Background-Intra-arterial cerebral angiography is associated with a low risk for neurological complications, but clinically silent ischemic events after angiography have been seen in a substantial number of patients. Methods and Results-In a prospective study, diffusion-weighted magnetic resonance imaging (DW-MRI) before and after intra-arterial cerebral angiography and transcranial Doppler sonography during angiography were used to evaluate the frequency of cerebral embolism. One hundred fifty diagnostic cerebral angiographies were randomized into 50 procedures, each using conventional angiographic technique, or systemic heparin treatment throughout the procedure, or air filters between the catheter and both the contrast medium syringe and the catheter flushing. There was no neurological complication during or after angiography. Overall, DW-MRI revealed 26 new ischemic lesions in 17 patients (11%). In the control group, 11 patients showed a total of 18 lesions. In the heparin group, 3 patients showed a total of 4 lesions. In the air filter group, 3 patients exhibited a total of 4 lesions. The reduced incidence of ischemic events in the heparin and air filter groups compared with the control group was significantly different (Pϭ0.002).Transcranial Doppler sonography demonstrated a large number of microembolic signals that was significantly lower in the air filter group compared with the heparin and control groups (PϽ0.01), which did not differ from each other. Conclusions-Air filters and heparin both reduce the incidence of silent ischemic events detected by DW-MRI after intra-arterial cerebral angiography and can potentially lower clinically overt ischemic complications. This may apply to any intra-arterial angiographic procedure.

Summary Mitoxantrone (MX) is a cytotoxic drug with proven clinical efficacy in active multiple sclerosis (MS). In this ex vivo

The reduction in cardiac high-energy phosphates in some patients with MS points to a subclinical involvement of the heart. This may be important for treatment with potentially cardiotoxic drugs. Longitudinal studies are need to understand the clinical relevance of our findings.

SUMMARYThe present study investigates the immunological effects of a combination treatment of mitoxantrone and the cardioprotector dexrazoxane in experimental autoimmune encephalomyelitis (EAE). Mitoxantrone, an anthracycline-derived immunosuppressive drug has been approved recently for treatment of very active multiple sclerosis (MS). Its prolonged use is limited due to its cardiotoxic properties. Dexrazoxane (DZR (S)-(+)-1,2-bis (3,5.dioxopiperazinyl)propane, ICRF-187) is an iron III chelator which in animal models and in cancer patients reduces anthracycline and mitoxantrone induced cardiotoxicity when given immediately before these agents. We examined the immunological effects of dexrazoxane in combination with mitoxantrone in experimental autoimmune encephalomyelitis (EAE) in Lewis rats. EAE was induced by active immunization with myelin basic protein (MBP) or by adoptive transfer of MBP specific T cells (AT-EAE). The clinical course, spinal cord pathology, activity of metalloproteinases (MMP-2 and MMP-9) and T cell apoptosis were assessed. Monotherapy with DZR ameliorated slightly the course of actively induced EAE and AT-EAE. The combination of DZR and mitoxantrone was superior to mitoxantrone given alone. Clinical amelioration ran in parallel with the marked reduction of inflammatory infiltration which was nearly abolished by the combination treatment. DZR did not affect the activity of metalloproteinase 9 and did not increase the proportion of apoptotic lymph node cells ex vivo or T cells in situ . We conclude that in addition to its cardioprotective role, DZR augments mitoxantrone-mediated immunosuppressive effects in animal models of human central nervous system (CNS) autoimmune disease. Clinical trials in MS patients are warranted to evaluate the unexpected immunosuppressive efficacy of DZR as add-on treatment.

People with post-stroke motor aphasia know what they would like to say but cannot express it through motor pathways due to disruption of cortical circuits. We present a theoretical background for our hypothesized connection between attention and aphasia rehabilitation and suggest why in this context, Brain-Computer Interface (BCI) use might be beneficial for patients diagnosed with aphasia. Not only could BCI technology provide a communication tool, it might support neuronal plasticity by activating language circuits and thereby boost aphasia recovery. However, stroke may lead to heterogeneous symptoms that might hinder BCI use, which is why the feasibility of this approach needs to be investigated first. In this pilot study, we included five participants diagnosed with post-stroke aphasia. Four participants were initially unable to use the visual P300 speller paradigm. By adjusting the paradigm to their needs, participants could successfully learn to use the speller for communication with accuracies up to 100%. We describe necessary adjustments to the paradigm and present future steps to investigate further this approach.

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In experimental autoimmune neuritis (EAN), T-cell receptor (TCR) variable (V)-region gene usage by neuritogenic T cells has been reported to be clonally restricted at the RNA level. This study was designed to verify TCR usage by neuritogenic T cells at the protein level. We generated two monoclonal antibodies (mAbs) 7H4 and 8G8 specific for a Vbeta4/Valpha11 associated idiotype expressed by the majority of neuritogenic cells of P2-specific T-cell lines. The remaining neuritogenic P2-specific T cells either exhibited a dominant usage of the TCR Vbeta13 chain recognized by the recently generated mAbs 17D5 and 18B1 or showed diverse Vbeta usage. Treatment of adoptive-transfer (AT)-EAN or of EAN actively induced with the neuritogenic P2 peptide by mAbs 7H4 and 8G8 led to a partial, but significant, reduction of clinical disease. Treatment with Vbeta13-specific mAb 17D5 had no clear effect on active EAN. Our data show that at least three different TCR are used by P2-specific pathogenic T cells in EAN, an animal model for human inflammatory neuropathies.

Background: Many studies showed that robot-assisted gait training might improve walking of patients after stroke. The question remains whether patients with other neurological diagnoses can improve their ability to walk by training in a gait center. Aim of the present study was therefore to investigate the effects of a gait center training in inpatient neurological rehabilitation on walking ability. Methods: We implemented a gait center training in addition to individual inpatient rehabilitation. Our primary outcome was walking ability based on the Functional Ambulation Categories (FAC). Our secondary outcomes were vital capacity and blood pressure. We predefined subgroups of patients with ischemic and hemorrhagic stroke and critical illness myopathy (CIM) and polyneuropathy (CIP). Results: We included 780 patients from our inpatient rehabilitation center in our cohort study. We analyzed 329 patients with ischemic, 131 patients with hemorrhagic stroke and 74 patients with CIP/ CIM. A large number of patients were able to improve their ability to walk. At the end of rehabilitation, patients with ischemic stroke and FAC 3 = increased theirFAC scores by 5%, FAC 4 = 4% and FAC 5 = 7%. Patients with hemorrhagic stroke and FAC 3 = increased by 5%, FAC 4 = 11% and FAC 5 = 9% and patients with CIP/CIM increased by FAC 3 = 3%, FAC 4 = 22% and FAC 5 = 26%. The largest improvement in walking ability during rehabilitation had patients with a FAC = 1 at baseline who improved by a median of 1.4 FAC points (p < 0.001). After adjusting for the number of gait training sessions, the largest improvement in walking ability during rehabilitation had patients with a FAC = 0 at baseline who improved by 1.8 FAC points (p < 0.001). Conclusions: Implementation of an additional gait center training may significantly improve walking ability in neurological rehabilitation.