RESUMEN
Objectives Intracranial penetration by foreign bodies entering via the orbit represent an unusual form of traumatic brain injury. Nevertheless, much is at stake with high risk for cranial nerve and neurovascular injury. We present a case where the bristled end of a toothbrush entered the brain as a projectile via the superior orbital fissure and discuss considerations for surgical management. Setting A 35-year-old woman suffered a periorbital injury after her husband threw an electric toothbrush at a wall and the head of the toothbrush became a missile that projected through her superior orbital fissure and into her right temporal lobe. She complained of headache and incomplete vision loss in the affected eye. Intervention After obtaining a cerebrovascular angiogram, we proceeded with emergent orbital decompression and anterograde extraction of the foreign body via a modified frontotemporal orbitozygomatic approach with drilling of the skull base allowing for en bloc removal of the toothbrush. Conclusions The patient recovered well with improvement in her vision and partial third and sixth nerve palsies. This report illustrates a unique mechanism of injury with a novel intracranial foreign body. We review the neurosurgeon's need for prompt management with an approach customized to the structure of the offending object, the damaged elements, and the surrounding cranial nerves and vascular anatomy.
RESUMEN
Asthma and mouse models of allergic respiratory inflammation are invariably associated with a pulmonary eosinophilia; however, this association has remained correlative. In this report, a causative relationship between eosinophils and allergen-provoked pathologies was established using eosinophil adoptive transfer. Eosinophils were transferred directly into the lungs of either naive or OVA-treated IL-5(-/-) mice. This strategy resulted in a pulmonary eosinophilia equivalent to that observed in OVA-treated wild-type animals. A concomitant consequence of this eosinophil transfer was an increase in Th2 bronchoalveolar lavage cytokine levels and the restoration of intracellular epithelial mucus in OVA-treated IL-5(-/-) mice equivalent to OVA-treated wild-type levels. Moreover, the transfer also resulted in the development of airway hyperresponsiveness. These pulmonary changes did not occur when eosinophils were transferred into naive IL-5(-/-) mice, eliminating nonspecific consequences of the eosinophil transfer as a possible explanation. Significantly, administration of OVA-treated IL-5(-/-) mice with GK1.5 (anti-CD4) Abs abolished the increases in mucus accumulation and airway hyperresponsiveness following adoptive transfer of eosinophils. Thus, CD4(+) T cell-mediated inflammatory signals as well as signals derived from eosinophils are each necessary, yet alone insufficient, for the development of allergic pulmonary pathology. These data support an expanded view of T cell and eosinophil activities and suggest that eosinophil effector functions impinge directly on lung function.
