scholarly journals Intracerebral steal phenomenon induced focal reversible vasogenic edema and decrease in cerebral blood flow after carotid endarterectomy

2020 ◽  
Vol 11 ◽  
pp. 161
Author(s):  
Yu Shimizu ◽  
Katsuhiro Tsuchiya ◽  
Norihiro Fujisawa

Background: Intracerebral steal phenomenon (ISP) is a rare complication following surgical treatment of carotid stenosis. However, the factors responsible remain unknown. We described the rear case of the ISP who had vasogenic edema and cerebral blood flow (CBF) decline and presented with hemiparesis after carotid endarterectomy (CEA). Case Description: A 72-year-old male with stenosis of the bilateral carotid artery (NASCET right 90% and left 70%) presented with cerebral hypoperfusion manifesting as right hemiparesis, after left CEA. Fluid-attenuated inversion recovery images showed edema of the motor area around an old infarction and a decrease in CBF. This lesion was an area of vasogenic edema caused by ISP and focal cerebral hypoperfusion. CBF of the contralateral cerebral hemispheres had increased. The treatment with an intravenous infusion of a free radical scavenger and glycerol improved the patient’s symptoms and brain edema. Magnetic resonance imaging showed a gradual decline in the brain edema, which completely disappeared 2 weeks after CEA. He was discharged with no neurological deficit. Conclusion: In this report, we described the case of a patient with ISP who had vasogenic edema induced by CBF decline and presented with hemiparesis following CEA. This is the first report of progressing focal vasogenic edema caused by ISP after endarterectomy.

2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Qian Liu ◽  
Mohammad Iqbal H. Bhuiyan ◽  
Ruijia Liu ◽  
Shanshan Song ◽  
Gulnaz Begum ◽  
...  

Abstract Background Chronic cerebral hypoperfusion (CCH) causes white matter damage and cognitive impairment, in which astrogliosis is the major pathology. However, underlying cellular mechanisms are not well defined. Activation of Na+/H+ exchanger-1 (NHE1) in reactive astrocytes causes astrocytic hypertrophy and swelling. In this study, we examined the role of NHE1 protein in astrogliosis, white matter demyelination, and cognitive function in a murine CCH model with bilateral carotid artery stenosis (BCAS). Methods Sham, BCAS, or BCAS mice receiving vehicle or a selective NHE1 inhibitor HOE642 were monitored for changes of the regional cerebral blood flow and behavioral performance for 28 days. Ex vivo MRI-DTI was subsequently conducted to detect brain injury and demyelination. Astrogliosis and demyelination were further examined by immunofluorescence staining. Astrocytic transcriptional profiles were analyzed with bulk RNA-sequencing and RT-qPCR. Results Chronic cerebral blood flow reduction and spatial working memory deficits were detected in the BCAS mice, along with significantly reduced mean fractional anisotropy (FA) values in the corpus callosum, external capsule, and hippocampus in MRI DTI analysis. Compared with the sham control mice, the BCAS mice displayed demyelination and axonal damage and increased GFAP+ astrocytes and Iba1+ microglia. Pharmacological inhibition of NHE1 protein with its inhibitor HOE642 prevented the BCAS-induced gliosis, damage of white matter tracts and hippocampus, and significantly improved cognitive performance. Transcriptome and immunostaining analysis further revealed that NHE1 inhibition specifically attenuated pro-inflammatory pathways and NADPH oxidase activation. Conclusion Our study demonstrates that NHE1 protein is involved in astrogliosis with pro-inflammatory transformation induced by CCH, and its blockade has potentials for reducing astrogliosis, demyelination, and cognitive impairment.


1972 ◽  
Vol 6 (1) ◽  
pp. 14-19 ◽  
Author(s):  
H.C. Engell ◽  
Gudrun Boysen ◽  
H.J. Ladegaard-Pedersen ◽  
H. Henriksen

2000 ◽  
Vol 92 (6) ◽  
pp. 1009-1015 ◽  
Author(s):  
Seiji Yamamoto ◽  
Weiyu Teng ◽  
Shigeru Nishizawa ◽  
Takeharu Kakiuchi ◽  
Hideo Tsukada

Object. The hydroxyl radical scavenger (±)-N,N′-propylenedinicotinamide (AVS) has been shown to ameliorate the occurrence of vasospasm following experimental subarachnoid hemorrhage (SAH) and to reduce the incidence of delayed ischemic neurological deficits (DINDs) in patients with SAH. The authors investigated whether prophylactic administration of AVS could improve cerebral blood flow (CBF) and cerebral glucose utilization (CGU) following SAH in rats.Methods. Anesthetized rats were subjected to intracisternal injection of blood (SAH group) or saline (control group). Either AVS (1 mg/kg/min) or saline (vehicle group) was continuously injected into the rat femoral vein. Forty-eight hours later, positron emission tomography scanning was used with the tracers 15O-H2O and 18F-2-fluoro-d-glucose to analyze quantitatively CBF and CGU, respectively, in the frontoparietal and occipital regions (12 regions of interest/group).In SAH rats receiving only vehicle, CBF decreased significantly (p < 0.05, Tukey's test) and CGU tended to decrease, compared with values obtained in control (non-SAH) rats receiving vehicle. In rats that were subjected to SAH, administration of AVS significantly (p < 0.05, Tukey's test) improved CBF and CGU in both the frontoparietal and occipital regions compared with administration of vehicle alone.Conclusions. Prophylactic administration of AVS improves CBF and CGU in the rat brain subjected to SAH, and can be a good pharmacological treatment for the prevention of DINDs following SAH.


DICP ◽  
1991 ◽  
Vol 25 (12) ◽  
pp. 1299-1301 ◽  
Author(s):  
Susan C. Fagan ◽  
James R. Ewing ◽  
Steven R. Levine ◽  
Gretchen E. Tietjen ◽  
Nabih M. Ramadan ◽  
...  

Dynamic cerebral blood flow (CBF) studies using acetazolamide or hypercapnia as a vasodilatory challenge have attempted to evaluate intracranial hemodynamics. We report two patients with asymptomatic internal carotid artery occlusion in whom the vasodilatory stimulus was a single oral dose of antihypertensive medication (prazosin hydrochloride or enalapril maléate). In both patients, changes in regional CBF occurred that were larger than those seen in nine normal controls. One patient experienced an improvement in regional CBF with a reduction in probe pair asymmetry. In the other patient, who had bilateral carotid artery disease, a decrease in regional CBF in all 16 probes (mean decrease 12 percent) and an accentuation of the predose asymmetry were observed. Both patients remained asymptomatic throughout the study. Assessing these effects on cerebral circulation may help identify patients at risk for iatrogenic focal cerebral ischemia and provide information regarding the functional status of the cerebral vasculature.


2018 ◽  
Vol 111 ◽  
pp. e686-e692
Author(s):  
Xu Wang ◽  
Bin Yang ◽  
Yan Ma ◽  
Peng Gao ◽  
Yabing Wang ◽  
...  

2019 ◽  
pp. 185-188
Author(s):  
Peter Novak

This case presents a patient with extreme fatigue and excessive sleepiness. The tilt test provoked decline in cerebral blood flow velocity (CBFv) associated with decline in end tidal CO2, indicative of hypocapnic cerebral hypoperfusion (HYCH). There was also mild small fiber neuropathy affecting predominantly autonomic fibers associated with mild autonomic dysfunction.


2019 ◽  
pp. 157-162
Author(s):  
Peter Novak

The tilt test showed orthostatic cerebral hypoperfusion syndrome (OCHOS) with intermittent reduction in cerebral blood flow velocity and vision loss. OCHOS is associated with reduced orthostatic cerebral blood flow velocity without orthostatic hypotension or arrhythmia.


2019 ◽  
pp. 153-156
Author(s):  
Peter Novak

The tilt test showed severe orthostatic cerebral hypoperfusion syndrome (OCHOS) with reduced cerebral blood flow velocity. OCHOS is associated with reduced orthostatic cerebral blood flow velocity without orthostatic hypotension or arrhythmia.


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