Early Diagnosis of Central Disorders Mimicking Horizontal Canal Cupulolithiasis.

BACKGROUND: Horizontal Canal Cupulolithiasis (hc-BPPV-cu) can mimic a pathology of central origin, so a careful examination is essential to prevent misdiagnosis. METHODS: Retrospective cross-sectional cohort study of 45 patients suffering from suspected hc-BPPV-cu. We recorded whether patients first presented through an ENT Emergency Department (ED) or through an Outpatient Otolaryngology Clinic (OC). RESULTS: We found statistically significant differences (p < 0.05) between the OC versus the ED in relation to the time between symptom onset and first assessment (79.7 vs. 3.6 days, respectively), the number of therapeutic maneuvers (one maneuver in 62.5% vs. 75.9%, and more than one in 25.1% vs. 13.7%), and multi-canal BPPV rate (43.8% vs. 3.4%). hc-BPPV-cu did not resolve in 2 patients (12.5%) from the OC and in 3 (10.3%) from de ED, all of which showed central pathology. DISCUSSION: There are no prior studies that analyze the approach to hc-BPPV-cu in the ED. The benefits of early specialist input are early identification of central positional nystagmus, a decrease in symptom duration, reduced number of therapeutic maneuvers required for symptom resolution, and lower rates of iatrogenic multi-canal BPPV. CONCLUSION: A comprehensive approach to hc-BPPV-cu in the ED allows both more effective treatment and early identification of central disorder mimics.

Epidemiology of Intracranial Haemorrhages Associated with Vitamin K Antagonist Oral Anticoagulants in Spain: TAC Registry.

BACKGROUND: Vitamin K antagonist oral anticoagulants (VKA-OACs) are effective for primary and secondary prevention of embolic events. The rate of haemorrhagic neurological complications in patients admitted to neurology departments in Spain is not yet known. AIMS: We aimed to determine the clinical and epidemiological characteristics of patients with intracranial haemorrhage secondary to VKA-OACs as well as the incidence of this severe complication. METHODS: We conducted a retrospective, descriptive, multi-centre study using information from the medical records of all patients admitted to neurology departments, diagnosed with spontaneous intracranial haemorrhage, and treated with VKA-OACs within a 1-year period. We collected demographic and care data from centres, patients' medical records [demographic data, medical history, haemorrhage origin, vascular risk factors, concomitant treatment, and National Institutes of Health Stroke Scale (NIHSS) scores], and patients' outcome at 3 months [independence (modified Rankin Scale score <3) and mortality rate]. RESULTS: Twenty-one hospitals serving a population of 8,155,628 inhabitants participated in the study. The total number of cases was 235, the mean age was 78.2 (SD 9.4) years, and the baseline NIHSS score was 11.6 (SD 9.5; median 9; interquartile range 14). The VKA-OACs used were acenocoumarol in 95.3% (224 patients) and warfarin in 4.7% (11 patients). The haemorrhage origin was deep in 29.8%, lobar in 25.5%, intraventricular in 11.5%, extensive in 17.4% (>100 ml), cerebellar in 12.3%, and in the brainstem in 3.4%. The international normalised ratio was within therapeutic ranges at admission (according to indication) in 29.4% (69 patients). The global incidence (cases per 100,000 inhabitants per year) is 2.88. The in-hospital mortality rate was 40%, and 24.3% of the patients were independent at 3 months, while the mortality at 3 months was 42.6%. CONCLUSION: VKA-OAC treatment is associated with a large percentage of all cases of spontaneous intracranial haemorrhage, an event leading to high dependence and mortality rates.

Neuroprotection or increased brain damage mediated by temperature in stroke is time dependent.

The control of temperature during the acute phase of stroke may be a new therapeutic target that can be applied in all stroke patients, however therapeutic window or timecourse of the temperature effect is not well established. Our aim is to study the association between changes in body temperature in the first 72 hours and outcome in patients with ischemic (IS) and hemorrhagic (ICH) stroke. We prospectively studied 2931 consecutive patients (2468 with IS and 463 with ICH). Temperature was obtained at admission, and at 24, 48 and 72 hours after admission. Temperature was categorized as low (<36°C), normal (36-37°C) and high (>37°C). As the main variable, we studied functional outcome at 3 months determined by modified Rankin Scale.Temperature in stroke patients is higher than in controls, and increases gradually in the first 72 hours after stroke. A positive correlation between temperature and stroke severity determined by NIHSS was found at 24 and 48 hours, but not at admission or 72 hours. In a logistic regression model, high temperature was associated with poor outcome at 24 hours (OR 2.05, 95% CI 1.59-2.64, p<0.0001) and 48 hours (OR 1.93, 95% CI 1.08-2.34, p = 0.007), but not at admission or 72 hours.Temperature increases in patients with stroke in the first 72 hours, with the harmful effect of high temperature occurring in the first 48 hours. The neuroprotective effect of low temperature occurs within the first 24 hours from stroke onset.

Cefalea secundaria a malformación de Chiari tipo I al soplar en controles de alcoholemia / Chiari type I malformation-related cephalea appearing at the time of blowing during alcohol controls

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