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When there is significant loss of spinal dura mater, dural substitution with synthetic or allogenic materials is essential. In the case of laminectomy, mechanical protection and reformation of the dorsal spinal canal may be useful. This is a report on a patient with total dura loss through tumour atrophy of the dura and laminae. In order to reconstruct the dorsal face of the spinal canal a polylactide sheet was cut and shaped to fit the physiological contour. A bovine dura substitute was firmly attached and sutured to the inner surface of the polylactide shield. The implant was wedged in between the pedicles and the facet joints and resulted in a water-tight dura substitute maintaining the shape of the spinal canal and protecting it against mechanical forces and intradural scar formation.

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The paper reports on auto fluorescence phenomena of inter-vertebral human discs. It systematically investigates the auto fluorescence effects of ex vivo disc specimen and reports on surgical cases to demonstrate the potential value of the new method. The paper offers biologic explanations of the phenomenon and discusses the potential value of the UV auto fluorescence technique as a diagnostic tool. Intra- and postoperative observations are made by a surgical microscope with an integrated UV light source. Quantitative measurements were carried out using a photon counter and a spectrometer ex vivo. The auto fluorescence phenomenon allows the differentiation of traumatized and degenerated disc tissue intraoperatively in some cases, it allows the differentiation of bony and collagen endplate in cervical disc surgery. The source of the auto fluorescent light emission are amino acids of the collagen molecules. The proteoglycan components and the liquid components of the disc do not show relevant auto fluorescence. Emission wavelength of disc material is equivalent to color perception. It differs due to different collagen composition of the intervertebral disc components from yellow-green to blue-green and can be visualized in situ by naked eye.UV-auto fluorescence of inter-vertebral discs is a new clinical tool that has the potential to differentiate disc material from the anatomical surrounding, to distinguish between different fractions of the disc and to give information on the quality and status of the disc material. Since the technology has just emerged, it needs further investigations to quantify the clinical observations reported in this paper.

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SUMMARY: Venous aneurysms so-called isolated cerebral varix, are known as a related pathology in arteriovenous malformations (AVM) due to the arterial pressure on venous drainage (16). They are also observed in combination with developmental venous anomalies (DVA) (2,4,8,15). However, isolated varix is a rare entity (1,7,11,13). They appear in most cases without neurological deficits. Some of the cases mimic a meningioma due to their manifestation in CT and MR imaging and their axial cortical localization. The case presented here is a isolated varix of a cortical vein located rostral to the motor strip. The patient was operated on successfully. The MRI and the histology of the case are presented.

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BACKGROUND: The 60 year old women with no prior history of arrhythmia or other cardiac symptoms was operated on for a cervical disc herniation at the level C7/D1. The C8 nerve root was visualized via a posterior approach. FINDINGS: Removal of the sequestrum and irritation of the anterior root with surgical instruments triggered cardiac arrest. INTERPRETATION: We offer the opinion that irritation of the anterior root led to diminished activity of the supraspinal sympathetic control system and consecutive hyper-activation of the parasympathetic system.

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Intraoperative neurophysiological mapping and monitoring of eloquent brain areas can be combined with image-guided localisation to enhance the safety and efficacy of surgical procedures in the motor cortex. We designed a new type of cortical electrode which can be repeatedly placed on the cortical surface and allows accurate and reproducible stimulation by means of a navigation pointer. The newly designed device consists of a monopolar electrode contact for direct cortical stimulation, housed in a holder which allows placement, easy removal, and precise repeated placement of a surgical navigation pointer. It can be used for navigation-guided, high-frequency anodal monopolar cortical stimulation (MCS) for the mapping of eloquent cortex, and for monitoring of motor pathways. While the cortex is stimulated, compound muscle action potentials (CMAP) are recorded from muscles of the contralateral extremities and are assessed both qualitatively and quantitatively. When the device is used in combination with intraoperative navigation, the stimulation sites may optionally be registered or displayed on the system monitor. This allows repeated pinpointing and obviates the need for strip or grid electrodes in the operative field; although such electrodes may be useful for continuous monitoring, they often are in the surgeon's way. In addition, the primary and supplementary motor cortex can be mapped by determining the location of the sites of stimulation on surface-projected images of the cerebral cortex.

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Intra-operative neurophysiological techniques allow reliable identification of the sensorimotor region and make their anatomical and functional preservation feasible. Monopolar cortical stimulation has recently been described as a new mapping technique. In the present study this method was compared to the "traditional" technique of bipolar stimulation. Functional mapping of the motor cortex was performed in 35 patients during surgery in the central region. The central sulcus (CS) was identified by somatosensory evoked potential (SEP) phase reversal. Cortical motor mapping was first performed by monopolar anodal stimulation with a train of 500 Hz (7-10 pulses) followed by bipolar stimulation (pulses at 60 Hz with max. 4 sec train duration). Surgery was performed under general anaesthesia without muscle relaxants. Of 280 motor responses elicited by bipolar cortical stimulation, 54.23% [152] were located in the primary motor cortex (PMC), 37.85% 106[ outside the motor strip in the secondary motor cortex (SMC), and 8% 22[ posterior to the CS. Of 175 motor responses elicited by monopolar cortical stimulation. 68.57% 120[ were located in the SMC, 23.42% 41[ in the SMC and 8% 14[ posterior to the CS. Contrary to the general clinical view, there is considerable overlapping of primary motor units over a cortical area much broader than the "classical" narrow motor strip along the CS. Bipolar cortical stimulation is more sensitive than monopolar for mapping motor function in the premotor frontal cortex. Both methods are equally sensitive for mapping the primary motor cortex.

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SUMMARY: This report describes three years of clinical experience with a new set of devices aimed at improving functional MRI of speech areas. They provide a valuable tool for pre-operative definition of hemispheric localization and spatial extension of these areas, especially in left-handed persons. The fibre-optic device described here transmits stimuli for cognitive tasks to patients undergoing MR investigations. Cognitive tasks elicit a defined brain activity lasting for several minutes. The resultant metabolic changes are detectable by functional MRI. The software (FIT ware) applied to process raw data allows semi-automated segmentation of the brain so as to obtain 3D images. Furthermore it allows the superposition of functional data. The effectiveness of the equipment was assessed on the basis of data from 140 fMRI studies. Intra-operative verification in eight patients with tumours located in the speech areas showed that the new set-up identified the speech-dominant side in each case and located speech areas in accordance with electrophysiological procedures.

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This study reports the development of a highly sensitive and reproducible RIA for the measurement of 3,5-diiodothyronine (3,5-T2) in human serum and tissue. The RIA employs 3-bromo-5-[125I]iodo-L-thyronine (3-Br-5-[125I]T1) as tracer, which was synthesized carrier free by an interhalogen exchange from 3,5-dibromo-L-thyronine (3,5-Br2T0). The detection limits were 1.0 fmol/g and 0.8 pmol/L in human brain tissue and serum, respectively. T3, diiodothyroacetic acid, and 3-monoiodothyronine cross-reacted with a 3,5-T2 antibody to the extent of 0.06%, 0.13%, and 0.65%, respectively. Serum concentrations of 3,5-T2 were measured in 62 healthy controls and 4 groups of patients with nonthyroidal illness, i.e. patients with sepsis (n = 24), liver diseases (n = 23), head and/or brain injury n = 15), and brain tumors (n = 21). The mean serum level of 3,5-T2 in the healthy subjects was 16.2 +/- 6.4 pmol/L. Concentrations of 3,5-T2 were significantly elevated in patients with sepsis (46.7 +/- 48.8 pmol/L; P < 0.01), liver diseases (24.8 +/- 14.9 pmol/L; P < 0.01), head and/or brain injury (24.1 +/- 11.3 pmol/L; P < 0.05), and brain tumors (21.6 +/- 4.8 pmol/L; P < 0.01). In all 4 patient groups, serum levels of T3 were significantly reduced, confirming the existence of a low T3 syndrome in these diseases. Serum concentrations of 3,5-T2 were significantly elevated in patients with hyperthyroidism (n = 9) and were reduced in patients with hypothyroidism (n = 8). The levels of T4, T3, and 3,5-T2 were measured in normal human tissue samples from the pituitary gland and various brain regions and in brain tumors. In normal brain tissue, the concentrations of 3,5-T2 ranged between 70-150 fmol/g, and the ratio of T3 to 3,5-T2 was approximately 20:1. In brain tumors, however, T3 levels were markedly lower, resulting in a ratio of T3 to 3,5-T2 of approximately 1:1. Recent findings suggest a physiological, thyromimetic role of 3,5-T2, possibly stimulating mitochondrial respiratory chain activity. Should this prove to be correct, then the increased availability of 3,5-T2 in nonthyroidal illness may be one factor involved in maintaining clinical euthyroidism in patients with reduced serum levels of T3 during nonthyroidal illness.

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In the present study we investigated the biochemical properties of in vitro phenolic (5'D) and tyrosyl (5D) ring deiodination and the tissue concentrations of T4, T3, and rT3 in adult human central nervous system (CNS) tissue. All samples were obtained from nontumoral tissue at autopsy (n = 6) or neurosurgical operation (n = 5). Both phenolic and tyrosyl ring deiodinase activities were demonstrable in all samples obtained intraoperatively, whereas only tyrosyl ring deiodination was evident in the tissues obtained postmortem. The phenolic ring deiodination pathway corresponded to the type II 5'-deiodinase isoenzyme with regard to its high affinity for T4 and rT3 (Km = 2.2 and 2.4 nmol/L, respectively), its insensitivity to 6-propyl-n-2-thiouracil (PTU), and the sequential reaction mechanism. No PTU-sensitive 5'-deiodination of rT3 was demonstrable. Tyrosyl ring deiodination of both T4 and T3 showed typical type III 5D kinetics (Ka, 6.5 nmol/L for T4 and 3.4 nmol/L for T3) and was PTU insensitive. Nanomolar concentrations of tissue T4, T3, and rT3 were detected in samples obtained both intraoperatively and postmortem. They were very similar to the absolute values of the apparent Km for T4, T3, and rT3 in the phenolic and tyrosyl ring deiodination pathways. In conclusion, we have demonstrated the coexistence of both phenolic and tyrosyl ring deiodinase activities in the human CNS. Their kinetic characteristics, substrate specificity, and reaction mechanisms are very similar to the corresponding type II 5'- and type III 5-iodothyronine deiodinase activities in rat brain. In contrast to the findings in the rat CNS, no PTU-sensitive phenolic ring deiodinase (i.e. type I 5'D) activity was found in the human CNS. This may explain the relatively high tissue concentrations of rT3.

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Medical examinations only insufficiently measure cognitive impairment in neurological and neurosurgical patients. Due to costs an personnel shortages, adequate neuropsychological test methods are typically bypassed. Indeed, the very size and methodological problems of current tests impede their application in clinical practice. To resolve this dissatisfying state of affairs, we have developed a standardized, scored form of initial neuropsychological examination. The Neuropsychological Screening Test (NST) comprises 45 items, is easy to handle, and can be conducted in 15-20 min. The NST measures psychic performance along functional parameters such as orientation in place and time, primary and secondary language, visuospatial ability, attention, and memory skills. We have assessed the validity and reliability of the NST in a prospective study. 129 neurosurgical patients (60% malignant or benign cerebral tumors, 21% vascular malformations with and without subarachnoid hemorrhage, 6% traumatic brain injury, 3% hydrocephalus, 10% others) and 52 control subjects were included in the study. The difference in average total NST-scores was highly significant for the two groups (t = -7.84, DF = 177.93, p < .001). In addition, two chronologically separate subsamples of NCH patients (N = 81) and controls (N = 35) were tested using the Mini-Mental State (MMS). The correlation between total NST-score and MMS results was r = .49 (p < .001). Cross-tabulation was used to set a cut-off score, by means of which 80% of the neurosurgical patients were identified as true positive and 74% of the controls as true negative. A 24-hour retest confirmed the NST as reliable to .85 (p < .001).(ABSTRACT TRUNCATED AT 250 WORDS)

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Although the loss of tumor suppressor genes and the activation of oncogenes have been established as two of the fundamental mechanisms of tumorigenesis in human cancer, little is known about the possible interactions between these two mechanisms. Loss of genetic material on chromosome 10 and amplification of the epidermal growth factor receptor (EGFR) gene are the most frequently reported genetic abnormalities in glioblastoma multiforme. In order to examine a possible correlation between these two genetic aberrations, the authors studied 106 gliomas (58 glioblastomas, 14 anaplastic astrocytomas, five astrocytomas, nine pilocytic astrocytomas, seven mixed gliomas, six oligodendrogliomas, two ependymomas, one subependymoma, one subependymal giant-cell astrocytoma, and three gangliogliomas) with Southern blot analysis for loss of heterozygosity on both arms of chromosome 10 and for amplification of the EGFR gene. Both the loss of genetic material on chromosome 10 and EGFR gene amplification were restricted to the glioblastomas. Of the 58 glioblastoma patients, 72% showed loss of chromosome 10 and 38% showed EGFR gene amplification. The remaining 28% had neither loss of chromosome 10 nor EGFR gene amplification. Without exception, the glioblastomas that exhibited EGFR gene amplification had also lost genetic material on chromosome 10 (p less than 0.001). This invariable association suggests a relationship between the two genetic events. Moreover, the presence of 15 cases of glioblastoma with loss of chromosome 10 but without EGFR gene amplification may further imply that the loss of a tumor suppressor gene (or genes) on chromosome 10 precedes EGFR gene amplification in glioblastoma tumorigenesis.

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