ライフサイエンスコーパス: neurological symptom

1 neuron populations required to ameliorate a neurological symptom.

2 nt two patients with COVID-19 and concurrent neurological symptoms.

3 bination with abnormal copper metabolism and neurological symptoms.

4 found between key brain findings and overall neurological symptoms.

5 stations of liver disease, but often worsens neurological symptoms.

6 episode of acute onset atypical or nonfocal neurological symptoms.

7 atory, gastrointestinal, cardiovascular, and neurological symptoms.

8 and in most of the cases subsequent multiple neurological symptoms.

9 both systemic disease and, in some patients, neurological symptoms.

10 od pressure <= 90 mm Hg) before the onset of neurological symptoms.

11 mild TBI, might be associated with long-term neurological symptoms.

12 e (CS) is a multisystem disorder with severe neurological symptoms.

13 Seventy patients (66.0%) developed severe neurological symptoms.

14 76) and were mostly mild; only 1 neonate had neurological symptoms.

15 There was absence of fever and neurological symptoms.

16 l dystonia compared to lesions causing other neurological symptoms.

17 raphic imaging within 3 months after LTx for neurological symptoms.

18 ler study and can predict the development of neurological symptoms.

19 oss of MeCP2 expression results primarily in neurological symptoms.

20 ood pressure <=90mmHg) prior to the onset of neurological symptoms.

21 pathways that may be modulated to treat the neurological symptoms.

22 t stroke in any patient with abrupt onset of neurological symptoms.

23 ll mice before and after the onset of severe neurological symptoms.

24 with genetic syndromes that frequently have neurological symptoms.

25 nd development of some of the characteristic neurological symptoms.

26 in some types, mental retardation and other neurological symptoms.

27 neuropil aggregate formation and ameliorates neurological symptoms.

28 s, myelin and axonal injury, and progressive neurological symptoms.

29 aine appear to reduce the risk for transient neurological symptoms.

30 and cattle, invariably die after exhibiting neurological symptoms.

31 ging abnormalities that accompany these same neurological symptoms.

32 0 infection with available clinical data had neurological symptoms.

33 usually fatal disease accompanied by severe neurological symptoms.

34 lting in an autoimmune attack on neurons and neurological symptoms.

35 with recurrent thrombosis, miscarriages, and neurological symptoms.

36 ronal nuclear inclusions and appeared before neurological symptoms.

37 and subcellular disease changes may mediate neurological symptoms.

38 ividuals for whom symptoms were reported had neurological symptoms.

39 deficits precede the onset of psychiatric or neurological symptoms.

40 In piglets and mice, Stx can induce fatal neurological symptoms.

41 stly affecting young children and leading to neurological symptoms.

42 w dysfunction in their absence underlies FXS neurological symptoms.

43 sorder characterized by immunodeficiency and neurological symptoms.

44 activity were observed, even after onset of neurological symptoms.

45 treatment, a growing number of cases present neurological symptoms.

46 with failure to thrive, immunodeficiency and neurological symptoms.

47 erature comparing PNES with other functional neurological symptoms.

48 netic disorders marked by severe somatic and neurological symptoms.

49 y, the patient experienced an improvement in neurological symptoms.

50 syndrome (GLUT1-DS) leads to a wide range of neurological symptoms.

51 creasing serum viral loads and resolution of neurological symptoms.

52 iscordance and escape may be associated with neurological symptoms.

53 kers, but there was no clear relationship to neurological symptoms.

54 n shown to contribute to the age at onset of neurological symptoms.

55 aplastic carcinoma), was admitted with focal neurological symptoms.

56 since murine models fail to mirror classical neurological symptoms.

57 g to motor neuron cell death and progressive neurological symptoms.

58 with some patients manifesting non-cognitive neurological symptoms.

59 nmental and genetic factors that cause these neurological symptoms.

60 ervous system nocardiosis, 13 (43.3%) had no neurological symptoms.

61 lowly growing VT in a woman with progressive neurological symptoms.

62 ll patients with meningovascular NS had only neurological symptoms.

63 lactosemia disease states manifest long-term neurological symptoms.

64 with time, peaking during the height of the neurological symptoms (1.5E copies/mL).

65 ith coexisting non-movement disorder-related neurological symptoms (100 [45%] of 222; excepting cases

66 ported a minor infection a few days prior to neurological symptoms, 2 patients presented criteria for

67 less than 10 months after the onset of their neurological symptoms (3.7 +/- 2.5 months, median +/- in

68 aining 30% had persistent hypertension (9%), neurological symptoms (4%), decreased glomerular filtrat

69 interfere with DNA repair but have only mild neurological symptoms [6-9], suggesting that the link be

70 logical cases were characterized by relevant neurological symptoms, a history of a past head injury w

71 gy of FMD (and by extension other functional neurological symptoms): abnormal attentional focus, abno

72 ctors of mortality include presentation with neurological symptoms (adjusted odds ratio, 16.0; P<0.00

73 ions with self-report measures of functional neurological symptoms, adverse life events and PTSD symp

74 Rebound syndrome was defined as new severe neurological symptoms after ceasing fingolimod treatment

75 Seven patients developed neurological symptoms; all of them had a positive RLS (P

76 r sibling was a 70-year-old man with minimal neurological symptoms and a mild depressive disorder.

77 sease correlate closely with the severity of neurological symptoms and age of the patient.

78 including an additional 10 items on specific neurological symptoms and an additional 5 items on menta

79 ain to environmental insult causes different neurological symptoms and behavioral outcomes depending

80 sclerosis (TSC), a hereditary syndrome with neurological symptoms and benign hamartoma tumours in th

81 agnosis and aggressive treatment can improve neurological symptoms and can substantially enhance a pa

82 ialic acid (SA) receptor specificity, caused neurological symptoms and death in ferrets inoculated wi

83 upper and lower motor neurons (LMNs) causes neurological symptoms and dysfunctions in motor neuron d

84 neuronal and glial cells display more severe neurological symptoms and earlier death than N171-82Q mi

85 PLP-150Q mice show progressive neurological symptoms and early death, as well as age-de

86 lase inhibitor prevents them from developing neurological symptoms and extends their life span threef

87 ve resulted in the subsequent improvement of neurological symptoms and impairments.

88 tion within glia may suffice to cause severe neurological symptoms and may even be the primary driver

89 individuals with GTPBP3 mutations developed neurological symptoms and MRI involvement of thalamus, p

90 nical course was complicated by debilitating neurological symptoms and multiple hospitalizations lead

91 These mice showed weight loss, progressive neurological symptoms and neurodegeneration before early

92 spectively; p < 0.0001) and experienced more neurological symptoms and other end-organ ischemic event

93 rol ligand, act in concert to delay onset of neurological symptoms and prolong the lifespan of npc1(-

94 n stress-related neuroplasticity, functional neurological symptoms and reduced insular volume was ide

95 diagnosis of multiple sclerosis is based on neurological symptoms and signs, alongside evidence of d

96 boratory-confirmed brucellosis cases who had neurological symptoms and signs, and 48 (37.5%) were dia

97 tt syndrome, a disease characterized by both neurological symptoms and systemic abnormalities.

98 linical interest in patients with functional neurological symptoms and the clear shift in diagnostic

99 ated the prevalences of various non-amnestic neurological symptoms and the contributions of age of on

100 We hypothesised that functional neurological symptoms and the magnitude of childhood abu

101 size >5 cm, tumour crossing the midline, or neurological symptoms), and without known HIV infection,

102 size >5 cm, tumour crossing the midline, or neurological symptoms), and without known HIV infection,

103 vivors, 4 (20%) reported at least 1 abnormal neurological symptom, and 3 (15%) had an abnormal neurol

104 All patients with late NS had neurological symptoms, and 2 (40%) also had ocular sympt

105 had ophthalmological symptoms, 14 (47%) had neurological symptoms, and 8 (26%) had both.

106 ncluding ichthyosis, primary hypothyroidism, neurological symptoms, and cryptorchidism.

107 treatment significantly delayed the onset of neurological symptoms, and improved deficits in PaGE per

108 ical characteristics, time to development of neurological symptoms, and modified Rankin Scale (mRS) s

109 ients manifested acute episodes of transient neurological symptoms, and neurological impairment was m

110 poor health, infectious diseases, insomnia, neurological symptoms, and suicide attempts during early

111 is, having a history of encephalitis, subtle neurological symptoms, and/or abnormal results on ancill

112 Although neurological symptoms are being reported worldwide, neur

113 Neurological symptoms are common manifestations of Lyme

114 identify carriers at risk before significant neurological symptoms are evident.

115 Functional (psychogenic) neurological symptoms are frequently encountered in neur

116 local anaesthetics with respect to transient neurological symptoms are limited and conflicting.

117 disease but they die from cancer before the neurological symptoms are manifested.

118 nt and postpartum patients with headache and neurological symptoms are often diagnosed with pre-eclam

119 Neurological symptoms are the predominant problem and th

120 (PNES) are classified with other functional neurological symptoms as 'Conversion Disorder', but ther

121 left anterior insular volume and functional neurological symptoms as measured by the Patient Health

122 ement alone (ie, pharmacological therapy for neurological symptoms as needed).

123 RBPs and associated factors lead to diverse neurological symptoms, as characterized by neurodevelopm

124 ity, and thus contribute to the emergence of neurological symptoms associated with ASD.

125 Patients can also have neurological symptoms associated with coagulopathies, im

126 However, in many cases it leads to neurological symptoms associated with haemodynamic distu

127 minergic systems in brain which may underlie neurological symptoms associated with human disorders su

128 g normal brain function, thus explaining the neurological symptoms associated with IP.

129 It is generally believed that the neurological symptoms associated with loss of PTEN and o

130 ed piglets had diarrhea and the severe fatal neurological symptoms associated with Stx2 intoxication.

131 after bacterial challenge, followed by fatal neurological symptoms at 48 to 96 h.

132 ich Mecp2 was deleted in brain showed severe neurological symptoms at approximately six weeks of age.

133 h MS more often show disabling and polyfocal neurological symptoms at disease onset than adults with

134 One patient (1.4%) still had major neurological symptoms at the latest follow-up.

135 inely done in patients presenting with acute neurological symptoms because this might shed light on t

136 Duration of neurological symptoms before diagnosis was 30 (interquar

137 Surprisingly, despite the lack of neurological symptoms, beta3A-deficient mouse brain poss

138 ainstem lesions on imaging, who had onset of neurological symptoms between Aug 1, 2014, and Oct 31, 2

139 This leads to severe neurological symptoms, but the mechanisms underlying bra

140 Forty percent of AIDS patients suffer from neurological symptoms, but the selective profile of dama

141 ll had a prodromal febrile illness preceding neurological symptoms by a median of 7 days (IQR 5.75-8)

142 plasmic mutant huntingtin and its associated neurological symptoms by preventing the accumulation of

143 tations range from itching and minor pain to neurological symptoms, cardiac collapse, and death.

144 eolysis, severe osteoporosis, short stature, neurological symptoms, cardiovascular defects, and polyc

145 Lesch-Nyhan syndrome encompasses a host of neurological symptoms, caused by a deficiency of the pur

146 tment with glucocorticoid analogues improved neurological symptoms characteristic of this syndrome.

147 g body of evidence indicating that transient neurological symptoms commonly occur after uneventful li

148 brains of infected mice, producing no major neurological symptoms, compared with the invariably leth

149 dults with low IQs than do those who develop neurological symptoms consistent with encephalopathy.

150 atients with acute Zika virus disease and no neurological symptoms (control group 2; n=70).

151 e dynamic neural mechanisms underlying acute neurological symptoms, cortical reorganization and treat

152 e accumulation of heparan sulfate results in neurological symptoms, culminating in extensive neurodeg

153 al diagnostic term for medically unexplained neurological symptoms (currently known as 'conversion di

154 The median delay from neurological symptom debut to first hospital contact was

155 ction, Catecholamines-up, delay the onset of neurological symptoms, dopaminergic neuron death, and mo

156 rful array of antiretroviral treatments, but neurological symptoms due to comorbid conditions, includ

157 atients with progressive subacute to chronic neurological symptoms due to congestive myelopathy cause

158 Patients often suffer from neurological symptoms due to obstruction of cranial fora

159 disorders that often display muscular and/or neurological symptoms due to the high-energy demands of

160 article reviews the treatment of functional neurological symptoms during World War I by Lewis Yealla

161 icrogyria is responsible for a wide range of neurological symptoms (e.g. epilepsy, intellectual disab

162 features range from none, to discrete focal neurological symptoms (eg, stroke), to insidious global

163 D50 of BoNT/C1 ad is 5 mg/kg, with transient neurological symptoms emerging at sub-lethal doses.

164 s a primary means by which seizure and other neurological symptoms ensue, our findings highlight oxLD

165 nal pain, vomiting, diarrhea, or nausea) and neurological symptoms (extremity paresthesia, arthralgia

166 Functional neurological symptoms (FNS) are commonly encountered but

167 Functional (conversion) neurological symptoms (FNS) are commonly encountered in

168 Neurocognitive function, neurological symptoms, functional independence, and heal

169 rity between this finding and recent work on neurological symptoms give rise to new hypotheses on the

170 Overt neurological symptoms have a relatively late onset (15-2

171 However, neurological symptoms have also been observed in some pa

172 However, recurrent episodes of focal neurological symptoms have been described after initial

173 ting the central nervous system, and several neurological symptoms have been described in patients wi

174 ions for RTT are limited to alleviating some neurological symptoms; hence, more effective therapeutic

175 tration of Cu(II)(atsm) delayed the onset of neurological symptoms, improved locomotive capacity and

176 with persistence of patient-reported sensory neurological symptoms in 25% of patients.

177 Cancer anteceded neurological symptoms in 4 of 28 patients.

178 costeroids induced the complete remission of neurological symptoms in 4 of 5 patients.

179 present in 65% of all patients with NS, and neurological symptoms in 60%.

180 A2AR activity therapeutically can attenuate neurological symptoms in ADK deficiency.

181 A2AR activity therapeutically can attenuate neurological symptoms in ADK deficiency.

182 partly protected against the development of neurological symptoms in an experimental autoimmune ence

183 xpression leads to striking loss of advanced neurological symptoms in both immature and mature adult

184 mutation should include questions regarding neurological symptoms in both older male and female carr

185 f gene regulatory networks as a cause of the neurological symptoms in CS.

186 were associated with a greater frequency of neurological symptoms in DLBCL and BL and with parenchym

187 of one volunteer and produced mild-to-severe neurological symptoms in four others.

188 ecently described the presence of late-onset neurological symptoms in male carriers of premutation (F

189 ATA box-binding protein causes age-dependent neurological symptoms in mice and the degeneration of ce

190 (160Q) in astrocytes is sufficient to induce neurological symptoms in mice.

191 to estimate the prevalences of non-amnestic neurological symptoms in participants with ADAD.

192 y in clinical dementia syndromes and complex neurological symptoms in patients with focal brain lesio

193 ic Gaucher disease (nGD) manifests as severe neurological symptoms in patients with no effective trea

194 should be considered in the setting of acute neurological symptoms in patients with renal failure, bl

195 Perfusion abnormalities are associated with neurological symptoms in patients with SCD, whether or n

196 entiate between the specific causes of acute neurological symptoms in pregnant and post-partum patien

197 Acute neurological symptoms in pregnant and post-partum women

198 lular LB/LN-like inclusions and the onset of neurological symptoms in recipient animals.

199 gen that causes congenital Zika syndrome and neurological symptoms in some adults.

200 (ADAD) is a rare disorder with non-amnestic neurological symptoms in some clinical presentations.

201 ciency, HIV-1 has been linked to a number of neurological symptoms in the absence of opportunistic in

202 d broadly applicable approach for localizing neurological symptoms in the setting of brain lesions.

203 etary modification partially rescued overall neurological symptoms in these mice after onset.

204 e neuronal dysregulation associated with the neurological symptoms in TSC.

205 Neurological symptoms in tuberous sclerosis complex (TSC

206 ), which causes flu-like symptoms leading to neurological symptoms in up to 14% of cases.

207 ve even when administered after onset of the neurological symptoms, in young adult mice, and without

208 disorder that targets NMDARs, causing severe neurological symptoms including hallucinations, psychosi

209 A common phenotype of severe neurological symptoms including intractable epilepsy and

210 ated in adulthood, the mice displayed severe neurological symptoms including tremors and hind-limb pa

211 encephalitis, particularly in the setting of neurological symptoms, including extrapyramidal side eff

212 ges on cerebral neuroimaging and progressive neurological symptoms, including movement disorders and

213 (+) embryos by doxycycline leads to multiple neurological symptoms, including severe epilepsy and pre

214 Individuals with CM1 can present with neurological symptoms, including severe headaches and se

215 tion of allopregnanolone delays the onset of neurological symptoms, increases Purkinje and granule ce

216 The etiology of these neurological symptoms is unclear and the function of the

217 ond phase of the disease, after the onset of neurological symptoms, magnetic resonance imaging (MRI)

218 These neurological symptoms may also be due to DST gene mutati

219 osquito-borne flavivirus, has induced severe neurological symptoms more frequently in the elderly pop

220 sented different developmental disorders and neurological symptoms - most often cerebral palsy and ep

221 In only one patient there were no neurological symptoms, most of the children presented di

222 osquito-borne flavivirus, has induced severe neurological symptoms, mostly in the elderly population.

223 rational explanation for the well-described neurological symptoms observed after allo-HSCT.

224 diseases and provides an explanation for the neurological symptoms observed in some patients with SLE

225 2 gene occur in the germ cells with onset of neurological symptoms occurring in early childhood, the

226 was strongly predictive of the occurrence of neurological symptoms (odds ratio, 204; 95% confidence i

227 The most common neurological symptom of tuberous sclerosis complex (TSC)

228 of brain ATM activity in the severity of the neurological symptoms of A-T.

229 The neurological symptoms of ataxia-telangiectasia may thus

230 ubsequent colonization of brain tissues with neurological symptoms of disease, we found similar resul

231 ording to one proposal, many psychiatric and neurological symptoms of FXS result from unchecked activ

232 ynaptic Fragile X proteins contribute to the neurological symptoms of FXS.

233 ant huntingtin in glia can contribute to the neurological symptoms of HD.

234 attack, which is clinically defined as focal neurological symptoms of ischaemic origin resolving spon

235 thrin-mediated membrane traffic leads to the neurological symptoms of Lowe syndrome.

236 ain functions and the dynamic changes in the neurological symptoms of RTT.

237 sleep and cognition recognised alongside the neurological symptoms of seizures and autonomic instabil

238 ous organs and the mechanisms underlying the neurological symptoms of the disease remain largely unkn

239 ceptual basis for linking the behavioral and neurological symptoms of the disease with the frequently

240 ely to contribute to the pathogenesis of the neurological symptoms of TSC.

241 lformation (molar tooth sign), together with neurological symptoms of variable expressivity.

242 tently, older SCA17 mice experienced earlier neurological symptom onset and more severe Purkinje cell

243 tients with subacute stroke (3-14 days after neurological symptom onset) underwent MRI examination.

244 detergent-soluble oligomers, which preceded neurological symptom onset, and were found at equivalent

245 ne (32%) were wheelchair-bound 1 month after neurological symptom onset.

246 progressing after previous radiotherapy, no neurological symptoms or corticosteroid requirement, and

247 e or reactive-like state before the onset of neurological symptoms or morphological changes.

248 Development of neurological symptoms or signs occurred in up to 30% of

249 n 5 and 20 mm in diameter without associated neurological symptoms or the need for corticosteroids.

250 ment for epidural abscesses in patients with neurological symptoms or who have not responded to medic

251 the knockout mice but did not cause obvious neurological symptoms, organomegaly, or a reduction in l

252 r mouse model of this disease, we found that neurological symptoms parallel progressive and severe ly

253 should be assessed for unexplained fever and neurological symptoms, particularly if they reside in ar

254 Focal neurological symptoms persisted in 22% of patients at di

255 Neurological symptoms preceded the tumour diagnosis in 6

256 esirable potential drug for the treatment of neurological symptoms present in most lysosomal storage

257 ubiquinone) Fe-S protein 4], delays onset of neurological symptoms, reduces neuroinflammation, and pr

258 Episodes of acute atypical or nonfocal neurological symptoms, referred to as transient neurolog

259 owever, once it manifests, particularly with neurological symptoms, reversal by dietary changes or su

260 light of better understanding of functional neurological symptoms, Sacks' experiences deserve to be

261 lanced XCI, which may affect the severity of neurological symptoms seen in these patients; however, w

262 , was independent of sensorimotor functional neurological symptom severity and motor FND subtype.

263 ions with self-report measures of functional neurological symptom severity or childhood abuse.

264 Terminally diseased mice with severe neurological symptoms showed extensive alterations in as

265 nhibitor of thiamine metabolism that induces neurological symptoms similar to that of Wernicke-Korsak

266 In most patients, recovery from neurological symptoms started within a few hours after o

267 ntial carotid artery narrowing but no recent neurological symptom (stroke or transient ischaemia), th

268 ic (ie, has caused no recent stroke or other neurological symptoms), successful carotid endarterectom

269 at pain spreading along the artery can cause neurological symptoms such as vertigo and syncope.

270 (IP) is a genetic disease leading to severe neurological symptoms, such as epileptic seizures, but n

271 While HF clearly shows neurological symptoms, such as fatigue, nausea, and dizz

272 ion of unesterified cholesterol and multiple neurological symptoms, such as vertical supranuclear oph

273 ian of 6 days (IQR 4-10) before the onset of neurological symptoms, suggesting recent Zika virus infe

274 nts conducted in a group of 65 patients with neurological symptoms suggestive of ischaemia in the are

275 RIAL/METHODS: Thirty-six patients with acute neurological symptoms suggestive of PRES were included i

276 This is readily evident in the neurological symptoms that accompany systemic acid/base

277 S) is a surgical procedure used to treat the neurological symptoms that are associated with certain n

278 s not cause histopathological CNS lesions or neurological symptoms that can be attributed to the viru

279 we presented a very rare eagle syndrome with neurological symptoms that occurred suddenly with cervic

280 racterized by rapid onset of psychiatric and neurological symptoms that often culminate in severe neu

281 ll patients had manifested acute or subacute neurological symptoms; the brain MRIs indicating diffuse

282 Neurological symptoms, time course of the disease, and i

283 itional and widely used approach for linking neurological symptoms to specific brain regions involves

284 'UK-Functional Neurological Symptoms (UK-FNS)' was an informal inaugura

285 who were potentially exposed and experienced neurological symptoms underwent evaluation at a US acade

286 Median age of onset of neurological symptoms was 14 years (range 0.5-55 years)

287 The most commonly occurring neurological symptoms were encephalopathy (57%), headach

288 s between these metabolites and clinical and neurological symptoms were examined at both time points.

289 to the Mayo Clinic (Rochester, MN, USA) with neurological symptoms were included.

290 Mild residual neurological symptoms were present in 21.7% of patients

291 inimal protein is able to prevent or reverse neurological symptoms when introduced into MeCP2-deficie

292 vement of other neurons can cause additional neurological symptoms, which define a diverse set of com

293 signs (prodromes) and aura (transient focal neurological symptoms) whose origin is thought to involv

294 mutations in CAPZA2 (HGNC: 1490) and exhibit neurological symptoms with shared phenotypes including g

295 infect multiple avian species, resulting in neurological symptoms with unknown routes of transmissio

296 lsant-withdrawal splenial abnormalities with neurological symptoms, with gabapentin-type anticonvulsa

297 Nine subjects (21%) had CTCAE grade 3 or 4 neurological symptoms, with no neurotoxicity-related dea

298 , but showed high antibody titers during the neurological symptoms, with the IgM decrease paralleling

299 Patients with development of neurological symptoms within 12 months of anti-PD-1 ther

300 umor burden manifested by the onset of focal neurological symptoms within 21 days.