The Risk of Symptomatic Intracranial Hemorrhage after Thrombolysis for Acute Stroke: Current Concepts and Perspectives

Background: Thrombolysis is the standard of treatment for acute ischemic stroke, with a time window of up to 4 1/2 h from stroke onset. Despite the long experience with the use of recombinant tissue plasminogen activator and the adherence to protocols symptomatic intracranial hemorrhage (SICH) may occur in around 6% of cases, with high-mortality rate and poor-functional outcomes. Many patients are excluded from thrombolysis on the basis of an evaluation of known risk factors, but there are other less known factors involved. Objective: The purpose of this work is to analyze the less known risk factors for SICH after thrombolysis. A search of articles related with this field has been undertaken in PubMed with the keywords (brain hemorrhage, thrombolysis, and acute ischemic stroke). Some risk factors for SICH have emerged such as previous microbleeds on brain magnetic resonance imaging, leukoaraiosis, and previous antiplatelet drug use or statin use. Serum matrix metalloproteinases have emerged as a promising biomarker for better selection of patients, but further research is needed. Conclusions: In addition to the already known risk factors considered in the standard protocols, an individualized evaluation of risks is needed to minimize the risk of brain hemorrhage after thrombolysis for ischemic stroke

The Interface between Depression and Alzheimer’s Disease. A Comprehensive Approach

Abstract Depression and Alzheimer’s disease (AD) are frequent interacting diseases in the elderly with a negative impact on the quality of life of patients and caregivers. Late-life depression may be regarded either as an early symptom of AD or a risk factor for AD, depending on the context. This review was focused on the latest developments in the fields of the neurobiological basis and treatment of depression in AD. We found that some plausible hypotheses are emerging to correlate with depression in AD, such as neuroinflammation and dysimmune regulation. It seems that depression is not related to amyloid deposition, but this issue is not completely resolved. The response to antidepressants is controversial according to the evidence from 10 small double-blind randomized placebo-controlled clinical trials with antidepressants in AD patients with depression: four with sertraline, one with three arms (sertraline, mirtazapine, placebo), one with fluoxetine, one with imipramine, one with clomipramine, one with escitalopram, and one with vortioxetine. The total number of treated patients completing the trials was 638. The main criterion of a positive response was a reduction in the scores of clinical scales for depression of at least 50%. The weighted OR (odds ratio) was calculated with the method of Mantel-Haenszel: 1.29; 95% CI: 0.77–2.16. No significant differences were found compared with placebo. Antidepressants did not have a meaningful negative influence on cognition, which was measured with the mini-mental state examination (MMSE) in 18 clinical trials. Alternatives other than drugs are also discussed. Although there have been important advances in this field, pathophysiology and treatment deserve further research

Magnetic resonance spectroscopy and brain volumetry in mild cognitive impairment. A prospective study

Objective To assess the accuracy of magnetic resonance spectroscopy (1H-MRS) and brain volumetry in mild cognitive impairment (MCI) to predict conversion to probable Alzheimer''s disease (AD). Methods Forty-eight patients fulfilling the criteria of amnestic MCI who underwent a conventional magnetic resonance imaging (MRI) followed by MRS, and T1-3D on 1.5 Tesla MR unit. At baseline the patients underwent neuropsychological examination. 1H-MRS of the brain was carried out by exploring the left medial occipital lobe and ventral posterior cingulated cortex (vPCC) using the LCModel software. A high resolution T1-3D sequence was acquired to carry out the volumetric measurement. A cortical and subcortical parcellation strategy was used to obtain the volumes of each area within the brain. The patients were followed up to detect conversion to probable AD. Results After a 3-year follow-up, 15 (31.2%) patients converted to AD. The myo-inositol in the occipital cortex and glutamate + glutamine (Glx) in the posterior cingulate cortex predicted conversion to probable AD at 46.1% sensitivity and 90.6% specificity. The positive predictive value was 66.7%, and the negative predictive value was 80.6%, with an overall cross-validated classification accuracy of 77.8%. The volume of the third ventricle, the total white matter and entorhinal cortex predict conversion to probable AD at 46.7% sensitivity and 90.9% specificity. The positive predictive value was 70%, and the negative predictive value was 78.9%, with an overall cross-validated classification accuracy of 77.1%. Combining volumetric measures in addition to the MRS measures the prediction to probable AD has a 38.5% sensitivity and 87.5% specificity, with a positive predictive value of 55.6%, a negative predictive value of 77.8% and an overall accuracy of 73.3%. Conclusion Either MRS or brain volumetric measures are markers separately of cognitive decline and may serve as a noninvasive tool to monitor cognitive changes and progression to dementia in patients with amnestic MCI, but the results do not support the routine use in the clinical settings

Familial Multiple Sclerosis with Repetitive Relapses of Manic Psychosis in Two Patients (Mother and Daughter)

The clinical presentation of multiple sclerosis (MS) with psychiatric symptoms is uncommon but it is believed that MS patients are twice as likely to be afflicted with bipolar disorder as the general population. We report two cases (mother and daughter) of MS presenting with bipolar disorder in the form of recurrent manic psychosis and whose outcome was favourable with neuroleptics and corticosteroids. In both cases we found multiple hypersignal lesions on brain magnetic resonance imaging (MRI), especially in the right frontal lobe where we observed signs of activity. Apart from clinical and radiological concordance, the patients exhibited similar class I HLA alleles and identical class II HLA alleles. We focused discussion on whether there may be a common genetic susceptibility to both illnesses or whether MS caused psychiatric manifestations. The coincidence of psychiatric and neurological symptoms in most relapses supports the second hypothesis

Plasmatic B-Type Natriuretic Peptide and C-Reactive Protein in Hyperacute Stroke as Markers of Ct-Evidence of Brain Edema

<p>OBJECTIVE. Plasmatic B-type-natriuretic peptide (NT-PBNP) and C-reactive protein (CRP) have been reportedly elevated in stroke patients; however their clinical significance remains uncertain. The purpose of this work is to investigate whether elevation of these proteins at baseline predicts CT-evidence of brain edema.</p> <p>METHODS. We recruited 41 consecutive patients with stroke and determined NT-PBNP and CRP at baseline (within 5 hours after onset), after 48-72 hours, and at discharge. Stroke severity was measured by means of the NIHS scale at baseline and at discharge. We also carried out brain CT at admittance and after 48 hours.</p> <p>RESULTS. There were 29 ischemic strokes and 12 hemorrhagic strokes. Evidence of brain edema on delayed scan was seen in 14 patients. Baseline levels of NT-PBNP did not predict CT-evidence of edema but CRP levels did so significantly (0.7 mg/dl in patients without edema versus 4.7 mg in patients with edema; p=0.001). Both NT-PBNP and PC levels correlated poorly to NIHSS score and increased markedly from baseline to the second determination in patients with edema. For these patients the NT-PBNP increase was 133.6 pmol/l in comparison to 1.58 pmol/l in patients without edema (p=0.002). Neither CRP nor NT-PBNP baseline levels were predictive of dependency or death.</p> <p>CONCLUSIONS. We conclude that CRP at baseline but not NT-PBNP predicts CT evidence of brain edema in stroke patients. We hypothesize that NT-PBNP levels elevated in response to edema after 48 hours of admission.</p

Une cause inhabituelle d’hyperCKémie

Les élévations du taux de créatine-phospho-kinase (CPK), ou hyperCKémies, constituent le lot quotidien de nombreux myologues. Leur grande diversité étiologique rend les choses difficiles en pratique clinique, plus encore lorsque l’hyperCKémie est isolée. Mis à part les élévations transitoires liées à certaines circonstances facilement identifiables (naissance, traumatisme, exercice musculaire extrême, exposition aux statines) ou certains facteurs ethniques, de nombreuses maladies neuromusculaires peuvent en être à l’origine. Il s’agit en premier lieu des dystrophies musculaires progressives et des myopathies métaboliques (glycogénoses surtout). Les progrès obtenus dans l’identification des causes des hyperCKémies ont sensiblement progressé ces dernières années grâce, notamment, à l’utilisation plus large du NGS. Dans l’observation ci-dessous, l’accent est mis sur une cause rare d’hyperCKémie pour laquelle un marqueur érythrocytaire simple permet d’évoquer le diagnostic