Determination of language dominance: Wada test confirms functional transcranial Doppler sonography.

OBJECTIVE: To determine the efficacy of the invasive Wada test in determining language dominance, and to validate the functional transcranial Doppler sonography (fTCD) examination in patients. BACKGROUND: Previous work shows that simultaneous bilateral fTDC may identify cognitive hemispheric dominance in healthy individuals. METHOD: fTDC and the Wada test were performed prospectively in 14 patients with various diseases (tumors, cerebrovascular events, head injury, intractable epilepsy). fTDC hemispheric dominance was determined based on the hemispheric blood flow velocity shift for language and visuospatial tasks. RESULTS: fTDC was performed easily in patients. One patient could not be examined by fTDC because of absent temporal bone window for ultrasonic transmission. Two Wada tests were inconclusive due to patient somnolence. One of these patients suffered from right frontal tumor and had aphasia remitted under steroids when examined. fTDC indicated a bilateral language dominance. In the remaining 11 patients the correlation between fTDC and Wada language lateralization indices was 0.75 (p = 0.008). If a post hoc cutoff score was taken for the fTDC language lateralization index, in eight patients, both fTDC and Wada testing determined the left hemisphere to be dominant for language; in the other three patients, language function was bilateral in both examinations. CONCLUSION: Although the current results are preliminary and require replication in a larger sample, fTDC seems to be able to assess hemispheric language dominance not only in healthy individuals, but also in patients. It might become an alternative noninvasive or complementary tool to the Wada test, particularly in patients in whom the Wada test is impractical or gives inconclusive results.

Antiganglioside GM1 antibodies and their complement activating capacity in central and peripheral nervous system disorders and in controls.

So far, the pathogenic significance and use for diagnosis of antiganglioside GM1 antibodies (anti-GM1) are unclear. We therefore compared serum IgM and IgG antimonosialo ganglioside GM1 levels of 33 patients with presumed immune-mediated neuropathies, 100 patients with various other central or peripheral neurological disorders, and 110 controls by ELISA. We also measured the complement-activating capacity of anti-GM1 by C5b-9-GM1-ELISA to evaluate its value to distinguish between pathogenic and nonpathogenic autoantibodies. Low levels of anti-GM1 were observed in all disease categories and in controls (healthy blood donors). Twenty-four of the controls including the 10 with the highest serum IgM or IgG anti-GM1 were examined for neurological disorders in a double-blind checkup study. In the patients, elevated IgM anti-GM1 levels were predominantly found in those with neuropathies (NP), but barely in patients with central nervous system disease (CNSD). We found elevated IgG anti-GM1 levels predominantly in patients with NP of inflammatory origin (multifocal motor neuropathy, chronic inflammatory demyelinating polyneuropathy or Guillain-Barré syndrome), rarely in patients with NP of noninflammatory origin or CNSD, but not in the control disease group myasthenia gravis (MG). Median levels of IgM-, IgG-, (IgM+IgG)-, and C5b-9-binding anti-GM1 were significantly higher in patients with inflammatory NP as compared to the controls (p < 0.025). In addition, median levels of IgG- and (IgM+IgG)-anti-GM1 were significantly higher in inflammatory NP versus CNSD. Elevated complement-binding activity was associated with low or elevated IgM and/or IgG anti-GM1. Nevertheless, there was a significant correlation between anti-GM1 level (IgM+IgG) and the respective complement-activating capacity (r = 0.758; n = 243). Estimation of anti-GM1 and their respective complement-activating capacity may be helpful in the diagnosis of inflammatory neuropathies. However, neither an elevated anti-GM1 level nor an increased C5b-9 binding seems specific for a given disease category (e.g. peripheral nerve disease) nor a disease process (e.g. demyelination or inflammation).

[Screening for sleep apnea: clinical use of Mesam IV and Apnoe-Check]. / Screening für Schlafapnoe: klinische Anwendung von Mesam IV und Apnoe-Check.

With the introduction of nasal continuous positive airway pressure as an effective treatment of the sleep apnea syndrome, the demand for costly polysomnographic investigations has markedly increased. Hence a reliable screening method would be desirable. Patients undergoing overnight oxymetry were simultaneously examined by MESAM (n = 54) and by Apnoe-Check (n = 23) in a prospective manner. The results were compared among themselves and with the complete overnight polysomnography (MESAM n = 38, Apnoe-Check n = 20). Simple overnight oxymetry, automatically assessed oxymetry by MESAM and apnea identification by Apnoe-Check correlated well with the polysomnographic findings. On the other hand, variation of heart rate, snoring events and changes of body position as identified by MESAM did not add relevant information. Only the detection of moderate to severe sleep apnea syndrome was satisfactory, though not infallible. Thus, there is still no screening method available to identify or exclude sleep apnea syndrome, particularly the milder form, which is nevertheless a significant disease.

Monitoring combined antithrombotic treatments in patients with prosthetic heart valves using transcranial Doppler and coagulation markers.

BACKGROUND AND PURPOSE: The combined use of coumarin and low-dose aspirin appears to reduce the risk of systemic embolism at a low risk of bleeding. The remaining incidence of embolism of approximately 2%/y is still high. Methods for real-time detection of embolic events have not been used thus far to monitor the efficacy of therapeutic strategies. They might permit individually tailored, effective treatments. METHODS: The frequency of embolic signals in both middle cerebral arteries was monitored using a two-channel 2-MHz transcranial Doppler system. We examined five patients with mechanical prosthetic heart valves suffering from recurrent cerebral ischemic symptoms despite adequate anticoagulant therapy (international normalized ratio, 3.0 to 4.3). Measurements were performed on coumarin alone (four baseline values) and subsequent to the addition of intravenous (500 mg bolus) and oral (100 mg/d for 10 days) aspirin or intravenous (5000 IU bolus) heparin. The prothrombotic markers thrombin-antithrombin III complex, fibrinopeptide A, D-dimer, and platelet beta-thromboglobulin were measured simultaneously. RESULTS: None of the combined drug regimens led to a significant reduction of the emboli count. The values of thrombin-antithrombin III complex, fibrinopeptide A, and D-dimer were already within normal limits with coumarin alone. The beta-thromboglobulin levels, however, were increased, and additional aspirin or heparin did not reduce them. There was no correlation between the emboli count and the prothrombotic markers or between the prothrombotic markers and the different drug regimens. CONCLUSIONS: The rate of cerebral emboli measured with transcranial Doppler in the group of high-risk patients studied was not influenced by additional antiplatelet therapy. The emboli are likely to be composed at least in part of platelets, and their generation seems not dependent on thrombin or cyclooxygenase. There is an apparent discrepancy between the unchanged rate of emboli during Doppler monitoring found in this and other studies and the partial efficacy of combined treatment with coumarin and aspirin in clinical long-term studies. This may be explained by differences in the composition or size of the emboli.

Determination of cognitive hemispheric dominance by "stereo" transcranial Doppler sonography.

BACKGROUND AND PURPOSE: Transcranial Doppler sonography (TCD) can assess blood flow velocity changes induced by focal brain activation. Therefore, TCD may have the potential to identify hemispheric dominance for cognitive tasks. METHODS: Using a system with two TCD probes ("stereo" TCD), we monitored simultaneously both middle cerebral arteries (MCAs) of 14 healthy right-handed volunteers while they performed cognitive tasks. The averaged blood flow velocity ratio of the two MCAs and the hemispheric blood flow velocity shift induced by the cognitive task were calculated. RESULTS: In every subject, language tasks resulted in blood flow velocity shift to the left compared with visuospatial tasks. Mean MCA blood flow velocity shift to the left was 1.67%, 2.01%, and 2.31% in three language tasks. Mean blood flow velocity shift to the right was 1.67% and 2.31% in two visuospatial tasks. CONCLUSIONS: Bilateral simultaneous MCA blood flow velocity monitoring and averaging during cognitive tasks can help to identify hemispheric dominance for cognitive tasks in individuals.

Motor-evoked responses to transcranial brain stimulation persist during cataplexy: a case report.

Magnetic brain stimulation was performed in a patient with the narcolepsy-cataplexy syndrome during and after a cataplectic status. Amplitudes and thresholds of responses in six muscles (diaphragm, lumbar erector spinae, trapezius, biceps, tibialis anterior and abductor digiti V) remained unchanged during cataplexy as compared to the normal state. Our data suggest that, similar to rapid eye movement (REM) sleep, an enhanced cortical excitability to magnetic brain stimulation may compensate for the postsynaptic spinal inhibition of muscle tone during cataplexy, and that there is no difference in this respect between axial and distal muscles. Our data agree well with other evidence of increased cortex activity during cataplexy and REM sleep.

Ultrasound findings in spontaneous extracranial vertebral artery dissection.

BACKGROUND AND PURPOSE: In this study we analyzed the value of ultrasound examination for diagnosis of vertebral artery dissection. METHODS: The vertebrobasilar arterial system was assessed in 14 patients using transcranial and extracranial pulsed-wave Doppler and duplex sonography. RESULTS: The dissections were verified by angiography (in 1 patient), magnetic resonance imaging (in 5), or both (in 8). The dissected segments were atlantoaxial (V-3) in 6, V-3 and intertransverse (V-2) in 3, V-3 and intracranial (V-4) in 3, and V-2 in 2 patients. Extracranial and transcranial Doppler examination of the atlas loop, involved in 12 patients, showed absent flow signal in 5, low bidirectional flow signal in 1, and poststenotic low blood flow velocities in 3 patients. Seven of these patients had high-grade stenosis or occlusion. The stenotic segment with increased flow signal could be identified directly in 2 patients. Duplex examination of the intertransverse segment confirmed absent flow in 4 patients, making technically insufficient examination unlikely. In the 2 patients with directly detected stenosis, duplex examination showed low flow velocities before the stenosis. The combined use of extracranial and transcranial Doppler and duplex sonography increases the diagnostic yield to detect vertebral artery pathology. If any abnormal sonographic finding was considered, the yield was 86%; relying only on definitively abnormal findings (absent flow signal, severely reduced vertebral artery blood flow velocities, no diastolic flow, bidirectional flow, and a stenosis signal), the yield was 64%. CONCLUSIONS: In most cases, there is no pathognomonic ultrasound finding for vertebral artery dissection. However, if a patient presents with suggestive symptoms, ultrasound may corroborate the clinical suspicion and aid in the decision regarding early anticoagulant treatment. A definite diagnosis can be made noninvasively when magnetic resonance imaging demonstrates hematoma in the vessel wall. Angiography yields additional information such as nature of underlying vascular disease, site and extent of dissection, intracranial extension, and presence of pseudoaneurysm.

Human oligodendrocytes in dissociated cell culture.

Human oligodendrocytes have been successfully maintained in cell cultures for 14 weeks using a modification of a method used previously for animal brain cell cultures. Dissociated cell cultures from spinal cords of human foetuses of 10 to 20 weeks gestional age were investigated for up to 98 days. Oligodendrocytes were identified by monoclonal human antiserum specific for myelin-associated glycoprotein, by polyclonal rabbit antiserum against myelin basic protein, and by the mouse monoclonal antibody I6G1. Astrocytes were identified by polyclonal antibodies against glial fibrillary acidic protein. Immunocytochemical cell identification was corroborated by electron microscopy, by which glial cells were investigated both in situ and in culture. Immunocytochemical staining of myelin-associated glycoprotein showed specifically labelled oligodendrocytes on electron microscopy. The present study indicates that human oligodendrocytes, a putative target in demyelinating disease, can be studied in dissociated cell culture of human foetal spinal cord for several weeks in vitro under stable conditions.