This study describes a method for performing diffusivity measures along and across a specific direction, derived from white matter in healthy controls. The diffusion tensor (DT) assigns a principal eigenvector (v₁) and eigenvalue (axial diffusivity, d(ax)) to each voxel. The average of the second and third eigenvalues is the radial diffusivity, d(rad) v₁ may be affected by pathology, therefore when comparing d(ax) and d(rad) in patients one has to consider the direction of the measurement and underlying anatomy. Here we created a representative super-DT dataset, DT(ref), whose eigenvector, v(1,ref), was considered the most likely direction of diffusivity per voxel. We defined the projected axial diffusivity, d(p-ax), as the projection of individual DTs along v(1,ref) and the projected radial diffusivity, d(p-rad), as the average of the projections along the second and third eigenvectors of DT(ref). The projected diffusivities are promising new parameters for studying white matter pathology.

The aim of this study was to assess the prevalence of chronic cerebrospinal venous insufficiency in an unselected cohort of multiple sclerosis (MS) patients. A total of 586 patients with clinically defined MS underwent catheter venography of the internal jugular veins, brachiocephalic veins and azygos vein. The following findings were regarded as pathologic: no outflow, slowed outflow, reversal of flow direction, prestenotic dilation accompanied by impaired outflow, outflow through collaterals, intraluminal structures obstructing the vein, hypoplasia, agenesia or significant narrowing of the vein. Venous abnormalities were found in 563 patients (96.1%). Lesions in one vein were found in 43.5%, in two veins in 49.5%, and in three veins in 3.1% of patients. Venous pathologies in the right internal jugular vein were found in 64.0% of patients, in the left internal jugular vein in 81.7%, in the left brachiocephalic vein in 1.0%, and in the azygos vein in 4.9%. Venous pathologies were found to be highly associated with MS, yet the clinical relevance of this phenomenon remains to be established.

Recent advances in the study of spontaneous brain activity have demonstrated activity patterns that emerge with no task performance or sensory stimulation; these discoveries hold promise for the study of higher-order associative network functionality. Additionally, such advances are argued to be relevant in pathological states, such as disorders of consciousness (DOC), i.e., coma, vegetative and minimally conscious states. Recent studies on resting state activity in DOC, measured with functional magnetic resonance imaging (fMRI) techniques, show that functional connectivity is disrupted in the task-negative or the default mode network. However, the two main approaches employed in the analysis of resting state functional connectivity data (i.e., hypothesis-driven seed-voxel and data-driven independent component analysis) present multiple methodological difficulties, especially in non-collaborative DOC patients. Improvements in motion artifact removal and spatial normalization are needed before fMRI resting state data can be used as proper biomarkers in severe brain injury. However, we anticipate that such developments will boost clinical resting state fMRI studies, allowing for easy and fast acquisitions and ultimately improve the diagnosis and prognosis in the absence of DOC patients' active collaboration in data acquisition.

Envisaged extensions of a functional magnetic resonance imaging (fMRI) technique allowing communication with patients affected by disorders of consciousness are here examined in connection with subjective symptom reporting, informed consent, and continued medical care decision-making. The principles of medical beneficence, personal autonomy protection, and the right to participate in social life are isolated as appropriate sources of ethical motivations for the use of fMRI-enabled communication. Consciousness requirements for each communication context are identified on the basis of qualitative distinctions between the access, phenomenal, and narrative varieties of consciousness. Ethically motivated uses of fMRI-enabled communication are hierarchically organized in terms of progressively more demanding consciousness requirements for successful communication. The outcomes of this analysis can be used to curb unrealistic expectations of these new scientific developments, and to promote mutual trust between medical doctors, patient surrogates and families.

Adaptive processes within cerebellar circuits, such as long-term depression and long-term potentiation at parallel fiber-Purkinje cell synapses, have long been seen as important to cerebellar motor learning, and yet little attention has been given to any possible significance of these processes for cerebellar dysfunction and disease. Several forms of ataxia are caused by mutations in genes encoding for ion channels located at key junctures in pathways that lead to the induction of synaptic plasticity, suggesting that there might be an association between deficits in plasticity and the ataxic phenotype. Herein we explore this possibility and examine the available evidence linking the two together, highlighting specifically the role of P/Q-type calcium channels and their downstream effector small-conductance calcium-sensitive (SK2) potassium channels in the regulation of synaptic gain and intrinsic excitability, and reviewing their connections to ataxia.

Genetic deletion of the plasma membrane calcium ATPase type 2 (PMCA2), a calcium transporter protein, is associated with an overtly ataxic phenotype in mice. PMCA2 is expressed at high levels in cerebellar Purkinje neurons (PNs) where functional integrity is essential for normal cerebellar function. Indeed, loss of PN function accompanies cerebellar ataxia in humans and mouse models. In the ataxic PMCA2 knockout (PMCA2-/-) mouse the ability of the PNs to control their cytosolic calcium levels was severely impaired; basal calcium levels were high and calcium recovery kinetics slow. Whole cell patch clamp recordings from PMCA2-/- PNs revealed that they possessed hyperpolarised membrane potentials, reduced frequency and increased irregularity of spontaneous action potential firing, curtailed complex spikes and sustained calcium-dependent outward K+ currents. We propose that these alterations limit pathological excursions in PN cytosolic calcium as an aid to survival but that they are insufficient to prevent loss of functional cerebellar output.

Surgical or interventional neurophysiology is a term commonly used to refer to a large number of neurosurgical procedures involving the brain, cranial nerves, spinal cord and peripheral nervous system which, to be efficient and safe, demand specific neurophysiological know-how. As a result of the development of these procedures and their increasing use in the operating room, the role of clinical neurophysiology, traditionally diagnostic, has been extended. With the advent of 'neurostimulation' and 'neuromodulation', some neurophysiological techniques have, in themselves, progressively become more therapeutic, the therapeutic alteration of nervous system activity being achieved not only by surgical ablation or medication but also through electrophysiological means via implanted or non-implanted devices, whose development was made possible by extensive studies in the field of neurophysiology. The first application of electrical stimulation in urology opened up the way for progress in the therapeutic direction. Moreover, with regard to the mechanism of action underlying neuromodulation, the application of neurophysiology and neuroimaging procedures has contributed to understanding of the neural control mechanism of visceral (e.g. lower urinary tract) function. In our experience, the advent of sacral neuromodulation for lower urinary tract dysfunction and the use of neurophysiology has made it possible to shed light on the pathophysiological mechanisms of neuro-urological disorders, allowing us to assess and validate new therapeutic approaches and finally to develop a new method and device for chronic pudendal nerve stimulation.

The constant ageing of the population has resulted in an increase in chronic conditions such as osteoporosis and neurodegenerative diseases as well as in patient comorbidity. Prolonged immobility, the use of osteopoenia-inducing drugs and an increased risk of falls in patients with neurological diseases have led to an increase in the incidence of fragility fractures, especially of the femur, in these patients. The consequences of these events are often dramatic, being associated with increased mortality, disability and worsening of cognitive and relational functions. Potent drugs are currently available that can reduce fracture risk by up to 50% with long-term safety and tolerability. Bisphosphonates are the agents most extensively used to prevent fragility fractures. Risedronate has been demonstrated to reduce fracture risk, also in patients with neurological conditions. Considering that osteoporosis requires chronic treatment, patient compliance is extremely important to obtain treatment efficacy.

Transcranial magnetic stimulation (TMS) was introduced nearly 20 years ago and has since been developed as a sophisticated tool for neuroscience research. It is an excellent technique that complements other non-invasive methods for studying human brain physiology. The aim of the present study was to review the basic concepts and principles of the repetitive TMS (rTMS) technique, gathering evidence of its applications in neurorehabilitation. Several clinical studies have reported that sessions of rTMS can improve some or all of the motor symptoms associated with Parkinson's disease, dystonia and stroke. However, since these changes are transient, it is premature to propose these applications as realistic therapeutic options, even though the rTMS technique has shown itself to be, potentially, a modulator of sensorimotor integration and neurogenesis. Future work in this area promises to advance our understanding of the pathophysiology of a wide range of neurological conditions, generate widely applicable diagnostic tools for clinical neurophysiology, and perhaps establish neuromodulation as a viable therapeutic option in neurorehabilitation.