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We report on a 49-year-old female patient suffering from recurrent carcinoma of the rectum, who underwent a palliative Hartmann operation for an anus praeter reconstruction. After a remifentanil bolus of 90 microg and a propofol bolus of 200 mg, anaesthesia was maintained with 0.25 microg/kg/min remifentanil and 4 mg/kg propofol, and after skin incision with 1.0 microg/kg/min remifentanil and 5 mg/kg/h propofol. Throughout the operation, the patient showed a stable blood pressure of 120-130/80 mmHg but 15 min after skin incision the heart rate suddenly rose to 140 beats/min, so remifentanil was increased to 1.8 microg/kg/min and propofol to 8 mg/kg/h. Over a time period of 15 min the heart rate decreased to 90 beats/min. Subsequently vegetative parameters stayed within the normal range (heart rate 90 beats/min, blood pressure 120-130/80 mmHg) so that continuous administration of remifentanil and propofol could be tapered. After completion of skin sutures, administration of remifentanil and propofol was terminated. After extubation the patient reported having heard conversations contributable to the end of the operation and the sentence: "now we're done" was clearly remembered. The patient stated that she had not been able to move any part of her body, that she had perceived the situation as extremely unpleasant and dangerous and that she had felt severe pain. At the postoperative rounds the patient refused any psychological and psychiatric help.

Background and Purpose: Cerebral sinus thrombosis (CST) needs to be considered in the differential diagnosis of all patients with acute headache. Early diagnosis is essential because early treatment may prevent morbidity and may even be life-saving. Definite exclusion, however, needs advanced neuroradiologic diagnostics, which are not readily available in many hospitals. Because measurement of D-dimers has been demonstrated to be helpful in excluding thromboembolic disease, our aim was to investigate whether D-dimers would be also sensitive enough to exclude CST., Methods: We undertook a prospective multicenter study over a 2.5-year period including all patients who came to the emergency departments with symptoms suggestive of CST. All patients were diagnosed either by magnetic resonance venography, spiral computed tomography scan venography, or intra-arterial digital subtraction angiography. D-dimer levels were measured at admission and analyzed by the same method in all patients., Results: A total of 343 patients were included. CST was diagnosed in 35 patients, of whom 34 had D-dimers above the cutoff value (>500 microg/L). From the 308 patients not having CST, D-dimers were elevated in 27. Sensitivity of D-dimers was 97.1%, with a negative predictive value of 99.6%. Specificity was 91.2%, with a positive predictive value of 55.7%. D-dimers were positively correlated with the extent of the thrombosis and negatively correlated with the duration of symptoms (Spearman rank correlation coefficients 0.76, -0.58, respectively)., Conclusions: D-dimer measurement is useful in patients with suspected CST. Normal D-dimers make the presence of CST very unlikely.

Chronic glutamate mediated excitotoxicity has been suggested to contribute to the pathogenesis of Huntington's disease (HD). Both, inhibition of glutamate release through stimulation of presynaptic metabotropic glutamate receptor (mGluR) 2 and blockade of postsynaptic mGluR5 have been demonstrated to be neuroprotective against excitotoxicity. R6/2 HD transgenic mice which express an expanded CAG triplet repeat serve as a well-characterized mouse model for HD with progressing neurological abnormalities and limited survival. We treated R6/2 HD transgenic mice with either the mGluR2 agonist LY379268 (1.2 mg/kg) or with the mGluR5 antagonist 2-methyl-6-(phenylethynyl)-pyridine (MPEP) (100 mg/kg) orally from a presymptomatic stage until death to investigate their potential disease modifying effects. We found that survival time in both the MPEP treated mice and the LY379268 treated mice was significantly increased in comparison to placebo treated transgenic controls (14.87+/-0.14 and 14.22+/-0.11 weeks versus 12.87+/-0.11 weeks, respectively). Additionally, the progressive decline in motor coordination of HD transgenic mice as tested with the rotarod test was significantly attenuated in MPEP- but not in LY379268-treated mice. Early pathological hyperactivity, which can be found in placebo treated HD transgenic mice, was significantly attenuated by both MPEP and LY379268 treatment. Immunohistologial examination of HD characteristic neuronal intranuclear inclusion (NII), however, demonstrated no effect on NII formation by either of the treatments applied. These data suggest that inhibition of glutamate neurotransmission via specific interaction with mGluRs might be interesting for both inhibition of disease progression as well as early symptomatic treatment in HD.

Glutamate excitotoxicity has been suggested to contribute to the pathogenesis of Huntington's disease (HD). Riluzole is a substance with glutamate antagonistic properties that is used for neuroprotective treatment in amyotrophic lateral sclerosis and which is currently tested in clinical trials for treatment of HD. R6/2 transgenic mice, which express exon 1 of the human HD gene with an expanded CAG triplet repeat, serve as a well-characterized mouse model for HD with progressing neurological abnormalities and limited survival. We treated R6/2 HD transgenic mice with riluzole orally beginning at a presymptomatic stage until death to investigate its potential neuroprotective effects in this mouse model and found that survival time in the riluzole group was significantly increased in comparison to placebo-treated transgenic controls. Additionally, the progressive weight loss was delayed and significantly reduced by riluzole treatment; behavioral testing of motor coordination and spontaneous locomotor activity, however, showed no statistically significant differences. We also examined the formation of the HD characteristic neuronal intranuclear inclusions (NII) immunohistologically. At a late disease stage, striatal NII from riluzole-treated transgenic mice showed profound changes in ubiquitination, i.e., NII were less ubiquitinated and surrounded by ubiquitinated micro-aggregates. Staining with antibodies directed against the mutated huntingtin revealed no significant difference in this component of NII. Taken together, these data suggest that riluzole is a promising candidate for neuroprotective treatment in human HD., (Copyright 2002 Movement Disorder Society)

This is a report of a new method for in vivo determination of the Young modulus of human os radii. The failure of the apparatus is +/- 1.86 per cent. The accuracy of the measuring procedure on healthy subjects bases on a variation coefficient of nearly 10 per cent. 124 forearms of healthy persons had been studied in relation to age, sex and to the right and the left os radii. There was a statistically significant higher elastic property of the bones of adolescent versus elder men (over 60 years), but no significant differences between male and female. Right and left os radii had nearly the same amounts for the Young modulus.