Causal Relation of Psychical Stress to Acute Back Pain.

PURPOSE OF THE STUDY There s a known relation between the chronical back-pain-syndrome and psychical problems. We suppose a direct causality between acute stress and onset of the backpain syndrome. MATERIAL AND METHODS A prospective cohort-study (IV/2014 - VIII/2014) of patients who came to our emergency department with acute backpain-syndrome, with no relevant previous history - such as operations or chronic pain. We questioned together 39 patients (19 female and 20 male). The patients filled in two charts: FW7, and also a modified HADS-D. In the later one the patients were questioned in two extra points regarding contingent excessive emotional or existential problems in their brief history. The Pain-Severity-Score was assessed as well. RESULTS Combined together, relevant score-results and / or anamnesis of excessive emotional or existential problem was found in 79.5% (SD 0.4%) of the whole cohort. CONCLUSIONS This could have implications for guidelines, introducing the psychotherapy-first into the concepts. Key words:stress; well-being; depression; back-pain-syndrome.

[Complex regional pain syndrome in nerve root compression and after spinal surgery]. / Komplexes regionales Schmerzsyndrom bei Nervenwurzelkompression und nach Wirbelsäulenoperation.

Complex regional pain syndrome (CRPS) is an extremely painful and partially disabling disease. It often occurs secondary to trauma, but also spontaneously. The emergence of CRPS has been reported following nerve root compression and/or spinal surgery, but its incidence is unknown. In this article, the present knowledge about the incidence of CRPS in the context of nerve root compression and spine surgery is reviewed and therapeutic and diagnostic consequences are discussed.

Complex regional pain syndrome following spine surgery: clinical and prognostic implications.

BACKGROUND: Complex regional pain syndrome (CRPS) has been reported following spinal surgery, but its frequency after spinal surgery is unknown. The aim of this study was to determine the frequency of spinal surgery preceding CRPS and to examine these patients regarding the course of the disease and prognostic factors. METHODS: We examined 35 CRPS patients regarding the symptoms and signs of CRPS, the type of CRPS (I or II), the origin and grade of the disease, the type of surgeries prior to CRPS onset, the course of the disease, and the therapies following diagnosis of CRPS. RESULTS: In 6 patients, CRPS began during the postoperative course (lumbar spine surgery, n = 5; cervical spine surgery, n = 1). Four of these patients suffered from CRPS II. The course of the disease in the 6 patients was not different from that of patients with CRPS of other origins. First symptoms of CRPS could be observed 1-14 days after surgery. CONCLUSIONS: CRPS is a rare complication after spinal surgery, but spinal surgery precedes the onset of CRPS of the lower limb in almost one-third of the cases. The first typical symptoms of CRPS emerge within 2 weeks after spinal surgery.

The many faces of chondrosarcoma of bone, own cases and review of the literature with an emphasis on radiology, pathology and treatment.

Chondrosarcoma is the third most frequent primary malignant tumor of bone, constituting up to 16% of the malignant osseous neoplasms. Up to date several genetic alterations and markers were described concerning the pathogenesis and the progression of the chondrosarcoma, which represents actually a heterogeneous group of different types including conventional intramedullary, clear cell, myxoid, mesenchymal, and dedifferentiated chondrosarcoma. The pathologic appearance varies, however, in general they grow with a lobulated pattern. Histologically the hyaline cartilage demonstrates high water content and typically enchondral ossification is apparent. Imaging reflect this while radiographic findings suggest the diagnosis when the typical "ring-and-arc" chondroid matrix mineralization, endosteal scalloping and soft-tissue extension were apparent. The CT is used for detecting the mineralization of the matrix, especially when it is subtle or when the lesion is located in complex areas. MRT is the method of choice to detect the high water content of these lesions with a high signal intensity with T2-weighting and its bone marrow extend. Surgical resection is the primary and preferred treatment modality for most individuals with localized disease. In selected cases of the Grad I conventional chondrosarcoma curettage should be discussed. Systemic chemotherapy may be considered in variant forms such as mesenchymal or dedifferentiated chondrosarcomas. In knowledge of the "many faces" of the primary chondrosarcoma individualized patient assessment and optimal clinical management is possible.

[Rational use of blood cell products in orthopedics and traumatology]. / Rationaler Einsatz von Blutkonserven in Orthopädie und Traumatologie.

STUDY DESIGN: The risk of transmission of human immunodeficiency virus (HIV), hepatitis B and C viruses as well as the development of costs has changed the use of homologous blood cell products. METHODS: The present investigation shows the state of the art of blood salvage in orthopedic and elective trauma surgery. RESULTS: In this investigation the established methods such as controlled hypotension (spine surgery), arrest of blood supply (extremity surgery) and the following methods of autotransfusion have been examined: acute normovolemic hemodilution (ANH), intra- (Cell-Saver, Haemonetics Corp.) and postoperative autotransfusion, autologous donor plasmapheresis and autologous predeposit. CONCLUSIONS: Using this method it is possible to reduce homologous blood transfusions particularly in elective procedures such as orthopedic surgery and elective trauma surgery to a minimum.

Surgical treatment of the spine at the cervicothoracic junction: an illustrated review of a modified sternotomy approach with the description of tricks and pitfalls.

The surgical treatment of burst fracture, tumour or spondylitis remains a challenge with regard to the surgical approach to the anterior aspect of the cervicothoracic junction. Many vital structures including osseus, articular, vascular and nervous ones hinder the exposure. Fortunately, indications for surgery in this region are rare. However, when it becomes necessary for the surgeon to expose this region, it is useful to be prepared to approach it carefully. In this investigation the anatomy and exposure of the cervicothoracic junction by means of a sternotomy are described. An illustrated review of the sternotomy approach to the cervicothoracic junction with a description of 'tricks and pitfalls' is provided.

[Transaxial spongiosa-plasty and ventral, temporary atlanto-axial fixation for therapy of dens pseudarthrosis]. / Transaxiale Spongiosaplastik und ventrale, temporäre atlantoaxiale Fixation zur Therapie der Denspseudarthrose.

PURPOSE: According to literature there is a pseudarthrosis rate of about 1% up to 64% depending on the treatment of the dens fracture (16). Generally the treatment of dens pseudarthrosis consists of the fusion of the joint C1/C2 with or without dens resection. Now, a method is presented whereby, on the one hand the pseudarthrosis is treated, while on the other hand the anatomical structures and physiological function of the joint C1/ C2 are restored. METHOD: The operation consists of a gradual outboring of the base of the dens and the dens axis and filling with autologous cancellous bone. Then follows a lateral, temporary transarticular screw fixation of C1/C2 which guarantees an immobilisation of the filled out dens. A halo-body-jacket is then applied. The removal of the screws of the temporary fixation follows three months post operatively after X-ray control. Then physiotherapy of the cervical spine follows. RESULTS: During 7/93 and 7/97 this operation was carried out on 11 patients. In 9 cases compression screw osteosynthesis was primarily conducted and in 2 cases conservative therapy had preceded. The X-ray follow ups showed on an average of 14 month a stable bony fusion in 10 patients, the clinical follow up examinations on an average of 14 month a normal function. CONCLUSION: The operation presented is indicated in case of dens pseudarthrosis because this accomplished a definite bony fusion without disturbance of the function of the joint C1/C2 in patients not older than 60 years. Disadvantages are to be found in the intraoperatively high X-ray radiation and the 3 month immobilisation.

[Paralysis of the foot as the first symptom of a herniated thoracic disc]. / Plegie der Fussheber und Fusssenker als Erstsymptom von thorakalen Bandscheibenvorfällen.

Herniated thoracic discs are uncommon entities that are difficult to diagnose. They may be associated with a myriad of symptoms, which often delays diagnosis. In general dorsal pain that radiats around the chest or abdomen are found. In case of spinal cord compression signs of thoracal myelopathy are common. This paper describes a patient with a complete paralysis of the left foot as the first symptom of a herniated thoracic disc. After frustrated diagnostic of the lumbar spine, the exact neurological examination showed a sensible cut at the level of D6/7, the MR tomography diagnosed a herniated thoracic disc at the same level. Four months later he was presented again with a plegia of the left foot and a sensible cut at the level D5/6. The MR tomography showed a herniated disc at the level above the spondylodesis. The immediately performed transthoracic disc excision and fusion of D6/7 was followed by complete remission of the plegia and the sensible cut. Four months later we performed a rethoracotomy, disc excision and decompression with a spondylodesis D5/6. The procedure was again followed by complete remission. In case of paralysis of the lower extremities one has to consider a herniated thoracic disc.

Candida albicans gene encoding resistance to benomyl and methotrexate is a multidrug resistance gene.

Candida albicans is not inhibited by a number of drugs known to affect fungal cells. The basis for this resistance in most cases is unknown but has been attributed to the general impermeability of the fungal cell envelope. A gene (BENr) formerly shown to be responsible for the resistance of C. albicans to benomyl and methotrexate was shown in the present study to confer resistance to four other inhibitory compounds: cycloheximide, benztriazoles, 4-nitroquinoline-N-oxide, and sulfometuron methyl. Analysis of the protein database revealed an apparent similarity of the C. albicans gene to membrane protein genes encoding antibiotic resistance in prokaryotes and eukaryotes and a high degree of identity to a recently cloned gene encoding cycloheximide resistance in Candida maltosa. We propose that BENr encodes a protein that operates in a fashion similar, but not identical, to that described for other multiple-drug resistance proteins.

Biochemical analysis of a human humoral fibroblast inhibitory factor associated with impaired vascular prosthetic graft incorporation.

A specific inhibitory factor was isolated from human serum of a patient who manifested impaired prosthetic graft tissue incorporation. The latter reaction was hypothesized to be related to inhibiting fibroblast proliferation by a specific humoral factor. The crude inhibitory serum was tested against a pool of normal human sera with different cell types in culture. Proliferation of human skin fibroblast and human smooth muscle cell cultures incubated in the presence of 50% inhibitory serum were inhibited up to 58% and 37%, respectively. Proliferation of bovine capillary endothelial cell cultures was stimulated under similar conditions. Isolation and purification of the inhibitory factor from crude serum were initiated by ammonium sulfate precipitation. The pellet was further fractionated by sepharose 6B gel filtration. The inhibitory activity was eluted from the column in a relatively purified form as indicated by gel electrophoresis of the inhibitory fractions, which demonstrated a specific band corresponding to the inhibitory protein, with an apparent relative molecular mass of 230 kDa. The inhibitory factor showed a high affinity to concanavalin A, indicating its nature as a glycoprotein not associated with albumin or immunoglobulin fractions of the serum.

Release of a small two-chain form of antithrombin III from a conformationally changed antithrombin III-thrombin complex.

Reaction of antithrombin III (AT) with thrombin results in the formation of stable antithrombin III-thrombin (AT-T) complex with a Mr of 92.5-kDa, accompanied by the appearance of a proteolytically modified form of the inhibitor (ATM). Under these conditions AT-T is also transformed to a smaller complex (AT-TS). This smaller complex (81-kDa), a product of a conformational change at the AT moiety of the AT-T complex, is further transformed to a very small complex (AT-TVS) with a Mr of 71-kDa. Along with this process, AT-TS slowly dissociates to a free enzyme and a small, presumably two-chain product of AT (ATMS) with a Mr of 49-kDa. The newly described component, ATMS, naturally occurs in plasma and serum and accumulates significantly in plasma of patients suffering from cardiovascular disease.

Characterization of the cellular binding domain and the effects of monoclonal antibodies and thrombin inhibitors on the binding and internalization of the antithrombin-III--thrombin complex by cultured cells.

Antithrombin III (AT) binds to cultured cells mainly as a complex with thrombin or other serine proteases rather than in its free form. This implies that, upon complex formation, a new determinant appears on the AT molecule which is recognized by the cells. Fragmentation of AT by cyanogen bromide exposes this determinant and an 8-kDa fragment is recognized by cultured cells. The binding of this fragment to cultured cells is inhibited by antithrombin-III-thrombin (AT-T) complex, but not by free AT. The putative cellular binding domain of AT-T is located over amino acid residues 253-314 of AT, in the large loop close to the carboxy-terminus of the molecule. The cell-associated AT-T is internalized and degraded, forming the thrombin-modified AT (ATM). This process is inhibited by lysosomal degradation inhibitors, such as chloroquine or benzamidine. Thus, the appearance of ATM in cells is not a result of its binding to the cell surface, but probably a result of lysosomal degradation of cell-associated AT-T. Another degradation product, with a molecular mass of 43 kDa, appears in cells along with the appearance of ATM. Hirudin, a specific inhibitor of thrombin, inhibits the cellular internalization of AT-T complexes, indicating a possible role for thrombin activity in the internalization process of complexes. Monoclonal antibodies (mAb) against AT, whose epitopes on the AT molecule have been located, affect the binding of AT-T to cultured cells. Two mAb, A10 whose epitope is found outside of the cellular binding site, and B108 whose epitope may overlap this sequence, totally inhibit the binding of the complex to cells. Inhibition of binding results either from steric hindrance or induced changes in the binding site.

The membrane-associated component of the amphiphile-activated, cytosol-dependent superoxide-forming NADPH oxidase of macrophages is identical to cytochrome b559.

The superoxide (O2-) forming NADPH oxidase complex of resting phagocytes can be activated in a cell-free system by certain anionic amphiphiles, such as sodium dodecyl sulfate (SDS). For O2- production to occur, the participation of both membrane-associated and cytosol-derived components is required. The purpose of this investigation was to isolate and characterize the membrane component of NADPH oxidase. For this purpose, guinea pig macrophage membranes were extracted with 1 M NaCl, solubilized by 40 mM octyl glucoside, and subjected to a purification sequence consisting of absorption with DEAE-Sepharose, affinity chromatography on heparin-agarose, and chromatography on hydroxylapatite. At each purification step, fractions were assayed for their ability to support SDS-elicited, cytosol-dependent O2- production, following incorporation in liposomes of phosphatidylcholine. We found that membrane oxidase activity copurified strictly with cytochrome b559. Peak hydroxylapatite fractions exhibited specific O2(-)-forming activity in the range of 81-115 mumol of O2-/mg protein/min and a specific cytochrome b559 content of 7-14 nmol of cytochrome b559/mg protein. SDS-polyacrylamide gel electrophoresis analysis of the peak oxidase activity fractions, derived by hydroxylapatite chromatography, revealed essentially two bands that were identified as the beta (54-60 kDa) and alpha (21/22 kDa) subunits of guinea pig cytochrome b559. The relation of the two polypeptides to cytochrome b559 was established by correlation with a spectral signal characteristic of cytochrome b559, immunoblotting with antibodies against defined human cytochrome b559 beta and alpha chain peptides, cross-linking studies, and deglycosylation experiments. Hydroxylapatite-purified membrane oxidase preparations did not contain FAD and were free of cytochrome c reductase activity. Purified membrane oxidase preparations were also capable of cooperating with purified cytosolic components in SDS-elicited cell-free O2- production. We conclude that the membrane-associated component of the O2- generating NADPH oxidase is identical to cytochrome b559.

Monoclonal antibodies against antithrombin III. Identification of their epitopes and effects on antithrombin III activities.

Four monoclonal antibodies with distinct epitopes were prepared against antithrombin III. None of them is directed against the heparin-binding region nor the active site, yet two mAb namely A36 and B108, interfere with antithrombin III inhibition of thrombin. The epitope of monoclonal antibody A36 is located within amino acid residues 1-393, at a site different from the active site since it recognizes antithrombin III and antithrombin-III-thrombin complexes with the same affinity. A36 partially prevents the intrinsic antithrombin III activity and has no effect on the heparin-enhanced antithrombin III activity when added to the antithrombin-III--heparin complex. If A36 is first reacted with antithrombin III and then heparin is added to the reaction mixture, A36 fixes the conformation of antithrombin III so that heparin binds to antithrombin III, but is not able to induce the conformational change in the antithrombin III molecule required for the enhanced activity. The epitope for monoclonal antibody B108 is located within residues 282-393, close to the active site. It does not recognize antithrombin-III-thrombin complexes by solid-phase radioimmunoassay. Its binding to antithrombin III induces a conformational change that enhances antithrombin III activity in a manner that resembles the heparin effect, but its effect is additive to the heparin effect, since when it was added to a reaction mixture which contained a saturating amount of heparin, inhibition of thrombin was enhanced. The epitope for monoclonal antibody A5 is located within residues 1-393, and its recognition of antithrombin III or antithrombin-III-thrombin is strongly dependent on the integrity of the disulfide bonds. A5 has no effect on antithrombin III activities. The epitope for monoclonal antibody A10 is well defined within a narrow range of 55 amino acid residues, 339-393, on the antithrombin III molecule, close to the active site, yet it has no effect on antithrombin III inhibitory activity. These monoclonal antibodies may be developed for various diagnostic or clinical purposes and offer a powerful tool for studying the conformational changes and structure/activity relationships in the antithrombin III molecule.

Isolation of a heme-controlled inhibitor of translation that blocks the interaction between messenger rna and eukaryotic initiation factor 2.

A heme-controlled inhibitor of translation was isolated from the S-100 of rabbit reticulocytes by a novel procedure including chromatography on double-stranded ribonucleic acid (dsRNA)-cellulose. The inhibitor thus purified is extremely active and functionally resembles previously studied heme-controlled inhibitor preparations in terms of kinetics and extent of inhibition of translation, relief of inhibition by eukaryotic initiation factor 2 (eIF-2), relief of inhibition by 2-aminopurine, and preferential inhibition of alpha-over beta-globin synthesis. The action of this inhibitor on translation is resistant to treatment with bacterial alkaline phosphatase, micrococcal nuclease, or trypsin and to incubation at 95 degrees C, pH 2 or pH 12. The inhibitor not only is retained on DEAE-cellulose, phosphocellulose, and dsRNA-cellulose but also exhibits a high affinity for the dye Cibacron Blue, properties that suggest that it may be a protein. Unlike previously described heme-controlled inhibitor preparations, or preparations that did not pass over dsRNA-cellulose, the inhibitor recovered upon dsRNA-cellulose chromatography does not exhibit eIF-2 kinase activity. The inhibitor does not block ternary complex formation between eIF-2, methionyl-tRNAfMet, and GTP but inhibits the ability of eIF-2 to form a complex with labeled globin mRNA. In the presence of inhibitor, the formation of mRNA/eIF-2 complexes can be restored effectively by an excess of eIF-2 but not by an excess of mRNA. The inhibitor thus appears to block the interaction between eIF-2 and mRNA not by competing with eIF-2 for a binding site on mRNA but, instead, by acting on eIF-2 itself.(ABSTRACT TRUNCATED AT 250 WORDS)