RESUMEN
Bilateral internal carotid artery dissection (ICAD) is a rare but important cause of stroke in young adults. Anticoagulant and/or antiplatelet agents are usually recommended for stroke prevention;however, such treatments remain highly controversial, and there are inadequate data to compare the efficacy of anticoagulation and antiplatelet therapy. We herein report the case of 30-year-old man presenting with progressive bilateral ICAD during antiplatelet treatment. This report suggests the possibility that intramural hematomas are enlarged by antiplatelet and anticoagulant agents and draws attention to the medications associated with ICAD.
Asunto(s)
Disección de la Arteria Carótida Interna/inducido químicamente , Disección de la Arteria Carótida Interna/diagnóstico , Progresión de la Enfermedad , Inhibidores de Agregación Plaquetaria/efectos adversos , Adulto , Humanos , MasculinoAsunto(s)
Angioplastia , Fístula Arteriovenosa/clasificación , Fístula Arteriovenosa/etiología , Infarto Encefálico/etiología , Enfermedades de las Arterias Carótidas/clasificación , Fístula del Seno Cavernoso de la Carótida/complicaciones , Fístula del Seno Cavernoso de la Carótida/terapia , Seno Cavernoso , Duramadre/irrigación sanguínea , Embolización Terapéutica , Hemorragias Intracraneales/etiología , Presión Venosa , Animales , Femenino , Humanos , MasculinoRESUMEN
Mouse embryonic stem cells (ESCs) can generate cerebellar neurons, including Purkinje cells (PCs) and their precursor cells, in a floating culture system called serum-free culture of embryoid body-like aggregates (SFEB) treated with BMP4, Fgf8b, and Wnt3a. Here we successfully established a coculture system that induced the maturation of PCs in ESC-derived Purkinje cell (EDPC) precursors in SFEB, using as a feeder layer a cerebellum dissociation culture prepared from mice at postnatal day (P) 6-8. PC maturation was incomplete or abnormal when the adherent culture did not include feeder cells or when the feeder layer was from neonatal cerebellum. In contrast, EDPCs exhibited the morphology of mature PCs and synaptogenesis with other cerebellar neurons when grown for 4 weeks in coculture system with the postnatal cerebellar feeder. Furthermore, the electrophysiological properties of these EDPCs were compatible with those of native mature PCs in vitro, such as Na(+) or Ca(2+) spikes elicited by current injections and excitatory or inhibitory postsynaptic currents, which were assessed by whole-cell patch-clamp recordings. Thus, EDPC precursors in SFEB can mature into PCs whose properties are comparable with those of native PCs in vitro.
Asunto(s)
Técnicas de Cocultivo/métodos , Células Madre Embrionarias/fisiología , Neurogénesis/fisiología , Células de Purkinje/fisiología , Potenciales de Acción/fisiología , Animales , Animales Recién Nacidos , Calcio/metabolismo , Línea Celular , Cerebelo/citología , Cerebelo/fisiología , Medio de Cultivo Libre de Suero , Células Madre Embrionarias/citología , Potenciales Postsinápticos Excitadores , Potenciales Postsinápticos Inhibidores , Ratones , Ratones Endogámicos ICR , Ratones Transgénicos , Neuronas/citología , Neuronas/fisiología , Células de Purkinje/citología , Sodio/metabolismo , Sinapsis/fisiologíaRESUMEN
Recently, patent foramen ovale(PFO) has been highlighted as an important risk factor of cerebral infarctions in young adults. We report a patient of multiple cerebral embolism associated with PFO and deep venous thrombosis caused by a uterine myoma. A 40-year-old woman suddenly suffered from right hemiparesis with motor aphasia. Brain angiography showed an occlusion of M2 portion of the left middle cerebral artery, but atherosclerotic changes were not seen. She developed left facial paresis 23 days later and admitted to our hospital. Brain MRI revealed multiple cerebral infarcts in the left insular cortex, the deep white matter of the right frontal lobe, and bilateral thalamus. Hypoxia with the perfusion defects of S1 and S2 sections of the right lung demonstrated by scintigraphy suggested pulmonary embolism. Transesophageal echocardiography showed a PFO with spontaneous left-to-right shunt and right-to-left shunt evoked by the Valsalva maneuver. Although venography could not detect thrombi, it revealed severe compression of the right external iliac vein by a uterine myoma. These findings suggested thrombi in the right external iliac vein were the embolic source when combined with elevated coagulation markers. An uterine myoma should be considered as an important risk factor for an embolic source in case of cerebral embolism with PFO.