%0 Case Reports
%T Acute Horner syndrome secondary to glandular fever due to Epstein Barr virus infection.
%A Schilt-Catafal MM
%A Manfreda-Domínguez L
%A Gil-Gimeno R
%A Duch-Samper AM
%A Schilt-Catafal MM
%A Manfreda-Domínguez L
%A Gil-Gimeno R
%A Duch-Samper AM
%J Arch Soc Esp Oftalmol (Engl Ed)
%V 97
%N 5
%D May 2022
%M 35526951
暂无%R 10.1016/j.oftale.2022.03.002
%X We present a clinical situation where a 47-year old female patient consulted with left partial ptosis and miosis that started, two weeks before, with an episode of glandular fever secondary to Epstein-Barr infection. Apraclonidine 0.5% and Phenylephrine 1% drop testing was performed with results consistent with suspected left Horner Syndrome (HS), with a probable postganglionic location. Magnetic Resonance Angiography (MRA) at the moment of the acute presentation did not show any image suggesting carotid arterial dissection but showed irregular narrowing of the left internal carotid artery on its paravertebral extracranial way, consistent to enlarged intra-carotid sheath lymphoid tissue. A week later, a Doppler ultrasound was performed, showing bilateral images compatible with internal carotid arterial dissection. When Postganglionar HS is suspected, the first aetiology to rule out is a carotid arterial dissection because of its potentially fatal outcome and for being a more described entity as postganglionic HS aetiology. However, it is also evidenced that a certain diagnose is not always possible. Furthermore, we describe the enlarged internal carotid artery sheath lymphoid tissue as a possible cause of sympathetic nerve disruption causing a Postganglionar HS, although not common.