Implementation of a gait center training to improve walking ability and vital parameters in inpatient neurological rehabilitation- a cohort study.

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.

Toward a P300 Based Brain-Computer Interface for Aphasia Rehabilitation after Stroke: Presentation of Theoretical Considerations and a Pilot Feasibility Study.

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.

Phagocytosis of apoptotic inflammatory cells downregulates microglial chemoattractive function and migration of encephalitogenic T cells.

Apoptosis of autoaggressive T cells in the central nervous system (CNS) and subsequent phagocytosis by microglia is probably crucial in the rapid resolution of the inflammatory infiltrate in T cell mediated neuroinflammatory diseases. In addition to mere clearance, phagocytosis of apoptotic leukocytes results in the downregulation of different microglial immune functions. Chemoattractive functions of Lewis rat microglia and secretion of chemokines and matrix-metalloproteinases (MMPs) were investigated after phagocytosis of apoptotic T cells in vitro. In a modified Boyden chamber assay migration of encephalitogenic T cells toward LPS-stimulated microglial supernatants after phagocytosis of apoptotic thymocytes was reduced by 24.9% in comparison to interaction with viable target cells (P < 0.001). Phagocytosis of apoptotic cells downregulated CC-chemokine ligand (CCL)-5-secretion by LPS-stimulated microglia by 66.2% (P < 0.001), whereas there was only a trend toward decreased CCL2-secretion. As determined by gelatinase-zymography, secretion of MMP-9 by microglia was decreased after phagocytosis of apoptotic cells, whereas MMP-2 secretion was not altered. These mechanisms may reduce further recruitment of pathogenic inflammatory cells into the CNS-lesion and thus contribute to the active resolution of the inflammatory infiltrate and termination of the autoimmune attack.

Heparin and air filters reduce embolic events caused by intra-arterial cerebral angiography: a prospective, randomized trial.

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 (P=0.002). 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 (P<0.01), 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.

Non-invasive functional and biochemical assessment of mitoxantrone cardiotoxicity in patients with multiple sclerosis.

As mitoxantrone is a recently approved immunosuppressant for managing multiple sclerosis, the number of patients treated with this effective but potentially cardiotoxic anthracenedione derivative will increase substantially. To detect subclinical mitoxantrone-induced cardiotoxicity, sensitive non-invasive diagnostic tools are required. Assuming that changes in myocardial high-energy phosphate metabolism and alterations in left ventricular (LV) diastolic performance might be early markers of mitoxantrone-induced cardiotoxicity we examined fifteen MS patients treated with mitoxantrone up to 100 mg/m2 compared with 15 matched control MS patients. 31P-magnetic resonance (MR) spectroscopy was employed to measure myocardial high-energy phosphate metabolism, MR imaging for morphometric evaluation of changes in LV geometry. Indices of diastolic performance were assessed by Doppler echocardiography. In this exploratory study, phosphocreatine/ATP ratios were comparable between mitoxantrone-treated and control patients (1.48 +/- 0.23 and 1.43 +/- 0.41). LV mass, LV end-diastolic and systolic volumes, wall motion score, EF and cardiac output did not differ between both groups. All parameters of diastolic performance (E/A-ratio, isovolumic relaxation time, and E-wave deceleration time) were not different and within normal limits.In conclusion, using advanced diagnostic methodology, including functional, morphometric, and biochemical measurements no cardiotoxic effect of mitoxantrone up to a cumulative dose range of 100 mg/m2 could be detected.

Does Down's syndrome protect against multiple sclerosis?

BACKGROUND: A higher incidence of certain autoimmune disorders has been reported in Down's syndrome (DS) but only 1 case of DS associated with multiple sclerosis (MS) has been published to date. METHODS: We performed a calculation based on population and prevalence data of each condition to estimate the expected coprevalence of both diseases. As no published data on DS prevalence are available, a rough estimate was calculated from live birth rates and published life tables. RESULTS: In a total of 116,939 assumed cases of patients with DS in Western Europe 102 patients with concordant MS would be expected at any time point according to the incidence of MS, but only 1 case was reported. CONCLUSION and HYPOTHESIS: We propose the hypothesis that despite a propensity in DS for certain autoimmune diseases there is a negative association of DS and MS. Genes located on chromosome 21 may thus confer protection against MS. Candidate genes for protective immunomodulation might include interferon receptor I and II and S100b. Substantiated by further epidemiologic data, the identification of these and other chromosome 21 gene products may provide new hints for the understanding of modulatory genes in the pathogenesis of MS. In more general terms, this negative association also may allow to study basic principles of how certain candidate genes might act on autoimmune disease expression.