Guillain-Barré syndrome following the 2009 pandemic monovalent and seasonal trivalent influenza vaccination campaigns in Spain from 2009 to 2011: outcomes from active surveillance by a neurologist network, and records from a country-wide hospital discharge database.

BACKGROUND: Studies have shown a slight excess risk in Guillain-Barré syndrome (GBS) incidence associated with A(H1N1)pdm09 vaccination campaign and seasonal trivalent influenza vaccine immunisations in 2009-2010. We aimed to assess the incidence of GBS as a potential adverse effect of A(H1N1)pdm09 vaccination. METHODS: A neurologist-led network, active at the neurology departments of ten general hospitals serving an adult population of 4.68 million, conducted GBS surveillance in Spain in 2009-2011. The network, established in 1996, carried out a retrospective and a prospective study to estimate monthly alarm thresholds in GBS incidence and tested them in 1998-1999 in a pilot study. Such incidence thresholds additionally to observation of GBS cases with immunisation antecedent in the 42 days prior to clinical onset were taken as alarm signals for 2009-2011, since November 2009 onwards. For purpose of surveillance, in 2009 we updated both the available centres and the populations served by the network. We also did a retrospective countrywide review of hospital-discharged patients having ICD-9-CM code 357.0 (acute infective polyneuritis) as their principal diagnosis from January 2009 to December 2011. RESULTS: Among 141 confirmed of 148 notified cases of GBS or Miller-Fisher syndrome, Brighton 1-2 criteria in 96 %, not a single patient was identified with clinical onset during the 42-day time interval following A(H1N1)pdm09 vaccination. In contrast, seven cases were seen during a similar period after seasonal campaigns. Monthly incidence figures did not, however, exceed the upper 95 % CI limit of expected incidence. A retrospective countrywide review of the registry of hospital-discharged patients having ICD-9-CM code 357.0 (acute infective polyneuritis) as their principal diagnosis did not suggest higher admission rates in critical months across the period December 2009-February 2010. CONCLUSIONS: Despite limited power and underlying reporting bias in 2010-2011, an increase in GBS incidence over background GBS, associated with A(H1N1)pdm09 monovalent or trivalent influenza immunisations, appears unlikely.

Evolution of cognitive impairment after stroke and risk factors for delayed progression.

BACKGROUND AND PURPOSE: Cognitive decline occurs in approximately 30% of stroke patients. Acute risk factors have been identified, but long-term risk has not been examined in large samples. The purpose of this research was to determine factors associated with the progression of cognitive impairment after stroke. METHODS: Consecutive stroke patients (193) without previous dementia were assessed 3 months after stroke with an extensive neuropsychological battery and diagnosed according to the Diagnostic and Statistical Manual of Mental Disorders Fourth Edition criteria and the Clinical Dementia Rating as normal (139), cognitive decline without dementia (18), or dementia (18 mild, 10 moderate, and 8 severe). After a 24-month follow-up, they were classified as stable, progressing, or improving, according to change in Clinical Dementia Rating score. The determinants of progression of cognitive decline were ascertained by logistic regression analysis of all clinical, neuroimaging, and complementary data. RESULTS: Cognitive status at 24 months was stable in most cases (151; 78.2%), decline progressed in 27 (14%; 6 demented and 21 nondemented), and improved in 15 (7.8%; 7 demented and 8 nondemented). Seven nondemented patients became demented at 24 months, and 5 demented became nondemented. The age (odds ratio [OR], 1.05; 95% CI, 1.01 to 1.1), mental decline before stroke (OR, 1.14; 95% CI, 1.02 to 1.27), number of prescribed drugs (OR, 1.34; 95% CI, 1.05 to 1.72), diastolic blood pressure on admission (OR, 0.96; 95% CI, 0.93 to 0.99), and episodes of hypotension during admission (OR, 7.61; 95% CI, 1.11 to 52.1) were significantly associated with cognitive deterioration. CONCLUSIONS: Cognition is rather stable for 2 years after stroke. Both progression and improvement of cognitive impairment are frequent in demented patients. Age, previous cognitive decline, polypharmacy, and hypotension during admission are risk factors for progression.

Cerebrospinal fluid markers in dementia with lewy bodies compared with Alzheimer disease.

BACKGROUND: Most patients with dementia with Lewy bodies (DLB) exhibit diffuse plaque-only pathology with rare neocortical neurofibrillary tangles (NFTs), as opposed to the widespread cortical neurofibrillary-tau involvement in Alzheimer disease (AD). Another pathological difference is the astrocytic and microglial inflammatory responses, including release of interleukins (ILs), around the neuritic plaques and NFTs in AD brains that are absent or much lower in DLB. We analyzed cerebrospinal fluid (CSF) markers that reflect the pathological differences between AD and DLB. OBJECTIVE: To determine CSF concentrations of tau, beta-amyloid, IL-1beta, and IL-6 as potential diagnostic clues to distinguish between AD and DLB. METHODS: We measured total tau, beta-amyloid1-42, IL-1beta, and IL-6 levels in CSF samples of 33 patients with probable AD without parkinsonism, 25 patients with all the core features of DLB, and 46 age-matched controls. RESULTS: Patients with AD had significantly higher levels of tau protein than patients with DLB and controls (P<.001). The most efficient cutoff value provided 76% specificity to distinguish AD and DLB cases. Patients with AD and DLB had lower, but not significantly so, beta-amyloid levels than controls. The combination of tau and beta-amyloid levels provided the best sensitivity (84%) and specificity (79%) to differentiate AD vs controls but was worse than tau values alone in discriminating between AD and DLB. Beta-amyloid levels had the best correlation with disease progression in both AD and DLB (P =.01). There were no significant differences in IL-1beta levels among patients with AD, patients with DLB, and controls. Patients with AD and DLB showed slightly, but not significantly, higher IL-6 levels than controls. CONCLUSIONS: The tau levels in CSF may contribute to the clinical distinction between AD and DLB. Beta-amyloid CSF levels are similar in both dementia disorders and reflect disease progression better than tau levels. Interleukin CSF concentrations do not distinguish between AD and DLB.

Previous and incident dementia as risk factors for mortality in stroke patients.

BACKGROUND AND PURPOSE: We sought to determine whether previous or incident dementia increases the risk of mortality after stroke. METHODS: We assessed clinical, functional, and cognitive status in 324 consecutive stroke patients who were followed up for 24 months. Prestroke dementia was diagnosed at admission (Diagnostic and Statistical Manual of Mental Disorders, Revised Third Edition criteria) and poststroke dementia 3 months after stroke (Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition criteria). The proportion of patients surviving in the groups with and without dementia and the relative risk of mortality were calculated with Kaplan-Meier and with Cox proportional hazards analyses, respectively, for prestroke, stroke-related, and poststroke dementia. RESULTS: Forty-nine patients (15.1% of the total sample) were found to have prestroke dementia. Three months after stroke, 75 cases had poststroke dementia: 50 incident cases (20% of 251 reexamined cases) with stroke-related dementia and 25 already demented before the stroke. After a mean follow-up of 16.1+/-9.9 months, the proportion of survivors was 20.4% in patients with and 72.6% in those without prestroke dementia. After a mean follow-up of 22.1+/-6.7 months, the proportion of survivors was 58.3% in patients with and 95.4% in those without stroke-related dementia. Using multivariate analysis and adjusting for age, sex, hypertension, diabetes, previous stroke, heart disease, and severity and recurrence of stroke, we found the relative risk of mortality associated with prestroke dementia to be 2.1 (95% CI, 1.2 to 3.6), with stroke-related dementia 6.3 (95% CI, 2.3 to 17.3), and with poststroke dementia 8.5 (95% CI, 3.4 to 20.9). CONCLUSIONS: Both previous dementia and incident dementia adversely influence long-term survival after stroke, even after adjustment for other predictors of stroke mortality.