Retraction notice to "Influence of different anticoagulation regimens on platelet function during cardiac surgery" [Br J Anaesth 73 (1994) 639-44].

This article has been retracted: please see Elsevier Policy on Article Withdrawal (https://www.elsevier.com/about/our-business/policies/article-withdrawal). This article has been retracted at the request of the Editor-in-Chief, Professor Hugh Hemmings, based on the recommendations of Justus-Liebig-University Giessen following an internal review of research conducted by Joachim Boldt at the University. This is further described in 'Further Retractions of Articles by Joachim Boldt', https://doi.org/10.1016/j.bja.2020.02.024.

[Can treatment with anesthetic anticonvulsive drugs worsen outcome in status epilepticus?] / Kann der Einsatz anästhetisierender Antikonvulsiva beim Status epilepticus das Outcome verschlechtern?

BACKGROUND AND OBJECTIVES: Nowadays, there is an ongoing discussion about the risks and benefits of anesthetic treatment concerning outcome in status epilepticus (SE). Therefore, we performed a retrospective database analysis to examine the influence of treatment with anesthetic drugs and narcosis in SE on mortality and disability. METHODS: All treatment episodes of SE at the Department of Neurology of the University of Rostock between 01 January 2000 and 31 December 2009 were evaluated. SE severity before treatment, mortality, and disability at discharge were taken into account. RESULTS: Of 167 treatment episodes of SE, 34 included treatment with anesthetic anticonvulsive drugs and narcosis. In the treatment episodes with use of anesthetic anticonvulsive drugs and narcosis, there was a more than twofold increased risk for death compared to the other treatment episodes. However, due to sample size this difference was not significant (p = 0.09). Cardiopulmonary complications were the cause of death in 4 of 5 patients dying during treatment episodes with anesthetic anticonvulsive drugs and narcosis. At discharge, disability as measured with the Modified Rankin Scale was higher in patients treated with anesthetic anticonvulsive drugs and narcosis than in the others (p = 0.03). A subgroup analysis revealed that especially in patients with nonconvulsive SE with impaired consciousness treatment with narcosis was associated with a higher rate of new deficits or mortality (p = 0.012). CONCLUSIONS: Especially when considering narcosis for treatment of nonconvulsive SE, risks and benefits should be carefully weighed. When treating SE with anesthetic drugs and narcosis, everything has to be done to avoid cardiopulmonary complications.

Neuromyelitis optica spectrum disorder coinciding with hematological immune disease: A case report.

INTRODUCTION: Recently defined consensus criteria for the diagnosis of neuromyelitis optica spectrum disorders (NMOSD) allow establishing the diagnosis in patients without elevated AQP4-Ab and optic nerve involvement. According to the new extended definition, NMOSD is closely associated with extensive spinal cord inflammation occurring in the course of systemic autoimmune diseases as sarcoidosis or lupus erythematodes. NMOSD occurring in the course of hematological disease have not yet been reported in the literature. CASE REPORT: A 38 year old male subsequently developed thrombocytopenia, hemolytic anemia and agranulocytosis over a 23 month period. Three months after an episode of agranulocytosis, he noticed ascending sensory disturbances and progressive weakness of his legs. Within two days, symptoms worsened to give almost complete paraplegia and loss of sensation below a midthoracic level. MRI revealed signal hyperintensity and edema in T2-weighted sequences reaching from the 2nd cervical to the 9th thoracic vertebral body. Two years later, he developed a second episode with lesions in the spinal cord and periventricular areas of brain stem and thalamus. CONCLUSION: The relapsing time course and the topographical pattern of central nervous system lesions restricted to axial brain structures and the spinal cord fulfill the criteria that have recently been defined for AQP4-Ab-negative NMO-spectrum disease. Systematic studies on the association of hematological autoimmune phenomena and spinal cord disease are needed to clarify whether this coincidence is just a casual phenomenon or whether it points to a yet undiscovered but perhaps therapeutically interesting link of immunological mechanisms affecting both organ systems.

Interhemispheric inhibition in different phenotypes of progressive supranuclear palsy.

Progressive supranuclear palsy (PSP) is the most common atypical parkinsonian syndrome and an important differential diagnosis of parkinson's disease (PD). The clinical diagnosis of PSP relies on characteristic symptoms. There is evidence of clinical subgroups within the entity of PSP interfering with making the firm diagnosis. It was the aim of the study to clarify the differences between phenotypical subtypes of PSP and PD focusing on transcallosal inhibition (TI). A systematic chart review of 67 patients supposed to have probable PSP was done in a standardized diagnostic work-up. As only complete data sets were included into further analysis, 26 PSP patients (mean age 68.6 ± 7.1 years) could be evaluated and subdivided into Richardson's syndrome (RS) (n = 15) or PSP of parkinsonian type (PSP-P) (n = 11). Fifteen PD patients served as controls. TI was evaluated by investigation of the ipsilateral silent period (iSP) with transcranial magnetic stimulation (TMS). Cognition was assessed by the Addenbrooke's cognitive examination (ACE-R). TMS revealed a significantly more severe affection of TI in RS patients as compared to PSP-P and PD patients who showed similar neurophysiological findings. 47 % of RS patient displayed an iSP loss, whereas PSP-P and PD did not. There was a significant correlation between iSP latency and ACE-R (Spearman's coefficient -0.369, P = 0.010). In conclusion, RS patients-contrary to PSP-P and PD patients-had pathological TI at least in one hemisphere indicating more severe involvement of transcallosally projecting output neurons in RS.

[Neurophysiological analysis of interhemispheric motor tracts in neurodegenerative diseases]. / Neurophysiologische Diagnostik interhemisphärischer motorischer Bahnen bei neurodegenerativen Erkrankungen.

The corpus callosum (CC) is the morphological correlate of inter-hemispheric connectivity. Its integrity is of great importance for motor function and inter-hemispheric coordination of bimanual movements. Callosal fibre tracts show a high vulnerability as they are involved in number of neurodegenerative disease like parkinsonian syndromes and amyotrophic lateral sclerosis, even at early stages of the diseases. The integrity of callosal fibre bundles may be investigated by magnetic resonance imaging techniques and electrophysiologically by transcranial magnetic stimulation (TMS) investigating the transcallosal inhibition (TI). TMS investigation of the TI may be performed by measurement of the ipsilateral silent period (iSP). Most common findings are a loss or a prolongation of the iSP latency. Alternatively, a double pulse paradigm may be used to demonstrate altered TI. Furthermore, the transcallosal conduction time may be lengthened. TMS investigation of TI may a helpful diagnostic tool and may give new insights into the pathophysiology.

Transcallosal inhibition in amyotrophic lateral sclerosis.

OBJECTIVE: Assessment of upper motor neuron (UMN) involvement is essential for the diagnosis of amyotrophic lateral sclerosis (ALS). In a number of ALS cases, mirror movements (MM) suggest an involvement of transcallosal fibre tracts in conjunction with UMN involvement. The present study analysed whether deficient transcallosal inhibition (TI) tested by TMS enables detection of cortical affection in ALS, even at early stages of the disease. METHODS: In three patients with definite ALS and 12 patients with early ALS (aged 64.1+/-7.8 years) TMS investigation included analysis of contralateral (cMEP) and ipsilateral (iMEP) motor evoked potentials as well as measurement of TI (latency, duration) with recording from both first dorsal interosseus muscles. RESULTS: Clinical UMN signs were present in four patients. 83.3% of patients showed a pathological TI (prolongation or loss of TI). Five out of eight ALS patients showing a pathological TI had no clinical UMN signs. Two of these patients showed MM. One patient displayed also pathological findings in TI investigation. CONCLUSIONS: Our findings suggest a functional deficit of transcallosal fibre tracts even at early stages of the disease still lacking clinical UMN signs. SIGNIFICANCE: Measurement of TI tested by TMS can detect an involvement of the cortical output system in ALS and may be helpful in an early assessment of the diagnosis.

Overactive bladder in Parkinson's disease: alteration of brainstem raphe detected by transcranial sonography.

Urinary dysfunction is very common in idiopathic Parkinson's disease (PD) and manifests primarily with symptoms of overactive bladder (OAB). Affection of central serotonergic systems has been suggested to play a role in OAB. The objective of this study was to evaluate whether in PD patients with OAB symptoms a specific alteration of the brainstem raphe (BR), which contains serotonergic neurons, can be detected with transcranial sonography (TCS). Of 116 PD patients enrolled, 19 had PD-related OAB symptoms (OAB+) unlike remaining 97 patients (OAB-). Patients were examined by a sonographer blinded to the clinical data. Reduced echogenicity of BR was found in 12 (63%) OAB+ patients but only in 18 (19%) of 93 assessable OAB- patients (Mann-Whitney U-test, P < 0.001). In OAB+ patients, lower raphe echogenicity score was associated with longer duration of OAB symptoms (anova, P = 0.033). Other TCS findings such as echogenicity of substantia nigra, thalami, lenticular and caudate nuclei, and widths of third and lateral ventricles did not differ between OAB+ and OAB- patients. TCS findings suggest a pathogenetic role of BR in OAB related to PD. Alterations may reflect disturbance of its central serotonergic system.

Modulation of transcallosally mediated motor inhibition in children with attention deficit hyperactivity disorder (ADHD) by medication with methylphenidate (MPH).

Motor hyperactivity is one of the most outstanding symptoms of attention deficit hyperactivity disorder (ADHD) which might be caused by a disturbed inhibitory motor control. Using focal transcranial magnetic stimulation (TMS) we tested the cortico-callosal inhibition (duration and latency of the ipsilateral Silent Period, iSP) in 23 children with ADHD (mean age 11+/-2.6 years) before and on treatment with methylphenidate (MPH). iSP latency was age correlated, whereas iSP duration as well as Conners scores were age independent. Analyses of mean differences revealed a significant prolongation of iSP duration (p=0.001), shortening of iSP latency (p=0.027) and reduction of Conners score (p=0.001) under medication. Increase of iSP duration and reduction of Conners score under medication were significantly correlated (t=-9.87, p=0.016). Reduced iSP duration and prolonged iSP latency in ADHD children could be the result of a disturbed transcallosally mediated inhibition, most probable due to a combination of maturation deficits of callosal fiber tracts as well as neuronal synaptical transmission within the neuronal network between ipsilaterally stimulated cortex layer III--the origin of transcallosal motor-cortical fibers--and contralateral layer V, the origin of the pyramidal tract. MPH may indirectly improve the dysbalance between excitatory and inhibitory interneuronal activities of this neuronal network via dopaminergic modulatory effects of the striato-thalamo-cortical loop.

[Diagnosis and therapy of Parkinson's disease]. / Parkinson-Symptome richtig deuten. Wann hilft eine dopaminerge Therapie?

The clinical diagnosis of Parkinson's disease is mainly based upon the principal symptoms bradykinesia, rigidity and tremor at rest. The differential diagnosis of idiopathic Parkinson's disease (IPD) from other parkinsonisms is from the prognostic and therapeutic standpoint of considerable importance because the Parkinson-Plus syndrome generally does not or only poorly responds to a dopaminergic therapy. The treatment of IPD comprises, in addition to, dopaminergic medications such as L-dopa or dopamine receptor agonists, operative therapeutic options such as deep brain stimulation and nondrug therapies.

Serum antibody reactivity against recombinant PrtC of Porphyromonas gingivalis following periodontal therapy.

OBJECTIVES: In 34 patients with chronic periodontitis, the presence of IgA, IgG, and IgG subclass serum antibodies against recombinant PrtC (rPrtC) of Porphyromonas gingivalis was assessed by immunoblot analysis 24 months after therapy. METHODS: rPrtC was produced from P. gingivalis ATTC 33277 using the plasmid pGEX-2T. In addition, intraoral colonization with P. gingivalis was detected by PCR in subgingival plaque and swab samples from buccal mucosae, tonsils and tongue at baseline, 10 d, and 3, 6, 9, 12, 18, and 24 months. RESULTS: All patients were found to harbor P. gingivalis in the oral cavity at least once during the observation period. The identified antibody responses against the rPrtC of P. gingivalis were IgA (97%, i.e. 33/34 patients) and IgG (100%, i.e. 34/34), with an IgG subclass distribution of IgG2 (65%, i.e. 22/34 patients) > IgG3 (47%, i.e. 16/34) > IgG1 (38%, i.e. 13/34) > IgG4 (29%, i.e. 10/34). Anti-rPrtC IgA and IgG antibody reactivity was found in all but one patients (anti-rPrtC IgA negative), who tested negative for P. gingivalis at all of the assessed intraoral sites for at least 6 months before sera collection. There was no association between IgG subclass reactivity against the rPrtC of P. gingivalis and progression of periodontal attachment loss. CONCLUSION: The results indicated that anti-rPrtC IgA and IgG antibodies may serve as an indicator for past or present intraoral colonization with P. gingivalis.

Substantia nigra echogenicity is normal in non-extrapyramidal cerebral disorders but increased in Parkinson's disease.

Transcranial sonography (TCS) revealed substantia nigra (SN) hyperechogenicity in idiopathic Parkinson's disease (IPD). To further evaluate specificity of this finding, we examined 30 IPD patients and 30 age-matched subjects with non-extrapyramidal cerebral disorders (NED). All IPD patients showed a SN hyperechogenicity, in 17 it was bilateral and in 13 unilateral. 7 NED patients had a SN hyperechogenicity, in all it was unilateral, confirming previous results in healthy subjects. Bilateral SN hyperechogenicity indicates IPD and normal SN echogenicity indicates NED. In 30% of patients TCS does not distinguish between IPD and NED. Data further support the assumption that bilateral SN hyperechogenicity is specific for IPD.

Heterogeneity of the prtC gene of Porphyromonas gingivalis.

In this study, the nucleotide sequences of the prtC genes of six clinical Porphyromonas gingivalis isolates obtained from patients with periodontitis and from reference strain 53977 were determined. All analyzed genes were heterogeneous in their nucleotide composition and differed in up to 13 nucleotides. Moreover, substantial differences were found in comparison to prtC of reference strain 53977. The prtC genes of 45 Porphyromonas gingivalis isolates were amplified by polymerase chain reaction (PCR) and the PCR products were also digested with restriction endonucleases Tsp509I, NlaIII and DraII (PCR-restriction fragment-length polymorphism). Nine different restriction pattern combinations were observed, with four being most frequent (28.9%, 26.7%, 17.8% and 11.1%). The data presented here demonstrates that prtC genes are heterogeneous in their nucleotide sequence and therefore may be used as a target for molecular epidemiological studies. The observed heterogeneity of prtC genes may be a result of microevolution processes.

Serodiagnosis of Porphyromonas gingivalis infection by immunoblot analysis with recombinant collagenase.

The Porphyromonas gingivalis collagenase-specific serum immunoglobulin A (IgA), IgM, and IgG responses from 20 patients with early-onset periodontitis (EOP), 20 patients with adult periodontitis, (AP), and 20 age- and sex-matched healthy controls were examined by immunoblot analysis. A recombinant collagenase antigen used for the immunoblot analysis was produced by using the plasmid pGEX-2T, which allows the fusion between the collagenase and glutathione S-transferase. There was no significant difference in collagenase-specific IgG antibody detection between samples from the EOP, AP, and control groups. In contrast, 85% of AP and EOP sera had collagenase-specific IgA antibodies, whereas only 20% of control sera showed collagenase-specific IgA reactivity. Plaque samples from all groups were assessed by PCR with primers complementary to the collagenase-encoding gene prtC. The results indicated that 90% of AP and EOP plaque samples and 10% of control samples were positive for P. gingivalis. All patients with collagenase-specific IgA antibodies were PCR positive. The results of the study indicate a nearly complete concordance (k = 0.856) between the presence of collagenase-specific IgA antibodies and PCR detection of P. gingivalis. By using PCR as the "gold standard," the sensitivity and specificity of the IgA immunoblot test were 94.7 and 90.9%, respectively. Therefore, the recombinant collagenase is a potential candidate for use in the serodiagnosis of periodontitis.

The effect of the anticoagulation regimen on endothelial-related coagulation in cardiac surgery patients.

Heparin is still the most commonly used anticoagulant in cardiac surgery necessitating cardiopulmonary bypass. In recent years, endothelial-related coagulation (e.g. thrombomodulin/protein C-system) has enlarged our knowledge of the regulation of haemostasis. In a controlled randomised study, the influence of different regimens of anticoagulation on the thrombomodulin/protein C-system was studied. Sixty patients undergoing elective coronary artery bypass grafting were randomly allocated into four groups (n = 15) to receive: 300 IU.kg-1 of heparin before bypass; 600 IU.kg-1 of heparin; 300 IU.kg-1 of heparin as bolus followed by a continuous infusion of 10 000 IU.h-1 until the end of bypass; or 600 IU.kg-1 of heparin plus 'high dose' aprotinin (2 million IU of aprotinin before bypass, 500 000 IU.h-1 until the end of the operation and 2 million IU added to the bypass pump prime). Grouping was blinded for the surgeon and the anaesthetist. Plasma concentrations of thrombomodulin, protein C and (free) protein S as well as thrombin/antithrombin III were measured by enzyme-linked-immunosorbent assays after induction of anaesthesia, during and after bypass, at the end of surgery, 5 h after bypass, and on the first postoperative day. Activated clotting time was significantly longer during bypass in group 2 (566 (60)s) and group 4 (655 (59)s), whereas standard coagulation parameters showed no differences between the four groups. Blood loss and use of homologous blood and blood products were highest in groups 2 and 3. Thrombomodulin plasma levels were similar (and normal) at baseline (< 40 ng.l-1), decreased during bypass and reached baseline values postoperatively without showing significant group differences. Protein C did not show any differences among the groups within the investigation period. 'Free' protein S plasma levels were most reduced in group 1 (from 68 (8)% to 48 (9)% after bypass). Thrombin/antithrombin III plasma concentrations increased most in groups 1 (to 69 (14) micrograms.l-1 after bypass) and 2 (to 48 (7) micrograms.l-1 after bypass), whereas they remained significantly lower in groups 3 and 4. The thrombomodulin/protein C-system was not significantly influenced by the regimen of anticoagulation. Administration of 'high-dose' heparin was associated with the highest blood loss, which could not be related to endothelial-associated coagulation.

Influence of different anticoagulation regimens on platelet function during cardiac surgery.

Qualitative platelet defects are of great importance as a cause of bleeding in cardiac surgery. We have studied the effects of different anticoagulation regimens on platelet function in 60 patients undergoing elective aorto-coronary bypass grafting with cardiopulmonary bypass (CPB). Patients were allocated randomly to four groups (each group n = 15) to receive either: bovine heparin 300 u. kg-1 (standard); heparin 300 u. kg-1 followed by a continuous infusion of 10,000 u. kg-1 until the end of CPB; heparin 600 u. kg-1; or heparin 600 u. kg-1 in addition to high-dose aprotinin 2 million iu before CPB, 500,000 iu h-1 until the end of operation and 2 million iu added to the prime. Platelet function was evaluated by aggregometry (turbidometric technique) using adenosine triphosphate (ADP) 2.0 mumol litre-1, collagen 4 microliters ml-1, adrenaline 25 mumol litre-1 and saline solution (control) as inducers. Both maximum aggregation and maximum gradient of aggregation were measured in arterial blood samples before, during and after CPB until the first day after operation. Mean total dose of heparin given in groups 2, 3 and 4 was more than 50,000 u. and differed significantly from that of group 1 (28,150 (SD 4700)u.). Platelet aggregation variables were most depressed during CPB and until the end of surgery in groups 2 and 3 (maximum aggregation - 54% to - 75% of baseline values). In the postoperative period, platelet function recovered but did not completely reach baseline values in these patients.(ABSTRACT TRUNCATED AT 250 WORDS)