canals

The semicircular canals are mechanoreceptors sensitive to angular acceleration/velocity.[9] They are arranged at right angles to one another (orthogonal) to detect rotation of the head, with each canal functionally paired with a coplanar canal in the opposite ear.[10] A simple way to remember each canal's main plane of movement is:

  • Anterior (superior) canal: activated by nodding the head, as in saying "yes".
  • Posterior canal: activated by tilting the head towards the shoulder. This is the canal most associated with benign paroxysmal positional vertigo (BPPV).
  • Lateral (horizontal) canal: activated by rotating the head, as in saying "no".

The planes of the semicircular canals lie close to the planes of the extraocular muscles, which allows the eyes and ears to "work as a team."[11] For more information on vestibular anatomy, see: Anatomy of the Peripheral Vestibular System.

Otolith organs

The otolith organs (utricle and saccule) detect linear acceleration and the position of the head relative to gravity. The utricle provides horizontal input while the saccule provides vertical input.[9]

Vestibular System and Concussion

While many concussion symptoms settle within a few weeks, symptoms such as vertigo, dizziness, and balance dysfunction can persist. Vestibular screening should therefore form part of the concussion evaluation.[1]

Visual System

The visual system is an important source of sensory information for balance, with postural stability influenced by the quality of visual input (i.e. it is better in a well-lit, stable visual environment and reduced when visual information is poor, such as in dim light or on a moving visual background). It is also particularly important at low frequencies of head movement: the vestibular system is less effective at detecting very slow rotational movements (below around 0.1 Hz), and the visual system contributes more to stability in this range.[12]

Classification of eye movements

Eye movements fall into two functional classes: gaze stabilisation and gaze shifting.

Gaze Stabilisation

Gaze stabilisation keeps the eyes stable when the head moves or appears to move. Two systems contribute to gaze stabilisation:[13]

  • Vestibulo-ocular reflex (VOR): an automatic brainstem reflex producing eye movement in the exact opposite direction to head movement, keeping the image steady on the retina.[11]
  • Optokinetic reflex: stabilises a moving image on the retina. The eyes follow the movement in a slow phase, then make a quick resetting movement.[14][15] For example, following the scenery when looking out of a moving vehicle.

Gaze stabilisation relies on conjugate movements, where both eyes move together in the same direction.

Clinical note: Oscillopsia refers to the visual field appearing to move when it should not. It is a highly distressing symptom that signals significant gaze stabilisation dysfunction.[16]

Watch these videos if you would like to learn more about VOR and the optokinetic response.


Gaze Shifting

Gaze shifting focuses the image on the fovea (the centre of the retina responsible for sharp, high-acuity vision) when the visual target changes. Three systems contribute to gaze shifting:[19]

  • Smooth pursuit: voluntary, smooth, conjugate eye movements that track a moving target (e.g. following a bird in flight).
  • Vergence: disconjugate eye movement (eyes move in opposite directions) that adjusts for distance. Eyes converge for near targets and diverge for far targets (e.g. looking from the classroom board to notes on a desk).
  • Saccades: short, rapid, ballistic eye movements that redirect gaze to a new target of interest (e.g. quickly shifting your gaze from one word to another while reading).


Visual System and Concussion

Vision impairments are common post-concussion.[22] Cranial nerves III, IV, and VI innervate the eye muscles and are vulnerable to injury anywhere along their course from brainstem to orbit.[9] Visual fallout after concussion can present as blurry or double vision, dizziness, nausea, headache, loss of balance while walking or turning the head, objects appearing to move or spin, and difficulty reading.[23]

Somatosensory System

The somatosensory system relays information about body position to the brain via mechanoreceptors, including the muscle spindles. This enables appropriate reflexive and voluntary motor responses.

The upper cervical spine, particularly the suboccipital region, contains a very high density of muscle spindles, far greater than in the limb muscles. This makes it an important source of proprioceptive information about head and neck position.[24][25]

Mechanoreceptor input from the upper neck travels via the C2–C3 dorsal root ganglia, which project to the vestibular nuclei. Input from C0–C2 also converges on the central cervical nucleus (CCN), where vestibular, ocular, and proprioceptive information is integrated.[26]

Clinical note: Sensorimotor dysfunction is more pronounced with upper cervical injury than lower cervical injury, because the upper region has greater muscle spindle density, stronger connections to the visual and vestibular systems, and greater reflex activity.[26][27] Because the forces that cause a concussion injure the neck at the same time, this upper cervical input is frequently disrupted after concussion. This is why an upper cervical assessment is essential for any patient with a concussion.

Central Processing

Sensory input from the vestibular, visual, and somatosensory systems is integrated centrally. Two sites are particularly important for vestibular processing:

  • Vestibular nuclear complex: provides fast, direct connections between afferent input and motor output. The superior and medial vestibular nuclei relay the vestibulo-ocular reflex. The medial nucleus also coordinates combined head and eye movement. The lateral vestibular nucleus is the principal relay for the vestibulospinal reflex (VSR).[28]
  • Cerebellum: coordinates and fine-tunes movement, including monitoring vestibular performance and adjusting central vestibular processing. Rather than initiating movement, it acts as a comparator, receiving intended motor plans from the cerebral cortex and checking them against real-time sensory feedback to correct errors and maintain precision.[29]

Key Reflexes

Several reflexes contribute to gaze, head, and postural stability. This section covers four of the most relevant: the vestibulo-ocular reflex (VOR), the cervicocollic reflex (CCR), the vestibulospinal reflex (VSR), and the vestibulosympathetic reflex (VSyR).[30]

Table 1. The Key Reflexes
Reflex Function Clinical Test Sign of dysfunction
Vestibulo-ocular reflex (VOR)[31] Stabilises gaze during head motion by moving the eyes an equal and opposite amount to head movement. Head thrust/impulse test. Corrective saccade.
Cervicocollic reflex (CCR)[32] Uses neck proprioceptors to detect head-on-trunk movement and trigger neck muscle contraction to stabilise the head. Trunk rotates beneath a stationary head. Head cannot stay steady on the target.
Vestibulospinal reflex (VSR)[33] Adjusts posture and neck muscle activity to maintain whole-body balance via the labyrinthine system. Balance/perturbation testing.

The Fukuda step test evaluates VSR function and uncovers unilateral vestibular imbalance by observing body rotation while marching in place with eyes closed.[1]

Dizziness, imbalance, nystagmus and falls.
Vestibulosympathetic reflex (VSyR)[34] Regulates blood pressure on postural change. Assess for orthostatic drop in blood pressure.

The NASA lean test can be used.[35] It measures the combined output of all orthostatic reflexes, including the VSR and arterial baroreflexes.[1]

Lightheadedness or symptoms on standing.

Summary

Postural control depends on the integration of visual, vestibular, and somatosensory input, processed centrally by the vestibular nuclear complex and fine-tuned by the cerebellum. Each system has clinically distinct anatomy, function, and failure signs, and several reflexes (such as the VOR and CCR) can be tested to assess the integrity of these pathways. Because concussion frequently affects more than one of these systems, a comprehensive, multi-system assessment is essential to accurately identify the source of a patient's dizziness, imbalance, or visual disturbance and to guide targeted rehabilitation.

Resources

Watch this video if you would like to learn more about the postural system:

References

  1. ↑ 1.0 1.1 1.2 1.3 1.4 1.5 1.6 Robertson M. Postural Control System Course. Physiopedia Plus, 2026.
  2. ↑ Ivanenko Y, Gurfinkel VS Human postural control. Frontiers in Neuroscience. 2018 Mar 20;12:171.
  3. ↑ Alcock L, O’Brien TD, Vanicek N. Association between somatosensory, visual and vestibular contributions to postural control, reactive balance capacity and healthy ageing in older women. Health care for women international. 2018 Dec 2;39(12):1366-80.
  4. ↑ Horak FB. Postural orientation and equilibrium: what do we need to know about neural control of balance to prevent falls? Age Ageing. 2006 Sep;35 Suppl 2:ii7-ii11.
  5. ↑ Möller CL. Overview of balance and the vestibular system. In Hartshorne TS, Hefner MA, Blake KD editors. CHARGE syndrome. 2nd edition. 2021, p.65-76.
  6. ↑ Appiah-Kubi KO, Galgon A, Tierney R, Lauer R, Wright WG. Concurrent vestibular activation and postural training recalibrate somatosensory, vestibular and gaze stabilisation processes. PLoS One. 2024 Jul 5;19(7):e0292200.
  7. ↑ Shin KH, Oh BM, Lee HY. Vestibular Rehabilitation for Post-Concussive Vestibular Dysfunction: Pathophysiology, Evidence-Based Practice, and Future Perspectives. Korean J Neurotrauma. 2026 Apr 24;22(2):119-134.
  8. ↑ Ray CA, Monahan KD; New Collective Author. Aging attenuates the vestibulosympathetic reflex in humans. Circulation. 2002 Feb 26;105(8):956-61.
  9. ↑ 9.0 9.1 9.2 Corbett R. Functional Visual Impairments from Concussion. Clinics in Sports Medicine. 2026 Apr 1;45(2):317-26.
  10. ↑ Khan S, Chang R. Anatomy of the vestibular system: a review. NeuroRehabilitation. 2013;32(3):437-43.
  11. ↑ 11.0 11.1 Cox PG, Jeffery N. Geometry of the semicircular canals and extraocular muscles in rodents, lagomorphs, felids and modern humans. J Anat. 2008 Nov;213(5):583-96.
  12. ↑ Thakkar RD, Kanase S. To Design and Investigate the Effectiveness of a Gaze Stabilization Application on Patients with Impaired Visual Vestibulo-ocular Reflex. Journal of Ecophysiology and Occupational Health. 2022 Jun;22(2):94-103.
  13. ↑ Frattini D, Rosén N, Wibble T. A proposed mechanism for visual vertigo: post-concussion patients have higher gain from visual input into subcortical gaze stabilization. Investigative Ophthalmology & Visual Science. 2024 Apr 1;65(4):26-.
  14. ↑ Turuwhenua J, Yu TY, Mazharullah Z, Thompson B. A method for detecting optokinetic nystagmus based on the optic flow of the limbus. Vision Res. 2014 Oct;103:75-82.
  15. ↑ Hale DE, Reich S, Gold D. Optokinetic nystagmus: six practical uses. Practical Neurology 2024;24:285-288.
  16. ↑ Kamath A, Huang WC, Madill SA. How should I approach and manage adult-onset oscillopsia? Eye (Lond). 2024 Aug;38(12):2246-2252.
  17. ↑ Neuro-Ophthalmology with Dr. Andrew G. Lee. VOR. Available from: https://www.youtube.com/watch?v=30xPZCbCBPw [last accessed 22/7/2026]
  18. ↑ Imagine X Functional Neurology. The Optokinetic Response. Available from: https://www.youtube.com/watch?v=ZbBqMBv5ml8 [last accessed 22/7/2026]
  19. ↑ Chen PY, Jheng YC, Huang SE, Po-Hung Li L, Wei SH, Schubert MC, Kao CL. Gaze shift dynamic visual acuity: A functional test of gaze stability that distinguishes unilateral vestibular hypofunction. J Vestib Res. 2021;31(1):23-32.
  20. ↑ UChicago Online. 14.2 Types of Eye Movements. Available from: https://www.youtube.com/watch?v=eb3h7oUqcTI [last accessed 13/8/2026]
  21. ↑ Australian Institute of Sport. Vestibular and Ocular Motor Screening. Available from: https://www.youtube.com/watch?v=y7SmycbgkAk [last accessed 13/8/2026]
  22. ↑ Treleaven J, Carberry K, Cook H, Fulcher D, Syme C, Galea O. Prevalence of cervical, vestibulo-ocular and or physiological impairments in symptomatic individuals 4 weeks to 6 months post-concussion. Musculoskelet Sci Pract. 2025 Oct;79:103381.
  23. ↑ Bell CA, Grossman SN, Balcer LJ, Galetta SL. Vision as a piece of the head trauma puzzle. Eye (Lond). 2023 Aug;37(12):2385-2390.
  24. ↑ Kulkarni V, Chandy MJ, Babu KS. Quantitative study of muscle spindles in suboccipital muscles of human foetuses. Neurol India. 2001 Dec;49(4):355-9.
  25. ↑ Moore CW, Fanous J, Rice CL. Fiber type composition of contiguous palmaris longus and abductor pollicis brevis muscles: Morphological evidence of a functional synergy. J Anat. 2021 Jan;238(1):53-62.
  26. ↑ 26.0 26.1 Kristjansson E, Treleaven J. Sensorimotor function and dizziness in neck pain: implications for assessment and management. J Orthop Sports Phys Ther. 2009 May;39(5):364-77.
  27. ↑ Treleaven J. Clinical recognition of the role of the cervical spine in signs and symptoms of altered sensorimotor control. Musculoskeletal Science and Practice. 2024 Nov 1;74:103187.
  28. ↑ Cullen KE. Research in Vestibular Science. Research in Vestibular Science. 2025 Sep 15;24(3):117-38.
  29. ↑ Popa LS, Ebner TJ. Cerebellum, Predictions and Errors. Front Cell Neurosci. 2019 Jan 15;12:524.
  30. ↑ MacDonald KC, Herman S, Katz LW. Vestibular rehabilitation following head injury. In Otologic and Lateral Skull Base Trauma 2024 Jan 1 (pp. 175-206). Elsevier.
  31. ↑ Bronstein AM, Patel M, Arshad Q. A brief review of the clinical anatomy of the vestibular-ocular connections—how much do we know?. Eye. 2015 Feb;29(2):163-70.
  32. ↑ Keshner EA, Peng G, Hain T, Peterson BW. Characteristics of head and neck stabilization in two planes of motion. In Multisensory control of posture 1995 (pp. 83-94). Boston, MA: Springer US.
  33. ↑ Angelaki DE, Cullen KE. Vestibular system: the many facets of a multimodal sense. Annu Rev Neurosci. 2008;31:125-50.
  34. ↑ Yates BJ, Bolton PS, Macefield VG. Vestibulo-sympathetic responses. Compr Physiol. 2014 Apr;4(2):851-87.
  35. ↑ Lee J, Vernon SD, Jeys P, Ali W, Campos A, Unutmaz D, Yellman B, Bateman L. Hemodynamics during the 10-minute NASA Lean Test: evidence of circulatory decompensation in a subset of ME/CFS patients. J Transl Med. 2020 Aug 15;18(1):314.