NGF-loaded PLGA microparticles for advanced multifunctional regenerative electrodes.

Nerve guide conduits are currently the elective device for peripheral nerve reconstruction applications, as nerve autograft often is hampered by procedure invasiveness and limited nerve availability. Many technological improvements have been approached to enhance nerve regeneration driven by these devices, whose main drawbacks are often disordered sprouting and ineffective axon guidance. Among the adopted solutions to overcome these problems, embedding of extracellular matrix (ECM) proteins and neurotrophic factors (NF) in nerve conduits has been a promising one. Using free NFs, however suffers from different drawbacks mainly due to diffusion, degradation and local concentration boosting. As part of a wider EU-funded program for next gen regenerative electrodes, we developed NGF-loaded PLGA microparticles to use them immersed in a gel biomatrix that is being embedded in nerve conduits before implant, and allow for timed-controlled delivery instead of an initial concentration boost. Here we report the technological steps for the synthesis and initial testing with mouse dorsal root ganglia (DRG) explants, towards their full integration with a complex three-dimensional biomatrix into next-gen regeneration electrodes.

Intracranial meningiomatosis causing foster kennedy syndrome by unilateral optic nerve compression and blockage of the superior sagittal sinus.

The original description of the Foster Kennedy syndrome included the clinical triad of optic disc pallor in one eye, optic disc edema in the other eye, and reduced olfaction caused by space-occupying anterior fossa masses. The optic disc pallor was attributed to direct compression of the intracranial optic nerve, the optic disc edema to increased intracranial pressure from mass effect, and the reduced olfaction to direct compression of the olfactory nerve. We report a patient with the ophthalmic features of the Foster Kennedy syndrome from meningiomatosis. A meningioma compressed one optic nerve to cause impaired visual function. Convexity meningiomas compressed the superior sagittal sinus to impair cerebral venous drainage, increased intracranial pressure, and papilledema in the other eye. This is the first report of the Foster Kennedy syndrome caused by this mechanism.

[Current aspects of nociceptive transmission: peripheral mechanisms and spinal modulation]. / Aspectos actuales de la transmisión nociceptiva: mecanismos periféricos y modulación espinal.

Nociceptive transmission shows unusual features of sensorial physiology, due to the complex modulation which occurs from the start of the impulse until its final perception. In recent years the dynamic role played in nociception by peripheral structures, such as the 7 and spinal nociceptors and the second order neurones, has been recognized. It is fairly clear how a number of modulators activate and make nociceptors sensitive, accounting for the appearance of clinical features such as primary hyperalgesia, and their persistance. Thus eico sanoides, histamine, bradykinin and others allow considerable control of nociceptor activity. Also, the dorsal horn neurones play an important part in other clinical signs associated with pain, such as mechanical (secondary) hyperalgesia. At this level, some neurotransmitters such as glutamate or the neurokinins seem to be important in central sensibilization phenomena which occur when a painful stimulus is maintained. In fact, continued release of these neurotransmitters implies the expression of certain genes and the production of certain proteins. Knowledge of the relationship between the different neurochemical systems and subsequent changes in their expression in different pathological situations may help to explain the pathophysiology of some clinical signs of neuropathic pain which are at present inexplicable.