Injuries deeper than the platysma are considered as penetrating neck injuries, constituting approximately 5% - 10% of all trauma. Many vital organs are at risk from a penetrating neck injury. These injuries in zone 1 have the highest mortality, because the injuries are close to the vital organs and difficult to access surgically. A 41-year-old male, a car mechanic by profession, presented to the emergency department with a penetrating neck injury on the right side. CT scan demonstrated a metallic foreign body in zone 1 between the right internal jugular vein and the common carotid artery. The patient was asymptomatic, and the foreign body was removed surgically. This case shows a rare presentation of a penetrating neck injury with a foreign body located in zone 1, where no vital internal structure was injured. As of now, no previous case report has been identified on such presentation. Thus, it will provide a valuable addition to the pre-existing literature.
Humans ; Male ; Adult ; Neck Injuries/diagnostic imaging* ; Wounds, Penetrating/diagnostic imaging* ; Foreign Bodies/diagnostic imaging* ; Jugular Veins ; Tomography, X-Ray Computed ; Carotid Artery Injuries/surgery* ; Carotid Artery, Common

Vasculature injury occurs rarely in traumatic brain injury but increases lifetime risk of ischemic or hemorrhage stroke. The diverse and nonspecific clinical manifestations make the diagnosis and treatment of these injuries highly challenging. With advancements in device design, endovascular treatments have become widely adopted, playing an increasingly vital role in the management of vascular diseases. The purpose of this review is to introduce and summarize endovascular treatments of traumatic cerebrovascular injury and other related pathological states after traumatic brain injury. Given the innovations of neuroendovascular devices and improvements in the techniques over the past decade, this review will outline several recent advancements in endovascular treatment strategies for cerebrovascular pathologies. Popularizing more treatment options to clinicians will benefit in dealing with a variety of clinical scenarios and reduce the overall morbidity of traumatic cerebrovascular injury.
Humans ; Endovascular Procedures/methods* ; Brain Injuries, Traumatic/complications* ; Cerebrovascular Trauma/therapy*

Pathological vascular remodeling is a hallmark of various vascular diseases. Previous research has established the significance of andrographolide in maintaining gastric vascular homeostasis and its pivotal role in modulating endothelial barrier dysfunction, which leads to pathological vascular remodeling. Potassium dehydroandrographolide succinate (PDA), a derivative of andrographolide, has been clinically utilized in the treatment of inflammatory diseases precipitated by viral infections. This study investigates the potential of PDA in regulating pathological vascular remodeling. The effect of PDA on vascular remodeling was assessed through the complete ligation of the carotid artery in C57BL/6 mice. Experimental approaches, including rat aortic primary smooth muscle cell culture, flow cytometry, bromodeoxyuridine (BrdU) incorporation assay, Boyden chamber cell migration assay, spheroid sprouting assay, and Matrigel-based tube formation assay, were employed to evaluate the influence of PDA on the proliferation and motility of smooth muscle cells (SMCs). Molecular docking simulations and co-immunoprecipitation assays were conducted to examine protein interactions. The results revealed that PDA exacerbates vascular injury-induced pathological remodeling, as evidenced by enhanced neointima formation. PDA treatment significantly increased the proliferation and migration of SMCs. Further mechanistic studies disclosed that PDA upregulated myeloid differentiation factor 88 (MyD88) expression in SMCs and interacted with T-cadherin (CDH13). This interaction augmented proliferation, migration, and extracellular matrix deposition, culminating in pathological vascular remodeling. Our findings underscore the critical role of PDA in the regulation of pathological vascular remodeling, mediated through the MyD88/CDH13 signaling pathway.
Mice ; Rats ; Animals ; Myeloid Differentiation Factor 88/metabolism* ; Vascular Remodeling ; Cell Proliferation ; Vascular System Injuries/pathology* ; Carotid Artery Injuries/pathology* ; Molecular Docking Simulation ; Muscle, Smooth, Vascular ; Cell Movement ; Mice, Inbred C57BL ; Signal Transduction ; Succinates/pharmacology* ; Potassium/pharmacology* ; Cells, Cultured ; Diterpenes ; Cadherins

Humans ; Neck Injuries/surgery* ; Carotid Artery Injuries/surgery* ; Neck ; Bone Screws/adverse effects* ; Carotid Artery, Common/surgery*

Aneurysm, False/etiology* ; Carotid Artery Injuries/therapy* ; Carotid Artery, Internal ; Embolization, Therapeutic ; Epistaxis/etiology* ; Humans

Carotid arterial dissections may result from spontaneous or traumatic causes. Postcoital arterial dissections have been reported in both the vertebral and coronary arteries. We report a rare case of spontaneous dissection on the extracranial internal carotid artery in a Filipino female after sexual intercourse, leading to a fulminant middle cerebral artery (MCA) territory infarct. Although postcoital carotid artery dissection is a very rare cause of neck vessel dissections, its rapid progressive course can lead to massive cerebral infarction and prompt management must be initiated.
Cerebral Infarction ; Carotid Artery, Internal, Dissection

PURPOSE: To explore the diagnosis and treatment of traumatic external carotid branch pseudoaneurysms. METHODS: Eleven cases of traumatic external carotid artery branch pseudoaneurysms were admitted in our hospital. Digital subtraction angiography was performed in all patients. It revealed that the pseudoaneurysms originated from the internal maxillary artery in 5 cases, superficial temporal artery in 5 cases and occipital artery in 1 case. Five cases of internal maxillary artery pseudoaneurysms and 2 cases of superficial temporal artery pseudoaneurysms were treated by embolization; the other 3 cases were surgically resected. RESULTS: Complete cessation of nasal bleeding was achieved in all the 5 pseudoaneurysms of internal maxillary artery after the endovascular therapies. Scalp bleeding stopped and scalp defect healed up in 2 patients with superficial temporal artery pseudoaneurysms treated by interventional therapy. All patients were followed up for 0.5-2.0 years without recurrence of nosebleed and scalp lump. CONCLUSION For patients with repeated severe epistaxis after craniocerebral injury, digital subtraction angiography should be performed as soon as possible to confirm traumatic pseudoaneurysm. Endovascular therapy is an effective method for traumatic internal maxillary artery pseudoaneurysms. For patients with scalp injuries and pulsatile lumps, further examinations including digital subtraction angiography should be performed to confirm the diagnosis. Surgical treatment or endovascular therapy for scalp traumatic pseudoaneurysm is effective.
Aneurysm, False/therapy* ; Angiography, Digital Subtraction ; Carotid Artery Injuries/therapy* ; Carotid Artery, External/diagnostic imaging* ; Embolization, Therapeutic ; Humans

Carotid Artery Injuries/etiology* ; Carotid Artery, Internal/diagnostic imaging* ; Foreign Bodies/complications* ; Humans ; Skull ; Skull Base/diagnostic imaging*

Carotid-cavernous fistula (CCF) is a rare and dangerous neurological disorder that arises due to an abnormal communication between the internal carotid artery (ICA) or the external carotid artery (ECA) and their branches and the cavernous sinus. It can either be a direct fistula (high-flow with acute symptoms) most commonly resulting from trauma (70-90%) or an indirect fistula (low-flow with insidious symptoms) secondary to hypertension, atherosclerosis and collagen vascular disorders. The shunting of arterial blood into the venous system leads to venous hypertension causing various clinical manifestations depending on the venous drainage patterns and the shunt flow. Increased anterior, posterior and superior venous drainage results to orbital/ocular, cavernous and cortical symptomatology, respectively. This paper aims to present a case of 58-year old Filipino female with a 2-day history of sudden, severe headache, vomiting and blurring of vision followed by decrease in sensorium and sudden proptosis and chemosis of the left eye. Patient had no co-morbidities, history of trauma, surgeries, facial skin infections or prior febrile illness. The left eye had exophthalmos, subconjunctival hyperemia, scleral edema/chemosis and ocular bruit. Neurologic examination showed a stuporous patient with multiple cranial nerve deficits (impaired direct and consensual pupillary reflex left, complete ptosis left, sluggish corneal reflex left, impaired oculocephalic reflex left), right hemiplegia and meningeal signs. Cranial Computed Tomography (CT) Angiogram revealed an acute parenchymal hemorrhage in the left frontotemporal lobe with subarachnoid component, with engorged left cavernous sinus and dilated left superior ophthalmic vein. Digital Subtraction Angiography (DSA) was done revealing a direct type of left carotid-cavernous fistula with massive ICA shunting to the cavernous sinus, superior ophthalmic vein and inferior petrosal sinus. The clinical and radiographic evidence were consistent with a Direct/Type A CCF. Unique in this case was a patient with no history of trauma presenting with simultaneous orbital/ocular, cavernous and cortical symptomatology – a clinical picture of CCF that has never been documented in any literature nor included in any classification system. The presence of all three symptomatology can be explained by a direct/highflow fistula that resulted to increased anterior, posterior and superior venous drainage as documented in the DSA. In addition, spontaneous intracranial hemorrhage in CCF is exceptionally rare and it is the most daunting symptomatology of this disease. With that, this specific case may pave the way to a new classification scheme and determine its corresponding treatment approach.
Carotid-Cavernous Sinus Fistula ; Cavernous Sinus

A carotid-cavernous sinus fistula is a rare condition in which an abnormal communication exists between the internal or external carotid artery and the cavernous sinus. It typically occurs within a few weeks after craniomaxillofacial trauma. In most cases, the carotid-cavernous sinus fistula occurs on the same side as the craniomaxillofacial fracture. We report a case of delayed carotidcavernous sinus fistula that developed symptoms 7 months after the craniomaxillofacial fracture. The fistula developed on the side opposite to that of the craniomaxillofacial fracture. Based on our experience with this case, we recommend a long follow-up period of 7–8 months after the occurrence of a craniomaxillofacial fracture. We also recommend that the follow-up should include consideration of the side contralateral to the injury.
Carotid Artery, External ; Carotid-Cavernous Sinus Fistula ; Cavernous Sinus ; Fistula ; Follow-Up Studies