Isolated Unilateral Blepharoptosis Associated with Influenza Infection

Sir, A 63-year-old male with a history of the right eye surgery (cataract extraction with intraocular lens implantation 2 years prior) presented with a 3-day history of right upper eyelid ptosis. He initially experienced cough, fatigue, malaise, rhinorrhea, fever, and chills, for which he self-administered ibuprofen (600 mg once daily) for 2 days. He reported frequently sleeping with the right side of his head resting on his outstretched hand but denied any direct ocular trauma. By the second day, his respiratory symptoms had improved; however, he developed painless right eyelid drooping, prompting medical evaluation on the third day. On presentation, his vital signs were stable. Neurological examination was unremarkable except for isolated right upper eyelid ptosis [Figure 1 and Video 1]. Ophthalmologic assessment, including fundoscopy and anterior chamber evaluation, was unremarkable. Cranial computed tomography (CT), CT angiography of the head and neck, brain magnetic resonance imaging (MRI), and orbital MRI showed no abnormalities. Laboratory investigations, including thyroid function tests, markers for giant cell arteritis, and myasthenia gravis testing, were unremarkable. He tested positive for influenza A but declined antiviral treatment with oseltamivir. The ptosis resolved completely within 30 days of symptom onset [Supplementary Material S1].Figure 1: Isolated right eyelid ptosis. (a) Primary gaze demonstrating right upper eyelid ptosis with a normal left eyelid position. (b) Activation of the levator palpebrae superioris muscle reveals a reduced margin reflex distance 1 (MRD1) in the right eye. The contralateral eyelid appears slightly retracted due to Hering's law of equal innervation, leading to apparent pseudo-ptosis of the left eye. Notably, the patient exhibits frontalis muscle activation even in primary gaze, likely as a compensatory effort to maintain eyelid elevation and prevent complete eye closure {"href":"Single Video Player","role":"media-player-id","content-type":"play-in-place","position":"float","orientation":"portrait","label":"Video 1.","caption":"","object-id":[{"pub-id-type":"doi","id":""},{"pub-id-type":"other","content-type":"media-stream-id","id":"1_qtnjwcvi"},{"pub-id-type":"other","content-type":"media-source","id":"Kaltura"}]} Blepharoptosis, or ptosis of the eyelid, is defined as an abnormal drooping of the upper eyelid. Elevation of the upper eyelid is primarily mediated by the levator palpebrae superioris (LPS) muscle, which is innervated by the oculomotor nerve (cranial nerve III). The LPS extends into a tendinous aponeurosis that inserts into the eyelid, forming the eyelid crease. Additionally, Müller's muscle, innervated by the sympathetic nervous system, contributes up to 2 mm of eyelid elevation, playing a secondary but essential role in maintaining eyelid position.[1] In our case, the patient exhibited normal levator function (12 mm), which is consistent with Horner syndrome or an aponeurotic etiology. Notably, reduced levator function is typically observed in neuropathic, myopathic, congenital, and neuromuscular causes of ptosis, distinguishing these conditions from aponeurotic and sympathetic dysfunction-related ptosis.[1] The patient's risk factors for aponeurotic ptosis include advanced age and a history of ocular surgery, as the use of a surgical speculum can contribute to eyelid damage. However, his eyelid crease margin was normal, making a purely aponeurotic etiology less likely. The most plausible explanation for his ptosis is incomplete Horner syndrome without anisocoria, supported by an apraclonidine test. Nevertheless, the possibility of an underlying aponeurotic component remains, given his history of prior ophthalmologic surgery and habitual lid rubbing. A comprehensive literature search was conducted using the PubMed (Medline) and Google Scholar databases with the search terms *ptosis* or *blepharoptosis* and *influenza*, without restrictions on language, year of publication, or article type. To the best of the authors' knowledge, no prior reports describing isolated ptosis associated with influenza have been documented in the literature. Basilious et al.[2] reported a case of unilateral ptosis following H1N1 influenza vaccination; however, the patient also exhibited ipsilateral orbital myositis affecting the superior rectus/levator complex, superior oblique, and medial rectus muscles. In another case, ptosis was observed after H1N1 influenza vaccination in a patient, who also developed cerebellar dysfunction and myelitis.[3] Notably, there are a few reports linking Miller-Fisher syndrome to influenza A infection.[4] Engelhardt et al.[5] described a pediatric patient with influenza A infection presenting with unilateral ptosis; however, neurological examination revealed concurrent ipsilateral superior rectus muscle paresis. Given the absence of orbital myositis, cerebellar findings, or other cranial neuropathies, our patient's isolated ptosis does not align with previously reported cases. While myasthenia gravis was a key differential diagnosis, serologic testing was negative, and the clinical course, including spontaneous resolution without treatment, further argued against an autoimmune etiology. Additionally, the absence of diplopia or anisocoria made an isolated oculomotor nerve palsy unlikely. This case highlights the importance of recognizing influenza A as a potential, albeit rare, trigger for transient autonomic dysfunction. While Horner syndrome is often associated with structural lesions along the oculosympathetic pathway, infectious etiologies should be considered, particularly in the setting of recent viral symptoms. The patient's complete resolution within a month without intervention suggests a self-limited process, reinforcing the role of conservative management in similar cases. Given the association between influenza and immune-mediated neurological sequelae, further research is warranted to elucidate the mechanisms linking viral infections to transient sympathetic dysfunction. Clinicians should maintain a high index of suspicion for underlying infectious triggers in cases of unexplained ptosis, particularly when initial imaging and laboratory studies are unremarkable. Declaration of patient consent The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed. Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest.