Biomedical subjects

Matthias Schilling

Publications and source records attributed to Matthias Schilling.

5 recordsLinked to original sources

PubMed2006

Neuroleptic-induced dysphagia: case report and literature review.

Neuroleptic medication may cause extrapyramidal symptoms (EPS) that can affect swallowing as well. This report describes a case of drug-induced dysphagia in a 53-year-old man receiving haloperidol for treatment of schizophrenia. The diagnosis was established by fiberoptic endoscopic evaluation of swallowing. After changing medication to fluphenazin, dysphagic symptoms resolved. The literature on EPS-related dysphagia, its demographic features, typical symptoms, diagnostic modalities, clinical course, and treatment options is reviewed.

Antipsychotic Agents↗

PubMed2006

Treatment for obstructive sleep apnoea: effect on peripheral nerve function.

BACKGROUND AND OBJECTIVE: Obstructive sleep apnoea (OSA) is suggested to be associated with peripheral nerve damage. A case-control study was conducted to provide further support to this observation. In a longitudinal intervention study, it was examined whether treatment for OSA has a possible beneficial effect on peripheral nerve function. METHODS: Participants were 23 patients with OSA and 23 controls matched for age and body mass index (BMI), all without any known cause of peripheral nerve damage. The sensory nerve action potential (SNAP) amplitudes of both sural nerves were determined. After 6 months of treatment for OSA, treatment compliance was evaluated and nerve conduction studies were repeated. RESULTS: Patients with OSA had significantly lower mean (standard deviation) sural SNAP amplitudes than controls (6.3 (3.5) v 11.2 (5.0), p < 0.001). Multivariate regression analysis including the variables age, BMI and Apnoea-Hypopnea Index (AHI) showed that both age (p < 0.01) and AHI (p < 0.05) were inversely related to the SNAP amplitude. On follow-up, the sural SNAP showed an increase of 2.6 mV on average (p < 0.001). Multivariate regression analysis including the variables age, BMI, AHI, pretreatment SNAP and treatment compliance identified only treatment compliance as being significantly related to the SNAP increase (p < or = 0.005). CONCLUSION: OSA is an independent risk factor for axonal dysfunction of peripheral sensory nerves. Impaired neural function is at least partly reversible with treatment for sleep apnoea.

Action Potentials↗

PubMed2005

Predominant phagocytic activity of resident microglia over hematogenous macrophages following transient focal cerebral ischemia: an investigation using green fluorescent protein transgenic bone marrow chimeric mice.

Activated microglia and hematogenous macrophages are known to be involved in infarct development after cerebral ischemia. Traditionally, hematogenic macrophages are thought to be the primary cells to remove the ischemic cell debris. However, phagocytosis is a well known property also of activated microglia. Due to a lack of discriminating cellular markers, the cellular origin of phagocytes and the temporal course of phagocytosis by these two cell types are largely unknown. In this study, we used green fluorescent protein (GFP) transgenic bone marrow chimeric mice and semithin serial sections after methyl methacrylate embedding of the brains to dissect in detail the proportion of identified activated resident microglial cells and infiltrating hematogenous macrophages in phagocytosing neuronal cell debris after 30 min of transient focal cerebral ischemia. Already at day one after reperfusion, we found a rapid decrease of neurons in the ischemic tissue reaching minimum numbers at day seven. Resident GFP-negative microglial cells rapidly became activated at day one and started to phagocytose neuronal material. By contrast, hematogenous macrophages incorporating neuronal cell debris were observed in the ischemic area not earlier than on day four. Quantitative analysis showed maximum numbers of phagocytes of local origin within 2 days and of blood-borne macrophages on day four. The majority of phagocytes in the infarct area were derived from local microglia, preceding and predominating over phagocytes of hematogenous origin. This recruitment reveals a remarkable predominance of local defense mechanisms for tissue clearance over immune cells arriving from the blood after ischemic damage.

Animals↗

PubMed2004

Acute and subacute intracerebral hemorrhages: comparison of MR imaging at 1.5 and 3.0 T--initial experience.

PURPOSE: To assess and describe the appearance of intracerebral hemorrhage (ICH) at 3.0-T magnetic resonance (MR) imaging as compared with the appearance of this lesion type at 1.5-T MR imaging. MATERIALS AND METHODS: Sixteen patients with 21 parenchymal ICHs were examined. ICHs were classified as hyperacute, acute, early subacute, late subacute, or chronic. Patients underwent 1.5- and 3.0-T MR imaging with T2-weighted fast spin-echo, fluid-attenuated inversion-recovery (FLAIR), and T1-weighted spin-echo (1.5-T) and gradient-echo (3.0-T) sequences within 4 hours of each other. The central (ie, core) and peripheral (ie, body) parts of the ICHs were analyzed quantitatively by using contrast-to-noise ratio (CNR) calculations derived from signal intensity (SI) measurements; these values were statistically evaluated by using the Mann-Whitney U test. Two readers qualitatively determined SIs of the cores and bodies of the ICHs, degrees of apparent susceptibility artifacts, and lesion ages. The chi(2) test was used to determine statistically significant differences. RESULTS: With the exception of the bodies of late subacute ICHs at 3.0-T T2-weighted imaging, which had increased positive CNRs and SI scores (P </=.05), all parts of the ICHs at all stages showed increased negative CNRs and SI scores at 3.0-T FLAIR and T2-weighted imaging, as compared with these values at 1.5 T (P </=.05). No significant CNR or SI score differences at any ICH stage were observed between 1.5-T spin-echo and 3.0-T gradient-echo T1-weighted imaging (P >.05). With the exception of minor susceptibility artifacts seen in acute and early subacute ICHs at 3.0-T T1-weighted gradient-echo imaging, no susceptibility artifacts were noticed. The ages of most lesions were identified correctly without significant differences between the two field strengths (P >.05), with the exception of the ages of acute ICHs, which were occasionally misinterpreted as early subacute lesions at 3.0 T. CONCLUSION: At 3.0 T, all parts of acute and early subacute ICHs had significantly increased hypointensity on FLAIR and T2-weighted MR images as compared with the SIs of these lesions at 1.5 T. However, 1.5- and 3.0-T MR images were equivalent in the determination of acute to late subacute ICHs.

Acute Disease↗

PubMed2003

Microglial activation precedes and predominates over macrophage infiltration in transient focal cerebral ischemia: a study in green fluorescent protein transgenic bone marrow chimeric mice.

Resident microglia and hematogenous macrophages play crucial roles in the pathogenetic cascade following cerebral ischemia but may functionally differ regarding neuroprotective and cytotoxic properties. Distinction between these cells has not been possible due to a lack of discriminating cellular markers. We generated bone marrow chimeric mice by transplanting bone marrow from green fluorescent protein (GFP) transgenic mice into irradiated wild-type recipients. Transient focal cerebral ischemia was induced by transient middle cerebral artery occlusion (MCAO) for 30 min. Resident microglia and infiltrating macrophages were identified by immunohistochemistry and GFP fluorescence after 1-28 days. The first blood-derived cells infiltrating the infarct area were seen on Day 1 and identified as granulocytes. Hematogenous GFP(+) macrophages were rarely observed on Day 2, reached peak numbers on Day 7, and decreased thereafter. In contrast, resident GFP(-) microglial cells rapidly became activated already on Day 1 after MCAO. Even on Days 4 and 7, most macrophage-like cells remained GFP(-), indicating their derivation from resident microglia. Hematogenous macrophages were able to acquire a ramified morphology indistinguishable from resident microglia while microglial cells could develop into a phagocytic phenotype indistinguishable from infiltrating macrophages. The vast majority of macrophages in the infarct area are derived from local microglia, revealing a remarkable predominance of local defense mechanisms over immune cells arriving from the blood. GFP bone marrow chimeric mice are a powerful tool to further differentiate the function of resident microglia and hematogenous macrophages following cerebral ischemia.

Animals↗