scholarly journals Deep cerebral veins

2018 ◽  
Author(s):  
Brian Di Giacinto ◽  
Mendel Castle
1997 ◽  
Vol 39 (11) ◽  
pp. 777-780 ◽  
Author(s):  
A. Madan ◽  
M. Sluzewski ◽  
W. J. J. van Rooij ◽  
C. C. Tijssen ◽  
J. L. J. M. Teepen

2014 ◽  
Vol 21 (3) ◽  
pp. 301-304
Author(s):  
Amit Agrawal

Abstract Meningiomas arising from the falcotentorial junction are the rarest subgroup of tentorial menigiomas. Because of the distance from the brain surface and the surrounding deep cerebral veins these lesions are difficult and dangerous to treat surgically. A 45-year-old female presented with the history of progressive headache, disorientation, unsteadiness, and urinary incontinence for over 6 months. The patient developed difficulty in swallowing, and weakness of all four limbs for the last 7 days. CT scan brain plain and contrast showed a large well defined, homogenously enhancing mass lesion in the peineal region with compression of the upper brain stem and obstructive hydrocephalus. Inspite of the good surgical decompression the patient did not do well. As described in the literature, the compression of the midbrain can cause severe respiratory disturbances with fatal outcome; probably the similar mechanism resulted in poor outcome in present case. As we noticed the diffuse hypodensity in midbrain on CT scan, similar findings have been described in literature in cases of transtentorial herniation with poorer outcome.


1976 ◽  
pp. 210-261 ◽  
Author(s):  
Georges Salamon ◽  
Yun Peng Huang ◽  
P. Michotey ◽  
N. Moscow ◽  
Ch. Raybaud ◽  
...  

Radiology ◽  
1955 ◽  
Vol 64 (2) ◽  
pp. 161-177 ◽  
Author(s):  
Bernard S. Wolf ◽  
Charles M. Newman ◽  
Benno Schlesinger

Author(s):  
Diederik O. Bulters ◽  
Andrew Durnford

The first part of this chapter describes normal neurovascular anatomy including its embryology, histology, and normal arterial variants. It includes angiographic arterial anatomy and also the structures and territories supplied by specific vessels. The anatomy of the venous sinuses and both the superficial and deep cerebral veins are described. The second part details normal cerebral neurophysiology, including autoregulation and the control of cerebral perfusion. It covers the myogenic, metabolic, and neurogenic mechanisms of cerebral blood flow and vessel diameter regulation. Finally, the role and influence of mannitol on cerebral blood flow is described, and how although it acutely reduces cerebral volume and intracranial pressure, its exact mechanism of action remains unclear.


2012 ◽  
Vol 27 (1_suppl) ◽  
pp. 107-113 ◽  
Author(s):  
P J Van Den Berg ◽  
L H Visser

A new venous disorder, chronic cerebrospinal venous insufficiency (CCSVI), has been proposed in patients with multiple sclerosis (MS). It is a vascular condition characterized by an impaired cerebrospinal venous drainage due to obstructions in the main extracranial cerebrovenous outflow routes (i.e. internal jugular veins [IJV] and/or azygos veins). In this review, the studies which assessed the prevalence of CCSVI in MS by echo colour Doppler (ECD) will be discussed. The technical aspects of determination of the five CCSVI criteria: (1) reflux in the IJV and/or vertebral veins in supine and upright position, (2) reflux in the deep cerebral veins, (3) high-resolution B-mode proximal IJV stenosis, (4) flow not Doppler detectable in IJVs and/or vertebral veins (VVs) and (5) reverted postural control of the main cerebrovenous outflow pathway are described in detail. We conclude that so far there are many studies with contradictory results, and as yet a strong scientific base to support the evidence for a causative relationship of CCSVI and MS is lacking. Recent studies call into question the validity of using ECD as a proper and reliable test for the diagnosis of CCSVI. One explanation for the variety in interpretation of the individual CCSVI criteria, with the wide-ranging percentages CCSVI, could be the different methods by using ECD to determine various criteria.


1955 ◽  
Vol 12 (3) ◽  
pp. 256-277 ◽  
Author(s):  
Paul M. Lin ◽  
John F. Mokrohisky ◽  
Herbert M. Stauffer ◽  
Michael Scott

2016 ◽  
Vol 175 (5) ◽  
pp. 18-25 ◽  
Author(s):  
L. M. Tibekina ◽  
T. A. Shumakova ◽  
A. A. Nikolaeva ◽  
Yu. A. Shcherbuk

Investigations were carried out in 24 patients in order to evaluate information value of the data of clinical, laboratory, neuroradiological methods of research and develop the diagnostic algorithm in case of cerebral venous thrombosis (CVT). The main group consisted of 11 patients (7 male, 4 female, average age 49,1±4,3) with CVT. The comparison group included 13 patients (6 male, 7 female; average age 68,1±9,5) with ischemic stroke (IS) of moderate severity. There were revealed changes in blood and cerebrospinal fluid (CSF) as form of leukocytosis of blood and moderately increased cell count with elevated protein in CSF and blood in case of CTV. The authors noted an elevated protein in CSF and blood and leukocytosis with predominant lymphopenia in blood and neurophilic predominance in CSF within the reference range of CSF in patient with ischemic stroke. The epileptic attacks, meningeal syndromes, headaches were more often among clinical syndromes at CTV than in case of ischemic stroke. The algorithm of neuroimaging research methods and modes of MRI were determined and allowed an effective diagnostics of damages of venous sinuses, superficial and deep cerebral veins in case of urgent hospitalization of patients. It was possible to suggest the venous pathology in 7 (63,6%) cases due to SKT (without contrast) and in case of application of MR venography (2D TOFmode), there were revealed 100% of cases.


PEDIATRICS ◽  
1993 ◽  
Vol 91 (6) ◽  
pp. 1219-1220
Author(s):  
ELKE H. ROLAND ◽  
OLOF FLODMARK ◽  
ALAN HILL

In Reply.— Rooman et al report on an infant who developed thalamic hemorrhage associated with a urinary tract infection caused by Escherichia coli. They speculate that E coli endotoxin may enhance clotting potential via the extrinsic cascade and decrease endothelial thrombomodulin expression, thus shifting the hemostatic balance and increasing the risk of cerebral venous infarction. In our article,1 we suggest that the most probable mechanism causing thalamic/intraventricular hemorrhage in the full-term newborn is thrombosis of the deep cerebral veins resulting in infarction and secondary hemorrhage in the thalamic region.


Sign in / Sign up

Export Citation Format

Share Document