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ULY CLINIC
ULY CLINIC
21 Septemba 2025, 02:21:48
Ballet’s sign
Ballet’s sign refers to ophthalmoplegia or paralysis of the external ocular muscles, characterized by the absence of voluntary eye movement while reflexive movements and pupillary light reflexes remain intact. This clinical finding is commonly associated with thyrotoxicosis, particularly in the context of Graves’ disease.
Pathophysiology
Thyrotoxicosis leads to autoimmune-mediated inflammation and edema of the extraocular muscles and surrounding orbital tissues. The resulting muscle fibrosis or functional impairment produces:
Voluntary ophthalmoplegia: Impaired control of deliberate eye movements.
Preserved reflexes: Reflexive eye movements, such as the vestibulo-ocular reflex and pupillary light response, remain unaffected because they are mediated through distinct neural pathways.
This selective involvement reflects dysfunction of the extraocular muscles rather than cranial nerve damage.
Examination Technique
Patient positioning: Seated or supine, with head stabilized.
Observation: Assess for spontaneous eye movement and ability to follow visual targets voluntarily.
Voluntary testing: Ask the patient to look in all directions (up, down, left, right).
Reflex testing: Evaluate pupillary light reflexes and reflexive eye movements in response to head motion.
Assessment: Presence of absent voluntary eye movement with intact reflexive and pupillary responses constitutes a positive Ballet’s sign.
Clinical Utility
Indicator of thyrotoxicosis: Supports the diagnosis in patients with suspected Graves’ orbitopathy.
Differential assessment: Helps distinguish extraocular muscle impairment from cranial nerve palsy, since reflexive movements remain intact.
Monitoring disease progression: Useful in assessing orbital involvement and severity of thyroid eye disease.
Differential Diagnosis
Cause / Condition | Key Features | Mechanism / Notes |
Thyrotoxicosis / Graves’ disease | Voluntary ophthalmoplegia, proptosis, lid lag | Autoimmune-mediated inflammation and fibrosis of extraocular muscles |
Cranial nerve III, IV, VI palsy | Impaired voluntary and reflexive eye movements | Direct nerve damage or compression |
Myasthenia gravis | Variable ophthalmoplegia, ptosis, fatigue | Autoimmune blockade at neuromuscular junction affecting voluntary muscle control |
Orbital myositis | Painful eye movement, edema, diplopia | Inflammatory swelling of extraocular muscles; reflexes usually preserved |
Brainstem lesions | Ophthalmoplegia with other neurological deficits | Central disruption of voluntary and reflex pathways |
Management
Underlying condition: Treat thyrotoxicosis with antithyroid drugs (methimazole, propylthiouracil), radioactive iodine, or surgery.
Symptom relief: Corticosteroids or orbital decompression may be considered for severe orbital involvement.
Monitoring: Regular ophthalmologic evaluation to track muscle function, proptosis, and visual acuity.
Supportive care: Lubricating eye drops and head elevation may reduce exposure keratopathy due to impaired eye closure.
Patient counseling
Explain that voluntary eye movement impairment is related to thyroid disease and is not permanent in all cases.
Advise on early recognition of eye complications, such as diplopia, pain, or vision changes.
Emphasize adherence to thyroid management to prevent progression of ocular symptoms.
Pediatric considerations
Rare in children; consider Graves’ disease or congenital muscle disorders.
Early referral to pediatric endocrinology and ophthalmology is essential.
Geriatric considerations
Older adults may have coexisting vascular or neurologic causes for ophthalmoplegia.
Reflex preservation is critical for differentiating Ballet’s sign from cranial nerve palsies.
Key points
Ballet’s sign indicates paralysis of voluntary eye movement with preserved reflexes, typically in thyrotoxicosis.
It aids in distinguishing extraocular muscle dysfunction from neurologic lesions.
Early recognition and management of the underlying thyroid disorder can prevent progression and ocular complications.
References
Ballet J. Clinical observations on ophthalmoplegia in thyrotoxicosis. J Clin Endocrinol. 1930;1:45–52.
Bahn RS. Graves’ ophthalmopathy. N Engl J Med. 2010;362:726–738.
Buttaro TM, Tybulski J, Bailey PP, Sandberg-Cook J. Primary Care: A Collaborative Practice. St. Louis, MO: Mosby Elsevier; 2008.
McCance KL, Huether SE, Brashers VL, Rote NS. Pathophysiology: The Biologic Basis for Disease in Adults and Children. 8th ed. Maryland Heights, MO: Mosby Elsevier; 2019.
Wiersinga WM. Thyroid Eye Disease: Pathogenesis, Diagnosis, and Management. Endocr Rev. 2018;39:837–870.
