Acute Horner syndrome secondary to glandular fever due to Epstein Barr virus infection.

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.

[Silent microhemorrhages in patients with symptomatic cerebrovascular disease]. / Microsangrados silentes en pacientes con enfermedad cerebrovascular sintomática.

INTRODUCTION: T2*-weighted gradient echo MRI sequences (T2*-MRI) have made it possible to detect cerebral microhemorrhages (MH) that have been considered as subclinical but whose clinical significance is largely unknown. OBJECTIVE: To establish the frequency of MH in a sample of consecutive symptomatic cerebrovascular disease (SCD) patients, analyzing its associations with different vascular risk factors (VRF) and its clinical significance. METHODS: A total of 198 patients with SCD were consecutively examined using T2*-MRI. Preferential location of MH and associations between MH presence and MH number with VRF, previous antithrombotic treatment and SCD subtypes were analyzed. RESULTS: A total of 52.5% of our patients had MH. The highest frequency of MH was found in hemorrhagic strokes (72.2%), Transitory ischemic attack (TIA) (42.9%) being the group with the lowest frequency. According to the bivariate analysis, the factors associated with the presence of MH were elderly age (72.4+/-10.5 vs 67.7+/-12.7; p 0.004), hypertension (65.4 vs 51.1%; p 0.041), diabetes (35.6 vs 22.3 %; p 0.041) and being under antithrombotic treatment (45.2 vs 28.7 %; p 0.017). According to the multivariate analysis, elderly age (p 0.019; OR: 1.03 [1.01- 1.06]), hypertension (p 0.032; OR: 1.97 [1.06-3.65]), use of antithrombotic treatment (p 0.038; OR: 1.95 [1.04-3.65]) and having a hemorrhagic stroke (p 0.028; OR: 3.63 [1.15- 11.46]) were predictors of MH presence. CONCLUSIONS: The presence of MH is frequent among patients with SCD, this being especially elevated in patients with hemorrhagic stroke. Cerebral MHs are classically associated with VRF classically related with small vessel disease and previously taking antithrombotic treatment.