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Background and Purpose— Many patients with acute ischemic stroke are not eligible for thrombolysis or mechanical reperfusion therapies due to contraindications, inaccessible vascular occlusions, late presentation, or large infarct core. Sphenopalatine ganglion (SPG) stimulation to enhance collateral flow and stabilize the blood-brain barrier offers an alternative, potentially more widely deliverable, therapy. Methods— In a randomized, sham-controlled, double-masked trial at 41 centers in 7 countries, patients with anterior circulation ischemic stroke not treated with reperfusion therapies within 24 hours of onset were randomly allocated to active SPG stimulation or sham control. The primary efficacy outcome was improvement beyond expectations on the modified Rankin Scale of global disability at 90 days (sliding dichotomy), assessed in the modified intention-to-treat population. The initial planned sample size was 660 patients, but the trial was stopped early when technical improvements in device placement occurred, so that analysis of accumulated experience could be conducted to inform a successor trial. Results— Among 303 enrolled patients, 253 received at least one active SPG or sham stimulation, constituting the modified intention-to-treat population (153 SPG stimulation and 100 sham control). Age was median 73 years (interquartile range, 64–79), 52.6% were female, deficit severity on the National Institutes of Health Stroke Scale was median 11 (interquartile range, 9–15), and time from last known well median 18.6 hours (interquartile range, 14.5–22.5). For the primary outcome, improved 3-month disability beyond expectations, rates in the SPG versus sham treatment groups were 49.7% versus 40.0%; odds ratio, 1.48 (95% CI, 0.89–2.47); P =0.13. A significant treatment interaction with stroke location (cortical versus noncortical) was noted, P =0.04. In the 87 patients with confirmed cortical involvement, rates of improvement beyond expectations were 50.0% versus 27.0%; odds ratio, 2.70 (95% CI, 1.08–6.73); P =0.03. Similar response patterns were observed for all prespecified secondary efficacy outcomes. No differences in mortality or serious adverse event safety end points were observed. Conclusions— SPG stimulation within 24 hours of onset is safe in acute ischemic stroke. SPG stimulation was not shown to statistically significantly improve 3-month disability above expectations, though favorable outcomes were nominally higher with SPG stimulation. Beneficial effects may distinctively be conferred in patients with confirmed cortical involvement. The results of this study need to be confirmed in a larger pivotal study. Clinical Trial Registration— URL: https://www.clinicaltrials.gov . Unique identifier: NCT03767192.

The guidelines on hypertension recently published by the European Societies of Hypertension and Cardiology (ESH/ESC), have acknowledged cognitive function (and its decline) as a hypertension mediated organ damage (HMOD). In fact, brain damage can be the only HMOD in more than 30% of hypertensive subjects, evolving undetected for several years if not appropriately screened; as long as undetected it cannot provide either corrective measures, nor adequate risk stratification of the hypertensive subject.The medical community dealing with older hypertensive patients should have a simple and pragmatic approach to early identify and precisely treat these patients. Both hypertension and cognitive decline are undeniably growing pandemics in developed or epidemiologically transitioning societies. Furthermore, there is a clear-cut connection between exposure to the increased blood pressure (BP) and development of cognitive decline.Therefore, a group of experts in the field from the European Society of Hypertension (ESH) and from the European Geriatric Medicine Society (EuGMS) gathered together to answer practical clinical question that often face the physician when dealing with their hypertensive patient in a routine clinical practice. They elaborated a Decision – making approach to help standardized such clinical evaluation. RUNNING TITLE: Cognitive screening in older hypertensive subjectsKEYWORDS Hypertension; Hypertension Mediated Organ Damage; Assessment; Cognition; Dementia; Prevention; Arterial Stiffness.

The aim of this paper was to assess the risk for depression in a 6-month-long post stroke follow up period as related to the stroke variables (i.e. stroke localisation, haemodynamic parameters).The stroke localisation was determined with CT and/or MRI. Subsequently all the examined individuals underwent SPECT examination. The follow up examinations were performed by the consultant psychiatrist in 6, 12 and 24 weeks subsequent to the stroke episode. The depressive episode diagnosis was established on the basis of ICD-10 diagnostic criteria.Only right-handed patients (43 men aged 57.3 +/- 11.6 and 17 women aged 62.5 +/- 14.4) with unilateral brain lesion were examined. 23 subjects (38%) developed depression in the follow-up period. 5 women (29%) and 18 men (ca. 42%) developed a depressive episode. Only one of the observed depressive episodes met ICD-10 criteria for severe depressive episode. 10 patients suffered from moderate depressive episode and 12 subjects exhibited a mild depressive episode.The results obtained with CT and/or MRI techniques revealed no correlation between the post-stroke depression and stroke lateralisation. However the localisation of the deep brain functional abnormalities revealed with SPECT correlated with the occurrence of the affective disorders as related to the asymmetry in regional blood flow measures.

The most common cause of hemispatial neglect (HN) is cerebral infarction. It can be induced by lesions in many different regions of the right hemisphere. The purpose of this article was to determine the prevalence of post-stroke HN, its clinical picture, and neuroanatomical correlates.Forty-six stroke patients with a focal right-hemisphere lesion were studied. Neglect in visual domain, assessed with a battery of drawing, line bisection and shape cancellation tests, was observed in 20 cases. The single-photon emission-computed tomography (SPECT) images of the brain were obtained with 740 MBq (20 mCi) of Tc-99m-labeled ECD on a triple-headed gamma camera.The most sensitive measure of HN was the cancellation test, which all neglect patients performed poorly. Twelve patients, classified as mildly impaired, showed no significant rightward deviation on line bisection, but they showed left visual neglect on the cancellation test. Reverse dissociation was not noted. Performance on a clock-drawing test revealed HN only in two patients, who showed also evidence of HN on other tests. Thereby, some of the tests seem to be more difficult or more sensitive to impairment. The critical area of perfusion abnormalities in all neglect patients were frontal lobe and striatum on the right. In severe HN, SPECT images evidenced the most extensive hypoperfusion throughout the perisylvian region and subcortical structures of the right hemisphere. Although parietal cortex was affected in patients with moderate to severe HN, it was spared in the rest.HN was a relatively common symptom of vascular right-hemisphere damage (43% of the patient population). HN was a complex disturbance in terms of its clinical manifestation and neuroimaging correlates. Our findings challenge the classical notion that damage to the parietal cortex is critically associated with HN. Instead, our results support the model attributing hemispatial neglect to a defect in a cortico-striato-thalamo-cortical loop. Also, the present study highlights the usefulness of cerebral blood flow SPECT imaging as a diagnostic aid in the post-stroke deficits of cognition following right-hemisphere damage.

Hemispatial neglect is characterised as a failure by a brain-damaged patient to attend to contralesional space. It is hypothesised to be a result of damage to a network involving the frontal, parietal and cingulated cortices, basal ganglia and thalamus.The aim of this preliminary study was to verify this model of neglect in 22 right hemisphere-damaged acute stroke patients, using single photon emission-computed tomography (SPECT). The presence of a single right-sided vascular brain lesion was confirmed on CT and/or MRI. Hemispatial neglect, assessed with a battery of drawings, line bisection and line and shape cancellation tests, was observed in 12 cases.Patients with neglect (compared with those without neglect) had more extensive hypoperfusion in the frontal and parietal cortex, as well as striatum and thalamus. Left-sided hypoperfusion in the parietal cortex and the thalamus was also significantly associated with neglect on SPECT imaging. Performance in three out of five psychological tasks commonly used to detect the presence of hemispatial neglect, such as drawing tests and line bisection test, was exclusively linked with damage to the parietal cortex of the right hemisphere, while the line cancellation test might be attributable to the lesion of the right striatum.These findings support the model attributing hemispatial neglect to a unilateral defect in a cortico-striatothalamo-cortical loop. CBF SPECT imaging may provide a reliable description of the brain pathology associated with hemispatial neglect.

This report describes the clinical, pathological, immunohistochemical and genetic data of two rare malignant neoplasms of the central nervous system (CNS)--a cerebral atypical teratoid/rhabdoid tumor (AT/RT) in a 5-month-old girl and a spinal canal primitive neuroectodermal tumor (PNET) in her father. Despite aggressive treatment, both tumors were fatal, displaying extensive local recurrence and diffuse neoplastic dissemination. The paraffin-embedded tumor tissue samples were analyzed using a dual-color FISH with a locus specific LSI22q (BCR) probe. In the AT/RT tissue, a loss of BCR locus was observed in a significant proportion of the cells in contrast to the PNET specimen where the majority of nuclei did not reveal any loss of the BCR region. No mutations in exon 5 and no changes in SNP of intron 5 of hSNF/INI1 gene were found. In addition, analysis of loss of heterozygosity (LOH) was performed using a panel of 15 microsatellite markers of chromosome 22. No LOH were found in both tumor tissues. In both cases no constitutional mutations of gene TP53 were found. Analysis of the TP53 mutations in the tumor tissues revealed that the PNET, not the AT/RT tumor, was homozygous for a missense mutation at codon 175 (CGC ==CAC). Thus, our findings emphasize the genetic differences between the two specimens and suggest that the occurrence of these two aggressive tumors of CNS in one family could be coincidental.