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1 evere stroke increasing the absolute risk of intracerebral haemorrhage).
2 lth Stroke Scale >3) versus those with acute intracerebral haemorrhage.
3 ical deficits without infarction, seizure or intracerebral haemorrhage.
4 in and is associated with dementia and lobar intracerebral haemorrhage.
5 age-matched stroke service referrals without intracerebral haemorrhage.
6 specialty practice can improve outcome after intracerebral haemorrhage.
7 ial conservative treatment for patients with intracerebral haemorrhage.
8 ay be a risk factor for thrombolysis-related intracerebral haemorrhage.
9 weighted scans) and lacunar infarcts, but no intracerebral haemorrhage.
10 traventricular haemorrhage size and thalamic intracerebral haemorrhage.
11 , and loss of functional independence) after intracerebral haemorrhage.
12 idence of dementia and risk factors after an intracerebral haemorrhage.
13 es on long-term functional performance after intracerebral haemorrhage.
14 ally invasive surgery (MIS) in patients with intracerebral haemorrhage.
15 cal management as a therapeutic strategy for intracerebral haemorrhage.
16 or people taking antiplatelet therapy before intracerebral haemorrhage.
17 s, does not improve functional outcome after intracerebral haemorrhage.
18 complications and no increase in symptomatic intracerebral haemorrhage.
19 in patients with probable CAA without lobar intracerebral haemorrhage.
20 redict a poor outcome in patients with acute intracerebral haemorrhage.
21 controls, though none had major CAA-related intracerebral haemorrhages.
22 idence declined by more than 50% for primary intracerebral haemorrhage (0.47, 0.27-0.83, p=0.01) but
24 lic blood pressure was much lower than after intracerebral haemorrhage (158.5 mm Hg [SD 30.1] vs 189.
25 eeded the absolute increase in risk of fatal intracerebral haemorrhage (2.2% [1.5% to 3.0%]) and the
28 bsolute excess 3.1% [2.4-3.8]); and of fatal intracerebral haemorrhage (91 [2.7%] of 3391 vs 13 [0.4%
29 changes in the population-based incidence of intracerebral haemorrhage according to age and likely ae
32 mortality (1.6, 0.8-3.4; p=0.27) or rates of intracerebral haemorrhage after treatment with thromboly
33 ognised as an important cause of spontaneous intracerebral haemorrhage and cognitive impairment in th
34 l disease and a largely untreatable cause of intracerebral haemorrhage and contributor to age-related
36 ploratory analyses to assess mortality after intracerebral haemorrhage and examine the absolute risks
37 gression models for association with primary intracerebral haemorrhage and ischaemic stroke subtypes.
40 loperoxidase levels increase risk of primary intracerebral haemorrhage and lacunar stroke, directly i
41 cerebrovascular permeability, development of intracerebral haemorrhage and neurovascular injury in ex
42 improve clinical management of patients with intracerebral haemorrhage and promise to reduce mortalit
43 t decreases in DBS complications, with fewer intracerebral haemorrhages and infections with general a
44 y participants or patients with non-CAA deep intracerebral haemorrhage) and patients with Alzheimer's
45 dwide (91.5% for ischaemic stroke, 87.1% for intracerebral haemorrhage), and were consistent across r
46 frequent but previously underestimated after intracerebral haemorrhage, and are three times more comm
47 of 14.2% (95% CI 10.0-19.3) at 1 year after intracerebral haemorrhage, and incidence reached 28.3% (
48 l burden of vascular-related brain damage in intracerebral haemorrhage, and may be a useful surrogate
49 have recently been described in spontaneous intracerebral haemorrhage, and may be important to under
50 separately for cerebral infarction, primary intracerebral haemorrhage, and subarachnoid haemorrhage.
51 dified Rankin scale [mRS]), the incidence of intracerebral haemorrhages, and technical observations.
55 as on cognition in the context of ageing and intracerebral haemorrhage, as well as in Alzheimer's and
56 are alone, reduced death or dependence after intracerebral haemorrhage associated with antiplatelet t
57 n older age-groups, in part due to a rise in intracerebral haemorrhage associated with antithrombotic
58 7, 0.20-0.69; p=0.002), but the incidence of intracerebral haemorrhage associated with antithrombotic
60 29-0.95; p=0.03), but the number of cases of intracerebral haemorrhage at all ages were similar in OX
61 mplications (cerebrospinal fluid leakage and intracerebral haemorrhage) at days 3-7 after AAV2 gene t
62 published arteriovenous malformation-related intracerebral haemorrhage (AVICH) score showed better ou
63 alteplase seems to be safe in patients with intracerebral haemorrhage, but increased asymptomatic bl
64 embolic events outnumbered warfarin-related intracerebral haemorrhages by about 15-fold (280 vs 19),
67 We used a discovery cohort of 1409 primary intracerebral haemorrhage cases and 1624 controls from t
68 d high-dose tinzaparin developed symptomatic intracerebral haemorrhage compared with one in the aspir
69 nd 138 controls (96 healthy elderly, 42 deep intracerebral haemorrhage controls) and 72 patients with
70 ulation aged under 75 years the incidence of intracerebral haemorrhage decreased substantially (rate
72 n, 3/52 [6%] vs 4/51 [8%], p=0.59) nor total intracerebral haemorrhage events (8/52 [15%] vs 14/51 [2
74 al cohort study in patients with spontaneous intracerebral haemorrhage from the Prognosis of Intracer
75 though the number of hospital admissions for intracerebral haemorrhage has increased worldwide in the
77 h systolic blood pressure were strongest for intracerebral haemorrhage (hazard ratio 1.44 [95% CI 1.3
80 mine the strength of the association between intracerebral haemorrhage (ICH) and cerebral amyloid ang
81 ERACT2 enrolled 2839 adults with spontaneous intracerebral haemorrhage (ICH) and high systolic blood
82 the relationship between laterality of acute intracerebral haemorrhage (ICH) and poor clinical outcom
83 onists oral anticoagulants (NOAC)-associated intracerebral haemorrhage (ICH) are largely unknown.
84 ilon2 and epsilon4 have an increased risk of intracerebral haemorrhage (ICH) in lobar regions, presum
85 study, we examined injury progression after intracerebral haemorrhage (ICH) induced by collagenase i
90 BACKGROUND AND Intraventricular extension of intracerebral haemorrhage (ICH) predicts poor outcome, b
93 ith arteriovenous malformation (AVM)-related intracerebral haemorrhage (ICH) than other AVM or ICH sc
94 dictor of poor outcome only in patients with intracerebral haemorrhage (ICH) volumes </=30 cm(3) (OR
95 (CAA)) is an important cause of spontaneous intracerebral haemorrhage (ICH), a devastating and still
106 Patients with spontaneous supratentorial intracerebral haemorrhage in neurosurgical units show no
107 s, but not in the overall number of cases of intracerebral haemorrhage in older age-groups, in part d
108 transfusion after acute spontaneous primary intracerebral haemorrhage in people taking antiplatelet
109 aemorrhage and examine the absolute risks of intracerebral haemorrhage in the context of functional o
110 e interventions (seizure after discharge and intracerebral haemorrhage in the recreational activity g
111 ital with acute stroke (ischaemic or primary intracerebral haemorrhage) in England and Wales between
112 than two times higher in patients with lobar intracerebral haemorrhage (incidence at 1 year 23.4%, 14
113 14.6-33.3) than for patients with non-lobar intracerebral haemorrhage (incidence at 1 year 9.2%, 5.1
114 ke severity, but the absolute excess risk of intracerebral haemorrhage increased with increasing stro
118 s use, improved data collection, low rate of intracerebral haemorrhage, low technical complications,
119 ow age 75 years, absolute number of cases of intracerebral haemorrhage might increase in future.
120 bsolute effects of alteplase on the risks of intracerebral haemorrhage, mortality, and functional imp
121 stroke), and outnumbered disabling or fatal intracerebral haemorrhage (n=45 vs n=18), with an absolu
123 9-60) in 2013; symptomatic post-thrombolysis intracerebral haemorrhages occurred in 28 of 675 patient
124 or conscious patients with superficial lobar intracerebral haemorrhage of 10-100 mL and no intraventr
125 -80 years with a non-traumatic (spontaneous) intracerebral haemorrhage of 20 mL or higher to standard
126 tratified by trial, to model the log odds of intracerebral haemorrhage on allocation to alteplase, tr
129 ia in dementia-free survivors of spontaneous intracerebral haemorrhage; our results suggest that unde
130 substantial fall in hypertension-associated intracerebral haemorrhage over the past 25 years, but no
131 sus 6/75 (8%) in the remaining patients with intracerebral haemorrhage (P = 0.024); no diffusion-weig
132 ients with infection at onset, patients with intracerebral haemorrhage (p=0.014), dysphagia (p=0.003)
133 racerebral haemorrhage from the Prognosis of Intracerebral Haemorrhage (PITCH) cohort who were admitt
135 creased steeply in the days and weeks before intracerebral haemorrhage (regression p<0.0001) but not
136 eria were pure intraventricular haemorrhage; intracerebral haemorrhage resulting from intracranial va
137 k (odds ratio, 1.07, P = 0.04) and recurrent intracerebral haemorrhage risk (hazards ratio, 1.45, P =
138 ase levels were associated with both primary intracerebral haemorrhage risk (odds ratio, 1.07, P = 0.
142 ture clinical trials including patients with intracerebral haemorrhage should assess cognitive endpoi
143 odels in a prospective cohort of 174 primary intracerebral haemorrhage survivors for association with
144 ective longitudinal follow-up of consecutive intracerebral haemorrhage survivors presenting to a sing
145 enrolled adults within 6 h of supratentorial intracerebral haemorrhage symptom onset if they had used
146 ommon in cerebral amyloid angiopathy-related intracerebral haemorrhage than in other intracerebral ha
148 ever, the risk of dementia after spontaneous intracerebral haemorrhage that accounts for about 15% of
149 th increasing stroke severity: for SITS-MOST intracerebral haemorrhage the absolute excess risk range
150 ubarachnoid haemorrhages and, of all primary intracerebral haemorrhages, they are responsible for 4%
151 ified assessment of three classifications of intracerebral haemorrhage: type 2 parenchymal haemorrhag
153 magnetic resonance imaging (<3 months after intracerebral haemorrhage) using diffusion-weighted imag
154 probable cerebral amyloid angiopathy-related intracerebral haemorrhage versus 6/75 (8%) in the remain
155 tensive care unit with stable, non-traumatic intracerebral haemorrhage volume less than 30 mL, intrav
158 e-phase blood pressure reading after primary intracerebral haemorrhage was more likely than after isc
159 owever defined, the proportional increase in intracerebral haemorrhage was similar irrespective of tr
160 the mean first systolic blood pressure after intracerebral haemorrhage was substantially higher than
161 ajor ischaemic stroke and those with primary intracerebral haemorrhage, we compared acute-phase and p
162 owever, alteplase also increases the risk of intracerebral haemorrhage; we aimed to determine the pro
163 only and those with frontal infarcts and/or intracerebral haemorrhage were both significantly more l
165 d compared with usual premorbid levels after intracerebral haemorrhage, whereas acute-phase systolic
166 ) to investigate changes in the incidence of intracerebral haemorrhage with time, above and below age
167 While the association between CAA and lobar intracerebral haemorrhage (with its high recurrence risk
168 Intraventricular haemorrhage is a subtype of intracerebral haemorrhage, with 50% mortality and seriou
169 st an association with a high risk of future intracerebral haemorrhage, with potential implications f
171 ge for patients with spontaneous superficial intracerebral haemorrhage without intraventricular haemo
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