acute-onset, severe, recurrent reversible vasoconstriction
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2 RCVS A clinical and radiologic syndrome Characterized by acute-onset, severe, recurrent headache and reversible vasoconstriction of the cerebral arteries RCVS accounts for most benign thunderclap headaches" (Ducroset al, 2013 BMJ) Vasoconstriction is crucial for the diagnosis of RCVS However Initial angiogram can be (=looks like) normal However 3 days after onset 10 days after onset 90 days after onset 2
3 Sometimes too subtle (=arguable) to detect At 6 days after onset After 3 mo Overlaps with atherosclerosis, dissection, moyamoya disease At 6 days after onset At 8 days after onset AJNR: 24, April 2003 Overlaps with atherosclerosis, dissection, moyamoya disease At 6 days after onset At 8 days after onset At 2 days after onset 3
4 Does NOT reflect pathophysiology(headache, brain hemorrhage, PRES ) Does NOT show us a disease-specific finding Noninvasive imaging (MRA) has intrinsic limitations Flow-related artifact In-plane saturation artifact Invasive Imaging may worsen vasospasm Luminographic findings are not specific for RCVS pathophysiology High prevalence of intracranial atherosclerosis/mmd/dissection in Asians RCVS no intraluminal pathology Initial angiogram can be normal 4
5 Vasoconstriction + something special Tentative mechanism: sympathetic dysregulation, failure to maintain arterial tone, BBB breakdown Vasodilation and/or BBB breakdown Can be documented by CSF enhancement in CE-FLAIR Delayed Contrast-Enhanced FLAIR protocol Moresensitive than CE-T1WI Does not show an enhancement of the normal vascular structures or normal meninges More sensitive to lower Gd concentrations Has been widely used in various conditions to test Wardlawet al, Ann neurol65(2): disruption of the BBB integrity Yang et al, Stroke 42(11): Ivenset al, J neurol257(4): Lee et al Korean J radiol17(1): Merino et al, AJNR 34(3): BBB disruption Passage of gadolinium to the CSF Gadolinium shortens T1 Disrupts the signal suppression of CSF in FLAIR imaging CSF appears hyperintense HARM Latour& Warachet al, 2004 Ann neurol 5
6 To document the presence of BBB breakdown in patients with RCVS To test the role of BBB breakdown for the diagnosis of RCVS and its complications Patients with thunderclap headache Onset <1mo Exclusion: aneurysmal SAH Recruited from ER, outpatient headache clinic, and inpatient consultation 6
7 Total 72 patients 29 (40%) showed angiographic findings compatible with RCVS (definite RCVS) 36 (50%) had normal neuroimaging 12 (17%): classified into probable RCVS by ICHD-3 beta 24 (33%): classified into primary thunderclap headache 7 (10%) had other secondary causes: arterial dissection, pituitary apoplexy, and ruptured cavernous angioma Noncontrast FLAIR CE-FLAIR 69.0% Enable the diagnosis of RCVS in angiogram-negative patients RCVS with typical angiogram (n=29) 25.0% 12.5% Normal angiogram (n=36) Probable RCVS (n=12) Primary Thunderclap Headache (n=24) 33.3% Probable RCVS by ICHD-3b 41.7% by ICHD-3 + BBB breakdown 0.0% Other secondary cause (n=7) 7
8 40.3% 48.6% 61.1% Angiographic finding BBB breakdown Clinical manifestation 0.0% 20.0% 40.0% 60.0% 80.0% Patients with RCVS+BBB breakdown are more likely to be/have Women (100%) Definite RCVS (87%) Neurological complications (26%) esp. SAH/PRES (22%) cf) None (0%) in patients with RCVS without BBB breakdown However, BBB breakdown was more extensive than the amount of hemorrhage/pres More number of vasoconstrictions However, BBB breakdown was not always located in the territory of narrowed artery 69.0% 25.0% 12.5% 0.0% 8
9 Univariable Multivariable OR 95% CI P OR 95% CI P Sex 0.43 ( ) Age 0.97 ( ) Mode of recruitment 1.67 ( ) Migraine 0.54 ( ) BP surge 5.44 ( ) ( ) Onset to MR (days) 0.88 ( ) Extent of BBB breakdown (per one territorial increase) 1.54 ( ) ( ) Number of vasoconstriction 1.15 ( ) Associated with csah Not restricted within the hemorrhaged region Associated with PRES Not restricted within the vasogenic edema Clinical implication BBB breakdown is present in 2/3 of patients with RCVS and specific for RCVS Enabled the diagnosis of RCVS in patients with diagnostic uncertainty Independently associated with increased risk of neurological complications Pathophysiological implication First study to document BBB breakdown in RCVS BBB breakdown as a bridging mechanism of neurological complications in RCVS The BBB breakdown implies an involvement of small vessels (cerebral capillaries/small arterioles) RCVS pathophysiology might not be limited to arteries 9
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