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1 ry of the upper extremity after a unilateral brain lesion.
2 hich revealed a non-specific enhancing focal brain lesion.
3 nd there is no clear relation to location of brain lesion.
4 ogical changes that occur distant to a focal brain lesion.
5 ulnerability of the behavior to a particular brain lesion.
6 chanisms that support brain recovery after a brain lesion.
7 ction in blood pressure and failed to reduce brain lesion.
8  approach to the LV developed at least 1 new brain lesion.
9 enotes brain dysfunction remote from a focal brain lesion.
10 ght intraorbital optic nerve tumor without a brain lesion.
11  may be indicated in HIV patients with focal brain lesion.
12  denial of motor deficits contralateral to a brain lesion.
13 zing neurological symptoms in the setting of brain lesions.
14 ls, thus contributing to tissue damage in MS brain lesions.
15 ially vulnerable to ischemic and hemorrhagic brain lesions.
16 mic disease have diminished efficacy against brain lesions.
17 lations and for understanding recovery after brain lesions.
18 erize the presence and extent of hippocampal brain lesions.
19  human neurological diseases with widespread brain lesions.
20 ould be monitored for cognitive problems and brain lesions.
21 nal outcome, and survival in adult rats with brain lesions.
22  heavily on the study of patients with focal brain lesions.
23 ry), demyelinating disorders, and infectious brain lesions.
24  mainly been tested by modelization of focal brain lesions.
25 0.81 versus 2.23 mm, P=0.05) of new ischemic brain lesions.
26 8 patients, who presented with new/enlarging brain lesions.
27 nance imaging of the brain revealed multiple brain lesions.
28 oms, reduces neuroinflammation, and prevents brain lesions.
29  mammalian target of rapamycin and disabling brain lesions.
30  led to a marked increase in necrosis of the brain lesions.
31 2009 to identify progression of MRI-measured brain lesions.
32 ne of ten patients had reductions in size of brain lesions.
33 tibility to heat-induced seizures and cystic brain lesions.
34 ics of early active demyelinating NMO and MS brain lesions.
35 ssociation of retinal microvascular signs to brain lesions.
36  the study of vascular and other acute focal brain lesions.
37  perceive than ungrouped ones after parietal brain lesions.
38 ic changes during recovery of function after brain lesions.
39 s distinguish CNS lymphoma from benign focal brain lesions.
40 etic variability, or to variable degree from brain lesions.
41  some cases are acquired, secondary to focal brain lesions.
42 ulting from clinically unrecognized vascular brain lesions.
43 om networks derived from patients with focal brain lesions.
44  roles in the repair process after traumatic brain lesions.
45 trasbourg and Liverpool) for the presence of brain lesions.
46 us indexes of cerebral blood flow with these brain lesions.
47 (212 males; 190 females) with chronic, focal brain lesions.
48  25 patients suffered from pre- or perinatal brain lesions.
49 12, respectively) than those without frontal brain lesions (1/11, P's < 0.05).
50     Clinical brain scans of 83 patients with brain lesions (67 in the training and 16 in the validati
51 evealed that 7 (12.5%) of the 56 total acute brain lesions after ablation formed a persistent glial s
52  incidence, number, and size of new ischemic brain lesions after CAS.
53         We describe the development of fetal brain lesions after Zika virus (ZIKV) inoculation in a p
54         There was a trend toward more severe brain lesions amongst patients with brain lesions and pl
55 ative disorder characterized by pathological brain lesions and a decline in cognitive function.
56 neurons from the postnatal SVZ contribute to brain lesions and abnormal circuit remodeling in forebra
57 mental brain ischemia as a paradigm of acute brain lesions and additionally investigated a large coho
58                                     Vascular brain lesions and atherosclerosis are two similar condit
59 ment is, in turn, associated with structural brain lesions and autonomic dysfunction, which may predi
60 gle course of rituximab reduced inflammatory brain lesions and clinical relapses for 48 weeks.
61 ynamic mechanisms contributing to structural brain lesions and cognitive impairment in the presence o
62 ses in which a temporal relationship between brain lesions and criminal behavior was implied but not
63 the brain at study entry for the presence of brain lesions and enhancing characteristics.
64 ined from 15 consecutive patients with focal brain lesions and from 14 healthy control subjects.
65            Evidence from patients with focal brain lesions and from healthy volunteers using function
66 rred for neurosurgical assessment of unclear brain lesions and had undergone (18)F-FET PET.
67 del replicates several features of human TSC brain lesions and implicates an important function of Ts
68  (CNTF) has been shown to be expressed after brain lesions and in particular after demyelination.
69 rx1(-/-) mice exhibited significantly larger brain lesions and increased motor deficits following CCI
70           Importantly, the pathognomonic MRI brain lesions and neurohistopathologic findings are reve
71      Of these 94 patients, 11 had measurable brain lesions and no previous radiotherapy to the brain,
72 and two control groups: SCD patients without brain lesions and non-sickle cell sibling controls (n =
73 ils the microstructural abnormalities of the brain lesions and of the morphologically normal appearin
74   Hoarding has been shown to be sensitive to brain lesions and pharmacological agents, and is a suita
75 e severe brain lesions amongst patients with brain lesions and placental abnormality (55% moderate/se
76  from the neonatal and juvenile SVZ generate brain lesions and structural abnormalities, which would
77 rmed to analyze the rate of ablation-related brain lesions and their effect on cognitive function.
78 psilateral hippocampal sclerosis as the only brain lesion, and underwent amygdalohippocampectomy.
79 nd overt cognitive impairment and structural brain lesions, and explored the role of autonomic dysfun
80 sodes of encephalopathy, bilateral symmetric brain lesions, and high excretion of organic acids that
81 ility of MSCs as OV carriers to disseminated brain lesions, and provides a clinically applicable ther
82           This data shows that demyelinating brain lesions are associated with the presence of microb
83                                        These brain lesions are associated with the symptom severity o
84                                    Ischaemic brain lesions are associated with white matter changes a
85                                        Focal brain lesions are assumed to produce language deficits b
86                                 MRI-detected brain lesions are common after left atrial catheter abla
87                            These parenchymal brain lesions are considered key contributors to cogniti
88 at the base of spontaneous regression of the brain lesions are discussed.
89                 Acute, subclinical ischaemic brain lesions are frequent but previously underestimated
90 ntibody-positive patients have revealed that brain lesions are not uncommon in NMO, and some patterns
91 reas and the disturbance introduced by focal brain lesions are poorly understood.
92                           Whereas multifocal brain lesions are present on MRI in many patients with a
93 ne in post-traumatic coma or when structural brain lesions are probable or possible causes.
94                                     Although brain lesions are readily detected, magnetic resonance i
95                       When clinically silent brain lesions are seen on MRI, the likelihood of develop
96 erous sclerosis complex (TSC) and associated brain lesions are thought to arise from abnormal embryon
97 n tremors, such as those induced by drugs or brain lesions, are also important to recognize because t
98  functional differentiation in breast cancer brain lesions as a novel therapeutic strategy.
99 apamycin (mTOR) activation in TSC-associated brain lesions as well as in various cancers.
100 e initiating event in the development of TSC brain lesions as well as underscore the importance of Ts
101 lanning resective surgeries in patients with brain lesions, as well as investigations into structural
102 d how and when dysfunctional MCT8 can induce brain lesions associated with the Allan-Herndon-Dudley s
103 , aberrantly activated Erk was also found in brain lesions associated with tuberous sclerosis (TSC).
104 fference in new positive postprocedure DWMRI brain lesions at 2 days after TAVI in potentially protec
105 had central veins visible in the majority of brain lesions at baseline.
106           CSF from MS patients with enhanced brain lesions at magnetic resonance imaging was able to
107 ledge of different types of hypoxic-ischemic brain lesions based on our personal experience and MR im
108 s expands, the utility of studying permanent brain lesions bears re-examination.
109                  Additionally, patients with brain lesions but not controls exhibited significant dif
110    Neglect signs do not only depend on focal brain lesions, but also on dysfunction of large-scale br
111                     In human demyelinated MS brain lesions, but not normal appearing white matter, ol
112 nce nitrogen) treatment following mechanical brain lesion by controlled cortical impact.
113                                   Mechanical brain lesion by controlled cortical impact.
114 phy as part of the Cardiac Abnormalities and Brain Lesions (CABL) study.
115 se from the Cardiovascular Abnormalities and Brain Lesions (CABL) study.
116 ing given powerful demonstrations that focal brain lesions can affect specific aspects of cognition.
117 curacy and the loss of such functions due to brain lesions can be catastrophic.
118 her differences between benign and malignant brain lesions can be depicted with fluorine 18 ((18)F) f
119 cal data from neurologic patients with focal brain lesions can be leveraged to advance our understand
120  evidence that propofol sedation after acute brain lesions can have a deleterious impact and implicat
121                                        Focal brain lesions can have important remote effects on the f
122  and we conclude that static models of adult brain lesions cannot be used to account for the dynamics
123                                In metastatic brain lesions carrying activated alpha(v)beta(3), VEGF e
124                              Here we analyze brain lesions causing acute onset freezing of gait to id
125 and use of antiepileptic drugs for different brain lesions causing epilepsy is not available.
126                                We studied 89 brain lesions causing hallucinations using a recently va
127 c resonance imaging measures of infarct-like brain lesions, cerebral microbleeds, total brain volume,
128  immune target is not the main substrate for brain lesion characteristics.
129                These results based on causal brain lesions complement prior neuroimaging studies in P
130 tic resonance imaging of angiomyolipomas and brain lesions, computed tomography of lung cysts, and pu
131 aine with clinical and sub-clinical vascular brain lesions, congenital heart defects, coronary heart
132 g outcome of having T2-weighted hyperintense brain lesions consistent with the 2010 McDonald MRI crit
133                                 How a single brain lesion could cause such a complex disorder is uncl
134 ; P=0.03), and significant reductions in the brain lesion count on magnetic resonance imaging (MRI) (
135                                              Brain lesion count was recorded from brain magnetic reso
136  were performed to determine whether age and brain lesion count were associated with adrenal findings
137                               Similar to the brain lesions described for human EEE, the NA EEEV-infec
138  (with 1 exception) were not associated with brain lesion development.
139 three main mechanisms of coma are structural brain lesions, diffuse neuronal dysfunction, and, rarely
140                                     Ischemic brain lesions discovered on DWI after CAS seem to be a m
141                                          MRI brain lesion distribution criteria were able to distingu
142                                              Brain lesions do not just disable but also disconnect br
143 ncluding psychiatric and neurologic disease, brain lesions, drug effect, and hearing impairment.
144 tive than flow reversal in reducing ischemic brain lesions during CAS through femoral approach.
145 iche of the adult brain, and in inflammatory brain lesions during experimental autoimmune encephalomy
146 umulative number of new gadolinium-enhancing brain lesions during the treatment phase and was analyse
147        The model also describes how specific brain lesions enhance the strength of the startle respon
148  A number of CD4(+) and CD8(+) T cells in MS brain lesions expressed GM-CSF.
149  fulminant encephalopathy and characteristic brain lesions following viral infection.
150 ciated with the clinical compensation of new brain lesion formation in RR-MS.
151 l giant cell astrocytomas (SEGAs) are common brain lesions found in patients with tuberous sclerosis
152 rst, we assessed ASIC1 expression in chronic brain lesions from post-mortem of patients with progress
153 eta(3) activation state that is critical for brain lesion growth.
154  extensive literature involving experimental brain lesions has implicated the hippocampus in context
155                   The study of patients with brain lesions has made major historical contributions to
156  new study mapping the functional effects of brain lesions has revealed a surprising map of human int
157                             Although various brain lesions have been found to affect performance on t
158  pure-tone thresholds and central MS-related brain lesions have not been assessed.
159 on-human animals with experimentally induced brain lesions have provided pivotal insights into the ne
160 ic brain areas and direct induction of focal brain lesions, human research has so far utilized predom
161 be assessed in patients suffering from focal brain lesions (i.e. connectomal diaschisis).
162  inattention to the side of space opposite a brain lesion in patients with unilateral neglect, primin
163                  These techniques detect new brain lesions in 25% to 50% of patients after both coron
164     Our observation of ZIKV-associated fetal brain lesions in a nonhuman primate provides a model for
165  used to precisely map and selectively model brain lesions in human and animals studies.
166 cm2 in adult mice recapitulates the CCM-like brain lesions in humans; the lesions display disrupted v
167 variants of these cells derived from bone or brain lesions in immunodeficient mice.
168 igraine with progression of any MRI-measured brain lesions in men.
169  spontaneously disseminate into the CSF from brain lesions in mice in a COX-2-dependent manner and ca
170 ) is the primary imaging technique to detect brain lesions in MS.
171                             Investigation of brain lesions in multiple sclerosis (MS) reveals a coord
172  of the nature, prognosis, and ways to treat brain lesions in neonatal infants has increased remarkab
173 hips between cognitive function and vascular brain lesions in patients with AF.
174          Establishing the diagnosis of focal brain lesions in patients with unexplained neurologic sy
175  MRI sequences is important to differentiate brain lesions in pediatric patients.
176 higher prevalence of asymptomatic structural brain lesions in people with migraine.
177 ction of CSF spermine reflects correction of brain lesions in these animals.
178  in CHD and may have a compounding effect on brain lesions in this high-risk population.
179 g has led to further characterization of the brain lesions in TSC.
180 iagnostic algorithms for the workup of focal brain lesions in which lymphoma is a consideration.
181      Eight patients with anterior prefrontal brain lesions including the FPC performed a four-armed b
182                                        Focal brain lesions increased EV release, and, following isola
183                                        Acute brain lesions induce profound alterations of the periphe
184                        We also observed that brain lesioning induced several metabolites with neuropr
185                                        Acute brain lesions induced dysbiosis of the microbiome and, i
186 ansplantation of fecal microbiota normalizes brain lesion-induced dysbiosis and improves stroke outco
187  of brain pathology by detecting any sign of brain lesions, infections, or dysfunction and can influe
188 predictable, and consistently sized necrotic brain lesions, inflammatory responses, and behavioral de
189 then test whether this network, derived from brain lesions, is abnormal in patients with idiopathic c
190 halopathy, which is characterized in part by brain lesions, lactic acidemia, excretion of ethylmaloni
191 , age of onset, disease severity, as well as brain lesion load and normalized brain volume from magne
192 neurological symptoms in patients with focal brain lesions localize to brain networks.
193 ne hundred three patients with focal, stable brain lesions mapped onto a reference brain were tested
194 hat language system organization after focal brain lesions may be marked by complex signatures of alt
195                       While it is known that brain lesions may selectively affect orthographic long-t
196 kely to be toxoplasmosis (n=8, 42.1%), focal brain lesion (n=5, 26.3%) or both (n=3, 15.8%).
197 ) with single or multiple contrast-enhancing brain lesions (n = 40) on MRI after radiation therapy of
198 g superior parietal cortex (n = 146), and no brain lesions (n = 55).
199  we assembled the largest known set of focal brain lesions (n = 581), derived from unselected patient
200                           Neither persistent brain lesions nor the ablation procedure itself had a si
201 leiotropic, clock-independent functions; and brain lesions not only disrupt cellular circadian rhythm
202                                      Typical brain lesions occurred in 50.9% of neuromyelitis optica
203 ncovered MCL- and MINCLE-expressing cells in brain lesions of MS patients and we further found an upr
204 n peripheral blood, cerebrospinal fluid, and brain lesions of MS patients.
205 cs, we observed that RAAS is up-regulated in brain lesions of MS.
206                                   In chronic brain lesions of patients with progressive multiple scle
207 al studies provide correlative evidence, and brain lesions often comprise both white and gray matter
208                                              Brain lesions on diffusion-weighted imaging (DWI) are fr
209 ent ischemic attack, and definitive ischemic brain lesions on fluid-attenuated inversion recovery mag
210 initial demyelinating event, had two or more brain lesions on MR images, and had two or more oligoclo
211 th AF have a high burden of LNCCIs and other brain lesions on systematic brain MRI screening, and mos
212       The UCCA and the number of hypointense brain lesions on T1-weighted images were the strongest M
213  parameters, including number of hypointense brain lesions on T1-weighted MR images, presence of diff
214                  UCCA, number of hypointense brain lesions on T1-weighted MR images, presence of diff
215 % with placebo (P=0.04); the total volume of brain lesions on T2-weighted magnetic resonance imaging
216               In previous follow-up studies, brain lesions on T2-weighted MRI are associated with inc
217 ere employed to test the mediating effect of brain lesions on the association of diabetes with cognit
218         This study showed that microvascular brain lesions on ultra-high field MRI are not significan
219 ansferring the three-dimensional volume of a brain lesion onto a reference brain; (ii) assessing the
220 ry obliterations associated with tumefactive brain lesions or nephropathy.
221 of fumarate-treated patients presenting with brain lesions or seizures even in the absence of severe
222 s can go unnoticed for years, and incomplete brain lesions or silencing of neurons often fail to prod
223 sue to resect, such as the location of focal brain lesions or the presence of epileptiform rhythms, d
224 orrelation with age (P < .001) and number of brain lesions (P < .001).
225 able regression model including all vascular brain lesion parameters, LNCCI volume was the strongest
226                       Here, we studied human brain lesion patients to determine whether the superior
227 the detection of awareness in anesthesia and brain-lesioned patients.
228 ssessment of patients with a newly diagnosed brain lesion; patients who had no radiotherapy, surgery,
229              Ablation-related acute ischemic brain lesions persist to some extent but do not cause co
230    Nesting has been shown to be sensitive to brain lesions, pharmacological agents and genetic mutati
231 as CAA may result in hemorrhagic or ischemic brain lesions potentially through 2 different mechanisti
232                                    While the brain lesions predominantly originate prenatally, it rem
233                                        These brain lesions present a mixed glioneuronal phenotype and
234 roach suboptimal for treatment of the global brain lesions present in most human neurogenetic disease
235                                     Vascular brain lesions, present in advanced atherosclerosis, shar
236                                    Following brain lesions, previously normal patients sometimes exhi
237              Much uncertainty has surrounded brain lesions producing deficits in these tests, with st
238      Eleven subjects with PBC had structural brain lesions quantified via magnetic resonance imaging.
239 hin 48 hours after ablation, showed that new brain lesions (range, 1-17) were present in 16 (43.2%) p
240 besity were not associated with infarct-like brain lesions (relative risk (RR) = 0.82, 95% confidence
241                  The treatment of metastatic brain lesions remains a central challenge in oncology.
242 onditions, of which neurological disease and brain lesions represent a substantial proportion, and th
243  rodents induces cortical neuronal migration brain lesions resembling those of autism.
244              Phosphoproteomic analysis of MS brain lesions revealed S1P1 phosphorylation on S351, a r
245 ical findings for patients with EEE included brain lesions, seizures that evolved to status epileptic
246                               Looking at the brain lesion should always be done from the whole patien
247          After adjusting for age, NIHSS, and brain lesion size (computed tomography), PENK-A predicte
248 r function after brain trauma, and decreases brain lesion size induced by trauma.
249 ody (0.8 mg/kg) caused a twofold decrease in brain lesion size, whereas that of tPA (10 mg/kg) had a
250 risk factors, vascular and neurodegenerative brain lesions, sleep patterns and cerebral haemodynamics
251 observations of visual-field scotomas across brain-lesioned soldiers to produce a schematic map of th
252 ved clinical-neuroanatomical predictions for brain lesion studies and provide a platform for explorat
253 m the CABL (Cardiovascular Abnormalities and Brain Lesions) study by traditional and tissue Doppler i
254 t in understanding functional recovery after brain lesions such as stroke.
255                               However, acute brain lesions, such as traumatic brain injury, reactivat
256 racterized by significant neurodevelopmental brain lesions, such as tubers and subependymal nodules.
257 ed to test the association between miRNA and brain lesions (T2 hyperintense lesion volume [T2LV]), th
258 ot significantly affected by the presence of brain lesions [T2 lesions (P = 0.918), periventricular T
259 emained obscure, which we addressed by using brain lesion techniques combined with modern immunohisto
260 were previously at high risk for destructive brain lesions that resulted in cystic white matter injur
261 6 men; age range, 26-79 years) with solitary brain lesions that were enhanced at magnetic resonance (
262 ctive response was reported in patients with brain lesions that were multiple or larger than 1 cm.
263                       Multiple, disseminated brain lesions, that are characterised by restricted diff
264 lthough chronic exposure is known to produce brain lesions, the influence of DA toxicosis on behavior
265 clinical relapses and new focal inflammatory brain lesions throughout the 2 years of immune monitorin
266 ing biomaterials for injection into cavitary brain lesions to recruit endogenous NPCs and enhance neu
267 distortions, contrasting patients with focal brain lesions to the ventromedial prefrontal cortex (vmP
268 tactic cues and structural support, cavitary brain lesions typically fail to recruit endogenous neura
269 rmance on the different tasks; patients with brain lesions under-produced but over-estimated time int
270 cal studies are important in determining the brain lesions underlying dementia.
271 ropathological information on the structural brain lesions underlying seizures is valuable for unders
272 asymptomatic NTZ-associated PML (NTZ PML, 18 brain lesions) underwent 3-T MR imaging.
273  isolated from rats after focal inflammatory brain lesions using IL-1beta, to activate a systemic APR
274                              PAI-039 reduced brain lesion volume by 26% at 24 hours and 43% at 5 days
275 roved motor function recovery, and decreased brain lesion volume compared with wild-type controls.
276 limited cerebral ischemic injury and reduced brain lesion volume significantly more effectively than
277  reflected by better motor function, reduced brain lesion volume, and diminished neurodegeneration.
278                             We also measured brain lesion volume, cervical spinal cord lesion number
279                     Significant reduction in brain lesion volume, neurodegeneration, microgliosis and
280 tical gray matter and cerebral white matter, brain lesion volume, spinal cord gray and white matter a
281 ic mice, BI-1 transgenic mice showed reduced brain lesion volumes and better performance in motoric t
282                                      The new brain lesion was treated with stereotactic radiosurgery,
283           GM-CSF production by T cells in MS brain lesions was analyzed by immunofluorescence.
284                          Using patients with brain lesions we show that, relative to nonfrontal lesio
285 velopmental perturbations that lead to these brain lesions, we created a mouse model that selectively
286 could inform on the origin of supratentorial brain lesions, we prospectively enrolled 23 patients wit
287  Studying a group of 192 patients with focal brain lesions, we show a significant association between
288 lated brainstem syndromes in whom multifocal brain lesions were absent, showed trajectories more clos
289                                     Ischemic brain lesions were assessed by a 3T magnetic resonance i
290                                   N = 302 MS brain lesions were detected, and generalized linear mixe
291                               No parenchymal brain lesions were evident on imaging, but transient cer
292               Neurological disease and focal brain lesions were found in 25% and 9% of the total subj
293                                   Structural brain lesions were found in PBC, the density of which co
294 ase reports of Holmes tremor caused by focal brain lesions were identified through a systematic liter
295                                  Intra-axial brain lesions were manually segmented in patients with M
296 12 s stimuli demonstrated that patients with brain lesions were more variable than controls on the es
297 erm equivalent age without focal parenchymal brain lesions were studied with 20 full-term control inf
298  The authors discussed a few T1-hyperintense brain lesions which did not include metastases (except f
299 th a post-neonatally acquired or progressive brain lesion who could grasp before the operation, and a
300 logical cost, we predicted that pathological brain lesions would be concentrated in hub regions.

 
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