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Antecedentes: El bloqueo neuroaxial obstétrico se emplea frecuentemente durante el trabajo de parto; sin embargo, como en todo procedimiento se han reportado complicaciones, dentro de las cuales se encuentra el síndrome de Horner. Objetivo: Caracterizar la incidencia, fisiopatología y manejo del síndrome de Horner durante la anestesia neuroaxial. Métodos: Se realizó una revisión de literatura mediante la búsqueda de artículos relacionados con el tema en PubMed y Web of Science. Resultados: La incidencia del síndrome de Horner tras bloqueo neuroaxial es muy variable siendo mayor en casos de cesárea que durante trabajo de parto (4% vs 0,4%-1,3%). Factores que promueven el esparcimiento cefálico del anestésico, la sensibilidad neuronal incrementada, los cambios fisiológicos y anatómicos inducidos por el embarazo, y en algunos casos el mal posicionamiento del catéter, explicarían esta asociación. La mayoría de veces se trata de un fenómeno benigno el cual se resuelve espontáneamente en menos de 4 horas; no obstante, se debe monitorizar la aparición de inestabilidad hemodinámica o sintomatología atípica que obliguen a ampliar los estudios diagnósticos y/o interrumpir el anestésico. Background: Obstetric neuraxial block is often used during labor; however, as in all medical procedures, complications have been reported, among which is Horner’s syndrome. Objective: Characterize the incidence, pathophysiology and management of Horner’s syndrome during neuraxial anesthesia. Methods: A review of literature was conducted by searching articles related to the subject in PubMed and Web of Science. Results: The incidence of Horner’s syndrome after neuraxial block is very variable being higher in cases of cesarean section than during labor (4% vs 0.4%-1.3%). Factors that promote cephalic spread of the anesthetic, increased neuronal sensitivity, physiological and anatomical changes induced by pregnancy, and in some cases poor positioning of the catheter, explain this association. Most of the time it is a benign phenomenon which resolves spontaneously in less than 4 hours; nevertheless, the onset of hemodynamic instability or atypical symptoms must be monitored, which obliges to expand the diagnostic studies and/or interrupt the anesthetic.

Purpose: To evaluate the clinical features of pediatric patients with acute-onset, unilateral transient acquired blepharoptosis. Methods: In this retrospective study, the clinical records of patients between April 2015 and June 2020 were reviewed for evaluation of demographic features, accompanying neurological and ophthalmologic manifestations, symptom duration, etiological cause, and imaging findings. Patients with congenital and acquired blepharoptosis with chronic etiologies were excluded. Results: Sixteen pediatric patients (10 boys and 6 girls) with acquired acute-onset unilateral transient blepharoptosis were included in this study. The patients’ mean age was 6.93 ± 3.16 years. The most commonly identified etiological cause was trauma in 7 patients (43.75%) and infection (para-infection) in 5 patients (31.25%). In addition, Miller Fisher syndrome, Horner syndrome secondary to neuroblastoma, acquired Brown’s syndrome, and pseudotumor cerebri were identified as etiological causes in one patient each. Additional ocular findings accompanied blepharoptosis in 7 patients (58.33%). Blepharoptosis spontaneously resolved, without treatment, in all the patients, except those with Miller Fisher syndrome, neuroblastoma, and pseudotumor cerebri. None of the patients required surgical treatment and had ocular morbidities such as amblyopia. Conclusion: This study demonstrated that acute-onset unilateral transient blepharoptosis, which is rare in childhood, may regress without the need for surgical treatment in the pediatric population. However, serious pathologies that require treatment may present with blepharoptosis. RESUMO Objetivo: Avaliar as características clínicas de pacientes pediátricos com blefaroptose adquirida unilateral, transitória e de início agudo. Métodos: Neste estudo retrospectivo, foram revisados prontuários clínicos entre abril de 2015 e junho de 2020. Os pacientes foram avaliados em termos de características demográficas, manifestações neurológicas e oftalmológicas associadas, duração dos sintomas, etiologia e achados de imagem. Foram excluídos pacientes com blefaroptose congênita e com blefaroptose adquirida de etiologia crônica. Resultados: Foram incluídos neste estudo 16 pacientes pediátricos (10 masculinos e 6 femininos) com blefaroptose adquirida transitória unilateral de início agudo. A média de idade dos pacientes foi de 6,93 ± 3,16 anos. As causas etiológicas mais comumente identificadas foram trauma em 7 pacientes (43,75%) e infecção (casos parainfecciosos) em 5 pacientes (31,25%). Além disso, a síndrome de Miller-Fisher, a síndrome de Horner secundária a neuroblastoma, a síndrome de Brown adquirida e pseudotumor cerebral foram determinados como causas etiológicas em um paciente cada uma. Achados oculares adicionais estavam associados à blefaroptose em 7 pacientes (58,33%). Foi observada a resolução espontânea da blefaroptose, sem tratamento, em todos os pacientes, exceto nos pacientes com síndrome de Miller-Fisher, neuroblastoma e pseudotumor cerebral. Nenhum paciente precisou de tratamento cirúrgico. Morbidades oculares, como ambliopia, não foram encontradas em nenhum paciente. Conclusão: Este estudo demonstrou que a blefaroptose transitória unilateral de início agudo, rara na infância, pode regredir sem a necessidade de tratamento cirúrgico na população pediátrica. No entanto, também não deve ser esquecido que patologias graves que requerem tratamento podem se apresentar com blefaroptose.

El síndrome de Horner causa ptosis, miosis y anhidrosis como resultado de una lesión en la vía simpática a nivel de cualquiera de sus tres neuronas de un largo recorrido, siendo muy poco frecuente a nivel central. Presentamos un caso clínico y realizamos una revisión bibliográfica del síndrome de Horner central a nivel subtalámico en un paciente que padece CADASIL, una rara enfermedad hereditaria que provoca infartos subcorticales y leucoencefalopatía. Horner syndrome causes ptosis, miosis, and anhidrosis due to a long-distance injury to the sympathetic pathway at the level of any of its three neurons, being very rare at the central level. We present a clinical case and carry out a bibliographic review of central Horner syndrome at the subthalamic level in a patient suffering from CADASIL, is a rare hereditary disease that causes subcortical infarcts and leukoencephalopathy. Medicina

Background: Thoracic paravertebral block can provide analgesia for unilateral chest surgery and is associated with a low complication rate. Horner syndrome also referred to as oculosympathetic paresis, is a classic neurologic constellation of ipsilateral blepharoptosis, pupillary miosis, and facial anhidrosis resulting from disruption of the sympathetic pathway supplying the head, eye, and neck. Case report: We present a patient with an ipsilateral transient Horner syndrome after ultrasound guided single shot of 15 mL 0.25% levobupivacaine for thoracic paravertebral block at T5–6 level. Conclusions: It should be kept in mind that even a successful ultrasound guided single shot thoracic paravertebral block can be complicated with Horner syndrome due to unpredictable distribution of the local anesthetic. Resumo: Justificativa: O bloqueio paravertebral torácico pode proporcionar analgesia para cirurgia torácica unilateral e está associado a um baixo índice de complicações. A síndrome de Horner (também denominada paralisia oculossimpática) é uma constelação neurológica clássica de blefaroptose ipsilateral, miose pupilar e anidrose facial devido a distúrbio da via simpática que fornece inervação para a cabeça, olhos e pescoço. Relato de caso: Apresentamos o caso de um paciente com síndrome de Horner transitória ipsilateral após a administração de injeção única de 15 mL de levobupivacaína a 0,25% para bloqueio paravertebral torácico ao nível de T5-6 guiado por ultrassom. Conclusões: Devemos considerar que mesmo um bloqueio paravertebral torácico bem-sucedido com a administração de injeção única e guiado por ultrassom pode ser complicado com a síndrome de Horner devido à distribuição imprevisível do anestésico local. Keywords: Horner's syndrome, Paravertebral block, Video assisted thoracic surgery, Palavras-chave: Síndrome de Horner, Bloqueio paravertebral, Cirurgia torácica videoassistida

Presentamos el caso de una mujer de 25 años que consulta por dolor en miembro superior izquierdo de inicio súbito. La isquemia arterial periférica aguda es la interrupción brusca del aporte sanguíneo a una extremidad, caracterizado por la aparición de dolor intenso, palidez, frialdad cutánea, impotencia funcional, junto con ausencia de pulsos distales. Se trata de una urgencia vital que requiere tratamiento precoz de permeabilización de la arteria afectada. El diagnóstico de isquemia aguda se basa en la historia clínica y la exploración física. La gravedad del cuadro estará determinada por el grado de obstrucción, velocidad de instauración, localización y la existencia de circulación colateral. El síndrome de Horner (oculo-simpatoparesis) consiste en la clásica triada de ptosis palpebral, miosis pupilar y anhidrosis facial ipsilateral. El síndrome resulta tras la interrupción de la inervación simpática del ojo y de los anexos oculares a diferentes niveles, siendo una complicación poco frecuente de la cirugía cervical. We present the case of a 25-year-old woman with sudden onset pain in upper extremity. Acute peripheral arterial ischemia is the sudden interruption of the blood flow to an extremity, characterized by the appearance of intense pain, pallor, skin coldness, functional impairment, together with absence of distal pulses. It is a life threatening emergency that requires early treatment of revascularization of the affected artery. The diagnosis of acute ischemia is based on clinical history review and physical examination. The severity of the clinical picture will be determined by the degree of obstruction, speed of onset, location, and presence of collateral circulation. Horner syndrome (oculosympathetic paresis) is characterized by the classic triad of palpebral ptosis, pupillary miosis and ipsilateral facial anhidrosis. The syndrome results from the interruption of sympathetic innervation to the eye and adnexa at various levels. It is a rare complication of cervical surgery.

Epidural analgesia is assumed to be the technique of choice for the relief of pain in labor. Multiple adverse neurological effects have been reported, one of which is the so-called Horner syndrome (ptosis, myosis, anhidrosis). Its evolution is usually benign and does not require specific management, except clinical monitoring for the more than probable cephalic spread of local anesthetic. Most of the cases that exist in the literature are isolated; in our work we present a series of 3 clinical cases and review the pathogenesis and management in the obstetric patient. La analgesia epidural supone la técnica de elección para el alivio del dolor del parto. Se han descrito múltiples efectos adversos a nivel neurológico, uno de ellos es el llamado Síndrome de Horner (ptosis,miosis, anhidrosis), suele presentar evolución benigna y no requiere manejo especifico, salvo vigilancia clínica por la más que probable difusión cefálica del anestésico local. La mayor parte de los casos existentes en la literatura son aislados, en nuestro trabajo presentamos una serie de 3 casos clínico y repasamos su etiopatogenía y manejo en la paciente obstétrica.

At times in clinical neurology, the identification of a subtle clinical or radiological sign can lead to prompt diagnosis of a very rare or difficult case. We report on a patient who presented with untreatable headache and unilateral ptosis. Computed tomography (CT) scan of the head did not reveal any structural cause. Magnetic resonance angiogram showed absence of left internal carotid artery, which was eventually confirmed by a catheter angiography. Reviewing the case, it emerged that a feature on the initial CT scan "bone window" would have confirmed the diagnosis, had it been searched for: the underdeveloped carotid canal, which is a consequence and a marker of internal carotid artery agenesis. Em algumas circunstâncias, o reconhecimento de um sinal clínico ou radiológico sutil pode tornar simples o diagnóstico de um caso raro ou muito difícil em neurologia clínica. Relatamos o caso de uma paciente que apresentava cefaleia intratável e ptose palpebral unilateral. A tomografia computadorizada (TC) de crânio não permitiu identificar nenhuma causa estrutural. A ressonância magnética evidenciou ausência da artéria carótida interna esquerda, posteriormente confirmada por arteriografia convencional. Retrospectivamente, descobriu-se que um dado da janela óssea da primeira TC de crânio teria confirmado o diagnóstico, tivesse ele sido pesquisado: o hipodesenvolvimento do canal carotídeo, que é uma consequência e um marcador de agenesia da artéria carótida interna.

Se describe un caso de síndrome de Horner contralateral luego de bloqueo de ganglio estrellado. Se trata de un varón de 56 años con diagnóstico de síndrome doloroso regional complejo tipo II en miembro superior derecho quien posterior a la aplicación de anestésico local guiado por ecografía en proximidad al ganglio estrellado derecho presenta síndrome de Horner izquierdo. El síndrome de Horner contralateral a un bloqueo de ganglio estrellado es una entidad de ocurrencia supremamente rara, en nuestra práctica se presentó uno de los pocos casos reportados en la literatura, de interés para la comunidad científica. We describe a case of contralateral Horner's syndrome following stellate ganglion block. A 56 years old man diagnosed with complex regional pain syndrome type II in right upper arm, who developed after the application of local anesthetic guided by ultrasound in proximity to the right stellate ganglion presented left Horner's syndrome. The contralateral Horner's syndrome following stellate ganglion block is a rare entity. In our practice occurred one of the few cases reported in the literature, which is of great interest for the medical community.

[ES]Se expone el caso de un paciente que, tras la realización de una amigdalectomía complicada por sangrado, presenta un cuadro de ptosis, miosis y enoftalmos junto con dolor ocular ipsilateral al lado del sangrado. El cuadro se circunscribe dentro del denominado síndrome de Horner y constituye una complicación poco frecuente de las amigdalectomías. [EN] There is exposed the case of a patient who, after the accomplishment of a tonsillectomy complicated for bled, presents ptosis, miosis and enoftalmos with ipsilateral ocular pain next to the bledding. The symptoms were inside Horner's syndrome called and constitutes a slightly frequent complication of tonsillectomy.

Casos clínicos: Se presentan cuatro casos: dos varones adultos con Síndrome de Horner clínico, diagnosticados mediante el test de apraclonidina 0,5% y el test de cocaína 4% respectivamente, y dos niños con anisocoria de los cuales, en uno de ellos el Síndrome de Horner se confirma con apraclonidina 1% y en otro el test de apraclonidina 1% descarta el Síndrome de Horner y el test de pilocarpina 0,125% confirma una pupila tónica de Adie. Discusión: La apraclonidina al 1% y al 0,5% pueden orientar el diagnóstico de Síndrome de Horner, siendo más fáciles de obtener que la cocaína. Case reports: We present four cases: two males with Horner Syndrome, who were diagnosed by means of apraclonidine 0.5% and cocaine 4% tests respectively. Two children with anysocoria, one of whom had Horner Syndrome confirmed with apraclonidine 1% and the other, in whom an apraclonidine test ruled out this syndrome but in whom pilocarpine 0.125% confirmed Adie’s pupil. Discussion: Apraclonidine drops (1% and 0.5%) may aid in the diagnosis of Horner Syndrome and are easier to obtain than cocaine.

Introducción: El bupropión se usa como deshabituante del hábito tabáquico. Puede provocar alteraciones visuales, pero hasta el momento no se había comunicado la aparición de anisocoria. Caso clínico: Mujer de 40 años con migrañas, en tratamiento con bupropión presentó midriasis monocular. Instilando cocaína al 5%, ambas pupilas dilataron de la misma manera. Con pilocarpina 0,025% ambas pupilas contrajeron de forma similar. La anisocoria cesó al suspender el tratamiento. Discusión: El bupropión es inhibidor selectivo de la recaptación de noradrenalina y dopamina. La vía pupilar simpática podría tener una cierta hipersensibilidad en pacientes migrañosos por denervación que podría estimularse con el tratamiento con estos fármacos, lo que explicaría la anisocoria. Por otra parte el estímulo midriático del bupropion podría haber desenmascarado una anisocoria fisiológica. Introduction: Bupropion is used to help people stop smoking. This drug can cause visual alterations but, up to now, its use was not associated with anisocoria. Case report: A 40 year-old woman with a personal history of migraines, presented with monocular mydriasis during treatment with bupropion. Both pupils dilated equally after a 5% cocaine test, and constricted equally after a 0.025% Pilocarpine test. The anisocoria disappeared after the treatment with bupropion was withdrawn. Discussion: Bupropion inhibits neural uptake of norepinephrine and dopamine. Patients with migraine could have a minor unilateral sympathetic pupillary deficit. This deficit could cause hypersensitivity in the oculosympathetic pathway that could be stimulated with bupropion treatment. This feature could explain the mydriasis in our patient. Another explanation could be that bupropion could unmask a physiological anisocoria.

Caso clínico: Se describe un caso documentado de síndrome de Horner como manifestación de un traumatismo cervical. Un varón de 33 años se presentó con ptosis y miosis derecha después de una lesión cervical incisa. Las imágenes de tomografía axial computerizada del cuello demostraron un hematoma a tensión con deformidad y estenosis de la tráquea. Discusión: Un traumatismo cervical puede interrumpir la vía simpática y cuando se realiza la exploración el síndrome de Horner puede ser la manifestación de un proceso potencialmente mortal. Case report: We present a case of Horner’s syndrome in a 33-year-old man who presented with ptosis and right pupil miosis after cervical trauma. Computed tomography revealed a tender haematoma in the neck, which was producing tracheal deformity and stenosis. Discussion: Cervical trauma may damage the sympathetic pathway and result in Horner’s syndrome. This may be a manifestation of a life-threatening condition.

A síndrome de Claude Bernard-Horner apresenta várias etiologias, ocorre por interrupção do estímulo nervoso em qualquer ponto do trajeto do nervo e pode ser intra ou extratorácica. É relatado um caso dessa síndrome causado por empiema pleural septado, localizado em região paravertebral, no terço superior do hemitórax direito. O paciente foi submetido à toracotomia para drenagem da cavidade pleural. A evolução foi satisfatória, com regressão do quadro infeccioso, expansão pulmonar e remissão da síndrome. Claude Bernard-Horner syndrome presents various etiologies and occurs as the direct result of interrupted nerve signaling at any point along the nerve trajectory, be it intrathoracic or extrathoracic. Herein, we report a case of Claude Bernard-Horner syndrome caused by loculated pleural empyema located in the paravertebral region of the upper third of the right hemithorax. The patient was submitted to thoracotomy in order to drain the infected fluids. The end result was satisfactory, including resolution of the infection, pulmonary expansion, and remission of the syndrome.

Background: Horner syndrome (HS) or oculosympathetic paresis is caused by the interruption of the sympathetic nervous pathway at any point from the brain to the eye. Clinical signs include miosis, upper lid ptosis, anhydrosis of the face, enophtalmus and iris heterochromia. Although it is usually a benign condition, the proximity of the sympathetic pathway to carotid arteries, thoracic structures and central nervous system requires a careful ruling out of life-threatening conditions. Objective: To describe the utility of clinical history and neurological examination in the assessment of the etiology and localization of lesions causing Horner syndrome. Methods: Review of cases presented at the Neurology Unit of Catholic University of Chile during 2003-2004. Results: 5 patients were identified with an age distribution of 2-72 months. 4 cases were congenital and 1 acquired. Neurological signs allowed to classify the cases of HS in peripheral (4) and central (1). Hemianhydrosis suggested that 3 cases were preganglionic and 2 postganglionic. Conclusions: History and neurological examination in cases of HS is usually enough to define the localization of the lesion. Further laboratory evaluation is unnecessary.

Introducción: El síndrome de Horner (SH) u oculosimpaticoparesia es causado por la interrupción de la vía simpática (VS) que va desde el cerebro hasta el ojo. Los signos clínicos son miosis, ptosis, enoftalmos, heterocromía del iris y hemianhidrosis facial ipsilateral, en su forma completa. Generalmente es benigno pero la proximidad arterias carotídeas, órganos torácicos y cerebro nos obliga a descartar patologías potencialmente riesgosas. Objetivo: Describir la utilidad de la historia clínica y el examen neurológico en la evaluación de la etiología y localización de la lesión en el SH. Pacientes y Método: 5 pacientes de sexo masculino entre 2-72 meses edad controlados en Neurología infantil de la Pontificia Universidad Católica de Chile entre los años 2003-2004. Resultados: Según tiempo de aparición, 4 casos fueron congénitos y 1 caso adquirido. Los signos neurológicos acompañantes clasificaban los casos como SH periférico (4) y SH central (1). La hemianhidrosis clasificaban 3 casos como preganglionares y dos postganglionares Conclusión: En niños con SH la anamnesis, el análisis de la signología propia y asociada del SH nos ayudan a localizar la lesión y reducen una extensa evaluación sistémica Background: Horner syndrome (HS) or oculosympathetic paresis is caused by the interruption of the sympathetic nervous pathway at any point from the brain to the eye. Clinical signs include miosis, upper lid ptosis, anhydrosis of the face, enophtalmus and iris heterochromia. Although it is usually a benign condition, the proximity of the sympathetic pathway to carotid arteries, thoracic structures and central nervous system requires a careful ruling out of life-threatening conditions. Objective: To describe the utility of clinical history and neurological examination in the assessment of the etiology and localization of lesions causing Horner syndrome. Methods: Review of cases presented at the Neurology Unit of Catholic University of Chile during 2003-2004. Results: 5 patients were identified with an age distribution of 2-72 months. 4 cases were congenital and 1 acquired. Neurological signs allowed to classify the cases of HS in peripheral (4) and central (1). Hemianhydrosis suggested that 3 cases were preganglionic and 2 postganglionic. Conclusions: History and neurological examination in cases of HS is usually enough to define the localization of the lesion. Further laboratory evaluation is unnecessary