Working memory signals in early visual cortex are present in weak and strong imagers.

It has been suggested that visual images are memorized across brief periods of time by vividly imagining them as if they were still there. In line with this, the contents of both working memory and visual imagery are known to be encoded already in early visual cortex. If these signals in early visual areas were indeed to reflect a combined imagery and memory code, one would predict them to be weaker for individuals with reduced visual imagery vividness. Here, we systematically investigated this question in two groups of participants. Strong and weak imagers were asked to remember images across brief delay periods. We were able to reliably reconstruct the memorized stimuli from early visual cortex during the delay. Importantly, in contrast to the prediction, the quality of reconstruction was equally accurate for both strong and weak imagers. The decodable information also closely reflected behavioral precision in both groups, suggesting it could contribute to behavioral performance, even in the extreme case of completely aphantasic individuals. Our data thus suggest that working memory signals in early visual cortex can be present even in the (near) absence of phenomenal imagery.

Changes in medication cost observed in chronic cluster headache patients treated with sphenopalatine ganglion (SPG) stimulation: Analysis based on 1-year data from the Pathway R-1 Registry.

Background On-demand stimulation of the sphenopalatine ganglion (SPG) by means of an implantable neurostimulation system has been shown to be a safe and effective therapy for treatment-refractory cluster headache patients. Our objective was to estimate changes in cluster headache medication cost observed in SPG-treated chronic patients. Methods Detailed patient-level data of 71 chronic patients treated with the Pulsante® SPG Microstimulator System were available from the Pathway R-1 Registry through 12 months' follow-up. We used utilization data of preventive and acute medications reported at baseline, 3, 6, 9, and 12 months to estimate annualized drug costs for SPG-treated patients and compared it to baseline. Cost estimates for all drug/dosage combinations were developed based on German medication prices for 2016. Results In the base case analysis, mean annual acute and preventive medication costs decreased from €14,178 to €6924 (-€7254; -51%), and €559 to €328 (-€231; -41%), respectively, leading to total estimated annual drug cost savings of €7484, 97% of which were attributable to acute medications. Conclusions Our analysis suggests that SPG stimulation for the treatment of chronic cluster headache is associated with pronounced reductions in cluster headache medication usage that might lead to sizable annual savings in medication costs.

Effect of long-acting nifedipine on mortality and cardiovascular morbidity in patients with stable angina requiring treatment (ACTION trial): randomised controlled trial.

BACKGROUND: Calcium antagonists are widely prescribed for angina pectoris but their effect on clinical outcome is controversial. We aimed to investigate the effect of the calcium antagonist nifedipine on long-term outcome in patients with stable angina pectoris. METHODS: We randomly assigned 3825 patients with treated stable symptomatic coronary disease to double-blind addition of nifedipine GITS (gastrointestinal therapeutic system) 60 mg once daily and 3840 to placebo. The primary endpoint was the combination of death, acute myocardial infarction, refractory angina, new overt heart failure, debilitating stroke, and peripheral revascularisation. Mean follow-up was 4.9 years (SD 1.1). Analysis was by intention to treat. FINDINGS: 310 patients allocated nifedipine died (1.64 per 100 patient-years) compared with 291 people allocated placebo (1.53 per 100 patient-years; hazard ratio 1.07 [95% CI 0.91-1.25], p=0.41). Primary endpoint rates were 4.60 per 100 patient-years for nifedipine and 4.75 per 100 patient-years for placebo (0.97 [0.88-1.07], p=0.54). With nifedipine, rate of death and any cardiovascular event or procedure was 9.32 per 100 patient-years versus 10.50 per 100 patient-years for placebo (0.89 [0.83-0.95], p=0.0012). The difference was mainly attributable to a reduction in the need for coronary angiography and interventions in patients assigned nifedipine, despite an increase in peripheral revascularisation. Nifedipine had no effect on the rate of myocardial infarction. INTERPRETATION: Addition of nifedipine GITS to conventional treatment of angina pectoris has no effect on major cardiovascular event-free survival. Nifedipine GITS is safe and reduces the need for coronary angiography and interventions.

Diagnosis and management of out-of-hospital cardiac arrest secondary to coronary artery spasm.

OBJECTIVE: The clinical features of coronary artery spasm as a cause of cardiac arrest were determined in a prospective study on out-of-hospital cardiac arrest (OHCA). METHODS: Coronary angiography was performed at admission in 300 consecutive patients with no obvious non-cardiac cause of OHCA. In survivors with no or minimal coronary artery stenosis, a second angiography with provocation test and electrophysiological testing were performed at 1 month. RESULTS: Spasm was demonstrated in ten patients. Diagnosis was based upon (1) spontaneous spasm on the admission angiogram (3 patients), (2) transient significative ST-segment elevation at follow-up in patients with no or non-significant coronary artery lesions (4 patients) and (3) spasm during the 1 month provocation test (3 patients). Six patients survived at 1 month; spasm occurred during a new provocation test in five despite treatment with high dosage calcium channel blockers leading to coronary stenting in two, an internal cardiovertor defibrillator in one, and increased drug therapy with prolonged hospitalization in the remainder. At a mean follow-up of 55+/-27 months, no recurrent cardiac arrest occurred. CONCLUSION: Systematic coronary angiograms and provocation tests in survivors of OHCA allow prompt diagnosis of coronary artery spasm. Residual spasm despite treatment with calcium channel blockers is frequent. Therapy should therefore be guided by repetitive provocation tests, and seems to avoid recurrence of cardiac arrest.