Background and Aims Stroke is the second leading cause of death around the globe. Studies examining the predictors of in‐hospital mortality and the impact of complications on early outcome of acute ischemic stroke are scant. The aim of this study was to identify predictors of in‐hospital mortality in patients with acute ischemic stroke. Methods This was a prospective, single‐center study of patients with acute ischemic stroke consecutively admitted to the Neurology Department of a general hospital during a 2‐year period (from January 1, 2010 to December 31, 2011). Prospective data from this single‐center study included variables related to sociodemographics, comorbidities, and medical complications, together with in‐hospital mortality. Since stroke mortality may impact differently by sex and is also influenced by hospital length of stay, we proceeded to stratify by these variables. Results Six‐hundred and seventy‐three patients were included. Overall, in‐hospital mortality rate was 7.13%. Stratifying by length of stay in‐hospital (< 7 days and ≥ 7 days), we observed that within the first week, overall mortality was related to a history of previous stroke, higher stroke severity, and to cardiovascular and respiratory complications. After 7 days, the main factor independently associated with overall in‐hospital mortality was stroke severity (National Institutes of Health Stroke Scale (NIHSS) ≥ 14, odds ratio (OR): 17.15; 95% CI, 3.06‐96.07). Stratifying by sex, we observed that females had a worse outcome if there was a history of prior stroke (OR: 3.29; 95% CI, 1.19‐9.10), higher stroke severity (NIHSS ≥ 14, OR: 16.63; 95% CI, 4.66‐59.31), and cardiovascular complications (OR: 29.70; 95% CI, 5.70‐154.8). Among men, stroke severity (NIHSS ≥ 14, OR: 23.19; 95% CI, 5.69‐94.56), respiratory infections (OR: 3.84; 95% CI, 1.32‐11.20), and older age had significant negative impact. Conclusions Stroke severity and potentially modifiable complications (respiratory infections and cardiovascular complications) confer an increased risk of in‐hospital death in both women and men, particularly during the first week of admission.

Migraine, epilepsy and stroke are highly prevalent neurological disorders, often comorbid. They share diverse pathophysiological mechanisms that explain the use of similar drugs on certain occasions (i.e., the use of antiepileptic drugs in migraine prevention). Migraine with aura represents a risk for ischemic stroke, and avoiding contraceptives, tobacco use, and ergot alkaloids should be advised in those patients. Epilepsy bears a bidirectional relationship with headache. Only three entities are considered as seizure-related headaches: migraine-triggered seizure (migralepsy), hemicrania epileptica, and post-ictal headache. Topiramate (100-200 mg daily) and valproic acid (500-1,000 mg daily) are first-line drugs in migraine prevention, while older antiepileptics have no use in this setting. Stroke is the most common cause of symptomatic epilepsy in the adult. Therapy with lamotrigine, gabapentine, and levetiracetam is advised in late-onset (2 weeks after stroke) stroke-seizures, while early-onset seizures usually do not require therapy.

We here describe an acute-onset amnesic syndrome with evidence of an embolic infarction in the distribution of the subcallosal artery, a proximal branch of the anterior communicating artery. The infarction involved the corpus callosum genu and both fornices, giving a peculiar image on MRI that resembled a goblet. Although infrequent, the subcallosal artery infarction should be considered in the differential diagnosis of patients with an acute amnestic syndrome. We propose "the goblet sign" for the peculiar diffusion-weighted MRI image of the brain in this syndrome.

A 69-year-old woman presented to the emergency department with dizziness and instability. She had a history of peripheral vertigo, tinnitus, and one episode of orthostatic syncope in recent years; her only daily medication was zolpidem. Her past medical history was unremarkable. She was cooking at home when she noticed sudden-onset dizziness with a sensation of impending fainting while standing. Dizziness was described as intense, without "room spinning," and was accompanied by unstable gait. She described the event as different from her prior episodes of vertigo. She went to bed without improvement; dizziness persisted in recumbent position.After calling emergency services, she was examined at home by a doctor who found her with skin pallor, garbled and slow speech, and bradypsychia. Blood pressure and capillary glucose levels were normal.The patient was referred to the hospital, where she was still dizzy. She was afebrile, alert, and disoriented to date, with scanning speech and very slow responses to the examiner's orders. Gait examination showed marked instability with a broad-based gait. Pupillary size was normal. There was a grade 1 bilateral gaze-evoked nystagmus. Strength was normal in all extremities, and Babinski sign was absent. There was no limb ataxia, meningeal signs, or any other abnormalities on neurologic and general examination. Recumbent blood pressure was 112/67 mm Hg and did not significantly change after 3 minutes of standing.Blood chemistry abnormalities were ruled out first. All of the following were normal in serum: urea, ammonium, creatinine, liver enzymes, lipid profile, protein electrophoresis, sodium, potassium, calcium, syphilis serology, erythrocyte sedimentation rate, and C-reactive protein.Considering the sudden onset and duration of the symptomatology with dysarthria, dizziness, and instability, an acute stroke in the vertebrobasilar territory was initially suspected, and the patient was placed on aspirin therapy. Cranial MRI was then performed and revealed no evidence of acute ischemic lesions. Magnetic resonance angiography showed only slight Practical ImplicationsConsider inadvertent cannabis consumption in elderly patients with neurologic and psychiatric disturbances of unclear origin.

Background: The quality of life of migraine patients, particularly mental domains, is severely diminished despite the preventive therapies available. We aimed to evaluate whether citalopram plus nadolol is superior to nadolol alone in terms of quality of life (QOL) in migraine patients.Methods: Adult patients with episodic migraine (! 3 headache days per month) were allocated by simple randomization to nadolol 40 mg daily plus citalopram 10 mg daily or to nadolol alone. Baseline visit confirmed the entry criteria and patients filled out a generic QOL (SF-36) as well a migraine-specific questionnaire (MSQoL), a measure of migraine-related disability (MIDAS), a headache calendar and Beck inventory for depression and anxiety. This battery was again completed after 16 weeks of therapy.Results: A total of 92 patients from a general neurology clinic completed the study, 85% females with migraine without aura. Fourty-four (47.83%) patients were allocated to nadolol therapy, and 48 (52.17%) to the combination of nadolol plus citalopram. After therapy, both groups had a similar gain in quality of life (SF-36 and MSQOL), but combination therapy was not superior to nadolol. Despite this improvement, all SF-36 domains remained below the population norms in both groups.Conclusion: Adding systematically citalopram 10 mg daily to a conventional migraine preventive drug (nadolol) does not result in an additional improvement in the QOL of migraine patients.