Cortical regional hyperperfusion in nonconvulsive status epilepticus measured by dynamic brain perfusion CT.

BACKGROUND AND PURPOSE: Nonconvulsive status epilepticus (NCSE) is associated with a mortality rate of up to 18%, therefore requiring prompt diagnosis and treatment. Our aim was to evaluate the diagnostic value of perfusion CT (PCT) in the differential diagnosis of NCSE versus postictal states in patients presenting with persistent altered mental states after a preceding epileptic seizure. We hypothesized that regional cortical hyperperfusion can be measured by PCT in patients with NCSE, whereas it is not present in postictal states. MATERIALS AND METHODS: Nineteen patients with persistent altered mental status after a preceding epileptic seizure underwent PCT and electroencephalography (EEG). Patients were stratified as presenting with NCSE (n = 9) or a postictal state (n = 10) on the basis of clinical history and EEG data. Quantitative and visual analysis of the perfusion maps was performed. RESULTS: Patients during NCSE had significantly increased regional cerebral blood flow (P > .0001), increased regional cerebral blood volume (P > .001), and decreased (P > .001) mean transit time compared with the postictal state. Regional cortical hyperperfusion was depicted in 7/9 of patients with NCSE by ad hoc analysis of parametric perfusion maps during emergency conditions but was not a feature of postictal states. The areas of hyperperfusion were concordant with transient clinical symptoms and EEG topography in all cases. CONCLUSIONS: Visual analysis of perfusion maps detected regional hyperperfusion in NCSE with a sensitivity of 78%. The broad availability and short processing time of PCT in an emergency situation is a benefit compared with EEG. Consequently, the use of PCT in epilepsy may accelerate the diagnosis of NCSE. PCT may qualify as a complementary diagnostic tool to EEG in patients with persistent altered mental state after a preceding seizure.

[Acute headache in a case of cerebral cavernomas]. / Akute Kopfschmerzen bei zerebralen Kavernomen.

We report a case of a 52-year-old female patient with known cerebral cavernomas and acute headache. A cranial CT scan excluded an intracranial bleeding. Cavernomas are rare vascular malformations of the venous blood system (synon. cavernous angiomas) with a slow blood flow. Clinical manifestation is presented between an age of 30-50 years with mostly unspecific neurological symptoms like headache, nausea, vomiting and dizziness, but also epileptic seizures and bleedings may occur. In general, therapy is symptomatic. In cases of seizures, however, anticonvulsive treatment is indicated. Operation can be discussed for peripheral localized cavernomas with bleeding or for refractory seizures. If antiplatelet or anticoagulation therapy is necessary due to other diseases (coronary heart disease, atrial fibrillation, thrombosis, pulmonary embolism), cerebral cavernomas are not considered as an absolute contraindication. The risk for an ischemic stroke under atrial fibrillation (5-20%), for example, is higher than the risk for bleeding of a cerebral cavernoma under anticoagulation therapy.

A cell culture assay for the detection of cardiotoxicity.

An important step in minimizing the number of animal experiments in medical research is the study of in vitro model systems. We propose the use of "shock protein" formation, which is a cellular response to cell-damaging stress as an assay to monitor cardiotoxicity. Isolated and cultured cardiac myocytes were prepared by a trypsin digestion method from 18-day-old fetal mice. These cells respond to typical substances inducing "shock protein" formation in other cellular systems as well as to known cardiotoxins with the de novo synthesis of "shock proteins." Pharmaceuticals relevant in transplant medicine were tested for possible cardiotoxic effects: Cyclosporine A evokes "shock protein" formation at subtherapeutic concentrations. Azathioprine and methyl-prednisolone exert the same effect but at concentration ranges highly above the therapeutic level. The ability to induce "shock protein" synthesis obviously seems to be restricted to toxic drugs. The data presented demonstrate that the proposed in vitro model system for cardiotoxicity is animal saving and sensitive.

In vitro studies on the cardiotoxicity of chemotherapeutics.

The de novo synthesis of 'shock proteins' is a cellular reaction towards toxic agents. Therefore, the induction of 'shock proteins' serves as a detector of toxicity on the level of protein synthesis. We investigated the effects of chemotherapeutics on cultured cardiac myocytes with this test system. Cisplatin (greater than or equal to 16 mumol/l) and methotrexate (greater than or equal to 1.4 mumol/l) evoked the de novo formation of a 30-kilodalton 'shock protein'. Doxorubicin (80-0.8 mumol/l) and daunomycin (90-0.9 mumol/l) inhibited protein synthesis almost completely. The other chemotherapeutic drugs tested did not influence heart cell protein formation even at concentrations widely above the pharmacological range. Our results indicate that the anthracyclines probably exert cardiotoxicity by depression of protein synthesis. Cisplatin and methotrexate are potentially cardiotoxic at high concentrations.