Republished: Primary intraventricular haemorrhage due to rupture of giant varix of the basal vein of Rosenthal in a patient with long-standing direct CCF: angiographic features and treatment considerations

2019 ◽  
Vol 12 (3) ◽  
pp. e3-e3
Author(s):  
Chinmay P Nagesh ◽  
Aneesh Mohimen ◽  
Santhosh K Kannath ◽  
Jayadevan E Rajan

Direct carotid cavernous fistulae (CCF) are often detected early and treated promptly resulting in a paucity of literature regarding its long-term evolution. We present a case of high flow post-traumatic direct CCF that was neglected for over 6 years and presented with a rare manifestation of primary intraventricular haemorrhage. Occlusions of the primary venous outlets likely resulted in engorgement of the deep venous system. The segmental anatomy of the shunting basal vein is critical to the clinical presentation and may range from basal ganglia or brainstem oedema/infarctions to uniquely, as in our case, isolated intraventricular haemorrhage secondary to variceal rupture. Treatment in such chronic cases requires a consideration of cerebral hyperperfusion syndrome necessitating deconstructive techniques with subsequent anticoagulation to avoid accelerated thrombosis of the venous varices.

2020 ◽  
Vol 83 (5) ◽  
pp. 453-457
Author(s):  
Montserrat González Delgado ◽  
Julien Bogousslavsky

Cerebral vasoconstriction is a normal physiological response under determined conditions to preserve a normal cerebral blood flow. However, there are several syndromes, with impaired cerebral autoregulation and cerebral vasoconstriction, not related with infection or inflammation, which share the same radiological and clinical presentation. We review here the cerebral hyperperfusion syndrome and related conditions such as hypertensive encephalopathy, posterior reversible encephalopathy syndrome, and reversible cerebral vasoconstriction syndrome. These syndromes might share the same pathophysiological mechanism with endothelial damage, cerebral vasoconstriction, blood-brain barrier disturbance, cerebral edema, and, occasionally, intracerebral hemorrhage, with fatal cases described in all. Despite knowledge of these syndromes, they still remain unknown to us. Why these entities present in some patients and not in others goes further than the actual understanding of these diseases. We have to consider that a genetic susceptibility and molecular disturbances may be involved. Thus, more studies are needed in order to better characterize such syndromes.


2002 ◽  
Vol 15 (5) ◽  
pp. 501-506
Author(s):  
G. Ferrari

An aneurysm is a swelling along a blood vessel. The majority of aneurysms are saccular in shape and result from a combination of factors. Prevalence of unruptured aneurysms varies from 0.4–3.6% to 3.7–6%. The frequency of asymptomatic aneurysm rupture is about 1–2%. The clinical presentation of aneurysms occurs due to: rupture (subarachnoid haemorrhage SAH, intraparenchymal haemorrhage, intraventricular haemorrhage); Warning Leak; nonhaemorrhagic manifestation. The incidence of SAH is steady at 10.5/100 000 per year. Clinical diagnosis of SAH may be straightforward if all major symptoms are present. However, in case of few symptoms or headache as the only symptom (Warning Leak) diagnosis may be difficult and the risk of misdiagnosis is high. In case of suspect SAH, CT is the first choice examination. However, lumbar puncture is still an indispensable step in the exclusion of SAH in patients with a convincing history and negative imaging. In case of untreated ruptured aneurysm there is a 3–4% risk of rebleeding in the first 24 hours, a 1–2% per day risk in the first month, and a long-term risk of 3% per year after three months. Urgent evaluation and treatment of patients with suspected SAH are strongly recommended.


2017 ◽  
Author(s):  
Beata Jurecka-Lubieniecka ◽  
Barbara Michalik ◽  
Grzegorz Bula ◽  
Jacek Gawrychowski ◽  
Dariusz Kajdaniuk ◽  
...  

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