scholarly journals Subclinical Brain Lesion in MRI is a Potential Indicative of PFO-Related Migraine in Younger Patients

Author(s):  
Fei Ma ◽  
Xiang Luo ◽  
Fan Lin ◽  
Rui Li ◽  
Qiang Zhou ◽  
...  

Abstract Background: The causal relationship of migraine with PFO remains controversial and a major question unresolved is how to define the PFO-attributable migraine.Objective: In this study, we evaluated diffusion-weighted-imaging (DWI) presentation in brain MRI and its association with PFO in patients with migraine. We aimed to define if brain lesion could be a potential indicative of PFO-related migraine. Methods: Consecutive migraine patients <60 years with or without aura from 2017 to 2019 who underwent transthoracic echocardiography (TTE) or transcranial Doppler (TCD) examination with agitated saline contrast (ASC) injection were assessed for right-to-left shunt (RLS). We then assessed brain DWI findings in the patients and tested the association of brain lesion with PFO. Results: A total of 424 patients with mean age 44.39±12.06 years were included in the study. Among them, 244 patients (57.5%) had PFO and 246 patients (58%) had subclinical brain lesion. The brain lesion presented as single or multiple scattered lesion. Although there was no association between PFO prevalence and brain lesion in the total cohort (OR 0.499, 95% CI 0.236-1.052), the association was significant in patients who were aged less than 46 years (OR 3.614 in group of age<34 years, 95% CI 1.128-11.580, and 3.132 in group of 34 years≤age<46 years, 95% CI 1.334-7.350, respectively). DWI lesion in patients with PFO was more coming from anterior or multiple than posterior vascular territory (p=0.033). DWI lesion numbers, location and RLS amounts were not affecting the association between DWI lesion and PFO. Conclusions: This study demonstrated that subclinical brain lesion are associated with PFO in migraineurs younger than 46 years. The DWI pattern of brain lesions may be used as a potential predictor of PFO-related migraine in patients who are aged less than 46 years and aids in selection of appropriate candidates for PFO closure.

2021 ◽  
Vol 29 (1) ◽  
pp. 230949902110011
Author(s):  
Kyoko Okuno ◽  
Yukihiro Kitai ◽  
Toru Shibata ◽  
Hiroshi Arai

Purpose: To investigate the risk factors for hip displacement in patients with dyskinetic cerebral palsy (DCP). Methods: We evaluated 81 patients with DCP, 45 males and 36 females, aged 10–22 years, risk factors for hip displacement were evaluated using multivariate logistic regression analysis with primary brain lesions, Gross Motor Function Classification System (GMFCS) level, gestational age, birth weight, Cobb’s angle, and complication of epilepsy as independent factors. Hip displacement was defined as migration percentage >30%. Primary brain lesions were classified into globus pallidus (GP), thalamus and putamen (TP), and others using brain magnetic resonance imaging (MRI). Perinatal and clinical features were compared between patients with GP lesions and those with TP lesions. Results: Hip displacement was observed in 53 patients (67%). Higher GMFCS levels (p = 0.013, odds ratio [OR] 2.6) and the presence of GP lesions (p = 0.04, OR 16.5) were independent risk factors for hip displacement. Patients with GP lesions showed significantly higher GMFCS levels, more frequent hip displacement, and lower gestational age and birth weight than those with TP lesions. Conclusion: Primary brain lesion location may be an important factor in predicting hip displacement among patients with DCP. Appropriate risk assessment using brain MRI may contribute to the early detection and intervention of hip displacement because brain lesion location can be assessed during infancy before GMFCS level is decided.


1998 ◽  
Vol 35 (5) ◽  
pp. 409-411 ◽  
Author(s):  
Y. Noda ◽  
Y. Uchinuno ◽  
H. Shirakawa ◽  
S. Nagasue ◽  
N. Nagano ◽  
...  

A bovine fetus aborted at 187 days of gestation was serologically and immunohistopathologically examined. Serum and cerebrospinal fluid samples had high titers of virus-neutralizing antibody for Aino virus. A severe necrotizing encephalopathy was noted. Aino virus antigen was demonstrated in neuroglial cells within the brain lesion. The destruction of developing neuronal cells appeared to be a significant feature of the pathogenesis of lesions due to Aino virus infection in the central nervous system.


2019 ◽  
Vol 1 (Supplement_1) ◽  
pp. i11-i11
Author(s):  
Joseph Megyesi ◽  
David Macdonald

Abstract INTRODUCTION: EGFR-targeted agents can be useful in the treatment of systemic metastatic cancer including that which has spread to the brain. We present the case of a patient with two different EGFR mutations that responded to receptor blockade. CASE REPORT: A 38 year old right-handed female presented with a one week history of progressive left-sided weakness and focal seizures. Neuroimaging revealed multiple enhancing brain lesions and a lesion in the left maxillary antrum. Body imaging revealed a right lung mass, hilar and mediastinal nodes and multiple bony lesions. Biopsy of the maxillary antrum lesion showed metastatic poorly differentiated adenocarcinoma, TTF-1 positive, suggesting a lung primary. ALK was not mutated but there was an EGFR mutation (exon 19 deletion). The patient underwent treatment with dexamethasone, levetiracetam, whole brain radiation and afatinib, an oral EGFR-targeted agent. Most of the brain lesions responded completely with only two small residual lesions. Seizures were controlled. There was major partial response from the systemic lesions. Two years later the patient was clinically well but the lung lesion, mediastinal nodes and bony lesions were all enlarging. A new pituitary lesion was identified on brain MRI. A liquid biopsy (blood) revealed a T790M mutation and the patient underwent stereotactic body radiation and EGFR-targeted therapy with osimertinib. All lesions responded to treatment and four years after initial diagnosis the patient is clinically well with stable disease. DISCUSSION: Successful treatment of widespread metastatic disease is possible with the use of multiple EGFR-targeted agents in certain patients.


Author(s):  
C. Cavestro ◽  
L. Richetta ◽  
M. R. L'Episcopo ◽  
E. Pedemonte ◽  
S. Duca ◽  
...  

Background:Some reports demonstrated vascular alterations in brain magnetic resonance imaging (MRI) in migraineurs and a relationship between circle of Willis (Circle) variants and lacunar brain infarcts. We examined anomalies of the whole circle of Willis and their relationship with vascular brain lesions in migraineurs, to identify any possible vascular mechanism in migraine.Methods:We studied, with a cohort controlled study, the circle of Willis in migraineurs seen consecutively in our Headache Center, and in non-headache controls, using angio-MRI of the brain. Statistical analysis used ANOVA, Scheffè's criterion, t-student test.Results:We recruited 270 migraineurs (204 without aura (MWOA), 66 with aura (MWA) and 159 controls. Migraineurs presented an anatomical variant in 108 (40%) cases with 34 controls (21.4%) presenting a variant. We found a significant association between MWOA and variants (OR=2.4 CI95% [1.5 to 3.9]) and between MWA and variants (OR=3.2 CI95% [1.6 to 4.1]). Unilateral posterior variants with basilar hypoplasia are statistically associated only with MWA compared to controls (OR=9.2, CI95% [2.3 to 37.2]). Thirty-three percent of MWOA and 24% of MWA sufferers present some kind of brain lesion, included 2% of infra-tentorial lesions. We did not find any statistical association between the presence of Circle variants and ischemic lesions on MRI (OR=1.5 CI95% [0.68; 1.94]), or with infratentorial lacunar lesions (OR=1.58 CI95% [0.48 to 5.24]).Conclusions:Anatomical variants of the Circle of Willis are significantly more frequent in migraineurs; posterior anomalies are more frequent in MWA, suggesting a vascular mechanism provoking changes in cerebral blood flow, thereby stimulating cortical spreading depression.


2011 ◽  
Vol 18 (1) ◽  
pp. 113-115 ◽  
Author(s):  
Ju-Hong Min ◽  
Byoung Joon Kim ◽  
Kwang Ho Lee

We report the case of a patient who developed extensive brain lesions during fingolimod (FTY720) treatment in the TRANSFORMS study. His initial diagnosis was multiple sclerosis, but after encephalopathy anti-aquaporin4 antibody (anti-AQP4 Ab) was detected, it was changed to neuromyelitis optica spectrum disorder. After treatment with fingolimod, he developed bilateral extensive brain lesions. The brain MRI showed lesions predominantly involving the right frontal and parietal lobes, with vasogenic edema and enhancement. He had residual encephalomalacia and no recurrence with steroid treatment over 3 years following withdrawal of fingolimod.


Author(s):  
Sun Jay Yoo ◽  
Jody Mou ◽  
Reena Elizebath ◽  
Ananyaa Sivakumar ◽  
Rene DeBrabander ◽  
...  

Abstract Access to deep-seated brain lesions (e.g., tumors, aneurysms, hematomas, and other malformations) is challenging due to the potential for retraction-induced injury. Traditionally, neurosurgeons use dissection and blade retractors to push apart tissue to visualize and operate on target lesions. These blades apply focal pressure onto the brain, resulting in ischemia, edema, and parenchymal trauma, leading to complications in up to 29% of cases. Tubular retractors were introduced to distribute forces radially and have led to improved safety and clinical outcomes. However, reports indicate that tubular retractors still led to complications in up to 9.1% of cases. Other concerns include significant pressure in the direction of insertion and the displacement of anatomic landmarks leading to inaccurate stereotaxis. We present a novel, minimally-invasive brain retractor that utilizes an expandable soft balloon to further reduce retraction-induced injury and increase stereotactic accuracy with a minimal port of entry. The device consists of a balloon catheter system, a clear sheath, and integration with neuronavigation stylets. This approach can reduce the rate of iatrogenic injury and improve clinical outcomes for brain lesion operations. Furthermore, we illustrate the efficacy of this device in use compared to those of conventional tubular and blade retractors in a pig cadaver.


2020 ◽  
Vol 154 (Supplement_1) ◽  
pp. S38-S38
Author(s):  
H Tomac Pavosevic ◽  
S Zaheer ◽  
G M Kleinman

Abstract Introduction/Objective Acute hemorrhagic leukoencephalitis (Weston-Hurst syndrome) is a rare, fulminant inflammatory hemorrhagic demyelination of the brain white matter, and it is considered to be the most severe form of acute disseminated encephalomyelitis (ADEM). Herein we describe a case of 6-year-old boy presenting with elevated intracranial pressure and uncal herniation. Brain MRI showed a large right temporoparietal T2 hyperintense lesion with edema, abnormal perivascular enhancement and midline shift. Emergent decompressive craniotomy with brain biopsy was performed. Results H&E sections of the brain lesion revealed neutrophilic small vessel vasculitis with extravasation of blood and fibrin. Predominantly in a perivascular distribution were infiltrates of neutrophils and in areas foamy macrophages. Additionally, the white matter was studded with hemorrhages of varying size. Sections stained with Luxol Fast Blue for myelin and with a neurofilament immunostain for axons were compared to reveal selective perivascular loss of myelin with relative sparing of axons. Conclusion The constellation of acute hemorrhages, neutrophilic infiltration and selective loss of myelin with relative sparing of axons is characteristic of this exceptional, hyperacute variant of acute disseminated encephalomyelitis. Histomorphologic diagnosis is characteristic and may be crucial for timely decision for treatment of this often fatal disease.


Author(s):  
Ian Q. Whishaw ◽  
Megan Okuma

A brain lesion is an area of damage, injury, or abnormal change to a part of the brain. Brain lesions may be caused by head injury, disease, surgery, or congenital disorders, and they are classified by the cause, extent, and locus of injury. Lesions cause many behavioral symptoms. Symptom severity generally corresponds to the region and extent of damaged brain. Thus, behavior is often a reliable indicator of the type and extent of a lesion. Observations of patients suffering brain lesions were first recorded in detail in the 18th century, and lesion studies continue to shape modern neuroscience and to give insight into the functions of brain regions. Recovery, defined as any return of lost behavioral or cognitive function, depends on the age, sex, genetics, and lifestyle of patients, and recovery may be predicted by the cause of injury. Most recovery occurs within the first 6 to 9 months after injury and likely involves a combination of compensatory behaviors and physiological changes in the brain. Children often recover some function after brain lesions better than adults, though both children and adults experience residual deficits. Brain lesion survival rates are improved by better diagnostic tools and treatments. Therapeutic interventions and treatments for brain lesions include surgery, pharmaceuticals, transplants, and temperature regulation, each with varying degrees of success. Research in treating brain lesions is progressing, but in principle a cure will only be complete when brain lesions are replaced with healthy tissue.


2019 ◽  
Vol 21 (Supplement_3) ◽  
pp. iii94-iii94
Author(s):  
J F Megyesi ◽  
D R Macdonald

Abstract INTRODUCTION EGFR-targeted agents can be useful in the treatment of systemic metastatic cancer including that which has spread to the brain. We present the case of a patient with two different EGFR mutations that responded to receptor blockade. CASE REPORT A 38 year old right-handed female presented with a one week history of progressive left-sided weakness and focal seizures. Neuroimaging revealed multiple enhancing brain lesions and a lesion in the left maxillary antrum. Body imaging revealed a right lung mass, hilar and mediastinal nodes and multiple bony lesions. Biopsy of the maxillary antrum lesion showed metastatic poorly differentiated adenocarcinoma, TTF-1 positive, suggesting a lung primary. ALK was not mutated but there was an EGFR mutation (exon 19 deletion). The patient underwent treatment with dexamethasone, levetiracetam, whole brain radiation and afatinib, an oral EGFR-targeted agent. Most of the brain lesions responded completely with only two small residual lesions. Seizures were controlled. There was major partial response from the systemic lesions. Two years later the patient was clinically well but the lung lesion, mediastinal nodes and bony lesions were all enlarging. A new pituitary lesion was identified on brain MRI. A liquid biopsy (blood) revealed a T790M mutation and the patient underwent stereotactic body radiation and EGFR-targeted therapy with osimertinib. All lesions responded to treatment and four years after initial diagnosis the patient is clinically well with stable disease. DISCUSSION Successful treatment of widespread metastatic disease is possible with the use of multiple EGFR-targeted agents in certain patients.


Neurology ◽  
2019 ◽  
Vol 92 (15) ◽  
pp. e1698-e1708 ◽  
Author(s):  
Afonso P. Liberato ◽  
Eric J. Mallack ◽  
Razina Aziz-Bose ◽  
Doug Hayden ◽  
Arne Lauer ◽  
...  

ObjectiveTo describe the brain MRI findings in asymptomatic patients with childhood cerebral adrenoleukodystrophy (CCALD).MethodsWe retrospectively reviewed a series of biochemically or genetically confirmed cases of adrenoleukodystrophy followed at our institution between 2001 and 2015. We identified and analyzed 219 brain MRIs from 47 asymptomatic boys (median age 6.0 years). Patient age, MRI scan, and brain lesion characteristics (e.g., contrast enhancement, volume, and Loes score) were recorded. The rate of lesion growth was estimated using a linear mixed effect model.ResultsSixty percent of patients (28/47) showed brain lesions (median Loes score of 3.0 points; range 0.5–11). Seventy-nine percent of patients with CCALD (22/28) had contrast enhancement on first lesional or subsequent MRI. Lesion progression (Loes increase of ≥0.5 point) was seen in 50% of patients (14/28). The rate of lesion growth (mL/mo) was faster in younger patients (r = −0.745; p < 0.0001). Older patients (median age 14.4 y/o) tended to undergo spontaneous arrest of disease. Early lesions grew 46× faster when still limited to the splenium, genu of the corpus callosum, or the brainstem (p = 0.001).ConclusionWe provide a description of CCALD lesion development in a cohort of asymptomatic boys. Understanding the early stages of CCALD is crucial to optimize treatments for children diagnosed by newborn screening.


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