Stroke syndromes: A case of an eight and a half syndrome

INTRODUCTION@#Eight and a Half syndrome: a combination of ipsilateral cranial nerve seven palsy plus one and a half syndrome is rare. Exact prevalence of the syndrome has not been reported as of yet. This syndrome is mostly attributed to a vascular etiology such as a pontine tegmental infarction. @*OBJECTIVE@#To present a rare case of a stroke syndrome : eight and a half syndrome (peripheral cranial nerve seven palsy plus a one and an half syndrome) in an adult male. To present the importance of its early clinical recognition in correlation of radiologic imaging, and management. @*CASE REPORT@#This is a case of a sixty-two year old male, who had a one day history of sudden double vision. Cranial nerve examination revealed a frozen right eye; unable to perform any movement on horizontal gaze, and with right sided facial asymmetry. He was hypertensive for more than ten years. Left eye was exotropic, with no adduction. Right eye was frozen on horizontal gaze, and primary gaze was at midline. Right sided peripheral facial palsy was seen on examination. Cranial non-contrast magnetic resonance imaging with time of flight was done revealing an infarct in the right posterior pontine area, and a narrow right vertebral artery due to a probable occlusion. Patient was started on antiplatelet cilostazol 100mg/tab 1 tablet twice daily. Atorvastatin 40mg/tab 1 tablet was given. Anti-hypertensives were started on his fourth hospital day. Smoking cessation, dietary modifications, and compliance to medications were emphasized prior to discharge. @*DISCUSSION@#Here we have a stroke syndrome presenting as an ipsilateral lower motor neuron: seventh nerve palsy, and an ipsilateral horizontal gaze palsy with internuclear ophthalmoplegia of the contralateral eye (failure of adduction) termed as CN VII, + 1 ½ syndrome or Eight and a Half Syndrome. This is caused by a lesion involving the paramedian pontine reticular formation (PPRF) which sends signals towards the ipsilateral abducens nerve and contralateral medial longitudinal fasciculus. These structures lie in close proximity to the nucleus and intraaxial fascicles of cranial nerve VII manifesting as facial weakness of the ipsilateral side to the lesion. An occlusion in the tip of the paramedian pontine artery, a branch of the basilar artery, is the most common etiology.

Síndrome del ocho y medio secundario a vasculopatía lúpica: presentación de un caso / Eight-and-a-half syndrome secondary to lupus vasculopathy: a case presentation

RESUMEN Introducción: El manejo diagnóstico y terapéutico en los pacientes con lupus eritematoso sistémico que desarrollan una afectación neuropsiquiátrica representa un reto, debido a la heterogeneidad de las formas en que puede presentarse y la ausencia de criterios diagnósticos. Objetivo: Reconocer las formas clínicas de presentación de los síndromes neuroftalmológicos que traducen afectación pontina. Presentación del caso: Hombre de 71 años con antecedente de lupus eritematoso sistémico con afectación neuopsiquiátrica, que de forma aguda desarrolla un cuadro emético en el curso de una emergencia hipertensiva seguido de una parálisis de la mirada horizontal hacia la izquierda, una oftalmoplejía internuclear posterior derecha y una parálisis facial izquierda. En la neuroimagen se constata una afectación multifocal con marcado daño pontino. Conclusiones: Reconocer las formas clínicas de presentación de estos trastornos neuroftalmológicos raros que generalmente se presentan de forma aguda/subaguda permite al neurólogo realizar el diagnóstico topográfico de la lesión a nivel protuberancial con elevada precisión desde la Sala de Urgencias, así como reducir los posibles diagnósticos diferenciales a una etiología vascular, desmielinizante u ocupativa de espacio(AU)

ABSTRACT Introduction: The diagnostic and therapeutic management of patients with systemic lupus erythematosus who develop a neuropsychiatric involvement represents one of the biggest challenges due to the heterogeneity of the ways in which it can occur and the absence of diagnostic criteria. Objective: To recognize the clinical forms of presentation of neurophthalmological syndromes that express pontine involvement. Case presentation: Seventy-one-year-old man with history of systemic lupus erythematosus with neuropsychiatric involvement who acutely develops an emetic episode in the course of a hypertensive emergency followed by a paralysis of the horizontal gaze to the left, a right-sided posterior internuclear ophthalmoplegia and a left facial palsy. In the neuroimaging, a multifocal involvement with marked pontine damage is observed. Conclusions: Recognizing the clinical forms of presentation of these rare neurophthalmological disorders that generally occur in an acute or subacute form allows the neurologist to perform the topographic diagnosis of the lesion at a protuberancial level with high precision from the time when the patient attends the Emergency Department and reduces the possible differential diagnoses to a vascular, demyelinating or occupational etiology of space(AU)

“Nine” syndrome and its MRI brain findings

We describe a rare presentation of pontine infarction in a lady who was on dual antiplatelet therapy.Her presentation includes one and a half syndrome, left facial nerve palsy and contralateral hemiataxia.Magnetic resonance imaging (MRI) of the brain revealed acute infarction of the dorsal pons. A diagnosisof “nine” syndrome secondary to lacunar stroke was made. She continued dual antiplatelet therapyand her symptoms resolved completely over three months.

Eight-And-a-Half Syndrome in Pontine Infarction

Eight-and-a-half syndrome is a clinical syndrome with the combination of a one-and-a-half syndrome and an ipsilateral seventh cranial nerve palsy usually due to a paramedian pontine tegmental lesion. A 57-year-old man presented with dizziness, diplopia, and a left facial palsy. Ocular motor manifestations showed combined left conjugate horizontal gaze palsy and left internuclear ophthalmoplegia (one-and-a-half syndrome). In addition, he had a left lower motor neuron pattern of facial palsy. Brain MR images showed an acute infarction in the left paramedian pontine tegmentum.