Cerebrovascular disease typically manifests with stroke, cognitive impairment, or both. Vascular cognitive impairment refers to all forms of cognitive disorder associated with cerebrovascular ...disease, regardless of the specific mechanisms involved. It encompasses the full range of cognitive deficits from mild cognitive impairment to dementia. In principle, any of the multiple causes of clinical stroke can cause vascular cognitive impairment. Recent work further highlights a role of microinfarcts, microhemorrhages, strategic white matter tracts, loss of microstructural tissue integrity, and secondary neurodegeneration. Vascular brain injury results in loss of structural and functional connectivity and, hence, compromise of functional networks within the brain. Vascular cognitive impairment is common both after stroke and in stroke-free individuals presenting to dementia clinics, and vascular pathology frequently coexists with neurodegenerative pathology, resulting in mixed forms of mild cognitive impairment or dementia. Vascular dementia is now recognized as the second most common form of dementia after Alzheimer’s disease, and there is increasing awareness that targeting vascular risk may help to prevent dementia, even of the Alzheimer type. Recent advances in neuroimaging, neuropathology, epidemiology, and genetics have led to a deeper understanding of how vascular disease affects cognition. These new findings provide an opportunity for the present reappraisal of vascular cognitive impairment. We further briefly address current therapeutic concepts.
Summary Cervical-artery dissection (CAD) is a major cause of cerebral ischaemia in young adults and can lead to various clinical symptoms, some of which are benign (eg, headache, neck pain, Horner's ...syndrome, and cranial-nerve palsy), but most patients have a stroke or transient ischaemic attack. In addition to trauma to the neck, other risk factors have been suggested, such as infection, migraine, hyperhomocysteinaemia, and the 677TT genotype of the 5,10-methylenetetrahydrofolate reductase gene ( MTHFR 677TT), although evidence is sparse. An underlying arteriopathy, which could in part be genetically determined, is believed to have a role in the development of CAD. Importantly, both research on and optimum management of CAD strongly rely on diagnostic accuracy. Although the functional outcome of CAD is good in most patients, socioprofessional effects can be important. Incidence of the disorder in the general population is underestimated. Mortality and short-term recurrence rates are low but possibly also underestimated. Further research is warranted to improve our understanding of the underlying pathophysiology, to assess the long-term outcome, and ultimately to provide treatment and prevention strategies.
Full text
Available for:
GEOZS, IJS, IMTLJ, KILJ, KISLJ, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UL, UM, UPCLJ, UPUK
3.
Stroke mimics and chameleons Moulin, Solène; Leys, Didier
Current opinion in neurology,
02/2019, Volume:
32, Issue:
1
Journal Article
Peer reviewed
A stroke mimic is a situation in which a diagnosis of stroke at admission is not confirmed, and a stroke chameleon is a situation in which a stroke is revealed by clinical symptoms that are not usual ...in stroke. The objective of this review is to identify the most frequent clinical situations in which stroke mimics and chameleons are encountered and consequences for the patient.
The safety profile of intravenous thrombolysis (IVT) in patients who have stroke mimics is excellent, and intracranial hemorrhages are rare. Modern neuroimaging techniques help identifying most mimics. For stroke chameleons the role of imaging may be less important, especially when the clinical presentation is not suggestive of a brain disorder that request immediate neuroimaging. Education of health providers to identify such situations is crucial.
Stroke mimics account for up to 25% of admissions for probable strokes. The proportion of patients with stroke mimics decreases with use of MRI at baseline. Mimics cannot always be ruled out in emergency. The problem with mimics is that stroke facilities are not properly used, and patients may receive IVT. However, thrombolysis is usually well tolerated in mimics and we should not spend much time in all patients to improve diagnostic accuracy, knowing that the time lost is harmful in all patients, and will only prevent treating one mimic out of 100 patients. The problem with chameleons is more serious, because patients are not identified, and are not properly treated.
In this trial, patients with stroke or TIA and atherosclerosis who received a statin with or without ezetimibe were randomly assigned to an LDL cholesterol target of less than 70 mg per deciliter or ...to a target range of 90 to 110 mg per deciliter. At a median follow-up of 3.5 years, the incidence of a composite cardiovascular end point was 12% lower in the lower-target group than in the higher-target group. The incidence of cerebral hemorrhage did not differ significantly between the two groups.
Summary Background Dementia occurs in at least 10% of patients within 1 year after stroke. However, the risk of dementia after spontaneous intracerebral haemorrhage that accounts for about 15% of all ...strokes has not been investigated in prospective studies. We aimed to determine the incidence of dementia and risk factors after an intracerebral haemorrhage. Methods We did a prospective observational cohort study in patients with spontaneous intracerebral haemorrhage from the Prognosis of Intracerebral Haemorrhage (PITCH) cohort who were admitted to Lille University Hospital, Lille, France. We included patients aged 18 years and older with parenchymal haemorrhage on the first CT scan. Exclusion criteria were pure intraventricular haemorrhage; intracerebral haemorrhage resulting from intracranial vascular malformation, intracranial venous thrombosis, head trauma, or tumour; haemorrhagic transformation within an infarct; and referral from other hospitals. Median follow-up was 6 years. We studied risk factors (clinical and neuroradiological MRI biomarkers) of new-onset dementia as per a prespecified subgroup analysis, according to intracerebral haemorrhage location. Dementia diagnosis was based on the National Institute on Aging-Alzheimer's Association criteria for all-cause dementia. We did multivariable analyses using competing risk analyses, with death during follow-up as a competing event. Findings From the 560 patients with spontaneous intracerebral haemorrhage enrolled in the PITCH cohort between Nov 3, 2004 and March 29, 2009, we included 218 patients (median age 67·5 years) without pre-existing dementia who were alive at 6 months follow-up. 63 patients developed new-onset dementia leading to an incidence rate of 14·2% (95% CI 10·0–19·3) at 1 year after intracerebral haemorrhage, and incidence reached 28·3% (22·4–34·5) at 4 years. The incidence of new-onset dementia was more than two times higher in patients with lobar intracerebral haemorrhage (incidence at 1 year 23·4%, 14·6–33·3) than for patients with non-lobar intracerebral haemorrhage (incidence at 1 year 9·2%, 5·1–14·7). Disseminated superficial siderosis (subhazard ratio SHR 7·45, 95% CI 4·27–12·99), cortical atrophy score (SHR per 1-point increase 2·61, 1·70–4·01), a higher number of cerebral microbleeds (SHR for >5 cerebral microbleeds 2·33, 1·38–3·94), and older age (SHR per 10-year increase 1·34, 1·00–1·79) were risk factors of new-onset dementia. Interpretation There is a substantial risk of incident dementia in dementia-free survivors of spontaneous intracerebral haemorrhage; our results suggest that underlying cerebral amyloid angiopathy is a contributing factor to the occurrence of new-onset dementia. Future clinical trials including patients with intracerebral haemorrhage should assess cognitive endpoints. Funding French Ministry of Education, Research, and Technology, Adrinord, Inserm U1171.
Full text
Available for:
GEOZS, IJS, IMTLJ, KILJ, KISLJ, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UL, UM, UPCLJ, UPUK
OBJECTIVE:To determine whether higher neutrophil counts before IV recombinant tissue plasminogen activator (rtPA) administration in ischemic stroke (IS) patients are associated with symptomatic ...intracerebral hemorrhages (sICH) and worse outcomes at 3 months.
METHODS:Blood samples for leukocyte, neutrophil, and lymphocyte counts were drawn before IV rtPA administration in IS patients included in the cohorts of Lille and Helsinki. The primary endpoint was sICH (European Cooperative Acute Stroke–II definition). Secondary endpoints were death and excellent (modified Rankin Scale mRS score 0–1 or equal to prestroke mRS) and good (mRS score 0–2 or equal to prestroke mRS) outcomes at 3 months.
RESULTS:We included 846 patients (median age 71 years; 50.8% men). The neutrophil count and neutrophil to lymphocyte ratio (NLR) were independently associated with the 4 endpointssICH (adjusted odds ratio adjOR for an increase of 1,000 neutrophils = 1.21 and adjOR 1.11, respectively), death (adjOR 1.16 and adjOR 1.08), and excellent (adjOR 0.87 and adjOR 0.85) and good (adjOR 0.86 and adjOR 0.91) outcomes. The total leukocyte count was not associated with any of the 4 endpoints. The best discriminating factor for sICH was NLR ≥4.80 (sensitivity 66.7%, specificity 71.3%, likelihood ratio 2.32). Patients with NLR ≥4.80 had a 3.71-fold increased risk for sICH (95% confidence interval adjOR1.97–6.98) compared to patients with NLR <4.80.
CONCLUSIONS:Higher neutrophil counts and NLR are independently associated with sICH and worse outcome at 3 months. The identification of mediators of this effect could provide new targets for neuroprotection in patients treated by rtPA.
Summary Spontaneous intracranial artery dissection is an uncommon and probably underdiagnosed cause of stroke that is defined by the occurrence of a haematoma in the wall of an intracranial artery. ...Patients can present with headache, ischaemic stroke, subarachnoid haemorrhage, or symptoms associated with mass effect, mostly on the brainstem. Although intracranial artery dissection is less common than cervical artery dissection in adults of European ethnic origin, intracranial artery dissection is reportedly more common in children and in Asian populations. Risk factors and mechanisms are poorly understood, and diagnosis is challenging because characteristic imaging features can be difficult to detect in view of the small size of intracranial arteries. Therefore, multimodal follow-up imaging is often needed to confirm the diagnosis. Treatment of intracranial artery dissections is empirical in the absence of data from randomised controlled trials. Most patients with subarachnoid haemorrhage undergo surgical or endovascular treatment to prevent rebleeding, whereas patients with intracranial artery dissection and cerebral ischaemia are treated with antithrombotics. Prognosis seems worse in patients with subarachnoid haemorrhage than in those without.
Full text
Available for:
GEOZS, IJS, IMTLJ, KILJ, KISLJ, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UL, UM, UPCLJ, UPUK
Stroke survivors typically experience varying degrees of motor and neuropsychological deficits. Although these deficits are frequently treated as separate entities in the cognitive and physical ...rehabilitation settings, there is considerable interaction between them. Cognitive-motor interference, for example, refers to the simultaneous performance of cognitive and motor functions that results in diminished execution of one or both of the tasks. Studies have demonstrated that when performing dual tasks, poststroke patients will typically favor the cognitive function over the motor task. Furthermore, only certain cognitive functions will interfere with motor abilities, while the intensity of the motor task may magnify the detriment in dual-task performance. Moreover, mood disorders, particularly depression, have also been shown to interact substantially with physical functioning. Consequently, poststroke patients with depression experience greater reductions in their activities of daily living and worse rates of recovery. Recent neuroimaging studies suggest an association between white matter hyperintensities and both motor and neuropsychological poststroke deficits. The relationship between spasticity and cognition deficits needs to be further explored with regard to the deleterious consequences of poststroke spasticity on quality of life and overall motor function. These insights, among others, contribute to a growing, if embryonic, body of knowledge about poststroke motor/cognitive interaction that will ultimately inform developments in treatment and rehabilitation.
Background
Intravenous thrombolysis with alteplase within a time window up to 4.5 h is the only approved pharmacological treatment for acute ischemic stroke. We studied whether acute ischemic stroke ...patients with penumbral tissue identified on magnetic resonance imaging 4.5–9 h after symptom onset benefit from intravenous thrombolysis compared to placebo.
Methods
Acute ischemic stroke patients with salvageable brain tissue identified on a magnetic resonance imaging were randomly assigned to receive standard dose alteplase or placebo. The primary end point was disability at 90 days assessed by the modified Rankin scale, which has a range of 0–6 (with 0 indicating no symptoms at all and 6 indicating death). Safety end points included death, symptomatic intracranial hemorrhage, and other serious adverse events.
Results
The trial was stopped early for slow recruitment after the enrollment of 119 (61 alteplase, 58 placebo) of 264 patients planned. Median time to intravenous thrombolysis was 7 h 42 min. The primary endpoint showed no significant difference in the modified Rankin scale distribution at day 90 (odds ratio alteplase versus placebo, 1.20; 95% CI, 0.63–2.27, P = 0.58). One symptomatic intracranial hemorrhage occurred in the alteplase group. Mortality at 90 days did not differ significantly between the two groups (11.5 and 6.8%, respectively; P = 0.53).
Conclusions
Intravenous alteplase administered between 4.5 and 9 h after the onset of symptoms in patients with salvageable tissue did not result in a significant benefit over placebo. (Supported by Boehringer Ingelheim, Germany; ISRCTN 71616222).
Full text
Available for:
NUK, OILJ, SAZU, UKNU, UL, UM, UPUK