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OBJECTIVE Dissection of the carotid and vertebral arteries can result in the development of aneurysmal dilations. These dissecting pseudoaneurysms can enlarge and cause symptoms. The objective of this study is to provide insight into the progression of dissecting pseudoaneurysms and the treatments required to manage them. METHODS A review of the electronic medical records was conducted to detect patients with carotid and vertebral artery dissection. An imaging review was conducted to identify patients with dissecting pseudoaneurysms. One hundred twelve patients with 120 dissecting pseudoaneurysms were identified. Univariate and multivariate analyses were conducted to assess the factors associated with undergoing further interventions other than medical treatment, pseudoaneurysm enlargement, pseudoaneurysms resulting in ischemic and nonischemic symptoms, and clinical outcome. RESULTS Overall, 18.3% of pseudoaneurysms were intracranial and 81.7% were extracranial, and the average size was 7.3 mm. The mean follow-up time was 29.3 months; 3.3% of patients had a recurrent transient ischemic attack, no patients had a recurrent stroke, and 14.2% of patients had recurrence of nonischemic symptoms (headache, neck pain, Horner syndrome, or cranial nerve palsy). Follow-up imaging demonstrated that 13.8% of pseudoaneurysms had enlarged, 30.2% had healed, and 56% had remained stable. In total, 20.8% of patients had an intervention other than medical treatment. Interventions included stenting, coiling, flow diversion, and clipping. Predictors of intervention included increasing size, size > 10 mm, location in the C2 (petrous) segment of the internal carotid artery (ICA), younger age, hyperlipidemia, pseudoaneurysm enlargement, and any symptom development. Significant predictors of enlargement included smoking, history of trauma, C2 location, hyperlipidemia, and larger initial pseudoaneurysm size. Predictors of pseudoaneurysm resulting in recurrent ischemic and nonischemic symptoms included increasing size and location in the petrous segment of the ICA. Smoking was a predictor of unfavorable outcome. CONCLUSIONS Dissecting pseudoaneurysms have a benign course and most will not cause symptoms or enlarge on follow-up. Medical treatment can be a sufficient, initial treatment for dissecting pseudoaneurysms.
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PMID:Dissecting pseudoaneurysms: predictors of symptom occurrence, enlargement, clinical outcome, and treatment. 2682 74

Carotid artery dissection secondary to cervical blunt trauma is a rare and potentially life-threatening condition that can cause a variety of clinical presentations, including stroke, headache, neck pain, tinnitus, Horner syndrome and cranial neuropathies and is associated with long-term sequelae. We report a case of a 49-year-old industrial vehicles mechanic who was projected to the ground by the explosion of the tire of a heavy truck he was inflating. In the following hours he presented various neurological signs and symptoms and was admitted to the Emergency Department. During hospitalization the patient underwent clinical and instrumental investigations with AngioCT and MR finding of left internal carotid artery dissection in correspondence of its cervical segment and three acute ischemic lesions in the left temporal, parietal and occipital lobes. Medical management was successful and the patient was discharged from the hospital three weeks after the admission but he wasn't able to get back to work due to neurological sequelae. This case report illustrates that traumatic carotid artery dissection, although rare, should be considered in patients who present neurological symptoms after an explosion, can meet the criteria for a work-related injury and may lead to a permanent decrease in the ability to work.
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PMID:Unusual case of traumatic carotid artery dissection occurred during a work-related activity. A case report. 3037 89

Harlequin syndrome is a disorder of the autonomic nervous system. It clinically presents as a distinct line of hemifacial sympathetic denervation. We describe a case of Harlequin syndrome with co-existing central first-order Horner syndrome in the setting of a large thalamic hemorrhage with intraventricular extension.
J Stroke Cerebrovasc Dis 2019 Sep
PMID:Harlequin Syndrome in Acute Thalamic Hemorrhage. 3130 85

Vertebral artery dissection can be insidious and is a leading cause of stroke in young patients, second only behind cardioembolic events [1]. We present the case of a 42-year-old patient who presented to the emergency department with diaphoresis and a complaint of neck pain one month after a low speed motor vehicle collision. The patient was transferred to a stroke center where cerebral angiography showed severe vertebral artery stenosis with likelihood of dissection after a noncontrast CT was negative for hemorrhage. She was definitively treated with antiplatelet therapy and discharged to rehab. By reviewing the most recent literature, we better define this illness. Most commonly, patients with arterial dissection present with head or neck pain, stroke, and Horner syndrome. It is now thought that vertebral artery dissection is a multifactorial disease process where certain intrinsic factors are present in the setting of an exacerbating extrinsic factor such as a low speed car accident, direct trauma, heavy lifting, or a rotational sports injury. And while our patient was treated with antiplatelet therapy and intravascular intervention, vertebral artery dissection is rare and further research is required to better guide treatment as there is no definitive data showing superiority of either anticoagulation or antiplatelet pharmaceutics.
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PMID:Delayed vertebral artery dissection after mild trauma in a motor vehicle collision. 3329 50


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