Search

Hemispherectomy (HS) is an effective surgical procedure aimed at managing otherwise intractable epilepsy in cases of diffuse unihemispheric pathologies. Neurological recovery in subjects treated with HS is not limited to seizure reduction, rather, sensory-motor and behavioral improvement is often observed. This outcome highlights the considerable capability of the brain to react to such an extensive lesion, by functionally reorganizing and rewiring the cerebral cortex, especially early in life. In this narrative review, we summarize the animal studies as well as the human neurophysiological and neuroimaging studies dealing with the reorganizational processes that occur after HS. These topics are of particular interest in understanding mechanisms of functional recovery after brain injury. HS offers the chance to investigate contralesional hemisphere activity in controlling ipsilateral limb movements, and the role of transcallosal interactions, before and after the surgical procedure. These post-injury neuroplastic phenomena actually differ from those observed after less extensive brain damage. Therefore, they illustrate how different lesions could lead the contralesional hemisphere to play the "good" or "bad" role in functional recovery. These issues may have clinical implications and could inform rehabilitation strategies aiming to improve functional recovery following unilateral hemispheric lesions. Future studies, involving large cohorts of hemispherectomized patients, will be necessary in order to obtain a greater understanding of how cerebral reorganization can contribute to residual sensorimotor, visual and auditory functions., (Copyright © 2017 Elsevier Inc. All rights reserved.)

Context/objective: Passive cycling (PC) may represent a potential alternative neurorehabilitation program for patients who are too weak or medically unstable to repeatedly practice active movements. We review here the most important animal and human studies addressing PC after spinal cord injury (SCI)., Methods: A MEDLINE search was performed using following terms: "passive", "cycling", "pedaling", "pedalling","spinal cord injury"., Results: Experimental studies revealed that PC modulated spinal reflex and reduced spasticity. PC also reduced autonomic dysreflexia and elicited cardio-protective effects. Increased levels of mRNA for brain-derived neurotrophic factor, glial cell line-derived neurotrophic factor and neurotrophin-4 were found. In contrast, human studies failed to show an effect of PC on spasticity reduction and did not support its application for prevention of cardiovascular disease-related secondary complications., Conclusion: Available evidence to support the use of PC as standard treatment in patients with SCI is still rather limited. Since it is conceivable that PC motion could elicit sensory inputs to activate cortical structures and induce cortical plasticity changes leading to improved lower limb motor performance, further carefully designed prospective studies in subjects with SCI are needed.

Background and Objective: Verticalization was reported to improve the level of arousal and awareness in patients with severe acquired brain injury (ABI) and to be safe in ICU. We evaluated the effectiveness of a very early stepping verticalization protocol on their functional and neurological outcome., Methods: Consecutive patients with Vegetative State or Minimally Conscious State were enrolled in ICU on the third day after an ABI. They were randomized to undergo conventional physiotherapy alone or associated to fifteen 30-minute sessions of verticalization, using a tilt table with robotic stepping device. Once stabilized, patients were transferred to our Neurorehabilitation unit for an individualized treatment. Outcome measures (Glasgow Coma Scale, Coma Recovery Scale revised -CRSr-, Disability Rating Scale-DRS- and Levels of Cognitive Functioning) were assessed on the third day from the injury (T0), at ICU discharge (T1) and at Rehab discharge (T2). Between- and within-group comparisons were performed by the Mann-Whitney U test and Wilcoxon signed-rank test, respectively., Results: Of the 40 patients enrolled, 31 completed the study without adverse events (15 in the verticalization group and 16 in the conventional physiotherapy). Early verticalization started 12.4±7.3 (mean±SD) days after ABI. The length of stay in ICU was longer for the verticalization group (38.8 ± 15.7 vs 25.1 ± 11.2 days, p = 0.01), while the total length of stay (ICU+Neurorehabilitation) was not significantly different (153.2 ± 59.6 vs 134.0 ± 61.0 days, p = 0.41). All outcome measures significantly improved in both groups after the overall period (T2 vs T0, p<0.001 all), as well as after ICU stay (T1 vs T0, p<0.004 all) and after Neurorehabilitation (T2 vs T1, p<0.004 all). The improvement was significantly better in the experimental group for CRSr (T2-T0 p = 0.033, T1-T0 p = 0.006) and (borderline) for DRS (T2-T0 p = 0.040, T1-T0 p = 0.058)., Conclusions: A stepping verticalization protocol, started since the acute stages, improves the short-term and long-term functional and neurological outcome of ABI patients., Trial Registration: clinicaltrials.gov NCT02828371.

We describe the case of a patient who underwent craniectomy for hemorrhage of the left parietal lobe. Three weeks later, orthostatic memory impairment was detected as initial symptom of sinking skin flap syndrome (SSFS). This deficit was examined by neuropsychological testing and associated with a posture-dependent increase in the delta/alpha ratio at the F3 electrode, an electroencephalographic (EEG) index related to brain hypoperfusion. This EEG spectral alteration was detected in a brain region that includes the left dorsolateral prefrontal cortex, an area known to be involved in memory processing; therefore we hypothesize that SSFS induced reversible hypoperfusion of this otherwise undamaged cortical region. Neither of these findings was present after cranioplasty. This case suggests that SSFS may induce neuropsychological deficits potentially influencing outcome in the postacute phase and is further evidence supporting the clinical benefits of early cranioplasty.

Background and Purpose: Nutrition is the result of a complex interaction among environmental, homeostatic and reward-related processes. Accumulating evidence supports key roles for the dopaminergic neurons of the ventral midbrain in regulating feeding behaviour. For this reason, in the present study, we have investigated the electrophysiological effects of two centrally acting anorexic agents, fenfluramine and sibutramine, on these cells., Experimental Approach: Rat midbrain slices were used to make intracellular recordings from dopaminergic neurons of the substantia nigra and the ventral tegmental area. Gamma-aminobutyric acid (GABA)-mediated synaptic transmission was assessed from the inhibitory postsynaptic potentials (IPSPs) mediated by GABA(A) and GABA(B) receptors., Key Results: Fenfluramine and sibutramine reduced, concentration-dependently, the GABA(B) IPSPs, without affecting the GABA(A)-mediated potentials. This effect is presynaptic, as postsynaptic membrane responses induced by application of a GABA(B) receptor agonist, baclofen, were not affected by the two drugs. Furthermore, the selective 5-hydroxytriptamine 1B (5-HT(1B)) receptor antagonist, SB216641, blocked the reduction of GABA(B) IPSPs caused by fenfluramine and sibutramine, indicating that the receptor mediating this effect is 5-HT(1B)., Conclusions and Implications: Two anorexic agents, fenfluramine and sibutramine, induced the activation of 5-HT(1B) receptors located on presynaptic GABAergic terminals, thus reducing the release of GABA. This action can alter the strength of synaptic afferents that modify the activity of dopaminergic neurons, inducing neuronal excitation. Our results reveal an additional mechanism of action for fenfluramine and sibutramine that might contribute to reducing food intake, by influencing the pleasurable and motor aspects of feeding behaviour.

The aims of this work are to assess the persistence of rotenone in oil and drupes of olive plants of cultivars Nocellara del Belice (NB) and Cassanese (CA), and to compare the quality of oils from rotenone-treated and untreated plants. Samples of drupes and oil were analyzed at 2, 12, 22 and 30 days after treatment. Rotenone levels in drupes of treated plants declined by about 50% after 22 days from treatment (0.037 mg kg(-1) in NB and 0.039 mg kg(-1) in CA), whereas the respective values in the oil were higher (0.209 mg kg(-1) in NB and 0.229 mg kg(-1) in CA) and had a lower decay half-life (4.02 days in NB and 4.71 days in CA). For both cultivars, no significant differences in oil physicochemical and nutritional parameters were found between the two treatments. The panel test of oils extracted after 22 days did not reveal significant differences in unpleasant aromatic notes nor defects between the two treatments. Our results confirm that serious doubts remain about the safety and healthiness of oils extracted from drupes treated with rotenone. This information could assess the real risk in the use of this product for plant protection in olive growing.

It is not yet clear how L-dopa, that is the most effective drug for the treatment of Parkinson's disease, enters into the dopaminergic neurons to be transformed into dopamine. It is suggested that L-dopa is mainly transported into cells by a group of L-amino acid carriers named "System L". Since these carriers are selectively inhibited by 2-aminobicyclo[2.2.1]heptane-2-carboxylic acid (BCH), we have applied this compound to electrophysiologically recorded dopaminergic neurons of the rat substantia nigra pars compacta to examine the possible modulation of the effects of L-dopa by System L. We have observed that BCH reduced, in a concentration-dependent manner, the membrane hyperpolarization/outward current caused by L-dopa. Interestingly, the actions of dopamine were not changed by this System L inhibitor, suggesting that the reducing effects on L-dopa are not due to a BCH-induced unspecific block of dopamine-mediated events. Therefore, our electrophysiological data that an l-type amino acid carrier, possibly System L, is involved in the transport of L-dopa into dopaminergic neurons.

Most anti-parkinsonian drugs produce a dopamine-like effect on single dopaminergic neurons. Using electrophysiological recordings, this effect is observed as an inhibition of the spontaneous firing activity. The firing activity of dopaminergic cells throughout dopamine-mediated mechanisms is inhibited not only by dopamine direct agonists but also by substances that increase the release or synthesis, or block the uptake or reduce degradation of dopamine in the brain. Here we propose the electrophysiological approach on dopaminergic neurons in in vitro slice preparation as a preliminary tool for selecting new potential anti-parkinsonian agents, before they are tested in more complex animal models.

Background: Although dopamine (DA) has been implicated in the psychostimulant properties of 3,4-methylenedioxymethamphetamine (MDMA), there is no detailed information on its modalities of action on single ventral midbrain dopaminergic neurons., Methods: We examined the actions of MDMA on intracellularly recorded dopaminergic neurons maintained in slices., Results: At 1 micromol/L, MDMA depolarized and excited the cells; at 3 micromol/L, either excited or inhibited the neurons. Interestingly, higher concentrations (10-30 micromol/L) inhibited firing through membrane hyperpolarization or caused an outward current. Whereas MDMA's excitatory effects were antagonized by pindolol, indicating involvement of 5-HT 1B receptors, the inhibitory effects were counteracted by sulpiride indicating involvement D2 receptors. Treatment of the cells with carbidopa eliminated MDMA-induced firing inhibition and membrane hyperpolarization. MDMA enhanced DA-induced cellular responses but reduced those of amphetamine. Cocaine-induced outward currents were not affected by MDMA. These actions are consistent with inhibition of the DA transporter. Moreover, MDMA depressed the GABA(B) IPSP by activating 5-HT 1B receptors., Conclusions: Our data demonstrate that 3-30 micromol/L MDMA preferentially inhibits the dopaminergic cells via indirect activation of D2 autoreceptors due to increased extracellular concentration of DA. In contrast, reduction of the GABA(B) IPSP could partially account for excitation caused by 1-3 micromol/L drug.