Síndrome de Horner agudo secundario a mononucleosis infecciosa por virus de Epstein Barr / Acute Horner syndrome secondary to glandular fever due to Epstein Barr virus infection

Presentamos el caso clínico de una mujer de 47 años que consultó por miosis y ptosis del ojo izquierdo cuyo inicio coincidió, 15 días antes, con un episodio de mononucleosis infecciosa con serología positiva para virus de Epstein-Barr. Se realizaron test con colirios de apraclonidina al 0,5% y fenilefrina al 1%, que apoyaron el diagnóstico de síndrome de Horner(SH) izquierdo posganglionar. En el momento agudo se practicó una angiografía por resonancia magnética que descartó disección carotídea, pero evidenció una imagen de arrosariamiento de la arteria carótida interna izquierda a lo largo de su trayecto extracraneal paravertebral compatible con inflamación del tejido linfático de la capa adventicia de la arteria. Una semana más tarde la ecografía Doppler de troncos supraaórticos con la que se completó el estudio mostraba una imagen compatible con disección de la arteria carótida interna bilateral. Ante un caso de SH posganglionar la primera causa a descartar por su gravedad, y por ser una entidad más ampliamente descrita como etiología del SH de 3.ª neurona, es la disección carotídea. Sin embargo, con este caso ponemos de manifiesto que no siempre se puede llegar a un diagnóstico certero. Asimismo, describimos la inflamación del tejido linfático carotídeo como posible etiología de una lesión de la cadena simpática cervical como causa infrecuente de SH posganglionar (AU)

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 (AU)

Horner syndrome in glandular fever: a case report.

OBJECTIVE: This study aimed to present and discuss the case of a patient with known glandular fever who presented with Horner syndrome. CASE REPORT: A 35-year-old patient with known glandular fever developed acute unilateral Horner syndrome, a previously undescribed complication of this common illness. Magnetic resonance imaging and magnetic resonance angiography showed that enlarged intra-carotid sheath lymphoid tissue was likely to be the underlying cause of sympathetic nerve disruption. The case is described, the anatomy of the sympathetic chain is discussed and possible alternative pathophysiological mechanisms are reviewed. CONCLUSION: This is the first report in the worldwide literature of Horner syndrome arising as a result of compression from enlarged lymph nodes in glandular fever.

[Acute myelitis of an unusual cause in a child: the lymphocytic choriomeningitis virus]. / Les myélites aiguës de l'enfant, à propos d'une cause rare: le virus de la chorioméningite lymphocytaire.

UNLABELLED: Acute transverse myelitis is a rare disorder in childhood. It usually occurs as a post-infectious disease, but a precise infectious agent is identified in only 20% of cases. OBSERVATION: The diagnosis of acute transverse myelitis was made in a 5.5-year-old girl who initially presented with left Claude-Bernard-Horner syndrome and meningitis. A few days later, motor and sensory tetraparesia with bladder dysfunction was observed. Magnetic resonance imaging showed a diffuse lesion in the medulla, with a hypersignal in the T2 and a hyposignal in the T1 sequences. Serum analysis showed the presence of a viral infection due to the lymphocytic choriomeningitis (LCM) virus. The outcome was marked by complete recovery of the sensorimotor deficit, but a persistence of the left Claude-Bernard-Horner syndrome. CONCLUSION: In rare cases, the LCM virus is responsible for myelitis. In the present case, the Claude-Bernard-Horner syndrome was secondary to the cervico-medullary lesion. Recent reports in the literature have been discussed, in particular as regards the use of immunomodulatory therapy, which clearly improves patient prognosis.

Horner's syndrome associated with mononeuritis multiplex due to cytomegalovirus as the initial manifestation in a patient with AIDS.

We report on a 60-year-old male with AIDS who presented Horner's syndrome that was associated with mononeuritis multiplex due to cytomegalovirus (CMV) infection. This is the first case who presented Homer's syndrome in the course of AIDS. Horner's syndrome associated with mononeuritis multiplex in this patient was the initial manifestation without any opportunistic infections. Since Horner's syndrome and mononeuritis multiplex in the present case were both improved by ganciclovir, it is important to consider CMV infection when Horner's syndrome or mononeuritis multiplex is observed in immunocompromised patients, such as those with HIV-1 infection or AIDS, even if they do not show any other opportunistic infections.

[Horner's syndrome secondary to ophthalmic herpes zoster]. / Síndrome de Horner secundario a herpes zoster oftálmico.

INTRODUCTION: Ophthalmoparesias is a frequent complication of ophthalmic herpes zoster. It occurs in 31% of all cases. However, the presence of Horner's syndrome during viral reactivation is a rarity which has only been previously described on two occasions, and never associated with cranial nerve involvement. CLINICAL CASE: We describe a patient with the first case of Horner's syndrome secondary to ophthalmic herpes zoster, with simultaneous, homolateral lesions of the third and sixth cranial nerves. Clinical evaluation, the course of the disorder, negative magnetic resonance studies and tests with cocaine and foledrin eye drops confirmed the presence of a post-ganglionar sympathetic lesion, probably situated in the ipsilateral cavernous sinus. CONCLUSIONS: Ophthalmoparesias as a complication of ophthalmic herpes zoster may have various origins. Diffusion of viral particles from the Gasserian ganglion and branches of the trigeminal nerve to adjacent structures, muscles, nerves and vessels, is the mechanism often mentioned. Presence of a simultaneous sympathetic lesion is very rare and of unknown pathology. However, it is probable that the origin of the lesion of the vegetative fibres is the same as that of the sensory or motor fibres, and adjacent inflammatory process caused by the virus extending. We analyze the factors involved in the low incidence of this association.