Why EU asylum standards exceed the lowest common denominator: the role of regulatory expertise in EU decision-making

While scholars traditionally expected EU policy-making in the area of asylum to produce lowest common denominator standards, recent studies on the first phase of the Common European Asylum System have observed higher asylum standards in some instances. This article aims at explaining this divergence. Drawing on concepts of regulatory expertise and ‘misfit’, it argues that the observed variation in policy output can be explained by the dominance of a few (Northern) member states which were highly successful in inserting their positions in the core EU directives. Government effectiveness and exposure to the phenomenon entailing regulatory expertise provide a powerful explanation for member states being effective policy-shapers. Characterized by low levels of government effectiveness and exposure in the asylum area, Southern European countries were, on the contrary, rather passive during the negotiations and barely left any mark on the EU directives

Effects of intermittent theta burst stimulation on spasticity after spinal cord injury

PURPOSE: Spasticity is a common disorder in patients with spinal cord injury (SCI). The aim of this study was to investigate whether intermittent theta burst stimulation (iTBS), a safe, non-invasive and well-tolerated protocol of excitatory repetitive transcranial magnetic stimulation (rTMS), is effective in modulating spasticity in SCI patients. METHODS: In this randomized, double-blind, crossover, sham-controlled study, ten subjects with incomplete cervical or thoracic SCI received 10 days of daily sessions of real or sham iTBS. The H/M amplitude ratio of the Soleus H reflex, the amplitude of the motor evoked potentials (MEPs) at rest and during background contraction, as well as Modified Ashworth Scale (MAS) and the Spinal Cord Injury Assessment Tool for Spasticity (SCAT) were compared before and after the stimulation protocols. RESULTS: Patients receiving real iTBS showed significant increased resting and active MEPs amplitude and a significant reduction of the H/M amplitude ratio. In these patients also the MAS and SCAT scores were significantly reduced after treatment. These changes persisted up to 1 week after the end of the iTBS treatment, and were not observed under the sham-TBS condition. CONCLUSION: These findings suggest that iTBS may be a promising therapeutic tool for the spasticity in SCI patients

Modulation of non-painful phantom sensation in subjects with spinal cord injury by means of rTMS

We aimed in this study to investigate whether repetitive transcranial magnetic stimulation (rTMS), given as theta burst stimulation (TBS), can interfere with non-painful phantom sensations in subjects with spinal cord injury (SCI). In double-blind, sham-controlled experiments in five subjects with cervical or thoracic traumatic SCI, we evaluated the effects of a single session of inhibitory (continuous) TBS, excitatory (intermittent) TBS, or placebo TBS, on simplex and complex non-painful phantom sensations. The interventions targeted the contralateral primary motor cortex (M1), the primary sensory cortex (S1) and the posterior parietal cortex (PPC). Measurements were carried out at baseline (T0), 5min (T1) and 30min later (T2) after the intervention. Descriptive evaluation of results shows that non-painful phantom sensations were not affected by rTMS applied over M1. Continuous (inhibitory) TBS over S1 induced a short-lasting decrease of simple non-painful phantom sensations, while continuous TBS over PPC induced a short-lasting decrease of both simple and complex phantom sensations. Intermittent (excitatory) TBS over PPC induced a slight increase of non-painful phantom sensations. Tests for significance confirm these observations, but must be interpreted with caution because of the small sample size. In conclusion, non-painful phantom sensations may be associated to a hyperexcitability of PPC and to a lesser extent of S1, which can be normalized by inhibitory rTMS. Our preliminary provide further evidence that neuromodulatory techniques are able to reverse phantom sensations not only after limb amputation but also in other conditions characterized by deafferentation such as SCI

Impaired cholinergic transmission in patients with Parkinson's disease and olfactory dysfunction

Olfactory dysfunction represents a frequent and disturbing non-motor manifestation of Parkinson's disease (PD). The pathophysiology of olfactory dysfunction in PD is still poorly understood. Experimental evidence suggests that olfactory impairment could be related to central cholinergic dysfunction. Short latency afferent inhibition (SAI) technique gives the opportunity to test an inhibitory cholinergic circuit in the human cerebral motor cortex. The objective of the study was to assess the cholinergic function, as measured by SAI, in PD patients with different degrees of olfactory dysfunction. We applied SAI technique in 31 patients with PD. These patients also underwent Olfactory Event-Related Potentials (OERPs) studies to objectively evaluate the olfactory system and a battery of neuropsychological tests to assess the cognitive functions. Absent OERPs indicated a severe olfactory dysfunction in 13 subjects. The presence of OERPs with an alteration in latency and/or amplitude can be considered as a borderline condition of slight alteration of smell and was found in other 15 patients. Only 3 patients showed normal OERPs. SAI was significantly reduced in the PD patients with absent OERPs compared with those with present but abnormal OERPs. Neuropsychological examination showed a mild cognitive impairment in 12 out of 13 PD patients with severe olfactory dysfunction, and in 3 out of the 15 patients with borderline olfactory dysfunction. SAI abnormalities and presence of severe olfactory impairment strongly support the hypothesis of cholinergic dysfunction in some patients with PD, who will probably develop a dementia. Longitudinal studies are required to verify whether SAI abnormalities in PD patients with olfactory dysfunction can predict a future severe cognitive decline

Abnormal cortical neuroplasticity induced by paired associative stimulation after traumatic spinal cord injury: a preliminary study

We aimed at assessing in this pilot study whether patients with spinal cord injury (SCI) show alterations of sensorimotor plasticity within the primary motor cortex (M1). Since learning in human M1 occurs through LTP-like mechanisms, we employed the paired associative stimulation (PAS) protocol by transcranial magnetic stimulation (TMS), which is able to induce LTP-like effects in M1, in subjects with chronic SCI. We found that PAS protocol significantly increased corticospinal excitability as long as 30minutes in healthy subjects and in SCI patients with good motor recovery, while it was followed by a non-significant increase of MEP amplitude in the SCI patients with poor functional recovery. These findings suggest that the level of LTP-like phenomena is correlated with long term recovery and support the correlation between the ability of inducing excitability changes using TMS and the process of motor recovery. Increased cortical plasticity might imply greater capability for neuromodulation

Effects of passive pedaling exercise on the intracortical inhibition in subjects with spinal cord injury

Cortical reorganization can be induced by exercise below the level of the lesion after spinal cord injury (SCI). The aim of the present study was to investigate the effect of passive and active pedaling exercise on leg motor cortical area excitability of subjects with traumatic SCI. Ten subjects with chronic cervical or thoracic SCI were enrolled in the study. We found a significant effect of pedaling on short-interval intracortical inhibition (SICI), which did not interact with the experimental condition (active vs. passive). This corresponded to a significant reduction of SICI in the subjects with SCI, together with no evidence that this pattern differed for passive vs. active pedaling. We found no significant effect of pedaling on intracortical facilitation. Our results showed that also passive cycling may be beneficial in activating motor cortical regions and possibly also facilitating motor recovery after SCI. The present study confirms and extends the findings of previous studies that have observed task-specific cortical activation during passive pedaling. Therefore passive exercise therapies when applied below the level of the lesion in subjects with SCI could promote cortical neuroplastic reorganization

Role of human prefrontal cortex in the modulation of conditioned eyeblink responses

Classical conditioning of the eyeblink reflex (EBC) is a simple form of associative motor learning. EBC is heavily dependent on cerebellar function, but experimental studies also suggest that the prefrontal cortex (PFC) orchestrates a neuronal network which interacts with the cerebellum to mediate the conditioned eyeblink responses (CR). To further investigate the role of PFC for EBC in humans, we aimed in this study at assessing whether acquisition of CR can be modulated by focal repetitive transcranial magnetic stimulation (rTMS) given as theta burst stimulation (TBS) over the dorsolateral PFC (DLPFC). A standard delay conditioning paradigm with a 540\u2009ms tone as conditioned stimulus (CS) coterminating with a 100\u2009ms air puff as unconditioned stimulus (US) was used in a total of 60 healthy subjects (35 female, 25 male, mean age 28.4\u2009\ub1\u20092.4 years). One hundred paired CS-US trials and 30 extinction CS alone trials were given. TBS was applied over the DLPFC ipsilaterally to the US during the acquisition phase. Subjects were randomly assigned to three groups (n\u2009=\u200920) using excitatory intermittent TBS (iTBS), inhibitory continuous TBS (cTBS) or sham stimulation. CR acquisition was significantly enhanced by iTBS (mean total CR incidence 63.1\u2009\ub1\u20096.5%) and significantly reduced by cTBS (13\u2009\ub1\u20092%) compared to sham stimulation (25.1\u2009\ub1\u20096.7%). We provide thus physiological evidence that the acquisition of this type of associative learning is critically modulated by PFC activity in humans