Styloidogenic Jugular Venous Compression Syndrome: Diagnosis and Treatment: Case Report
Norton Neuroscience Center, Norton Healthcare, Louisville, Kentucky, USA. Neurosurgery
(Impact Factor: 3.62).
08/2011; 70(3):E795-9. DOI: 10.1227/NEU.0b013e3182333859
Intracranial venous hypertension is known to be associated with venous outflow obstruction. We discuss the diagnosis and treatment of mechanical venous outflow obstruction causing pseudotumor cerebri.
We report 2 patients presenting with central venous outflow obstruction secondary to osseous compression of the internal jugular veins at the craniocervical junction. The point of jugular compression was between the lateral tubercle of C1 and a prominent, posteriorly located styloid process. In both cases, catheter venography showed high-grade jugular stenosis at the level of C1 with an associated pressure gradient. The dominant jugular vein was decompressed after the styloid process was resected. Postoperative imaging confirmed resolution of the jugular stenosis and normalization of preoperative pressure gradients. In both cases, the symptoms of intracranial hypertension resolved.
Intracranial venous hypertension may result from extrinsic osseous compression of the jugular veins at the skull base. Although rare, this phenomenon is important to recognize because primary stenting not only is ineffective but also may actually exacerbate the outflow obstruction. The osseous impingement of the dominant jugular vein can be relieved via a decompressive styloidectomy, and the clinical results can be excellent.
Available from: PubMed Central
- "Subsequent compression impedes flow, which may contribute to thrombus formation, particularly if there is a thrombogenic foci already present, such as a central venous catheter. Additionally, there are a number of rigid and semi-rigid structures abutting the SVC, including vertebrae, ribs, and the aorta, which can cause compression.7,8 "
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ABSTRACT: Superior vena cava (SVC) syndrome is most commonly the insidious result of decreased vascular flow through the SVC due to malignancy, spontaneous thrombus, infections, and iatrogenic etiologies. Clinical suspicion usually leads to computed tomography to confirm the diagnosis. However, when a patient in respiratory distress requires emergent airway management, travel outside the emergency department is not ideal. With the growing implementation of point-of-care ultrasound (POCUS), clinicians may make critical diagnoses rapidly and safely. We present a case of SVC syndrome due to extensive thrombosis of the deep venous system cephalad to the SVC diagnosed by POCUS.
The western journal of emergency medicine 09/2014; 15(6):715-8. DOI:10.5811/westjem.2014.6.14006
Available from: Chun-Yu Cheng
- "There are studies demonstrating etiologies of IJV stenosis, such as external compression from bony structure
[28,29] or adjacent muscle
. Truncular venous malformation involving the venous system of the head and neck, an embryological defect, has also been reported as one of the causes of CCSVI
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ABSTRACT: The etiology of transient monocular blindness (TMB) in patients without carotid stenosis has been linked to ocular venous hypertension, for their increased retrobulbar vascular resistance, sustained retinal venule dilatation and higher frequency of jugular venous reflux (JVR). This study aimed to elucidate whether there are anatomical abnormalities at internal jugular vein (IJV) in TMB patients that would contribute to impaired cerebral venous drainage and consequent ocular venous hypertension.
Contrast-enhanced axial T1-weighted magnetic resonance imaging (MRI) was performed in 23 TMB patients who had no carotid stenosis and 23 age-and sex-matched controls. The veins were assessed at the upper IJV (at C1-3 level) and the middle IJV (at C3-5 level). Grading of IJV compression/stenosis was determined bilaterally as follows: 0 = normal round or ovoid appearance; 1 = mild flattening; 2 = moderate flattening; and 3 = severe flattening or not visualized.
There was significantly more moderate or severe IJV compression/stenosis in the TMB patients at the left upper IJV level and the bilateral middle IJV level. Defining venous compression/stenosis scores [greater than or equal to]2 as a significant cerebral venous outflow impairment, TMB patients were found to have higher frequency of significant venous outflow impairment at the upper IJV level (56.5% vs. 8.7%, p=0.0005) and the middle IJV level (69.6% vs. 21.7%, p=0.0011).
TMB Patients with the absence of carotid stenosis had higher frequency and greater severity of IJV compression/stenosis which could impair cerebral venous outflow. Our results provide evidence supporting that the cerebral venous outflow abnormality is one of the etiologies of TMB.
BMC Neurology 07/2013; 13(1):94. DOI:10.1186/1471-2377-13-94 · 2.04 Impact Factor
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ABSTRACT: Obstructive sleep apnea has been shown to increase intracranial pressure, and to be a secondary cause of intracranial hypertension. There are a few theories that attempt to explain this relationship, however there is little data, and even less recognition among physicians that this actually occurs. This paper discusses multiple pieces of data, from anatomical correlates to biochemical information involving neuro-excitotoxicity, as well as hematologic factors and issues surrounding brain edema and blood–brain barrier dysfunction. A complex paradigm for how obstructive sleep apnea may lead to increased intracranial pressure is thus proposed. In addition, suggestions are made for how obstructive sleep apnea must as a result be managed differently in the setting of idiopathic intracranial hypertension.
Medical Hypotheses 10/2014; 83(6). DOI:10.1016/j.mehy.2014.10.011 · 1.07 Impact Factor
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