Endovascular treatment of traumatic azygous vein injuries: a case report.

BACKGROUND: Management of thoracic vascular injury predominantly focuses on the aorta and its tributaries while reports of venous injury are less frequent. Although rare, traumatic azygous vein injuries are associated with high mortality. Prompt treatment is required and has traditionally been open surgery. We present a case of an endovascular repair of an azygous vein injury. CASE PRESENTATION: A female patient presented to our trauma center following ejection after a motor vehicle collision (MVC). CT imaging workup revealed mediastinal and periaortic hematoma with active contrast extravasation adjacent to the azygos vein. She was referred to interventional radiology for vascular evaluation and potential endovascular intervention. The patient met criteria for class III hypovolemic shock upon arrival in the endovascular suite. Aortography demonstrated no arterial injury. Venography revealed a pseudoaneurysm on the superior aspect of the azygos arch and contrast extravasation from the inferior margin of the azygous arch. A stent-graft was deployed and post-deployment venogram showed no extravasation and successful exclusion of the injuries. The patient did not have further signs of bleeding. She left the interventional suite with improved vital signs, yet her condition remained guarded. Follow-up CT chest confirmed continued patency of the stent-graft at 8 days and 2 years post-procedure. CONCLUSION: Historically, azygos vein injuries are a rare occurrence and managed with open surgery. Swift management is necessary to prevent the increased morbidity and mortality associated with azygous vein injury, particularly in polytrauma patients such as the one presented here. We believe endovascular stent-graft treatment offers an innovative alternative to the current standard of operative management of azygos vein injury.

Successful endovascular coil embolization of large pseudoaneurysm of ductus arteriosus diverticulum.

BACKGROUND: Pseudoaneurysm of the ductus arteriosus diverticulum, although rare in adults, may have catastrophic consequences if left untreated due to erosion and rupture of the pseudoaneurysm into adjacent thoracic structures. Although thoracic endovascular aortic repair (TEVAR) is the standard treatment method for aneurysm closure of the ductus arteriosus diverticulum, it was not possible in our patient secondary to marked aortoiliac access vessel tortuosity, significant vascular calcific burden, and an abdominal aortic aneurysm. We describe the first reported case of endovascular coil embolization being successfully used as the definite repair of a ductus arteriosus diverticulum pseudoaneurysm. CASE PRESENTATION: An 85-year-old man with history of severe coronary arterial disease presented with an enlarging pseudoaneurysm of a ductus arteriosus diverticulum. The diverticulum and thoracic aortic junction demonstrated the typical obtuse angles and wide neck, differentiating it from otherwise similar-appearing diagnostic considerations. Repair was attempted with conventional aortic stent graft but the patient's infrarenal abdominal aortic aneurysm and his heavily calcified, tortuous iliac vessels could not accommodate the 24Fr introducer sheath necessary for stent graft placement. Therefore, endovascular coil embolization was successfully completed through a 4Fr directional catheter. The patient tolerated the procedure well and was discharged from the hospital in good condition on post-embolization day six. CONCLUSIONS: Endovascular coil embolization is an alternative treatment for ductus arteriosus diverticulum pseudoaneurysm closure in cases where the standard TEVAR method is unsuccessful. Instead of the wide entry point at the aorta we used the junction of the diverticulum and pseudoaneurysm as the "neck" for satisfactory and stable coil placement. Endovascular coil embolization alone may be a viable definitive therapy for occlusion of the ductus pseudoaneurysm component of the diverticulum in cases where complex anatomy or extensive vascular disease makes stent graft repair impractical if not impossible.

Cortical control of affective networks.

Transcranial magnetic stimulation and deep brain stimulation have emerged as therapeutic modalities for treatment refractory depression; however, little remains known regarding the circuitry that mediates the therapeutic effect of these approaches. Here we show that direct optogenetic stimulation of prefrontal cortex (PFC) descending projection neurons in mice engineered to express Chr2 in layer V pyramidal neurons (Thy1-Chr2 mice) models an antidepressant-like effect in mice subjected to a forced-swim test. Furthermore, we show that this PFC stimulation induces a long-lasting suppression of anxiety-like behavior (but not conditioned social avoidance) in socially stressed Thy1-Chr2 mice: an effect that is observed >10 d after the last stimulation. Finally, we use optogenetic stimulation and multicircuit recording techniques concurrently in Thy1-Chr2 mice to demonstrate that activation of cortical projection neurons entrains neural oscillatory activity and drives synchrony across limbic brain areas that regulate affect. Importantly, these neural oscillatory changes directly correlate with the temporally precise activation and suppression of limbic unit activity. Together, our findings show that the direct activation of cortical projection systems is sufficient to modulate activity across networks underlying affective regulation. They also suggest that optogenetic stimulation of cortical projection systems may serve as a viable therapeutic strategy for treating affective disorders.

A role for repressive histone methylation in cocaine-induced vulnerability to stress.

Substance abuse increases an individual's vulnerability to stress-related illnesses, which is presumably mediated by drug-induced neural adaptations that alter subsequent responses to stress. Here, we identify repressive histone methylation in nucleus accumbens (NAc), an important brain reward region, as a key mechanism linking cocaine exposure to increased stress vulnerability. Repeated cocaine administration prior to subchronic social defeat stress potentiated depressive-like behaviors in mice through decreased levels of histone H3 lysine 9 dimethylation in NAc. Cre-mediated reduction of the histone methyltransferase, G9a, in NAc promoted increased susceptibility to social stress, similar to that observed with repeated cocaine. Conversely, G9a overexpression in NAc after repeated cocaine protected mice from the consequences of subsequent stress. This resilience was mediated, in part, through repression of BDNF-TrkB-CREB signaling, which was induced after repeated cocaine or stress. Identifying such common regulatory mechanisms may aid in the development of new therapies for addiction and depression.