Cardiocerebral infarction presenting as Opalski Syndrome: A case report

Introduction@#Opalski Syndrome is a rare type of stroke variant presenting with signs of lateral medullary syndrome plus ipsilateral hemiparesis. A confirmed myocardial infarction simultaneously occurring with this acute ischemic stroke syndrome makes this an even more challenging case of Cardiocerebral infarction.@*Case@#The patient is a 48-year-old female, a known diabetic and asthmatic, and was seen due to a 3-day history of sudden onset of non-rotatory dizziness associated with diplopia, non-projectile vomiting, numbness of the left side of the face and lingual dysarthria. She was initially admitted in a primary hospital wherein she developed chest pain, dyspnea and diaphoresis. She was transferred and was received with findings of miosis of the left eye, rotational nystagmus, left dysmetria, decreased pain and temperature sensation on the right extremities, left central facial palsy, tongue deviation to the left side, left hemiparesis and upward Babinski on the left. We localize this lesion on the left lateral medullary area with involvement of the caudal left corticospinal tract. Hence, a clinical impression of Opalski Syndrome was made. This was confirmed with cranial MRI findings of T2/FLAIR hyperintense focus involving the left lateral aspect of the medulla. The patient’s Troponin I was also elevated and she was managed as a case of acute coronary syndrome - NSTEMI. Hence, a diagnosis of Type III Cardiocerebral infarction was made. Medical intervention was started with dual antiplatelet therapy and anticoagulation with noted clinical improvement. @*Conclusion@#This case report highlights the diagnosis of Opalski Syndrome in a patient also presenting with Cardiocerebral infarction. There should be prompt recognition of the following disease entities to have an effective treatment, avoid cardiac and neurologic sequelae, and achieve an overall favorable prognosis.

Revisão de anatomia e correlações clínicas do tronco encefálico, parte i: bulbo / Review of brain anatomy and clinical correlations, part i: medulla

O Tronco encefálico (TE) é uma estrutura singular do sistema nervoso central, pois nele passam tratos sensoriais ascendentes da medula espinal, tratos sensoriais da cabeça e do pescoço, os tratos descendentes motores originados no prosencéfalo (divisão mais rostral do encéfalo), e as vias ligadas aos centros de movimento dos olhos. Contém ainda os núcleos dos nervos cranianos e está envolvido na regulação do nível de consciência através de projeções ao prosencéfalo oriundas da formação reticular. Todas essas estruturas coexistem em um espaço muito exíguo, o que faz com que o TE seja um local muito sensível às alterações patológicas, sendo que os pacientes apresentam muitos sinais neurológicos mesmo com lesões muito pequenas nesse local. Compreender a anatomia interna do TE é essencial para o diagnóstico neurológico e a prática da medicina clínica. Outros profissionais da saúde também se beneficiam desse conhecimento para melhor manejo dos seus pacientes neurológicos. Essa revisão apresenta detalhes da anatomia macroscópica e microscópica do bulbo, bem como seus correlatos clínicos frente às lesões mais comuns dessa divisão particular do TE, conhecidas como síndromes bulbares.

The brainstem is a unique structure in the central nervous system, since it gives way to ascending sensory tracts from the spinal cord, sensory tracts from the head and neck, motor descending tracts originating from the forebrain, and the pathways connected to the eye movement centers. It also contains the cranial nerve nuclei and is involved in the regulation of consciousness levels through projections to the forebrain originating in the reticular formation. All these structures coexist in a very small space, which makes the brainstem very sensitive to pathological changes, with patients presenting several neurological symptoms even with very small brainstem lesions. Understanding the internal anatomy of the brainstem is essential for neurological diagnosis and the practice of clinical medicine. Other health professionals also benefit from this knowledge to better manage their neurological patients. This review presents detailed information on the macroscopic and microscopic anatomy of the medulla, as well as its clinical correlates in the face of the most common lesions of this particular division of the brainstem, known as medullary syndromes.

Blepharoptosis and dysarthria in a boy aged 2 years / 中国当代儿科杂志

A boy, aged 2 years and 4 months, had a sudden onset of blepharoptosis of the right eyelid, accompanied by the mouth deviated to the right side, drinking cough, nystagmus, and developmental regression. Cranial MRI showed softening lesions formed after infarction of the right dorsolateral medulla oblongata, while head CT angiography showed no imaging of the proximal part of the V4 segment of the right vertebral artery. The child was diagnosed with dorsolateral medulla oblongata syndrome and was treated with gamma globulin to regulate immune function, with mannitol to reduce neuronal edema, with low-molecular-weight heparin sodium to improve local hypercoagulation of occluded blood vessels, with hyperbaric oxygen to improve local ischemia and hypoxia and promote the recovery of brain function, and with neuromuscular electrical stimulation to promote the recovery of neuromuscular function. Before discharge, only mild right ataxia and Horner syndrome remained. This article reports the first case of infantile dorsolateral medulla oblongata syndrome and provides experience for the diagnosis and treatment of the disease.

Origin of the Posterior Inferior Cerebellar Artery over the C1 Posterior Arch / Origem da artéria cerebelar inferoposterior sobre o arco posterior de C1

Resumo The posterior inferior cerebellar artery usually arises from the intracranial segment (V4) of the vertebral artery. Despite its mean diameter of 2 mm, it usually irrigates important areas of the brain. When occluded, whether due to trauma or surgery, it may cause infarction in the brain stem and cerebellum. The present report describes a case of incidental finding of a posterior inferior cerebellar artery arising from the cervical segment (V3) of the vertebral artery, demonstrated by angiography. The findings were recorded and compared to those of earlier publications. Brief explanations regarding anatomy, vascular anomalies and embryology were provided. A literature review showed that anomalous branches of the cervical segment of the vertebral artery are infrequent andmust be known. A better understanding of anatomy and its variations enables an accurate topographic diagnosis, as well as the planning of the optimal surgical approach and therapy. Knowledge of this anatomical variation is essential because, if it is mistaken for a muscle branch and coagulated, this can cause ischemia and disabling sequelae.

Resumo A artéria cerebelar inferoposterior geralmente nasce do segmento intracraniano (V4) da artéria vertebral. Apesar de ter diâmetro médio de 2 mm, usualmente irriga áreas eloquentes do encéfalo. Quando ocluída, seja por trauma ou cirurgia, pode causar infarto no tronco encefálico e no cerebelo. Apresentamos um caso de artéria cerebelar inferoposterior com origem anômala no segmento cervical (V3) da artéria vertebral, demonstrado por angiografia. Os resultados foram registrados e comparados com os de publicações anteriores. Foram fornecidas breves explicações sobre a anatomia, anomalias vasculares e embriologia. A revisão da literatura mostrou que os ramos anômalos do segmento cervical da artéria vertebral são infrequentes e devem ser conhecidos. Uma melhor compreensão da anatomia e suas variações permite fazer um diagnóstico topográfico preciso, bem como planejar a abordagem e a terapia cirúrgicas ideais. O conhecimento dessa variação anatômica é essencial, pois, se confundida com um ramo muscular e coagulada, pode causar isquemia com sequelas incapacitantes.

Opalski Syndrome Presenting as Sensorimotor Deficits Ipsilateral to Cerebral Infarction

Opalski syndrome is a rare lateral medullary infarction variant presenting with ipsilateral motor deficits known to be caused by involvement of the post-decussating pyramidal tract. Here, we report two rare cases of Opalski syndrome presenting as ipsilateral sensorimotor deficits in cerebral infarction.

Una propuesta de clasificación del complejo arteria cerebelosa anteroinferior ­ arteria subarcuata basada en el desarrollo embriológico / A proposed classification of the anteroinferior cerebellar artery - subarcuate artery complex based on embryological development

Introducción: El recorrido del "loop subarcuato" de la arteria cerebelosa anteroinferior (ACAI) presenta múltiples variaciones que condicionan además su principal eferencia, la arteria subarcuata (ASA). El espectro de variaciones de este complejo ha sido referido en la literatura de forma inconexa y desorganizada. Material y Métodos: Se propuso una clasificación sistematizada de las variantes del complejo ACAI-ASA, basada en la interacción del hueso petroso y la ACAI en el periodo embrionario. La misma fue aplicada en una serie de pacientes estudiados mediante secuencia CISS (constructive interference in steady state) de resonancia magnética para categorizar las relaciones presentes en el ángulo pontocerebeloso (APC). Resultados: Se evaluaron 84 pacientes, incluyendo 161 APC. Todos los grados propuestos fueron identificados en la serie evaluada. Las proporciones encontradas en la gradación propuesta se mantuvieron en el rango de las publicaciones aisladas. Conclusión: La clasificación propuesta para el complejo ACAI-ASA permitió distinguir y objetivar consistentemente el espectro de variaciones.

Introduction: The pathway of the anterior inferior cerebellar artery's (AICA) "subarcuate loop" can vary extensively. This variability also affects its main branch, the subarcuate artery (SAA). The spectrum of variations observed with this combination of vessels is inadequately described in the literature. Methods and Materials: A systematized classification system for AICA-SAA complex variants was proposed, based upon interactions between the petrosal bone and the AICA in embryos. This classification scheme then was applied to a series of patients assessed by magnetic resonance CISS (constructive interference in steady state) sequences, to categorize the cerebellopontine angle (CPA) relationships. Results: Eighty-four patients were evaluated, encompassing 161 CPA. All the proposed grades were identified in the evaluated series. The proportions found with the proposed gradation system were within the range of previous publications. Conclusions: The AICA-SAA complex classification system that we proposed allowed for consistently distinguishing and objectifying the spectrum of variations seen in the subarcuate loop.

Accidente cerebrovascular bulbar lateral con trayecto extracraneal de la arteria cerebelosa póstero-inferior / Lateral medullary stroke with extracranial course of the postero- inferior cerebellar artery

Presentamos dos casos de accidente cerebrovascular en sujetos con trayecto extracraneal de la arteria cerebeloso póstero-inferior. Caso 1: varón de 21 años, quien presentó ataxia y dismetría derecha luego de un traumatismo cervical en un partido de rugby. Caso 2: mujer de 56 años, quien inició con vértigo y hemiparesia izquierda luego de esfuerzo físico intenso. En ambos casos, los estudios angiográficos mostraron un trayecto extracraneal de la arteria cerebelosa póstero-inferior. Este vaso raramente se origina por debajo del foramen magno, en relación cercana con las primeras tres vértebras cervicales y la articulación atlanto-axial. En este nivel, está expuesta a daño mecánico causante de disección, como por ejemplo trauma directo, manipulación cervical abrupta o extensión cefálica prolongada. Por lo tanto, en pacientes con accidente cerebrovascular de región lateral de bulbo y trayecto extracraneal de la arteria cerebelosa póstero-inferior se debería considerar esta asociación.

We present two cases of lateral medullary stroke in subjects with extracranial trajectory of the postero-inferior cerebellar artery. Case 1: a 21-year-old male who presented ataxia and right dysmetria after cervical trauma in a rugby match. Case 2: 56-year-old woman, who started with vertigo and left hemiparesis after intense physical effort. In both cases, the angiographic studies showed an extracranial trajectory of the posterior inferior cerebellar artery. This vessel rarely originates below the foramen magnum, in close relationship with the first three cervical vertebrae and the atlanto-axial joint. At this level, it is exposed to mechanical damage causing dissection, such as direct trauma, abrupt cervical manipulation or prolonged cephalic extension. Therefore, this association should be considered in patients with stroke of the lateral region of the bulb and extracranial trajectory of the posterior-inferior cerebellar artery.

A Case of Posterior Inferior Cerebellar Artery Infarction after Cervical Chiropractic Manipulation / 대한신경손상학회지

We describe the case of a patient who had infarction of the posterior inferior cerebellar artery (PICA) after a chiropractic cervical manipulation. A 39-year-old man visited the emergency room with signs of cerebellar dysfunction, presenting with a 6-hour history of vertigo and imbalance. Two weeks ago, he was treated by a chiropractor for intermittent neck pain. At the time of admission, brain computed tomography, magnetic resonance imaging, and angiography revealed an acute infarction in the left PICA territory and occlusion of the extracranial vertebral artery (VA; V1/2 junction) as a result of the dissection of the VA. Angiography revealed complete occlusion of the left PICA and arterial dissection was shown in the extracranial portion of the VA. He was treated with antiplatelet therapy. Three weeks later, he was discharged without any sequelae. The possibility of VA dissection should be considered at least once in patients presenting with cerebellar dysfunctions with a recent history of chiropractic cervical manipulation.

Stellate ganglion block for the treatment of intractable hiccups: A case report

Hiccups are an involuntary contraction of the diaphragm that may repeat several times per minute. In general, hiccups are very common, transient, and self-limited. However, if the condition persists longer than days or months, it impacts a patient's quality of life. Pharmacologic and non-pharmacologic methods are used for the treatment of persistent or intractable hiccups. Nerve block and stimulation have been shown to be effective through neural pathway interruption or stimulation of the hiccup reflex arc. Stellate ganglion block (SGB) is an injection of local anesthetic adjacent to a group of nerves in the neck known as the stellate ganglion. The authors report a case of SGB as an effective treatment for a patient with intractable hiccups resulting from right lateral medullary syndrome.

Síndrome de Opalski / Opalski síndrome

El síndrome de Opalski es la presencia de hemiplejia ipsilateral asociada con síntomas del síndrome medular lateral. Diferentes estudios confirman que el infarto en tales casos ocurre a un nivel más bajo que el encontrado en el síndrome de Wallenberg. Se localiza debido a la presentación característica, el territorio único de suministro de sangre y el área pequeña de lesión. La implicación del tracto corticoespinal ipsilateral después de la decusación piramidal, o compresión de la decusación, podrían causarlo. Presentamos el caso de una mujer de 71 años que desarrolló hemiplejia izquierda y dificultad repentina para caminar, acompañada de diplopía, cefalea, disfagia y vómito recurrente. La imagen de resonancia magnética demostró un infarto lateral medular izquierdo. La angiografía reveló estenosis distal y proximal de la arteria vertebral izquierda e hipoplasia de la arteria vertebral derecha.

Opalski syndrome is the presence of ipsilateral hemiplegia which is associated with symptoms of a lateral medullary syndrome. Studies confirm that the infarction, in such cases, occurs at a lower level than that found in Wallenberg syndrome. This syndrome is localized because of characteristic presentation, the unique territory of blood supply and small area of lesion. The involvement of the ipsilateral corticospinal tract after the pyramidal decussation, or compression of the decussation, could cause the syndrome. We present a case of Opalski syndrome in a 71-year-old woman developed left hemiplegia and sudden difficulty for walking, accompanied by diplopia, headache, dysphagia and recurrent vomiting. Magnetic resonance image demonstrated a left lateral-medullary infarction. Angiography revealed distal and proximal stenosis of left vertebral artery and hypoplasia of right vertebral artery.

Síndrome de Opalski, una variante del síndrome de Wallenberg: reporte de caso y revisión de la literatura / Opalski Syndrome, a variant of Wallenberg Syndrome: Case report and literature review

RESUMEN Se presenta un caso local de la variante de Opalski, del síndrome medular lateral (síndrome de Wallenberg) y se hace una revisión de la literatura sobre los síntomas de este cuadro clínico, así como las posibles razones que explican esta modificación en la expresión clínica. La variante de Opalski fue descrita en 1948, ochenta y nueve años después de la descripción original del síndrome por Adolf Wallenberg, su principal característica es la presencia de hemiparesia o hemiplejía del cuerpo del mismo lado de la lesión del bulbo raquídeo. La etiología es vascular en la mayoría de casos, por obstrucción de la arteria cerebelosa postero-inferior o de los ostium de vasos penetrantes que se originan en la arteria. No hay estudios que reporten la incidencia exacta de este cuadro clínico a nivel mundial, sin embargo, su presentación no es tan infrecuente. Lo más interesante al analizar cada caso, es que los hallazgos semiológicos son una muestra de la profunda organización del sistema nervioso.

SUMMARY A clinical case of the Opalski variant of the lateral medullary syndrome (Wallenberg's syndrome) is presented and a literature review about the symptoms of this clinical picture is done, as well as the possible reasons explaining this modification in the clinical expression. The Opalski variant was described in 1948, eighty-nine years after the original description of the syndrome by Adolf Wallenberg, its main feature is the presence of hemiparesis or hemiplegia of the ipsilateral side of the injury in the medulla oblongata. In most cases the etiology is vascular when the postero-inferior cerebellar artery is occluded or there is an obstruction of the ostium of penetrating vessels originating in the artery. There are no studies that accurately report the worldwide incidence of this clinical variant, however, its presentation is not uncommon. The most interesting discovery of each case is that semiological findings are a good example of the profound organization of the nervous system.

Síndrome de Wallenberg: reporte de caso / Wallenberg Sindrome: a case report

El Síndrome de Wallenberg representa el 36% de los infartos del tronco cerebral. Se debe a la oclusión de la Arteria cerebelosa posterior inferior, afectando estructuras encontradas en el cerebelo y la parte lateral del bulbo raquídeo. El principal factor de riesgo es la aterosclerosis. El caso se trata de paciente masculino de 57 años de edad con antecedente de Infartos lacunares en cerebelo, Diabetes mellitus tipo 2No controlada, tabaquismo y dislipidemia. Inicia con cuadro clínico de cefalea occipital, intensa, súbita, sin atenuantes concomitantemente vértigo, hipo, nauseas, vómitos y parestesia de miembros inferiores. Al examen físico pulsos periféricos disminuidos, presenta Síndrome de Horner, hipo, hipoestesia en hemicara izquierda y hemicuerpo contralateral, con ataxia, dismetría y disdiadococinesia. Se realiza IRM con difusión con conclusión diagnostica: Imagen hiperintensa de morfología irregular en el contorno lateral izquierdo del bulbo raquídeo por restricción molecular, compatible con evento isquémico (Síndrome Wallenberg). Se indica tratamiento antitrombótico y terapia física. Paciente es evaluado 2 meses después mostrando amplia mejoría de su cuadro. Es un síndrome muy específico, cuya manifestación clínica depende de la región anatómica afectada y abstrae al clínico de otros diagnósticos.

Wallenberg's Syndrome represents 36 % of strokes in the brainstem. It is due to occlusionof the inferior cerebellar artery, affecting structures found in the cerebellum and the lateral part of themedulla oblongata. The main risk factor is atherosclerosis. The case is about a 57-year-old male patient witha history of lacunar infarcts in the cerebellum, type 2 diabetes mellitus, smoking and dyslipidemia. It beginswith an intense and sudden occipital headache, without attenuating, concomitantly vertigo, hiccups, nausea,vomiting and paresthesia of lower limbs. At the physical examination, decreased peripheral pulses presentHorner's syndrome, hypoesthesia, hypoesthesia in left hemiface, and contralateral hemibody, with ataxia,dysmetria and dysdiadochokinesia. MRI was performed with diffusion with diagnostic Hyperintense image ofirregular morphology in the left lateral contour of the medulla oblongata, compatible with ischemic event(Wallenberg syndrome). Antithrombotic treatment and physical therapy was indicated. Patient was evaluated2 months later showing ample improvement. It is a very specific syndrome, whose clinical manifestationdepends on the anatomical region affected and abstracts the clinician from other diagnoses.

Response to Letter by Dr. Cristina Brandolini / 대한뇌졸중학회지

No abstract available.

Trigeminal Neuralgia Presenting as Transient Ischemic Attack in a Patient with Lateral Medullary Infarction

No abstract available.

Isolated Axial Lateropulsion in Lateral Medullary Infarction

The Wallenberg's syndrome is produced by infarction of lateral medulla. Isolated ipsilateral axial lateropulsion without other common symptoms of Wallenberg syndrome has rarely been reported as manifestation of lateral medullary infarction. The responsible anatomical structure of ipsilateral axial lateropulsion is still uncertain. We describe a patient with lateral medullary infarction who present with isolated ipsilateral axial lateropulsion without other symptoms of Wallenberg syndrome.

Unilateral Punctate Keratitis Secondary to Wallenberg Syndrome

We studied three patients who developed left unilateral punctate keratitis after suffering left-sided Wallenberg Syndrome. A complex evolution occurred in two of them. In all cases, neurophysiological studies showed damage in the trigeminal sensory component at the bulbar level. Corneal involvement secondary to Wallenberg syndrome is a rare cause of unilateral superficial punctate keratitis. The loss of corneal sensitivity caused by trigeminal neuropathy leads to epithelial erosions that are frequently unobserved by the patient, resulting in a high risk of corneal-ulcer development with the possibility of superinfection. Neurophysiological studies can help to locate the anatomical level of damage at the ophthalmic branch of the trigeminal nerve, confirming the suspected etiology of stroke, and demonstrating that prior vascular involvement coincides with the location of trigeminal nerve damage. In some of these patients, oculofacial pain is a distinctive feature.

Esclerosis Lateral Amiotrófica. Experiencia quirúrgica en 13 pacientes / Amyotrophic Lateral Sclerosis. Surgical experience in 13 patients

Introducción: En agosto del 2009 operamos el primer paciente con esclerosis lateral amiotrófica (ELA). Sin embargo, hasta la fecha, todo los investigadores informan que no hay cura para esta enfermedad. Objetivo: Demostrar que la ELA puede ser detenida y mejorada mediante un transplante de epiplón. Material y Método: Presentamos a 13 pacientes con formas bulbar y espinal de ELA. Durante la cirugía encontramos: 1) variantes anatómicas del segmento V4 de las arterias vertebrales, 2) aterosclerosis moderada o severa en ambos segmentos V4, 3) algunas arterias circunflejas originadas desde las arterias espinales anteroventrales (AEAVs) exsangües, 4) hipotrofia de raicillas nerviosas en la hilera de los nervios IX, X y XI, 5) en algunos casos, hipotrofia de la superficie anterior de las pirámides e 6) hipotrofia de raíces anteriores en C5 - C6.Todos ellos recibieron transplante de epiplón a la superficie anterior, lateral y posterior de la medula oblongada y en 5 pacientes, un transplante adicional a nivel C5-C6. Resultados: La mejoría neurológica fue observada desde el primer día de la operación y fue mayor durante los primeros días o semanas de la cirugía que en los siguientes meses. Actualmente, 2 pacientes con 8 y 12 meses de evolución postoperatoria han mejorado en un 90% los síntomas de la forma bulbar de ELA. Conclusión: Estos resultados indican que la forma bulbar de ELA es originada por isquemia progresiva en el territorio intraparenquimatoso de las AEAVs y la forma espinal por isquemia en la arteria espinal anterior, pero a nivel C5 a T1. Eso explicaría porque su revascularización por medio del epiplón produjo mejoría neurológica.

Introduction: In August 2009 we performed surgery for the first time in a patient with amyotrophic lateral sclerosis (ALE). However, every published report about ALE mentions there is no cure for this condition. Objective: To prove that the progression of ALE may be stopped and the condition may be improved using an epiplon transplant. Material and Method: This report presents our experience with 13 ALE patients, affected by the bulbar and spinal forms of the disease. During the surgical procedures, we made the following findings: 1) anatomical variants in the V4 segment of vertebral arteries, 2) moderate or severe atherosclerosis in both V4 segments, 3) some circumflex blood vessels originating from the low-flow anterior and ventral spinal arteries, 4) hypothrophy of small nerve roots in the pathway of IX, X, and XI cranial nerves, 5) in some cases, hypothrophy of the anterior surface of the pyramids, and 6) hypothrophy of the anterior roots in C5 - C6. Every patient underwent an epiplon transplant upon the anterior, lateral, and posterior aspects of the medulla oblongata, and 5 patients underwent an additional transplant performed upon the C5-C6 territory. Results: Neurological improvement was seen from the first postoperative day, and it reached its maximum level during the first few days or weeks after surgery. Nowadays, 2 patients after eight and twelve months after surgery have had a 90% symptomatic improvement of the bulbar form of ALE. Conclusion: These results indicate that the bulbar form of ALE is caused by progressive ischemia in the parenchymal territory irrigated by the anterior and ventral spinal arteries, and that the spinal form is caused by ischemia in the anterior spinal artery, affecting the area between C5 and T1. This may explain why this revascularization procedure using epiplon tissue led to neurological improvement.

A Case of Posterior Inferior Cerebellar Artery Infarction Presenting with Sudden Hearing Loss and Vertigo / 대한평형의학회지

Sudden hearing loss and vertigo are the typical presentation of anterior inferior cerebellar artery infarction, but may rarely occur in posterior inferior cerebellar artery (PICA) infarction. Here we describe a 65-year-old man who presented with sudden hearing loss in his left ear and severe vertigo. The diffusion-weighted magnetic resonance imaging revealed acute infarction in the territory of PICA and cerebral angiography showed non-visualization of left vertebral artery. Sudden hearing loss and vertigo may be a presentation of PICA infarction.

Lateral medullary infarct/Wallenberg Syndrome: Jamaica / Síndrome de Wallenberg/Infarto medular lateral: Jamaica

We describe two cases of lateral medullary syndrome at the University Hospital of the West Indies, Mona, Jamaica. This diagnosis is often missed and not well understood, so we will discuss the underlying pathophysiology.

Se describen dos casos de síndrome medular lateral en el Hospital Universitario de West Indies, Mona, Jamaica. Este diagnóstico pasa a menudo inadvertido y no es bien entendido. Por esa razón se discute aquí la patofisiología subyacente.

A Case of Airway Obstruction Caused by Bilateral Vocal Cord Palsy in a Patient with Lateral Medullary Infarction / 대한뇌졸중학회지

Lateral medullary infarction can lead to central respiratory failure. However, in Wallenberg's syndrome, obstructive respiratory failure rarely develops. Here, we report a case of obstructive respiratory failure with stridor caused by unilateral lateral medullary infarction. A 74-year-old woman was admitted for acute right lateral medullary infarction. On the 12th day after the stroke, the patient developed respiratory failure necessitating endotracheal intubation. She could maintain good oxygen saturation and ventilation in intubated status without the assistance of mechanical ventilator, even during sleep. The pharyngo-laryngoscopy demonstrated the hypomobility of bilateral vocal cords. This case suggests that unilateral medullary infarction might be a cause of bilateral vocal cord palsy.