In the present study, we report sICAM-1 concentration in the cerebrospinal fluid (CSF) and serum of patients with neuroborreliosis (NB, n = 11), compared to the data from a control group of patients with corresponding blood/CSF barrier dysfunction but without inflammation in the central nervous system (disc prolaps, DP, n = 11). In NB, the sICAM-1 concentration in CSF was increased up to six-fold (ranges: 6.6-42.8 ng/ml and 2.2-9.8 ng/ml for NB and DP respectively) with no change in serum sICAM-1. The corresponding sICAM-1 CSF/serum concentration quotients (Q(ICAM)) were in the ranges: 22.5-171.3 X 10(-3), and 8.8-27.8 X 10(-3) for NB and DP respectively. This finding can be explained by increase of the brain-derived fraction of sICAM-1 in NB. In one case we observed increased Q(ICAM) on 6th day after admission to the hospital (171.3 X 10(-3) at the time of the first lumbar puncture slightly increasing to 243.6 x 10(-3) five days later), followed by normalization, in two remaining repunctured patients we observed decreasing QICAM with normalizing Q(Alb).

We present four cases of iatrogenic epidural spinal abscess directly caused by externally introduced catheters or probes. In two patients the infection spread per continuum, in the other two patients due to haematogenous dissemination. Clinical presentation in each case included generalized malaise with fever, signs of meningeal inflammation and focal neurological signs at the spinal level. The diagnosis was made on the basis of inflammatory changes in the cerebral spinal fluid and localization of the abscess by means of computer and magnetic resonance tomography. A broad-spectrum antibiotic regimen included a penicillinase-resistant preparation because of the frequent involvement of Staphylococcus aureus. It is our experience that a good outcome is dependent on early and specific treatment.

beta-Trace, a protein that represents a major constituent of human cerebrospinal fluid with unknown function has been purified to apparent homogeneity by gel chromatography and electrophoresis. After sodium dodecylsulfate electrophoresis on polyacrylamide gels (SDS-PAGE) and Western blotting, the N-terminal sequence (28 amino acids) has been determined. The high degree of identity with the corresponding sequences of prostaglandin D synthetase from rat (68%) and human (93%) suggests a strong relationship if not identity with this enzyme. Thus, 30 years after its discovery beta-trace might unravel as a well-known protein of the prostaglandin metabolism.

Abstract: P0, the most abundant glycoprotein of PNS myelin, is a homophilic and heterophilic adhesion molecule. P0 is known to contain a glycofonn population that expresses the L2/HNK‐1 carbohydrate epitope found on other neural adhesion molecules, and to be functionally implicated centrally in neural cell adhesion and neurite outgrowth. This carbohydrate epitope has been characterized previously from glycolipid structures and contains a sulphated glucuronic acid residue. However, the L2/HNK‐1 carbohydrate epitope has not been characterized in glycoproteins. Because P0 possesses only one glycosylation sequon, the number of P0 glycoforms is equal to the heterogeneity of the glycan species. Here we report that the carbohydrate analysis of L2/HNK‐1‐reactive P0 showed the presence of anionic structures containing sialic acid and sulphate in various combinations. At least one sulphate residue was present in 80% of the monosaccharide sequences, and 20% contained three sulphates. High‐resolution P4 gel chromatography of the desialylated and desulphated oligosaccharides showed substantial heterogeneity of monosaccharide sequences. Sequential exoglycosidase digestions indicated that the majority of the structures were of the hybrid class, although the sulphated structures were found to be en‐doglycosidase H‐resistant.

Involvement of the cervical spine is seen in 40%-60% of all patients with rheumatoid arthritis. Consequences are instability of the upper cervical column with pain and neurological deficits, in some cases tetraplegia, and sudden death. From this reason special care has to be taken in the management of those patients, even when they are comatose or anesthetized, to avoid sudden spinal cord compression with irreversible neurological deficits. We report a 49-year-old female with a history of rheumatoid arthritis for more than 10 years. Because of an adhesive ileus complicated by septicemia, she underwent abdominal surgery twice followed by prolonged mechanical ventilation under high doses of sedative drugs. After reduction of the tranquilizer doses tetraplegia with respiratory insufficiency was found. Neurophysiological and X-ray examinations showed spinal cord compression due to dislocation of the odontoid process, a rare but typical complication in patients with rheumatoid arthritis. It was not possible to determine the date of the dislocation, but it might have been caused by intubation or respositioning. Although the patient underwent immobilization and surgical fusion of the upper cervical spine, there was no improvement in the neurological status and she died 5 months later. In patients with advanced rheumatoid arthritis a detailed medical history, clinical examination, and radiography are necessary before general anesthesia or intensive care with intubation is considered. If an unstable cervical spine is suspected, intubation should be performed by fiberoptic technique under light sedation. Regional anesthesia should be preferred over general anesthesia. Surgical stabilization of the cervical spine should be considered in prolonged intensive care treatment of comatose or anesthetized patients with rheumatoid arthritis and an unstable cervical spine.

The use of MRI in the diagnosis of vascular anomalies of the basilar artery is demonstrated in two cases. The first patient had a partially thrombosed giant aneurysm of the basilar artery; the second had an atypical course of the basilar artery. MRI is indicated whenever other imaging procedures do not provide a definite diagnosis or the use of contrast medium for conventional X-ray examination or computed tomography is contraindicated.

We present a 71-year-old male in whom an epidural abscess developed within a short temporal interval after an epidural anesthetic. Due to different locations of the abscess and the site of the epidural puncture, the diagnosis was quite problematic. The initial symptoms consisted of pain in the shoulder-neck region, elevated temperature, and leucocytosis 1 week after the puncture was performed. The further course presented a picture of high spinal paralysis with respiratory insufficiency and massive cardiovascular problems. Magnetic resonance imaging of the cervical spine confirmed the suspected diagnosis of an epidural abscess (Fig. 1). Due to the reduced general condition of the patient, an operation was initially not possible. After the patient's condition had stabilized under antibiotic therapy with penicillin G, vancomycin, and gentamycin, exploration of the abscess area was performed. Histologic studies showed granulomatous tissue resulting from the previous inflammation. During the subsequent course of the disease, the clinical symptoms did not regress significantly. The patient required prolonged mechanical ventilation and died of recurrent bronchopulmonary infections after 5 months of intensive care treatment. The probable pathogenesis of the abscess as well as the diagnostic and therapeutic aspects are discussed in summary.

Involvement of the cervical spine is seen in 40%-60% of all patients with rheumatoid arthritis. Consequences are instability of the upper cervical column with pain and neurological deficits, in some cases tetraplegia, and sudden death. From this reason special care has to be taken in the management of those patients, even when they are comatose or anesthetized, to avoid sudden spinal cord compression with irreversible neurological deficits. We report a 49-year-old female with a history of rheumatoid arthritis for more than 10 years. Because of an adhesive ileus complicated by septicemia, she underwent abdominal surgery twice followed by prolonged mechanical ventilation under high doses of sedative drugs. After reduction of the tranquilizer doses tetraplegia with respiratory insufficiency was found. Neurophysiological and X-ray examinations showed spinal cord compression due to dislocation of the odontoid process, a rare but typical complication in patients with rheumatoid arthritis. It was not possible to determine the date of the dislocation, but it might have been caused by intubation or respositioning. Although the patient underwent immobilization and surgical fusion of the upper cervical spine, there was no improvement in the neurological status and she died 5 months later. In patients with advanced rheumatoid arthritis a detailed medical history, clinical examination, and radiography are necessary before general anesthesia or intensive care with intubation is considered. If an unstable cervical spine is suspected, intubation should be performed by fiberoptic technique under light sedation. Regional anesthesia should be preferred over general anesthesia.(ABSTRACT TRUNCATED AT 250 WORDS)

The broad spectrum of CNS listeriosis is expanded by the observation of an intracerebral infarction associated with meningoencephalitis. Sequential CCT scans in a 66-year-old immuno-compromised woman led to the clinical diagnosis of brain abscess. Autopsy revealed an infected intracerebral infarction most probably due to temporal occlusion of the middle cerebral artery by septic microemboli or septic endothelial damage.

Several monoclonal antibodies were generated against the major glycoprotein P0 of human peripheral nervous system myelin. Antibodies were selected for their reactivity with P0 in Western blots. The antibodies were of the immunoglobulin G subclass and reacted with the glycopeptidase F-treated P0, indicating that the reactive epitope resides in the protein backbone. In fresh frozen and paraffin-embedded sections of central and peripheral nervous system of rat and human, P0 antibody 592 reacted with myelin sheaths of peripheral, but not central, nervous system.

The adenylate kinase (AK) enzyme activity in plasma and CSF of acute brain infarctions was examined. The normal values of enzyme activity in plasma reached from 1.7-5.6 U/l, and in CSF from 0.23-0.71 U/l. According to this present classification a significant CSF increase in AK activity was found with semi-severe and severe brain infarctions. With the CCT an increased enzyme activity was shown with infarction in or close to the cortex. In no case was an alteration of AK activity in the serum sample. CSF samples showing blood contamination or pleocytosis led to false pathological results with examination of AK activity.

A patient with motor neuropathy associated with monoclonal IgM protein is reported. Using enzyme-linked immunosorbent assays, the antibody activity of the monoclonal IgM was shown to be directed against GD1a ganglioside, a new and so far unreported specificity.

Immunocytological localization of the major glycoprotein of peripheral myelin P0 and its associated carbohydrate structures L2/HNK-1 and L3 was performed at the light- and electron-microscopic levels in mouse sciatic nerves at several developmental stages and in adulthood. P0 was first expressed on Schwann cells at the time that Schwann cells associated with axons on a 1:1 basis. P0 remains expressed at all times of myelin formation and in compact myelin. After cessation of myelination P0 is no longer detectable in the uncompacted parts of myelin, i.e., Schmidt-Lanterman incisures, paranodal loops, and outer and inner mesaxons. P0 is not detectable on basement membranes, interstitial collagens, and non-myelin-forming Schwann cells. The associated carbohydrate epitope L2 does not follow the expression of P0 at any developmental or adult stage. Until 21 days the L2 epitope is confined to nonmyelinated fibers. In sciatic nerves of mice older than 8 weeks, however, only a few nonmyelinated fibers remain L2-positive. L2 immunoreactivity is clearly seen in a subpopulation of compact myelin figures largely associated with motor fibers. The L3 epitope is never detectable on nonmyelinated fibers and becomes first visible when compact myelin is discerned. Unlike the L2 epitope L3 is present in most, if not all, compact myelin figures. These observations suggest that P0 may be involved in ensheathment of axons by Schwann cells at the decisive stages of initiation of myelination and later on, possibly in conjunction with the L3 carbohydrate structure, in maintenance of compact myelin. The appearance of the L2 carbohydrate epitopes in compact myelin of largely motor and fewer sensory nerve fibers at times when morphogenesis of myelin has ceased remains to be elucidated in functional terms.

The major glycoprotein Po from human and bovine peripheral nerves carries the L2/HNK-1 and L3 carbohydrate epitopes and is recognized by serum from patients with IgM gammopathy and polyneuropathy. Only serum from patients with reactivity toward the myelin-associated glycoprotein (MAG) was reactive with Po, while serum that did not react with MAG also did not recognize Po. Furthermore, the neural adhesion molecules L1, N-CAM, and J1 were also recognized by the serum that reacted with MAG, while the L3 carbohydrate-carrying cell adhesion molecule AMOG was not recognized. These observations indicate a restricted specificity in carbohydrate reactivity of IgM paraproteins and implicate yet another and, for the first time, peripheral myelin-specific glycoprotein in the pathogenesis of demyelinating neuropathy.

On the basis of recent evidence that the carbohydrate structures L2/HNK-1 and L3 are shared by several neural cell adhesion molecules, we have suggested that other glycoproteins carrying these carbohydrate structures are adhesion molecules. We have isolated P0, the major glycoprotein of peripheral myelin, from human sciatic nerve by immunoaffinity chromatography using a monoclonal L2 antibody column and tested it, along with bovine P0, in Western blots for the presence of the two carbohydrate structures. Here we show that P0 expresses the L2/HNK-1 and L3 carbohydrates.

Wohl erlaubt die Computer-Tomographie nahezu problemlos die Diagnostik von intrazerebralen und subarachnoidalen Blutungen unmittelbar nach der Klinikeinweisung. Dies trifft jedoch nicht für den durch lokale Ischämie bedingten Hirninfarkt und die durch globale Perfusionsstörung hervorgerufene zerebrale Hypoxie zu. Der ischämische Hirninfarkt wird einschließlich der besonders ungünstig verlaufenden Krankheitsbilder, wie Basilaristhrombose und Mediaverschluß, in den ersten Tagen meistens nur klinisch diagnostiziert. Die Abschätzung von Ausmaß und Größe des Gewebsunterganges war bisher nicht möglich. Die bildgebenden Verfahren blieben hierfür unergiebig: Im kranialen CT stellt sich innerhalb der ersten 24 Std. nur bei 20% und bis Ende des 2. Krankheitstages lediglich bei ca. 55% der Fälle der geschädigte Gewebsbereich dar (1,2).

Hirnödem, intrakranielle Drucksteigerung und schließlich transten-torielle Einklemmung mit Kompression des Hirnstamms stellen die häufigste Todesursache in der ersten Woche nach Hirninfarkten dar. Wie neuropathologische Untersuchungen zeigen, ist die Frühmortalität nach einem Hirninfarkt unmittelbar Folge des Hirnödems, das um den vierten Tag nach dem akuten Ereignis das Maximum seiner Ausbildung erreicht und sich in vier Wochen wieder weitgehend zurückbildet (14). Der Behandlung des Hirnödems kommt daher in der Frühphase des Hirninfarkts eine entscheidende Bedeutung zu.