Universality of Performance Indicators based on Citation and Reference Counts

We find evidence for the universality of two relative bibliometric indicators of the quality of individual scientific publications taken from different data sets. One of these is a new index that considers both citation and reference counts. We demonstrate this universality for relatively well cited publications from a single institute, grouped by year of publication and by faculty or by department. We show similar behaviour in publications submitted to the arXiv e-print archive, grouped by year of submission and by sub-archive. We also find that for reasonably well cited papers this distribution is well fitted by a lognormal with a variance of around 1.3 which is consistent with the results of Radicchi, Fortunato, and Castellano (2008). Our work demonstrates that comparisons can be made between publications from different disciplines and publication dates, regardless of their citation count and without expensive access to the whole world-wide citation graph. Further, it shows that averages of the logarithm of such relative bibliometric indices deal with the issue of long tails and avoid the need for statistics based on lengthy ranking procedures.Comment: 15 pages, 14 figures, 11 pages of supplementary material. Submitted to Scientometric

Abnormal cortical responses to somatosensory stimulation in medication-overuse headache

BACKGROUND: Medication-overuse headache (MOH) is a frequent, disabling disorder. Despite a controversial pathophysiology convincing evidence attributes a pivotal role to central sensitization. Most patients with MOH initially have episodic migraine without aura (MOA) characterized interictally by an absent amplitude decrease in cortical evoked potentials to repetitive stimuli (habituation deficit), despite a normal initial amplitude (lack of sensitization). Whether central sensitization alters this electrophysiological profile is unknown. We therefore sought differences in somatosensory evoked potential (SEP) sensitization and habituation in patients with MOH and episodic MOA. METHODS: We recorded median-nerve SEPs (3 blocks of 100 sweeps) in 29 patients with MOH, 64 with MOA and 42 controls. Episodic migraineurs were studied during and between attacks. We measured N20-P25 amplitudes from 3 blocks of 100 sweeps, and assessed sensitization from block 1 amplitude, and habituation from amplitude changes between the 3 sequential blocks. RESULTS: In episodic migraineurs, interictal SEP amplitudes were normal in block 1, but thereafter failed to habituate. Ictal SEP amplitudes increased in block 1, then habituated normally. Patients with MOH had larger-amplitude block 1 SEPs than controls, and also lacked SEP habituation. SEP amplitudes were smaller in triptan overusers than in patients overusing nonsteroidal anti-inflammatory drugs (NSAIDs) or both medications combined, lowest in patients with the longest migraine history, and highest in those with the longest-lasting headache chronification. CONCLUSIONS: In patients with MOH, especially those overusing NSAIDs, the somatosensory cortex becomes increasingly sensitized. Sensory sensitization might add to the behavioral sensitization that favors compulsive drug intake, and may reflect drug-induced changes in central serotoninergic transmission

Triptans attenuate capsaicin-induced CREB phosphorylation within the trigeminal nucleus caudalis: a mechanism to prevent central sensitization?

The c-AMP-responsive element binding protein (CREB) and its phosphorylated product (P-CREB) are nuclear proteins expressed after stimulation of pain-producing areas of the spinal cord. There is evidence indicating that central sensitization within dorsal horn neurons is dependent on P-CREB transcriptional regulation. The objectives of the study were to investigate the expression of P-CREB in cells in rat trigeminal nucleus caudalis after noxious stimulation and to determine whether pre-treatment with specific anti-migraine agents modulate this expression. CREB and P-CREB labelling was investigated within the trigeminal caudalis by immunohistochemistry after capsaicin stimulation. Subsequently, the effect of i.v. pre-treatment with either sumatriptan (n = 5), or naratriptan (n = 7) on P-CREB expression was studied. Five animals pre-treated with i.v. normal saline were served as controls. CREB and P-CREB labelling was robust in all animal groups within Sp5C. Both naratriptan and sumatriptan decreased P-CREB expression (p = 0.0003 and 0.0013) within the Sp5C. Triptans attenuate activation of CREB within the central parts of the trigeminal system, thereby leading to potential inhibition of central sensitization. P-CREB may serve as a new marker for post-synaptic neuronal activation within Sp5C in animal models relevant to migraine

Current and prospective pharmacological targets in relation to antimigraine action

Migraine is a recurrent incapacitating neurovascular disorder characterized by unilateral and throbbing headaches associated with photophobia, phonophobia, nausea, and vomiting. Current specific drugs used in the acute treatment of migraine interact with vascular receptors, a fact that has raised concerns about their cardiovascular safety. In the past, α-adrenoceptor agonists (ergotamine, dihydroergotamine, isometheptene) were used. The last two decades have witnessed the advent of 5-HT1B/1D receptor agonists (sumatriptan and second-generation triptans), which have a well-established efficacy in the acute treatment of migraine. Moreover, current prophylactic treatments of migraine include 5-HT2 receptor antagonists, Ca2+ channel blockers, and β-adrenoceptor antagonists. Despite the progress in migraine research and in view of its complex etiology, this disease still remains underdiagnosed, and available therapies are underused. In this review, we have discussed pharmacological targets in migraine, with special emphasis on compounds acting on 5-HT (5-HT1-7), adrenergic (α1, α2, and β), calcitonin gene-related peptide (CGRP 1 and CGRP2), adenosine (A1, A2, and A3), glutamate (NMDA, AMPA, kainate, and metabotropic), dopamine, endothelin, and female hormone (estrogen and progesterone) receptors. In addition, we have considered some other targets, including gamma-aminobutyric acid, angiotensin, bradykinin, histamine, and ionotropic receptors, in relation to antimigraine therapy. Finally, the cardiovascular safety of current and prospective antimigraine therapies is touched upon

Chirp stimulation:H-response short and dynamic

Background Migraine patients have an increased photic-driving response. This ‘H-response’ (HR) has potential diagnostic value but it is time consuming. Aim The aim of the study was to establish a fast and standardized test for the study of migraine biology and treatment. Methods We studied 11 migraine patients and 11 matched control participants. We used stroboscope flashes with a ‘chirp’-like linear frequency-increase from 10 to 40 Hz. EEG was recorded from occipital electrodes. Power spectral density was calculated for the stimulus response and corrected for baseline. An HR-estimator was calculated as the average power between 18 and 26 Hz in the stimulation-frequency window. Results There was a significant difference for single ( p &lt; 0.05) and for 10 averaged recordings ( p &lt; 0.01) between migraineurs and controls, and a high inter-test reliability (Cronbach’s alpha = 0.94). Conclusion Chirp-like stimulation to study the H-response is reliable and efficient and might therefore have a potential for acute interventional studies in migraine research. </jats:sec

Sensory information processing may be neuroenergetically more demanding in migraine patients

Electrophysiological studies of stimulus-evoked brain activation suggest that sensory processing in migraine patients is abnormal between attacks. The main findings are increased amplitudes and decreased habituation of cortical evoked potentials. Recent findings in healthy individuals showed that evoked potentials result mainly from phase resetting of background electroencephalographic activity. We recorded single trial visual evoked potentials during repetitive visual stimulation in migraine patients and healthy controls and analyzed these in the frequency domain for amplitude and phase. Increases in visual evoked potential amplitudes in migraine patients are explained almost entirely by increases in local amplitude, rather than increases in phase synchrony across trials. As amplitude modulation is generally considered more energy demanding than phase synchronization, this may explain the increased vulnerability of migraine patients to sensory stressors and the effectiveness of drugs that reduce evoked potential amplitudes or enhance aerobic energy metabolism