[Quality parameters in the treatment of acute stroke: comparison of various regional treatment concepts]. / Qualitätsparameter der akuten Schlaganfallversorgung: Gegenüberstellung unterschiedlicher regionaler Versorgungskonzepte.

BACKGROUND: The long-term prognosis of stroke patients is still dependent in particular on the timing of a correct diagnosis, immediate initiation of a suitable specific therapy and competent treatment in a stroke unit. Therefore, nationwide attempts are being made to establish a comprehensive coverage of the necessary specific competence and infrastructural requirements. Divergent regional circumstances and economic viewpoints determine the characteristics of the various healthcare concepts and the interplay between participating cooperation partners. This article compares the development with respect to three qualitative treatment parameters exemplified by four regional healthcare models during the time period 2008-2011. METHODS: The hospitalization rates for patients with transitory ischemic attacks, ischemic and hemorrhagic stroke, the case numbers for stoke unit treatment and the rates of systemic thrombolysis and mechanical thrombectomy in the regions of Berlin, the Ruhr Area, Ostwestfalen-Lippe and southeast Bayern (TEMPiS) are presented based on the data from the DRG statistical reports for the years 2008 and 2011. RESULTS: The average hospitalization rates for ischemic stroke patients (brain infarct ICD 163) in the time period from 2008 to 2011 were 294 per 100,000 inhabitants for the Ruhr Area, 257 per 100,000 inhabitants for Ostwestfalen-Lippe and 265 per 100,000 inhabitants each for Berlin and southeast Bayern. The complex stroke treatment quota for southeast Bayern in 2008 was 31 % and 47 % in 2011 and the respective quotas for the other regions studied were 42-44 % and 58-59 %. The rate of systemic thrombolysis in 2008 ranged between 4.2 % and 7.4 % and in 2011 the increase in the range for the 4 regions studied was between 41 % and 145 %. In 2011 the thrombectomy quota of 2 % in the Ruhr Area was the only one which was above the national average of 1.3 % of all brain infarcts. DISCUSSION: Stroke is a common disease in the four regions studied. For the established forms of therapy, complex treatment of stroke and systemic thrombolysis, the positive effect of structurally improved approaches in the four different regional treatment concepts could be confirmed during the course of the observational time period selected. Mechanical thrombectomy which is currently still considered to be an individual healing attempt, was used significantly more often in the Ruhr Area in 2011 than in the other three regions studied. A standardized referral procedure had previously been established in the metropolitan regions.

Recanalization after intravenous thrombolysis: does a recanalization time window exist?

BACKGROUND: To evaluate the time course of major vessel recanalization under IV thrombolysis in relation to functional outcome in acute ischemic stroke. METHODS: A total of 99 patients with an acute anterior circulation vessel occlusion who underwent IV thrombolysis were included. All patients had a standardized admission and follow-up procedure. Color-coded duplex sonography was performed on admission, 30 minutes after thrombolysis, and at 6 and 24 hours after onset of symptoms. Recanalization was classified as complete, partial, and absent. Functional outcome was rated with the modified Rankin Scale on day 30. RESULTS: Complete recanalization occurred significantly more frequently in patients with multiple branch occlusions compared to those with mainstem occlusion (OR 5.33; 95% CI, 2.18 to 13.05; p < 0.0001) and was associated with lower NIH Stroke Scale (NIHSS) scores (p < 0.001). Not the specific time point of recanalization at 6 or 24 hours after stroke onset, but recanalization per se within 24 hours (OR 7.8; 95% CI 2.2 to 28.2; p = 0.002) was significantly associated with a favorable outcome. Multivariate analysis revealed recanalization at any time within 24 hours and NIHSS scores on days 1 and 7 together explaining 75% of the functional outcome variance 30 days after stroke. CONCLUSIONS: Complete recanalization up to 24 hours after stroke onset is significantly associated with the short-term clinical course and functional outcome 30 days after acute stroke.

Detection of cerebral perfusion abnormalities in acute stroke using phase inversion harmonic imaging (PIHI): preliminary results.

Phase inversion harmonic imaging (PIHI) with newer contrast agents can display parameters of cerebral perfusion either using the established ipsilateral approach, or the novel bilateral approach in which both hemispheres are assessed in one examination. The aim of this study was to evaluate the potential of PIHI in detecting pathological perfusion in acute stroke, using the bilateral approach. Patients with a hemispheric syndrome presenting within 12 hours after symptom onset were examined with PIHI (SonoVue; bolus kinetics, fitted model function) using the bilateral approach if possible. Semi-quantitative perfusion related parameters (time to peak intensity (TPI) and peak width (PW)) were evaluated, and results correlated to follow up cerebral computed tomography (CCT) scans. In these four preliminary cases (one ipsilateral, three bilateral), PIHI was able to identify the ischaemic region because the function could not be fitted to the data. In one case, there was a difference between a core region where no perfusion was seen, and a surrounding region where hypoperfusion was detected (prolonged TPI and reduced PW). PIHI was able to predict the localisation and size of the eventual infarction even if no early CCT signs were seen. Furthermore, in one case, a surrounding hypoperfused region was identified, where tissue survived after recanalisation of the initially occluded middle cerebral artery. Using the bilateral approach, two advantages in comparison with the ipsilateral approach were obvious: cortical structures could be evaluated, and only one examination was needed to compare unaffected (ipsilateral) with affected (contralateral) tissue. These results should be confirmed by more cases, and should also be correlated to acute perfusion/diffusion weighted MRI data.

Feasibility and validity of transcranial duplex sonography in patients with acute stroke.

OBJECTIVES: To evaluate in a prospective multicentre setting the feasibility of transcranial colour coded duplex sonography (TCCS) for examination of the middle cerebral artery (MCA) in patients with acute hemispheric stroke, and to assess the validity of sonographic findings in a subgroup of patients who also had a correlative angiographic examination. METHODS: TCCS was performed in 58 consecutive patients within six hours of the onset of a moderate to severe hemispheric stroke. Ultrasound contrast agent (Levovist) was applied if necessary. Thirty two patients also had computed tomography angiography (n=13), magnetic resonance angiography (n=18), or digital subtraction angiography (n=1). In 14 of these patients, both the sonographic and corresponding angiographic examination were performed within six hours of stroke onset (mean time difference between TCCS and angiography 0.8 hours). Eighteen patients, in whom angiography was carried out more than 24 hours after stroke onset, had a follow up TCCS for method comparison (mean time difference 6.1 hours). RESULTS: Initial unenhanced TCCS performed 3.4 (SD 1.2) hours after the onset of symptoms depicted the symptomatic MCA mainstem in 32 patients (55%) (13 occlusions, one stenosis, 18 patent arteries). After signal enhancement, MCA status could be determined in 54 patients (93%) (p<0.05), showing an occlusion in 25, a stenosis in two, and a patent artery in 27 patients. In 31 of the 32 patients who had correlative angiography, TCCS and angiography produced the same diagnosis of the symptomatic MCA (10 occlusions, three stenoses, 18 patent arteries); TCCS was inconclusive in the remaining one. CONCLUSION: TCCS is a feasible, fast, and valid non-invasive bedside method for evaluating the MCA in an acute stroke setting, particularly when contrast enhancement is applied. It may be a valuable and cost effective alternative to computed tomography and magnetic resonance angiography in future stroke trials.

Recanalization of acute symptomatic occlusions of the internal carotid artery.

BACKGROUND: Little is known about the natural course of internal carotid artery (ICA) occlusion and its possible recanalization. The present study was designed to evaluate recanalization rates of extracranial ICA occlusions in acute stroke patients by means of color-coded duplex sonography (CCDS). METHODS: 305 patients with acute ischemia in the territory of the middle cerebral artery were included in this study. All patients had a neurological examination on admission and on discharge and were rated by means of the European Stroke Scale (ESS). Extracranial color-coded duplexsonography, transcranial Doppler sonography and cranial computed tomography were immediately performed after admission and within 7 days. RESULTS: 254 patients showed no sign of hemodynamic relevant stenosis greater than 70% of the ICA. 21 patients had symptomatic high grade ICA stenosis. 20 patients had an acute occlusion and 10 patients an old ICA occlusion as judged by duplex sonographic criteria. Six patients (5 male, 1 female; age range 57 to 77 years) with an acute atherothrombotic or cardioembolic occlusion showed a recanalization of the ICA in the follow-up ultrasonography. Two patients with cardiogenic embolic occlusion of the ICA had the most favorable outcome and these patients showed no residual stenosis. 4 patients who had ultrasound findings consistent with atherosclerosis on follow-up examination (2 high-grade stenosis, 2 with carotid plaques) did not show a notable improvement of their ESS-score. Patients with carotid plaques developed complete MCA infarctions; the other 4 patients had partial anterior circulation infarction on follow-up CT. CONCLUSIONS: The present study showed that recanalization of the occluded ICA in acute stroke patients is more frequent than generally presumed. CCDS should be routinely performed in the follow-up of stroke patients as spontaneous recanalization may influence clinical outcome.

Autonomic nervous system function in Huntington's disease.

OBJECTIVE: To investigate whether Huntington's disease (HD) affects autonomic nervous system (ANS) functioning. METHODS: Twenty patients with HD who had positive genetic test results underwent standardised ANS function tests including sympathetic skin responses (SSRs) of the hands and feet, measurements of heart rate variability (HRV), both during five minutes of resting and deep respiration, and an orthostatic blood pressure test. Patients were classified according to the motor subscale of the unified Huntington's disease rating scale (UHDRS; mean (SD) score 26.4 (13.6)) and divided into two subgroups: UHDRS <25 points (early stages, E-HD) and UHDRS > or =25 points (mid stages, M-HD). Autonomic indices were compared with those obtained for a group of well matched healthy controls (n=60). RESULTS: Overall, patients showed lower HRV indices than controls. Multivariate analysis with the independent factor of "group" (controls, E-HD, M-HD) showed a significant group effect on both the high frequency power (F=4.32, p=0.017) and the coefficient of variation (F=4.23, p=0.018), indicating a significant reduction in vagal modulation in the M-HD group. There was a shift in autonomic neurocardiac balance towards sympathetic predominance in the M-HD group compared with controls (F=2.89, p=0.062). Moreover, we found an inverse correlation between the severity of clinical HD symptoms (assessed by the UHDRS) and the modulation of cardiovagal activity (p=0.028). Vagal dysregulation was present in two patients; one of them also showed a pathological blood pressure test and a latency prolongation in the SSRs of the hands. Two other patients had pathologically reduced SSR amplitudes. Only patients of the M-HD group were affected. CONCLUSION: Autonomic dysfunction is present even in the middle stages of HD and affects both the sympathetic and parasympathetic branch of the ANS.

Relation between electroconvulsive therapy, cognitive side effects, neuron specific enolase, and protein S-100.

OBJECTIVE: To investigate whether electroconvulsive therapy (ECT) induces brain tissue damage expressed as an increase in neuron specific enolase and protein S-100. METHODS: A total of 179 serial measurements of S-100 and NSE serum concentrations were performed on 14 patients during the course of a bilaterally stimulated ECT series. Cognitive performance was assessed by psychometric testing carried out on the day before the start of ECT as well as on the days after the third, sixth, and last ECT. Pre-ECT and post-ECT concentrations of NSE and S-100 were compared by non-parametric tests. RESULTS: On average, 9.5 (SD 2.9) (range 3-12) ECTs were applied; 13 of 14 patients received at least six ECTs. The average duration of convulsion (computed for all ECTs) was 29.0 (SD 10.5) seconds. At no point during the ECT series was there a significant increase in the average NSE or S-100 concentrations compared with the baseline investigation before the start of the ECT series. The maximal measured post-ECT values of NSE and S-100 were 26.6 ng/ml and 0.46 ng/ml, respectively. The cumulative energy doses applied, seizure durations, and ECT induced changes in cognitive performance scores were never significantly correlated with the NSE or S-100 serum concentrations. CONCLUSION: This pattern of findings suggests that a modern ECT, fulfilling current quality standards, induces no brain tissue damage detectable by changes in NSE or protein S-100.

Distribution of artificially-produced microembolic signals into the cerebral circulation.

According to clinical observations, cardiogenic embolism occurs more often in the anterior than in the posterior cerebral circulation. An ultrasound (US) contrast agent was used to artificially produce microembolic signals (MES) to imitate the intracranial distribution of systemic emboli. Systemic microemboli were simulated by IV administered US agent (Levovist(R) 300 mg/mL as bolus). A total of 20 patients were monitored by means of transcranial Doppler sonography (TCD), 3 min after the injection, with a 2-MHz transducer simultaneously at 50 mm (middle cerebral artery, MCA, on one side) and 90 mm (basilar artery, BA). Four 3-min recordings were done (two of the right MCA, two of the left MCA, with the BA, respectively). Three observers and an automatic detection system independently performed an off-line analysis. A total of 160 recordings were analyzed. The mean numbers of detected high-intensity transient signals (HITS) were 34.5 +/- 28.2 in the right MCA (simultaneously registered HITS in the BA: 9.4 +/- 16.8) and 39.1 +/- 34.2 in the left MCA (simultaneously registered HITS in the BA: 12.2 +/- 14.5). Only 21.4 to 23.7% of all HITS were recorded in the BA. Microembolic signals artificially produced by means of US contrast agent made it possible to mimic the physiologic distribution of small embolic particles. In future, these might help to investigate the distribution of systemic emboli in different vascular territories in various pathologic conditions of the cerebral blood flow.

Ultrasonic assessment of physiological echo-contrast agent distribution in brain parenchyma with transient response second harmonic imaging.

OBJECTIVES: The present study was designed to provide normal data of transient response second harmonic imaging (TRSHI) examinations of cerebral echo contrast enhancement using different modes of electrocardiogram (ECG) gating and echo-contrast agent doses. MATERIALS AND METHODS: Fifty-five patients were examined in an axial diencephalic plane of section using the transtemporal acoustic bone window. TRSHI examinations (ECG gating: systolic, frame-rate once every 2 cardiac cycles = "basical instrument setting") could be performed in 50 individuals with adequate insonation conditions after application of 4 g of a galactose-based microbubbles suspension in a concentration of 400 mg/ml. For comparison, diastolic ECG gating (20 patients), cardiac-cycle triggering frequency of once every 2 seconds (15 patients), or an echo contrast agent dose of 2 g Levovist (15 patients) were used. Analysis of peak intensities (PIs) and areas under the curve (AUCs) was done in posterior (region of interest [ROI]a) and anterior (ROIb) parts of the thalamus, in the lentiform nucleus (ROIc), and the white matter (ROId). RESULTS: In 41 patients with basical instrument setting, characteristic time intensity curve (TIC) could be detected in all ROIs. In ROIa (90%) and ROIb (82%), focal contrast enhancement was most difficult to visualize, and in ROIc and ROId, characteristic TICs were observable in more than 90% of the examinations. Background subtracted PIs and AUCs were significantly higher in ROIc (mean PI: 12.2 +/- 8 acoustic units [AUs]; mean AUC: 598.8 +/- 451.1 AU x Cardiac cycles), and ROId (11.8 +/- 6.9; 559.2 +/- 404) as compared to ROIa (8.3 +/- 5.2; 368.9 +/- 242.7) and ROIb (7.1 +/- 4.7; 298.2 +/- 199.1) (P < .0001). Values for corresponding examinations with a diastolic ECG gating and a cardiac cycle triggering frequency of once every 2 seconds were not different as compared to the basical instrument setting. A 4 g Levovist dose increased the portion of typical TIC in all ROIs. PI of 4 g examinations were significantly higher in ROId and ROIb as compared to the 2 g examination. CONCLUSION: Our findings indicate that TRSHI allows noninvasive assessment of focal cerebral contrast enhancement in the majority of patients with adequate insonation conditions. This study provides data about normal quantitative and qualitative TRSHI values in patients without cerebrovascular diseases. A dose of 4 g Levovist is recommended in those individuals with inaccurate echo contrast enhancement using the 2 g dose.

Autonomic neurocardiac function in patients with major depression and effects of antidepressive treatment with nefazodone.

BACKGROUND: Major depression (MD) is associated with an augmented risk of cardiovascular mortality. One possible explanation for this association is that MD influences autonomic neurocardiac regulation (ANR). However, previous studies on this subject revealed conflicting results. METHODS: Using an autonomic test battery, which consisted of standardised measurements of heart rate variability (HRV) and blood pressure, we (1) compared ANR between 25 patients with DSM-III-R diagnosed MD and 60 healthy controls, and (2) investigated the autonomic effects of antidepressive treatment with nefazodone. RESULTS: Following multivariate analysis of all tests a significant reduction in HRV could only be shown for the Valsalva ratio amongst the depressives compared to controls. There was a significant inverse correlation between the HRV during deep respiration and both the severity of depression and the duration of the depressive episode. Serial HRV recordings revealed that both the mean resting heart rate and systolic blood pressure significantly decreased after 21 days of nefazodone treatment (average dosage 413 mg/day), whereas after 10 days (average dosage 270.8 mg/day) there were no striking changes compared to the pre-treatment values. During nefazodone treatment no significant changes in parasympathetic tone occurred. LIMITATIONS: ANR was not assessed in a randomised, placebo-controlled fashion. CONCLUSIONS: (1) Patients with MD may suffer from functional disturbances in the interaction between the sympathetic and parasympathetic autonomic tree. (2) The pattern of autonomic changes during treatment suggests that nefazodone induced a dose dependent, serotonergically-mediated down-regulation of the sympathetic tone. This mechanism might be responsible for nefazodone's properties of reducing anxiety.

Contrast agent specific imaging modes for the ultrasonic assessment of parenchymal cerebral echo contrast enhancement.

Previous work has demonstrated that cerebral echo contrast enhancement can be assessed by means of transcranial ultrasound using transient response second harmonic imaging (HI). The current study was designed to explore possible advantages of two new contrast agent specific imaging modes, contrast burst imaging (CBI) and time variance imaging (TVI), that are based on the detection of destruction or splitting of microbubbles caused by ultrasound in comparison with contrast harmonic imaging (CHI), which is a broadband phase-inversion-based implementation of HI. Nine healthy individuals with adequate acoustic temporal bone windows were included in the study. Contrast harmonic imaging, CBI, and TVI examinations were performed in an axial diencephalic plane of section after an intravenous bolus injection of 4 g galactose-based microbubble suspension in a concentration of 400 mg/mL. Using time-intensity curves, peak intensities and times-to peak-intensity (TPIs) were calculated off-line in anterior and posterior parts of the thalamus, in the region of the lentiform nucleus, and in the white matter. The potential of the different techniques to visualize cerebral contrast enhancement in different brain areas was compared. All techniques produced accurate cerebral contrast enhancement in the majority of investigated brain areas. Contrast harmonic imaging visualized signal increase in 28 of 36 regions of interest (ROIs). In comparison, TVI and CBI examinations were successful in 32 and 35 investigations, respectively. In CHI examinations, contrast enhancement was most difficult to visualize in posterior parts of the thalamus (6 of 9) and the lentiform nucleus (6 of 9). In TVI examinations, anterior parts of the thalamus showed signal increase in only 6 of 9 examinations. For all investigated imaging modes, PIs and TPIs in different ROIs did not differ significantly, except that TVI demonstrated significantly higher PIs in the lentiform nucleus as compared with the thalamus and the white matter (P < 0.05). The current study demonstrates for the first time that CBI and TVI represent new ultrasonic tools that allow noninvasive assessment of focal cerebral contrast enhancement and that CBI and TVI improve diagnostic sensitivity as compared with CHI.

Ultrasonic evaluation of pathological brain perfusion in acute stroke using second harmonic imaging.

OBJECTIVE: To evaluate the use of transient response second harmonic imaging (HI) by means of ultrasound to assess abnormalities of cerebral echo contrast agent enhancement in patients with acute stroke. METHODS: The study comprised 25 patients with acute onset of hemispheric stroke (<24 h) with sufficient insonation conditions and 14 control subjects without cerebrovascular disease. All stroke patients had HI, extracranial and transcranial colour coded duplex examinations of the arteries supplying the brain, and clinical examinations (European stroke scale) performed in the acute phase, on day 2, and within 1 week. Acute CT was repeated within 1 week and facultatively accompanied by angiography. Examinations using HI were performed in an axial diencephalic plane of section using the transtemporal acoustic bone window. After bolus application of galactose based microbubbles, 61 ultrasound images with a cardiac cycling triggering frequency of once every 2 seconds were recorded and evaluated off line. Focal perfusion deficit was identified if no contrast enhancement was visualised in a circumscribed region of interest and insufficient temporal bone window was excluded. In cases of reappearance of contrast enhancement reperfusion was assessed. RESULTS: Adequate cerebral contrast enhancement could be seen in 21 subjects. In seven, a large hemispheric deficit of contrast enhancement affecting the entire middle cerebral artery (MCA) territory was detectable; the lentiform nucleus was affected in three subjects. Assessment of cerebral contrast abnormalities was possible in two patients with superficial MCA infarctions but in none of the patients with lacunar ischaemias. None of the control persons had focal deficits of cerebral echo contrast enhancement. In all patients with complete MCA infarction and striatocapsular infarction, presumed ischaemic areas in HI examinations correlated with final CT findings. Overall sensitivity and specifity of HI examinations for predicting size and localisation of the infarction were 75 and 100%, respectively. During follow up, reappearance of contrast enhancement was determined in three patients, in two patients circulatory arrest due to malignant brain oedema with missing contrast enhancement in the entire cerebral hemisphere could be seen. Extent of contrast enhancement deficits significantly correlated with the clinical status on admission and after 1 week (p<0.01). CONCLUSIONS: Second harmonic imaging is the first ultrasonic technique that enables visualisation of pathological cerebral echo contrast enhancement. Because this method identifies deficits of focal contrast enhancement in patients with acute stroke and allows estimation of the final infarct size and clinical prognosis, it may help to select and monitor patients for invasive therapies.

DIAS I: duplex-sonographic assessment of the cerebrovascular status in acute stroke. A useful tool for future stroke trials.

BACKGROUND AND PURPOSE: A number of controlled trials have evaluated the benefit of intravenous thrombolysis in acute stroke with inconsistent results. None of these studies assessed the initial vascular status or provided information regarding the recanalization rate after therapy. Further trials need to clarify whether certain subgroups might possibly benefit more than others from intravenous thrombolysis. Therefore, a fast and valid method for assessment of cerebrovascular status is needed. In this multicenter study, we evaluated the potentials and limitations of color-coded duplex sonography (TCCS) for cerebrovascular status assessment in acute stroke patients before and after therapy. Furthermore, we compared the recanalization rate for patients referred to thrombolytic and conservative medical therapy. METHODS: Fifty-eight patients suffering from hemispheric stroke were enrolled consecutively in 8 centers. Duplex sonography was performed on admission, 2 hours after start of therapy, and 24 hours after onset of symptoms. Therapy was started within 6 hours. RESULTS: Intravenous thrombolysis was performed in 18 patients, conservative medical therapy in 39 patients, and early thromboendarterectomy in 1 patient. The middle cerebral artery (MCA) mainstem was patent in 29 patients (53.7%), occluded in 25 (46.3%), and was not assessable in 4 patients. Recanalization of the occluded MCA after 2 and 24 hours was diagnosed in 50% and 78% of the patients treated with rtPA and in 0% and 8% in the conservatively treated patients. CONCLUSIONS: Intravenous thrombolysis is highly effective in restoring blood flow after MCA occlusion. TCCS is suitable for assessment of the cerebrovascular status in acute stroke and therefore might define therapeutically relevant subgroups of patients in future stroke trials on the basis of their vascular pathology.

Acute brainstem symptoms associated with cervical syringomyelia.

Syringomyelia classically presents with slowly progressing dissociated sensory and upper and lower motor deficits. Atypical and acute manifestations have rarely been described. We report here on 3 patients with syringomyelia, who had acute and atypical brainstem symptoms with regard to the underlying disease. These symptoms occurred after acute elevation of the intrathoracic and intra-abdominal pressure, respectively, and remitted subsequently. Vertebrobasilar ischemia was initially suspected.

Basal ganglia alterations and brain atrophy in Huntington's disease depicted by transcranial real time sonography.

OBJECTIVES AND METHODS: Transcranial real time sonography (TCS) was applied to 49 patients with Huntington's disease and 39 control subjects to visualise alterations in the echotexture of the basal ganglia. For comparison T1 weighted, T2 weighted, and fast spin echo MRI was performed in 12 patients with Huntington's disease with and in nine patients without alterations of the basal ganglia echotexture as detected by TCS and T1 weighted, T2 weighted, and fast spin echo MRI. Furthermore, the widths of the frontal horns, third ventricle, and the lateral ventricles were depicted in TCS examinations and correlations examined with corresponding CT slices. RESULTS: Eighteen out of 45 (40%) of the patients with Huntington's disease with adequate insonation conditions showed hyperechogenic lesions of at least one basal ganglia region. In 12 patients TCS depicted hyperechogenic lesions of the substantia nigra; in six patients the head of the caudate nucleus was affected. The lentiform nucleus (n=3) and the thalamus (n=0) were less often affected or spared. Hyperechogenic lesions were significantly more frequent in patients with Huntington's disease than in 39 control subjects, who had alterations of the echotexture in 12.8% (4/39) of the examinations. The number of CAG repeats and the clinical status correlated with the identification of hyperechogenic lesions of the substantia nigra (p<0.01). Hyperechogenic lesions of the caudate nucleus were associated with an increased signal intensity in T2 weighted MR images (p<0.05). All TCS parameters indicating brain atrophy correlated with CT findings (p<0.0001). CONCLUSIONS: TCS detects primarily abnormalities of the caudate nucleus and substantia nigra in Huntington's disease. These changes in the echotexture may represent degenerative changes in the basal ganglia matrix and are partially associated with CAG repeat expansion and the severity of clinical findings.

Contrast-enhanced transcranial color-coded sonography in acute hemispheric brain infarction.

PURPOSE: The aim of the present study was to investigate the diagnostic potential of contrast-enhanced transcranial color-coded real-time sonography (CE-TCCS) in otherwise ultrasound-refractory acute stroke patients with an ischemia in the territory of the middle cerebral artery (MCA). Furthermore, correlations of CE-TCCS findings with clinical, angiographic, and CT results were investigated. METHODS: In 90 acute stroke patients with inadequate insonation conditions in unenhanced transcranial color-coded real-time sonography (TCCS) examinations, CE-TCCS, clinical, angiographic, and CT examinations were performed within 12 hours, 36 hours (CE-TCCS only), and 1 week after onset of clinical symptoms. A CT angiography (CTA) as reference method was available in 39 individuals. After application of a galactose-based echo-enhancing agent, the portion of conclusive ultrasound examinations of the MCA, as manifested by an MCA occlusion, decreased or increased flow velocity (FV), and symmetrical MCA FV, was evaluated. CE-TCCS findings on admission and during follow-up were correlated with infarction size as demonstrated on follow-up CT, and clinical findings were assessed by use of the European Stroke Scale. RESULTS: Adequate diagnosis was achieved in 74 of 90 patients (82%) by the use of echo contrast agents. MCA occlusion or reduction of MCA FV was found in 20 and 27 patients, respectively. MCA occlusion was confirmed by CTA in 17 cases. In one individual, false-positive diagnosis of MCA occlusion was made according to ultrasound criteria. In 5 patients with MCA occlusion, vessel recanalization was observed during follow-up; 15 of 27 patients with decreased flow velocities showed normalization after the third examination that was associated with a significantly better clinical outcome (P<0.0001). Furthermore, MCA occlusion or decreased FV in the first 12 hours were associated with significantly larger infarctions in the MCA territory compared with normal CE-TCCS findings (P<0.0001). CONCLUSIONS: CE-TCCS enables adequate diagnosis in approximately 80% of acute hemispheric stroke patients with insufficient unenhanced TCCS examinations. It is a reliable diagnostic tool regarding MCA mainstem and branch occlusions. Because this method conveys useful information concerning cerebral tissue and clinical prognosis, it may be useful to identify those patients who benefit most from local or intra-arterial thrombolytic therapy.

Second harmonic imaging In acute middle cerebral artery infarction. Preliminary results.

BACKGROUND: Second harmonic imaging (SHI) is a new ultrasound technique that is able to detect microbubbles in the tissue vascular space. The aim of this pilot study was to prove that this technique may detect focal abnormalities of cerebral echo-contrast enhancement in acute hemispheric stroke. CASE DESCRIPTIONS: Two male patients (aged 72 and 64 years) were included who presented with acute onset of severe hemiparesis and no established demarcation of the ischemic area in CT scans. After bolus application of galactose-based microbubbles, axial SHI examinations in a diencephalic plane of sections were performed using the transtemporal approach. Ultrasound investigations were recorded and evaluated offline. In both individuals demarcated focal abnormalities of cerebral contrast enhancement were detectable: in patient 1 the region of the lentiform nucleus and the adjacent parts of the temporoparietal lobe was affected, and in patient 2 a large region including the lentiform nucleus and cortical white matter was involved for at least 24 hours. Follow-up CT scans demonstrated a striatocapsular infarct in patient 1 and complete MCA infarction in patient 2, correlating with the presumed ischemic area in acute ultrasound examinations. The patient with complete MCA infarction showed missing contrast enhancement in the entire hemisphere of the affected side in follow-up SHI examinations. He died of malignant space-occupying brain edema. In the patient with the striatocapsular infarction, reappearance of echo-contrast enhancement in the ischemic area was assessable after 1 week. CONCLUSIONS: SHI may identify focal abnormalities of cerebral echo-contrast enhancement in acute hemispheric stroke. Furthermore, this technique helps to determine size, localization, and prognosis of the ischemic region and could be useful for bedside assessment of echo-contrast agent distribution related to brain tissue perfusion.

Serum levels of neuron-specific enolase and s-100 protein after single tonic-clonic seizures.

Serum neuron-specific enolase (s-NSE) and s-100 protein (s-100) are sensitive markers of various brain diseases. We investigated both of these markers in nine patients within 5 min, 6 h, 12 h, and 48 h after a single tonic-clonic seizure. The mean peak s-NSE level was significantly higher after 5 min (11.97 +/- 8.56 microg/l) and 48 h (10.31 +/- 8.92 microg/l, P < 0.05) than the levels of seizure-free, age-matched controls. Five patients had increased s-NSE levels regarding the upper limit of normal as mean + 3 SD. s-100 was not detected either in controls or epileptic patients. These data indicate that s-NSE in contrast to s-100 may be an in vivo marker after generalized seizures in some patients.