INTRODUCTION:Early cognitive screening, although recommended, can be challenging in acute stroke settings. In patients with acute stroke, we aimed to evaluate (1) reasons and predictors of non-applicability of the Montreal Cognitive Assessment (MoCA) and (2) MoCA score performance, focusing on sex-related differences. PATIENTS AND METHODS:We conducted a single-centre study on patients consecutively admitted to our stroke unit (June 2019-June 2023). Reasons for MoCA non-applicability and MoCA scores were compared between sexes. Univariate and multivariable analyses explored associations between MoCA applicability and sociodemographic/clinical characteristics. RESULTS:Out of 637 admitted patients (median age 78.8 years; 54.3% male; 81.2% ischemic stroke), 445 (69.8%) completed the MoCA (76.3% of males, 62.2% of females, P <.001). Reasons for non-applicability were acute stroke-related in 63.5% of cases (mainly altered consciousness and aphasia), prestroke conditions-related in 22.9% and other (refusal/unreported) in 13.5%. Stroke-related reasons were more frequent in females (P =.002) and refusal in males (P =.005). Variables associated with MoCA non-applicability were: NIHSS on admission in both females (adjusted odds ratio [adj.OR] 1.25, 95% CI, 1.16-1.34) and males (adj.OR 1.24, 95% CI, 1.14-1.34); pre-stroke mRS in females (adj.OR 1.58, 95% CI, 1.15-2.17) and years of education and left-hemisphere lesion in males (adj.OR 0.91, 95% CI, 0.84-1.00 and adj.OR 2.38, 95% CI, 1.16-4.86, respectively). Among tested patients, females showed lower raw and adjusted MoCA scores (P <.001 and P =.022, respectively). CONCLUSION:Sex-specific factors influence feasibility and interpretation of early cognitive screening in the acute stroke phase: recognising these differences might guide future efforts towards more inclusive and individualised protocols.

INTRODUCTION:Post-stroke depressive symptoms are heterogeneous and variably associated with other psycho-cognitive features. We employed cluster analysis to identify distinct profiles of post-stroke depressive symptomatology and their association with cognitive performance. METHODS:We included consecutive patients undergoing neuropsychiatric evaluation 6 months after stroke. Cluster analysis incorporated the Center for Epidemiologic Studies Depression Scale, along with the apathy and anxiety items from the Neuropsychiatric Inventory questionnaire. Baseline clinical/neuroimaging variables and 6-months cognitive outcomes were compared across profiles. RESULTS:We included 189 patients with acute cerebrovascular events (median age 75.4 years, 62% male, 80% ischemic strokes). Three profiles emerged: (A) low-depressive symptoms (n = 108), (B) moderate-depressive symptoms plus anxiety (n = 41), (C) high-depressive symptoms plus apathy (n = 40). Regarding baseline predictors of 6-month depressive symptoms profiles, patients with high-depressive symptoms plus apathy exhibited lower Montreal Cognitive Assessment scores at baseline (16.0 vs. 21.5; adjusted odds ratio [adj.OR] per 1-point increase 0.91, 95% confidence interval [95% CI] 0.83-0.99) compared to patients with low-depressive symptoms; moderate-depressive symptoms plus anxiety patients had less cortical atrophy compared to both low-depressive symptoms (adj.OR 0.92, 95% CI 0.86-0.99) and high-depressive symptoms plus apathy (adj.OR 0.89, 95% CI 0.81-0.97) profiles. Regarding 6-month cognitive performance, high-depressive symptoms plus apathy patients showed higher rates of post-stroke dementia and attention/executive function impairment compared with the two other groups (both p < 0.05), and higher rates of language impairment compared with low-depressive symptoms profile (p < 0.05). CONCLUSION:By integrating apathy and anxiety in our model, depressive symptoms after stroke emerged as heterogeneous neuropsychiatric syndromes, showing different baseline predictors and distinctive cognitive patterns.

Background: In patients with cryptogenic stroke (CS) or transient ischemic attack (TIA), prolonged cardiac monitoring is recommended to improve detection of atrial fibrillation (AF). Prediction scores have been proposed to identify patients with a high likelihood of post-stroke AF detection and some of them have been used to guide the selection of patients for implantable loop recorders (ILR), but few studies have externally assessed their performances. Aims: aim of this prospective cohort study was to assess the performance of nine AF prediction scores in a cohort of CS and TIA monitored with ILR. Methods: Patients were included after a diagnosis of CS or TIA and ILR implantation between July 2018 and December 2023. Nine AF prediction scores were evaluated: STAF, LADS, HAVOC, Brown-ESUS AF, AS5F, C2HEST, CHASE-LESS, AF-ESUS, and Empoli ESUS-AF. For each score we calculated sensitivity, specificity, negative (NPV) and positive predictive value (PPV), overall accuracy, and area under the receiver operating characteristic curve (AUROC). AUROCs were compared with DeLong’s test. Results: Of 1032 admitted patients, 270 (26.2%) were defined cryptogenic, 194 of whom (71.9%) received an ILR (43.3% women; median age 74.0 years [IQR 65.8-82.0]; median NIHSS score on admission 3.0 [1.0-6.0]; 182 (93.8%) ischemic stroke and 12 (6.2%) TIA). Median time from index event to ILR implant was 10 days (7-37). During long-term monitoring (median follow-up 23.0 months [12.0-37.3]), AF was detected in 62 patients (32%), with a median time from index stroke to AF diagnosis of 4.0 months (1.0-11.3). Sensitivity of the scores ranged between 12.9 and 95.2%, specificity 12.9-67.7%, PPV 37.3-48.1%, NPV 68.6-90.6%, and overall accuracy 45.4-66.3%. The Brown ESUS-AF score reached the highest AUROC (0.697 in the whole cohort, 0.707 in the ischemic stroke subgroup). In patients with ischemic stroke, AUROC was higher for Brown ESUS-AF compared to HAVOC (p=0.014), CH2EST (p=0.002), and Empoli ESUS-AF (p=0.015) and for LADS (AUROC=0.690) compared to CH2EST (p=0.039) and Empoli ESUS-AF (p=0.015). Conclusions: AF prediction scores based on clinical and cardiovascular imaging parameters do not predict AF detection with adequate accuracy in patients with CS or TIA and ILR. Brown ESUS-AF and LADS scores demonstrated a better performance compared to other prediction scores.

BACKGROUND:Some patients with stroke have prestroke cognitive impairment (pre-SCI), but its etiology is not clear. The aim of this cross-sectional study was to assess the frequency of pre-SCI and its association with premorbid neuropsychiatric, functional, and neuroimaging features. METHODS:Patients hospitalized in stroke unit with an informant who could complete IQCODE (Informant Questionnaire for Cognitive Decline in the Elderly) were included. Pre-SCI was diagnosed if the IQCODE score was >3.3. Prestroke assessment also included NPI-Q (Neuropsychiatric Inventory Questionnaire), the basic Activities of Daily Living and Instrumental Activities of Daily Living scales, and the Clinical Dementia Rating scale. A multivariate logistic regression model was used to evaluate the association of pre-SCI with age, sex, education, arterial hypertension, atrial fibrillation, white matter lesions, cerebral microbleeds, and pathological medial temporal lobe atrophy. RESULTS:IQCODE was available in 474 of 520 patients (91.2%; 45% women; mean age 75.5 +/- 13.3 years). Pre-SCI had a prevalence of 32.5% and was associated with prestroke NPI-Q (pre-SCI absent versus present, 1.7 +/- 2.3 versus 5.5 +/- 4.9; P<0.001), Activities of Daily Living scale (0.3 +/- 0.8 versus 1.8 +/- 1.9; P<0.001), Instrumental Activities of Daily Living scale (0.6 +/- 1.3 versus 3.8 +/- 4.0; P<0.001), and Clinical Dementia Rating scale score (0.7 +/- 1.7 versus 7.2 +/- 6.2; P<0.001). In the 271 patients with a magnetic resonance imaging available, the multivariate logistic regression showed that age (odds ratio [OR], 1.05 [95% CI, 1.62-9.73]), white matter lesions (OR, 1.26 [95% CI, 1.003-1.58]), and a pathological medial temporal lobe atrophy score (OR, 3.97 [95% CI, 1.62-9.73]) were independently associated with pre-SCI. In the 218 patients with ischemic stroke, white matter lesions (OR, 1.34 [95% CI, 1.04-1.72]) and medial temporal lobe atrophy (OR, 3.56 [95% CI, 1.38-9.19]), but not age, were associated with pre-SCI. CONCLUSIONS:One-third of patients admitted to a stroke unit have pre-SCI that is associated with preexisting neuropsychiatric symptoms and functional performance. White matter lesions and medial temporal lobe atrophy are associated with pre-SCI, suggesting that both small vessel disease and neurodegeneration might be involved in its etiology.

BACKGROUND AND PURPOSE:Post-stroke dysphagia affects outcome. In acute stroke patients, the aim was to evaluate clinical, cognitive and neuroimaging features associated with dysphagia and develop a predictive score for dysphagia.METHODS:Ischaemic stroke patients underwent clinical, cognitive and pre-morbid function evaluations. Dysphagia was retrospectively scored on admission and discharge with the Functional Oral Intake Scale.RESULTS:In all, 228 patients (mean age 75.8 years; 52% males) were included. On admission, 126 (55%) were dysphagic (Functional Oral Intake Scale ≤6). Age (odds ratio [OR] 1.03, 95% confidence interval [CI] 1.00-1.05), pre-event modified Rankin scale (mRS) score (OR 1.41, 95% CI 1.09-1.84), National Institutes of Health Stroke Scale (NIHSS) score (OR 1.79, 95% CI 1.49-2.14), frontal operculum lesion (OR 8.53, 95% CI 3.82-19.06) and Oxfordshire total anterior circulation infarct (TACI) (OR 1.47, 95% CI 1.05-2.04) were independently associated with dysphagia at admission. Education (OR 0.91, 95% CI 0.85-0.98) had a protective role. At discharge, 82 patients (36%) were dysphagic. Pre-event mRS (OR 1.28, 95% CI 1.04-1.56), admission NIHSS (OR 1.88, 95% CI 1.56-2.26), frontal operculum involvement (OR 15.53, 95% CI 7.44-32.43) and Oxfordshire classification TACI (OR 3.82, 95% CI 1.95-7.50) were independently associated with dysphagia at discharge. Education (OR 0.89, 95% CI 0.83-0.96) and thrombolysis (OR 0.77, 95% CI 0.23-0.95) had a protective role. The 6-point "NOTTEM" (NIHSS, opercular lesion, TACI, thrombolysis, education, mRS) score predicted dysphagia at discharge with good accuracy. Cognitive scores had no role in dysphagia risk.CONCLUSIONS:Dysphagia predictors were defined and a score was developed to evaluate dysphagia risk during stroke unit stay. In this setting, cognitive impairment is not a predictor of dysphagia. Early dysphagia assessment may help in planning future rehabilitative and nutrition strategies.

We showed that the Clock Drawing Test (CDT) performed during the acute phase of cerebrovascular diseases predicted worsening of cognitive function defined based on a clinical judgement at a 3-month follow-up. The aim of this study was to verify the predictivity of the CDT on the worsening of cognitive status assessed with an extensive neuropsychological evaluation 6 months after the acute event. Patients with a stroke or transient ischemic attack underwent a baseline clinical, neuroimaging, and neuropsychological assessment, including the CDT. Premorbid cognitive status was evaluated by means of the Clinical Dementia Rating scale. Between 6 and 7 months after the acute event, all patients underwent a neuropsychological evaluation that included tests for executive function, attention, language, memory, and visuospatial abilities. Fifty patients (29 males; mean age 72.2 years) were enrolled: 28 (56%) had no premorbid cognitive impairment, 15 (30%) had premorbid mild cognitive impairment (MCI), and 4 (8%) had premorbid dementia; for 3 patients, evaluation of premorbid status was not available. At follow-up, 11 (22%) had no cognitive impairment, 28 (56%) were diagnosed with MCI, and 11 (22%) dementia. In patients who were non-demented before the event, on regression analysis, the score obtained at CDT was predictive of decline of cognitive status at the 6-month follow-up (OR 1.65; 95% CI 1.08–2.52). Our study confirms that administering the CDT during the acute phase of cerebrovascular diseases is informative with regard to the worsening of cognitive function after 6 months.

Introduction Different mechanisms may underlie cryptogenic stroke, including subclinical atrial fibrillation (AF), nonstenotic carotid plaques (NCP), and aortic arch atherosclerosis (AAA). In a cohort of cryptogenic stroke patients, we aimed to: (1) evaluate the prevalence of subclinical AF, NCP, and AAA, and reclassify the etiology accordingly; (2) compare the clinical features of patients with reclassified etiology with those with confirmed cryptogenic stroke. Methods Data of patients hospitalized for cryptogenic stroke between January 2018 and February 2021 were retrospectively analyzed. Patients were included if they received implantable cardiac monitoring (ICM) to detect subclinical AF. Baseline computed tomography angiography (CTA) was re-evaluated to assess NCP and AAA. Since aortic plaques with ulceration/intraluminal thrombus were considered pathogenetic during the initial workup, only patients with milder AAA were included. Stroke etiology was reclassified as "cardioembolic", "atherosclerotic", or "mixed" based on the detection of AF and NCP/AAA. Patients with "true cryptogenic" stroke (no AF, ipsilateral NCP, or AAA detected) were compared with those with reclassified etiology. Results Among 63 patients included, 21 (33%) were diagnosed with AF (median follow-up time of 15 months), 12 (19%) had ipsilateral NCP, and 6 (10%) had AAA. Stroke etiology was reclassified in 30 patients (48%): cardioembolic in 14 (22%), atherosclerotic in 9 (14%), and mixed in 7 (11%). Patients with true cryptogenic stroke were younger compared to those with reclassified etiology (p = 0.001). Discussion One or more potential covert stroke sources can be recognized in half of the patients with a cryptogenic stroke through long-term cardiac monitoring and focused CTA re-assessment.

Background: In patients with atrial fibrillation who suffered an ischemic stroke while on treatment with nonvitamin K antagonist oral anticoagulants, rates and determinants of recurrent ischemic events and major bleedings remain uncertain. Methods: This prospective multicenter observational study aimed to estimate the rates of ischemic and bleeding events and their determinants in the follow-up of consecutive patients with atrial fibrillation who suffered an acute cerebrovascular ischemic event while on nonvitamin K antagonist oral anticoagulant treatment. Afterwards, we compared the estimated risks of ischemic and bleeding events between the patients in whom anticoagulant therapy was changed to those who continued the original treatment. Results: After a mean follow-up time of 15.0±10.9 months, 192 out of 1240 patients (15.5%) had 207 ischemic or bleeding events corresponding to an annual rate of 13.4%. Among the events, 111 were ischemic strokes, 15 systemic embolisms, 24 intracranial bleedings, and 57 major extracranial bleedings. Predictive factors of recurrent ischemic events (strokes and systemic embolisms) included CHA 2 DS 2 -VASc score after the index event (odds ratio [OR], 1.2 [95% CI, 1.0–1.3] for each point increase; P =0.05) and hypertension (OR, 2.3 [95% CI, 1.0–5.1]; P =0.04). Predictive factors of bleeding events (intracranial and major extracranial bleedings) included age (OR, 1.1 [95% CI, 1.0–1.2] for each year increase; P =0.002), history of major bleeding (OR, 6.9 [95% CI, 3.4–14.2]; P =0.0001) and the concomitant administration of an antiplatelet agent (OR, 2.8 [95% CI, 1.4–5.5]; P =0.003). Rates of ischemic and bleeding events were no different in patients who changed or not changed the original nonvitamin K antagonist oral anticoagulants treatment (OR, 1.2 [95% CI, 0.8–1.7]). Conclusions: Patients suffering a stroke despite being on nonvitamin K antagonist oral anticoagulant therapy are at high risk of recurrent ischemic stroke and bleeding. In these patients, further research is needed to improve secondary prevention by investigating the mechanisms of recurrent ischemic stroke and bleeding.

BACKGROUND:Multiple sclerosis (MS) is characterized by phenotypical heterogeneity, partly resulting from demographic and environmental risk factors. Socio-economic factors and the characteristics of local MS facilities might also play a part.METHODS:This study included patients with a confirmed MS diagnosis enrolled in the Italian MS and Related Disorders Register in 2000-2021. Patients at first visit were classified as having a clinically isolated syndrome (CIS), relapsing-remitting (RR), primary progressive (PP), progressive-relapsing (PR), or secondary progressive MS (SP). Demographic and clinical characteristics were analyzed, with centers' characteristics, geographic macro-areas, and Deprivation Index. We computed the odds ratios (OR) for CIS, PP/PR, and SP phenotypes, compared to the RR, using multivariate, multinomial, mixed effects logistic regression models.RESULTS:In all 35,243 patients from 106 centers were included. The OR of presenting more advanced MS phenotypes than the RR phenotype at first visit significantly diminished in relation to calendar period. Females were at a significantly lower risk of a PP/PR or SP phenotype. Older age was associated with CIS, PP/PR, and SP. The risk of a longer interval between disease onset and first visit was lower for the CIS phenotype, but higher for PP/PR and SP. The probability of SP at first visit was greater in the South of Italy.DISCUSSION:Differences in the phenotype of MS patients first seen in Italian centers can be only partly explained by differences in the centers' characteristics. The demographic and socio-economic characteristics of MS patients seem to be the main determinants of the phenotypes at first referral.

Background and Purpose- Despite treatment with oral anticoagulants, patients with nonvalvular atrial fibrillation (AF) may experience ischemic cerebrovascular events. The aims of this case-control study in patients with AF were to identify the pathogenesis of and the risk factors for cerebrovascular ischemic events occurring during non-vitamin K antagonist oral anticoagulants (NOACs) therapy for stroke prevention. Methods- Cases were consecutive patients with AF who had acute cerebrovascular ischemic events during NOAC treatment. Controls were consecutive patients with AF who did not have cerebrovascular events during NOACs treatment. Results- Overall, 713 cases (641 ischemic strokes and 72 transient ischemic attacks; median age, 80.0 years; interquartile range, 12; median National Institutes of Health Stroke Scale on admission, 6.0; interquartile range, 10) and 700 controls (median age, 72.0 years; interquartile range, 8) were included in the study. Recurrent stroke was classified as cardioembolic in 455 cases (63.9%) according to the A-S-C-O-D (A, atherosclerosis; S, small vessel disease; C, cardiac pathology; O, other causes; D, dissection) classification. On multivariable analysis, off-label low dose of NOACs (odds ratio [OR], 3.18; 95% CI, 1.95-5.85), atrial enlargement (OR, 6.64; 95% CI, 4.63-9.52), hyperlipidemia (OR, 2.40; 95% CI, 1.83-3.16), and CHA2DS2-VASc score (OR, 1.72 for each point increase; 95% CI, 1.58-1.88) were associated with ischemic events. Among the CHA2DS2-VASc components, age was older and presence of diabetes mellitus, congestive heart failure, and history of stroke or transient ischemic attack more common in patients who had acute cerebrovascular ischemic events. Paroxysmal AF was inversely associated with ischemic events (OR, 0.45; 95% CI, 0.33-0.61). Conclusions- In patients with AF treated with NOACs who had a cerebrovascular event, mostly but not exclusively of cardioembolic pathogenesis, off-label low dose, atrial enlargement, hyperlipidemia, and high CHA2DS2-VASc score were associated with increased risk of cerebrovascular events.

In older patients with recurrent unexplained focal neurologic episodes, an EEG and brain MRI may reveal that they are a treatable manifestation of CAA.

Paroxysmal atrial fibrillation (AF) represents one of the main mechanisms underlying cryptogenic stroke (CS). Trials have shown that prolonged cardiac monitoring through Implantable Loop Recorders (ILR) allows higher AF detection frequency after CS compared with routine follow-up and 24 h Holter monitoring, reaching 30% rate at 3 years. We aimed at assessing whether these data are reproducible in clinical practice.

Introduction: Cluster headache (CH) is a trigeminal autonomic cephalalgia characterized by extremely painful, strictly unilateral, headache attacks accompanied by ipsilateral autonomic symptoms.Only few studies investigated a possible role of right-to-left shunt (R-to-LS) and sleep apnea (OSA) in cluster pathogenesis or expression and no prior studies were located that combined the two conditions in CH patients.Objective: To define the potential combined effect of right-to-left shunt and obstructive sleep apnea in patients with cluster headache and their possible influence on the frequency of attacks and on response to oxygen therapy of headache attacks.Methods: 33 patients with cluster headache were recruited and subsequently invited to undergo polysomnography and a transcranial doppler bubble study.Polysomnography is used for the diagnosis of obstructive sleep apnea whereas transcranial doppler bubble study can help diagnose a cardiac right-to-left shunt.Results: Transcranial doppler results demonstrated that 10 out of 31 patients in our cohort had a right-to-left shunt (RLS).Polysomnography revealed that 10 out of 32 patients had obstructive sleep apnea (OSAS).Nineteen out of 33 subjects had one of the two conditions but only one of our 33 patients had both conditions simultaneously.In this sample patients with clear seasonality to their cluster attacks had a higher frequency of obstructive sleep apnea than patients without seasonality.Also a good response to oxygen treatment of the attacks was higher in OSAS patients.Conclusion: the presence of RLS or OSAS, by their possible influence on blood oxygenation, seems to be independently able to predispose to cluster headache or to make it clinically manifest, while the hypothesizable synergistic role between them in favoring cluster headache was not put in evidence.Additionally, our study suggested that the seasonality of cluster headache, may be influenced by the seasonal nature of obstructive sleep apnea.Finally, the presence of sleep breathing alterations seems to be also able to modulate the efficacy of oxygen inhalation on cluster headache attacks.

INTRODUCTION:Cognitive impairment is a common and disabling consequence of stroke. Its prevalence, the best way to screen for it in the acute setting, and its relation with premorbid status have not been thoroughly clarified.MATERIALS AND METHODS:Ischemic and hemorrhagic stroke patients admitted to our stroke unit underwent a baseline assessment that included a clinical and neuroimaging assessment, two cognitive tests (clock-drawing test, CDT; Montreal Cognitive Assessment-Basic, MoCA-B) and measures of premorbid function (including the Clinical Dementia Rating Scale). A follow-up examination was repeated 3-4 months after the acute event.RESULTS:Two hundred and twenty-three patients (52.5% women, mean age ± SD 75.8 years ± 12.3) were evaluated. Prestroke cognitive impairment was present in 91 patients (40.8%). At follow-up, the prevalence of cognitive impairment was 49%, while its incidence among patients who did not have any prestroke cognitive impairment was 38.8%. Of the originally admitted 223 patients (71 were lost to follow-up), only 60 (26.9%) were still cognitively intact at follow-up. On regression analysis, age and baseline CDT were associated with worsening of cognitive status at follow-up. In patients without cognitive impairment at baseline, a cutoff of 23 for MoCA-B and of 8.7 for CDT scores predicted the diagnosis of post-stroke cognitive impairment with sufficient accuracy.DISCUSSION AND CONCLUSION:Prestroke and post-stroke cognitive impairment affect a large proportion of patients with stroke. Our findings suggest that a neuropsychological screening during the acute phase might be predictive of the development of post-stroke cognitive impairment.

Giant cell arteritis (GCA) is the most common vasculitis in patients older than 50 years, and it is occasionally a cause of ischemic stroke. GCA as a paraneoplastic manifestation has been rarely described. We describe a 77-year-old man with a sudden onset of dizziness, vomiting, and gait disturbances. Following imaging studies, a diagnosis of bulbar ischemic stroke with left vertebral artery stenosis was made. Based on a history of polymyalgia rheumatica, on laboratory tests, and brain digital subtraction angiography, a diagnosis of GCA was advanced and the patient underwent high-dose steroidal therapy. After a total body 18-FGD PET imaging, a pulmonary adenocarcinoma was found. Vertebral artery involvement is a rare but important occurrence in GCA as it carries a high mortality rate, and may require a vigorous therapeutic approach. The association of lung cancer and GCA is infrequent, and the relationship between malignancy and GCA remains unclear. Whereas the search for a malignancy in the setting of a GCA is not routinely performed, the use of total body PET when a large vessel vasculitis is suspected may provide useful information on disease and help recognize occult neoplasms. (C) 2019 Elsevier Ltd. All rights reserved.

Platypnea-orthodeoxia syndrome is a condition of dyspnea and hypoxia whilst in the upright position, which improves in the recumbent position.We present a case of platypnea-orthodeoxia due to a fenestrated atrial septal aneurysm that induced recurrent strokes and a recent condition of fluctuating confusion and cognitive impairment, modified by position, associated with rapid variations of O 2 saturation position related.The suspect of platypneaorthodeoxia syndrome may be hypothesized in case of patients with recurrent cerebral ischemia and fluctuating cognitive disturbances induced by change of position.In those cases a careful echocardiographic evaluation and O 2 saturation determination in up and downright position are required.

Background and Purpose: About half of the dysphagic stroke patients have persistent swallowing dysfunction after 7 days from symptom onset. The aim of the study was to evaluate incidence, prognosis, clinical and neuroradiological correlates of post-stroke dysphagia. Methods: We prospectively examined consecutive patients with acute ischemic or hemorrhagic stroke. Patients' clinical and neuroradiological data were collected. Swallowing function was assessed by the water swallow test upon admission and after 14 days; patients were then classified as persistent dysphagic, non-persistent dysphagic or non-dysphagic. Results: We recruited 275 patients, 121 of whom were dysphagic upon admission and 254 patients attended follow-up at 14 days; 141 never presented dysphagia, 21 had a non-persistent pattern of dysphagia and 92 had a persistent one. Stroke type, leukoaraiosis degree, previous cognitive impairment and stroke severity upon admission independently predicted the occurrence of dysphagia after stroke and its persistence as well. At receiver operating characteristic (ROC) analysis, the National Institutes of Health Stroke Scale (NIHSS) score of 11.5 was the best predictive value of persistent dysphagia, with a specificity of 90.1% and a sensitivity of 72.4%. Conclusion: Stroke severity is an important predictor of a persistent pattern of dysphagia, with a suggested NIHSS cutoff value of ≥12. An independent correlation was observed with leukoaraiosis and with previous cognitive impairment.

Activation of NADPH oxidase and superoxide anion release in human neutrophils has been shown to be dependent on Na+/H+ exchange, and inhibition of intracellular alkalinisation has been proposed as a mechanism of action for some anti-inflammatory drugs. The effect of nimesulide, a novel nonsteroidal anti-inflammatory drug, on intracellular pH (pHi) regulation by the Na+/H+ antiport in human neutrophils was examined using the pH-sensitive fluorescent probe 2,7-biscarboxyethyl-5(6)-carboxyfluorescein (BCECF), When stimulated by formylmethionylleucyl-phenylalanine (fMLP) or phorbol-12-myristate-13-acetate (PM A), neutrophils displayed changes in pHi consisting of an initial acidification followed by a sustained alkalinising phase indicative of antiport activation. Nimesulide did not change the pHi of resting neutrophils and did not affect the pHi response to stimulation, It is concluded that the anti-inflammatory effect of nimesulide is not directly linked to interactions with the Na+/H+ antiport or other pathways affecting the regulation of pHi.