[1, 13] In dilated vessels, spontaneous thrombosis can lead to a fast rise in venous system pressure and therefore result in venous hypertension and subsequent SAH.[1] Vasospasm of the vertebrobasilar system in the context of rupture of an anterior spinal artery aneurysm has been described in the literature.[14] Vasospasm of anterior spinal artery has been postulated as a complication of transforaminal nerve root injections, resulting selleck chemical in spinal cord infarctions and subsequent paraplegia.[15]

The onset of vasospasm in this patient was coincident with the development of an anterior spinal artery syndrome, resulting in acute paresis and dissociated sensory loss. The poor flow through the anterior spinal artery resulting in spinal cord ischemia may have been secondary to either vasospasm of the vertebral arteries

or of the anterior spinal artery itself, or both. Target Selective Inhibitor Library In the first case, spasm of the vertebral arteries may have resulted in poor inflow into the anterior spinal artery, whereas in the second case poor flow through the anterior spinal artery may have been due to the increased resistance of the segment in spasm. We present a case of vasospasm following rupture of a cervical DAVF. Although an uncommon location for a DAVF, one must consider this entity in the workup for intracranial SAH when an intracranial source cannot be found. Treatment consists of surgical, endovascular, and radiosurgical modalities. However, the presence of vasospasm in this case was an unexpected complication, since vasospasm after rupture 上海皓元 of a DAVF had not been reported. This finding warrants further study to discover the incidence of this phenomenon, and may warrant prolonged monitoring for vasospasm as is currently practiced with SAH secondary to intracranial aneurysms.

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“Papillary glioneuronal tumor (PGNT) was newly classified as a Grade I neuronal-glial tumor by 2007 revision of the World Health Organization (WHO) classification of tumor of central nervous system (CNS) because of its characteristic pseudopapillae and diphase differentiation features. Previous literature has laid particular emphasis on pathology manifestations, and radiological features were only briefly mentioned. The purpose of this study was to describe magnetic resonance imaging (MRI) features through reporting 2 cases of PGNT and literature review. MRI findings and pathology features in 2 cases of PGNT were reported and the literature was reviewed. Both patients were confirmed as PGNT by surgery and pathology. Seizure was the main clinical manifestation. Histopathological examination revealed characteristic pseudopapillary structure with astrocytes and neurons. Both lesions were located in the temporal lobe, and one case was closely related with the lateral ventricle. MRI showed cystic-solid mass or cystic lesion with mural nodule. The solid component enhanced strikingly after contrast agent administration.