Post stroke sleep apnea hypopnea syndrome: a series of 12 consecutive stable stroke cases.

OBJECTIVES: Sleep Disordered Breathing (SDB) is a negative prognostic factor for stroke patients. In order to reveal: (1) the frequency of Sleep Apnea-Hypopnea Syndrome (SAHS) in the stable phase of the illness; (2) the type of SAHS, either obstructive (OSAHS) or central (CSAHS); (3) the possible association between SAHS and daily sleepiness, cardiac arrhythmias, stroke / TIA recurrence and location of the brain lesion, an observational study is on-going at Sapienza University of Rome. We report here the results of cases included in the feasibility study. PATIENTS AND METHODS: clinical evaluations, brain images and polisomnographic study were performed at discharge and after 4 and 9 months of stroke. RESULTS: Eleven out of the 12 patients included (91.6%) had an Apnea/Hypopnea Index-AHI >= 5. In 5 cases, the majority of total respiratory events were purely central in origin. In 3 of these 5 cases, a concomitant obstruction of the upper airways was revealed; the 2 remaining had risk factors for OSAHS (smoke, hypertension, BMI > 25). A significant association was found between central apnea/hypopnea events and cardiac arrhythmias (p value 0.017). CONCLUSIONS: These findings confirm the high prevalence of SDB, either obstructive or/and central, even in the stable phase of the illness, which in those patients who had accumulated risk factors for OSAHS result in Complex-sleep apnea/hypopnea syndrome (CompSAHS). As patients with CompSAHS are left with very disrupted breathing on continuous positive airway pressure, in order to select cases with stable stroke who benefit from continuos-positive airway pressure (C-PAP) treatment, further and more detailed clinical studies are needed to better distinguish CompSAHS from mixed SAHS.

Embolism to the brain during carotid stenting and surgery.

UNLABELLED: The aim of this study was to assess the prevalence and clinical relevance of microembolism in one hundred unselected patients submitted to 50 carotid endarterectomy (CEA) and 50 carotid stenting (CAS) procedures from January 2005 to January 2006 for hemodynamic lesions of the carotid bifurcation (> 70% stenosis). MATERIAL AND METHODS: High-resolution Colour-Flow Mapping (CFM), Transcranial Doppler (TCD), cerebral computed tomography (CT) or magnetic resonance (MR) and four psychometric tests (Mini mental state, Beck depression inventory, Zung anxiety inventory, SF-12) were carried out in the preoperative evaluation in all the patients. In the CEAs loco-regional anesthesia (100%), patch angioplasty (84%) and Pruitt- Inahara shunt (4%) were employed; in the CASs local anesthesia (100%), three different carotid stents (Precise-Cordis, Acculink-Guidant and Carotid Wallstent-Boston Scientific) and three temporary distal filter protection devices (Angioguard-Cordis, Accunet-Guidant, Filterwire-EZ- Boston Scientific), without pre-dilatation, were employed. TCD monitoring was used intra-operatively and 12 hours post-operatively to evaluate the presence and the number of microembolic events (ME's) and to investigate the efficiency of neuroprotective filter devices. The efficacy of the in situ opened filter was judged evaluating the decrease of mean blood velocity in ipsilateral middle cerebral artery and the reduction rate of microembolic events (number of microemboli detected during the entire procedure/number of microemboli detected during the filter positioning). Diffusion-weighted magnetic resonance imaging (DWI) of the brain was obtained within 24 to 48 hours after the procedures to detect new ischemic brain lesions. Psychometric tests were repeated at the discharge of the patient and after two months to evaluate cognitive faculties. RESULTS: During postoperative period (30 days) and follow-up, no procedure-related death and three regressive minor strokes occurred : 1 in CEA (2%) and 2 in CASs (4%) ; a cranial nerve lesion occurred in CEA (2%). TCD monitoring showed ME's (a mean of five events) in 37 CEAs (74%) and in 50 CASs (100%) (a mean of 60 ME's). In five patients submitted to CAS repeated microemboli occurred during one hour postoperative TCD control (10%). A 10-30% decrease of mean blood velocity basal value was recorded in the ipsilateral middle cerebral artery when the filter device was opened. A mean 70% reduction of ME's was obtained with a cerebral protection system deployed. Postoperative DWI detected new focal ischemic lesions in 24 patients [22 after CAS (44%) (a mean of 5 new ipsi and contra-lateral lesions) , and 2 after CEA (4%). Cognitive capability worsened in 20 patients [18 after CAS (36%) e 2 after CEA (4%)]. CONCLUSIONS: Mortality and morbidity rates of patients submitted to CAS are comparable to the results obtained by CEA. A great number of ME's are recorded by TCD during endovascular procedures, more than during open surgery. ME's due to CAS are reduced by filter protection devices, but the cognitive faculties in a great number of "asymptomatic" patients are decreased after CAS.

Resting state functional thalamic connectivity abnormalities in patients with post-stroke sleep apnoea: a pilot case-control study.

OBJECTIVE: Sleep apnoea is common after stroke, and has adverse effects on the clinical outcome of affected cases. Its pathophysiological mechanisms are only partially known. Increases in brain connectivity after stroke might influence networks involved in arousal modulation and breathing control. The aim of this study was to investigate the resting state functional MRI thalamic hyper-connectivity of stroke patients affected by sleep apnoea (SA) with respect to cases not affected, and to healthy controls (HC). PATIENTS AND METHODS: A series of stabilized strokes were submitted to 3T resting state functional MRI imaging and full polysomnography. The ventral-posterior-lateral thalamic nucleus was used as seed. RESULTS: At the between groups comparison analysis, in SA cases versus HC, the regions significantly hyper-connected with the seed were those encoding noxious threats (frontal eye field, somatosensory association, secondary visual cortices). Comparisons between SA cases versus those without SA revealed in the former group significantly increased connectivity with regions modulating the response to stimuli independently to their potentiality of threat (prefrontal, primary and somatosensory association, superolateral and medial-inferior temporal, associative and secondary occipital ones). Further significantly functionally hyper-connections were documented with regions involved also in the modulation of breathing during sleep (pons, midbrain, cerebellum, posterior cingulate cortices), and in the modulation of breathing response to chemical variations (anterior, posterior and para-hippocampal cingulate cortices). CONCLUSIONS: Our preliminary data support the presence of functional hyper connectivity in thalamic circuits modulating sensorial stimuli, in patients with post-stroke sleep apnoea, possibly influencing both their arousal ability and breathing modulation during sleep.

Differential Influence of Carotid Stenosis and White Matter Disease on Motor and Cognitive Activation.

BACKGROUND: Cognitive and motor performance can be supported, especially in older subjects, by different types of brain activations, which can be accurately studied by functional magnetic resonance imaging (fMRI). Vascular risk factors (VRFs) are extremely important in the development of cognitive impairment, but few studies have focused on the fMRI cortical activation characteristics of healthy subjects with and without silent cerebrovascular disease including white matter hyperintensities (WMH) and carotid stenosis (CS) performing cognitive tasks. METHODS: Thirty-five volunteers with and without asymptomatic unilateral carotid stenosis above 70% and variable degrees of WMH underwent performance of a simple motor and cognitive task during an fMRI session. RESULTS: While the performance of the motor task resulted in a cortical activation dependent of age but not of WMH and carotid stenosis, performance of the cognitive task was accompanied by a significantly increased activation independently correlated with age, presence of WMH as well as of carotid stenosis. CONCLUSIONS: in this study, cognitive domains regulating attention and working memory appear to be activated with a pattern influenced by the presence of carotid stenosis as well as by white matter hyperintensities. The impairment of these cognitive abilities is of high relevance in Alzheimer's disease pathology. The fMRI pattern shown in patients with asymptomatic but significant carotid stenosis might be related to chronic cerebrovascular hypoperfusion, a critical pathophysiological mechanisms in AD. In these patients, carotid endoarterectomy should be considered also for AD prevention and might be recommended.

Morphological and functional characteristics of patent foramen ovale and their embolic implications.

BACKGROUND AND PURPOSE: Transesophageal echocardiography (TEE) has detected a high prevalence of patent foramen ovale (PFO) in stroke patients, but the clinical implications of the distinctive characteristics of this patency are still a matter of debate. METHODS: We studied 350 patients with acute ischemic stroke or transient ischemic attack (TIA) within 1 week of admission. Of these, 101 (29%) were identified by contrast TEE to have a PFO; 86 patients (25%) were cryptogenic stroke patients, and 163 were excluded because of the presence of a definite or possible arterial or clinical evidence of a source of emboli or small-vessel disease. Thirteen PFO subjects without a history of embolism were designated as the control group. All PFO and cryptogenic stroke patients were followed up by neurological visits. RESULTS: Compared with controls, PFO patients with acute stroke or TIA more frequently presented with a right-to-left shunt at rest and a higher membrane mobility (P:<0. 05). Patients with these characteristics were considered to be at high risk. During a median follow-up period of 31 months (range, 4 to 58 months), 8 PFO and 18 cryptogenic stroke patients experienced recurrent cerebrovascular events. The cumulative estimate of risk of cerebrovascular event recurrence at 3 years was 4.3% (95% confidence interval [CI], 0% to 10.2%) for "low-risk" PFO patients, 12.5% (95% CI, 0% to 26.1%) for "high-risk" PFO patients, and 16.3% (95% CI, 7. 2% to 25.4%) for cryptogenic stroke patients (high-risk PFO versus low-risk PFO, P:=0.05). CONCLUSIONS: The association of right-to-left shunting at rest and high membrane mobility, as detected by contrast TEE, seems to identify PFO patients with cerebrovascular ischemic events who are at higher risk for recurrent brain embolism.

Hemorrhagic transformation of ischemic brain tissue: asymptomatic or symptomatic?

BACKGROUND AND PURPOSE: The term symptomatic hemorrhage secondary to ischemic stroke implies a clear causal relationship between clinical deterioration and hemorrhagic transformation (HT) regardless of the type of HT. The aim of this study was to assess which type of HT independently affects clinical outcome. METHODS: We used the data set of the European Cooperative Acute Stroke Study (ECASS) II for a post hoc analysis. All patients had a control CT scan after 24 to 96 hours or earlier in case of rapid and severe clinical deterioration. HT was categorized according to radiological criteria: hemorrhagic infarction type 1 and type 2 and parenchymal hematoma type 1 and type 2. The clinical course was prospectively documented with the National Institutes of Health Stroke Scale and the modified Rankin Scale: The independent risk of each type of HT was calculated for clinical deterioration at 24 hours and disability and death at 3 months after stroke onset and adjusted for possible confounding factors such as age, severity of stroke syndrome at baseline, and extent of the ischemic lesion on the initial CT. RESULTS: Compared with absence of HT, only parenchymal hematoma type 2 was associated with an increased risk for deterioration at 24 hours after stroke onset (adjusted odds ratio, 18; 95% CI, 6 to 56) and for death at 3 months (adjusted odds ratio, 11; 95% CI, 3.7 to 36). All other types of HT did not independently increase the risk of late deterioration. CONCLUSIONS: Only parenchymal hematoma type 2 independently causes clinical deterioration and impairs prognosis. It has a distinct radiological feature: it is a dense homogeneous hematoma >30% of the ischemic lesion volume with significant space-occupying effect.

PET study of changes in local brain hemodynamics and oxygen metabolism after unilateral middle cerebral artery occlusion in baboons.

Local cerebral hemodynamics and oxygen metabolism were measured by positron emission tomography (PET) with the oxygen-15 (15O) steady-state method in baboons, immediately before (T0), 1 (T1), and 3-4 (T2) h after permanent middle cerebral artery occlusion (MCAO). At T1, there was a marked fall in both cerebral blood flow (CBF) and the CBF/cerebral blood volume (CBV) ratio in the occluded territory; these changes were sustained at T2, indicating stable reduction in cerebral perfusion pressure and lack of spontaneous reperfusion within this time range. Compared with preocclusion conditions, the oxygen extraction fraction (OEF) in the occluded territory was elevated at both T1 and T2, indicative of a persistent oligemia/ischemia for up to 3 h after MCAO. At T2, however, this OEF increase had lessened, concomitantly with a decline in cerebral metabolic rate of oxygen (CMRO2). This impairment of oxidative metabolism occurred earlier in the deep, compared with the cortical, MCA territories; in the latter, the CMRO2 was essentially preserved at T1 and only moderately reduced at T2, possibly suggesting prolonged viability. Finally, no significant changes in CBF or CMRO2 were observed in the contralateral MCA territory in this time range after MCAO. Despite methodological limitations (mainly partial volume effects related to PET imaging, which may have resulted in an underestimation of true changes and an overlooking of heterogeneous changes) our study demonstrates the feasibility of the combined PET-MCAO paradigm in baboons; this experimental approach should be valuable in investigating the pathophysiology and therapy of acute stroke.

Prediction of long-term outcome in the early hours following acute ischemic stroke. Italian Acute Stroke Study Group.

OBJECTIVE: To develop a model for predicting outcome in the first few hours after the onset of an ischemic stroke on the basis of the clinical findings obtained during a rapid bedside examination. DESIGN: Clinical records were retrieved from the data bank of a randomized multicenter trial. The resulting case series was split into two subgroups that served as a "training set" and a "test set." Logistic regression was applied to the training set to select the prognostic predictors among baseline clinical findings. The performances of the model based on independent prognostic predictors were then validated in the test set. SETTING: Eleven primary care institutions (either hospitals or university clinics) participating in the Italian Acute Stroke Study on the efficacy of hemodilution and monosialoganglioside in acute ischemic stroke. PATIENTS: Consecutive noncomatose patients (N = 300) observed within the first 6 hours after the onset of a first supratentorial ischemic stroke. MAIN OUTCOME MEASURE: Death or disablement 4 months after the index stroke. Disablement was defined as a score of 3 or higher on the Rankin Scale. RESULTS: Age and CNS score defined six risk groups with a predicted 4-month poor outcome rate ranging from 10% (patients aged 70 years or younger and with an initial CNS score of 7 or higher) to 89% (patients older than 70 years and with a CNS score of 4.5 or lower). When a risk of poor outcome of 60% was taken as a cutoff, the accuracy of the prediction was 78% +/- 6% in the training set and 72% +/- 9% in the test set. CONCLUSION: Long-term outcome can be predicted in the first few hours following an acute ischemic stroke by means of a simple model based on age and CNS score.

Progressing neurological deficit secondary to acute ischemic stroke. A study on predictability, pathogenesis, and prognosis.

OBJECTIVES: To identify predictors and possible pathogenetic mechanisms of early neurological deterioration in patients with acute ischemic strokes and to evaluate their impact on clinical outcome. DESIGN: Case series. SETTING: University hospital's stroke unit. PATIENTS: A continuous series of 152 patients with first-ever ischemic hemispheric strokes were hospitalized within 5 hours of onset, evaluated with the Canadian Neurological Scale, and underwent a computed tomographic (CT) scan. The initial subset of 80 patients also underwent angiography. A repeated CT scan or autopsy was performed within 5 to 9 days of a patient's stroke. Progressing neurological deficit was defined as a decrease of one point or more in the global neurological scale score during hospitalization, when compared with that at entry. RESULTS: The conditions of 39 patients (26%) deteriorated during the initial 4 days; 20 patients (51%) had an impaired level of consciousness, and 19 patients (49%) had impaired limb strength and/or speech. They had been hospitalized earlier and had higher serum glucose levels at admission; the baseline CT scans of these patients showed an early focal hypodensity and initial mass effect more frequently. On the repeated CT scan (144 patients) or at autopsy (eight patients), patients with a progressing course more frequently had large infarcts, severe mass effect, and hemorrhagic infarction. We found no differences with regard to demographic data, medical history, and treatments that were given; only subcutaneous heparin calcium was more frequently administered to patients with a progressing course. Twenty-two (27%) of the 80 patients who underwent angiography had a progressing course, of whom 20 (91%) had an intracranial and/or extracranial arterial occlusion, with collateral blood supply in seven patients (35%). Logistic regression analysis showed that the independent predictors of progression were the serum glucose levels at admission and the early focal hypodensity with cortical and corticosubcortical locations, with the positive predictive values of the latter being 34% (95% confidence interval [CI], 26% to 42%) and 57% (95% CI, 47% to 67%), respectively. Among patients who underwent angiography, logistic regression analysis showed a significant correlation between carotid siphon occlusion and a progressing course. The 30-day case-fatality ratio and disability (Barthel index, < 60) were higher in patients with a progressing course (36% and 54% vs 12% and 35%, respectively). CONCLUSIONS: Early stroke deterioration is still an event that is difficult to predict; it is largely determined by cerebral edema following an arterial occlusion, as indicated by an early focal hypodensity and initial mass effect on the baseline CT scan. Since early deterioration anticipates a bad outcome in 90% of patients, it might be used as an early surrogate end point in therapeutic trials.

Decreased cerebral glucose utilization in myotonic dystrophy.

To test the hypothesis that cerebral metabolism is altered in myotonic dystrophy (MyD), we investigated cerebral glucose kinetics and utilization in 11 adult patients with MyD and 14 healthy controls, using 18F-labeled 2-fluoro-2-deoxy-D-glucose (FDG) and dynamic positron emission tomography. Estimation of rate constants in MyD revealed a reduction of FDG delivery to the brain. Cortical glucose utilization rate was reduced by about 20% in MyD. These findings may be related to the presence of neurologic impairment in MyD and prompt further investigations on the metabolic and clinical features of brain dysfunction in this disease.

Natural history of cardiac involvement in myotonic dystrophy: correlation with CTG repeats.

The authors prospectively studied the natural course of cardiac involvement and its relationship to cytosine-thymine-guanine (CTG) expansion in 50 patients with myotonic dystrophy who were submitted to periodic cardiovascular EKG and EKG-Holter monitoring during a median follow-up of 56 months. Nineteen patients (38%) developed major EKG changes. CTG length was not correlated with the frequency of EKG abnormalities, but was inversely correlated with the age at onset of EKG abnormalities (p < 0.0001). CTG length influences the timing of cardiac complications in myotonic dystrophy.

Early neurologic complications following allogeneic bone marrow transplant for leukemia: a prospective study.

BACKGROUND: Bone marrow transplant (BMT) is used for both neoplastic and nonneoplastic diseases. Following BMT, particularly during the first 3 months, patients have a number of neurologic complications. We evaluated the early neurologic complications following BMT and their influence on survival. METHODS: We prospectively followed 115 consecutive patients having BMT for leukemia, for a median period of 90 days after transplantation. RESULTS: Sixty-four patients (56%) had neurologic complications. Sixteen developed more than one complication. Twenty-seven patients (25%) had major neurologic complications: metabolic encephalopathy (8), seizures (8), psychiatric symptoms (3), cerebral hemorrhage (1), cerebral abscess (1), leukemic meningitis (1), peripheral neuropathies (5), and myopathies (2). Forty patients (35%) had minor complications, including headache (16) and tremor (31). Major neurologic complications occurred after engraftment in most patients. Metabolic encephalopathy correlated with graft-versus-host disease (GVHD) (p < 0.03). Seven percent of patients had generalized seizures that occurred without signs of structural cerebral lesions. Probability of survival at day 90 was lower in patients with than in those without major central nervous system complications (63% versus 87.5%, p < 0.01). CONCLUSIONS: Neurologic complications are frequent during the first 3 months following BMT and affect patient survival. Drug neurotoxicity and acute GVHD are the main factors influencing their occurrence.

Hemorrhagic transformation of brain infarct: predictability in the first 5 hours from stroke onset and influence on clinical outcome.

OBJECTIVE: To identify, in the first 5 hours of acute brain infarct, clinical and radiologic predictors of subsequent hemorrhagic transformation (HT), and to evaluate its influence on the clinical course. BACKGROUND: The identification of early predictors of HT might be important to plan antithrombotic or thrombolytic treatments. PATIENTS: One hundred fifty consecutive patients with cerebral anterior circulation infarct systematically underwent a first CT within 5 hours of onset. During the first week after stroke, we performed a repeat CT or autopsy to look for HT. Outcome measures were early neurologic deterioration within the first week of onset and 30-day case fatality rate and disability. RESULTS: HT was observed in 65 patients (43%): 58 (89%) had a petechial HT and seven (11%) a hematoma. Among initial clinical an CT findings, the only independent predictor of HT was early focal hypodensity. Its presence was associated with subsequent HT in 77% of cases (95% CI, 68 to 86%), whereas its absence predicted the absence of subsequent HT in 94% of cases (95% CI, 89 to 99%). No baseline clinical or CT characteristic differentiated patients with petechial HT from those with hematoma. Antithrombotic and antiplatelet agents did not influence the occurrence of either type of HT. The frequency of early neurologic deterioration and of 30-day death or disability in HT patients was twice as high as in those without HT. However, a large-sized infarct and the presence of mass effect at the repeat CT or autopsy were the only factors independently linked to both the outcome events, irrespective of the development of HT. Clinical evolution of HT patients given antithrombotics was comparable with that of HT patients not receiving these drugs. CONCLUSIONS: HT of a brain infarct is a common event that occurs independently of anticoagulation and can be reliably predicted as early as 5 hours from stroke onset by the presence of focal hypodensity at CT. Apart from the infrequent cases of massive hematoma, HT does not influence prognosis, whereas a poor outcome in HT patients is correlated with a higher frequency of large edematous infarcts in this subgroup. The clinical course and final outcome of HT in anticoagulated patients does not differ from that of non-anticoagulated HT patients.

Right motor neglect associated with dynamic aphasia, loss of drive and amnesia: case report and cerebral blood flow study.

A 30-year-old right-handed man had right motor neglect, amnesia, aphasia and loss of drive following bilateral thalamic and subthalamic infarctions. Serial resting cerebral blood flow (CBF) measurements with either Xenon 133 inhalation or positron emission tomography at 1, 8 and 10 months post-onset showed a widespread and long-lasting low CBF in the cortex. An additional CBF measurement, during motor tasks, showed a marked interhemispheric asymmetry in the pattern of activation: whereas left hand movement resulted in a CBF increase in contralateral superior rolandic and prerolandic areas, no significant regional CBF changes were seen during right hand movement, despite recovery from motor neglect. This loss of CBF increase in cortical motor and premotor areas during voluntary movement of the previously neglected side points to a disruption of cortico-subcortical pathways subserving motor activation. The pathophysiology of aphasia, loss of drive and amnesia as well as their relationships to motor neglect, may also be discussed on the basis of thalamo-cortical disconnections.

Impaired cerebral glucose metabolism in myotonic dystrophy: a triplet-size dependent phenomenon.

Myotonic dystrophy (DM) is caused by an expansion of a CTG triplet repeat sequence in the 3'-noncoding region of a protein kinase gene, yet the mechanism by which the triplet repeat expansion causes disease remains unknown. Impaired glucose penetration into brain tissues has been described in DM patients and is a phenomenon that remains unexplained. The present study shows that altered brain glucose metabolism is triplet repeat dependent. We studied brain glucose metabolism (CMRGlu, mumol/100 g/min) by the use of positron emission tomography and 18F-fluoro-2-deoxy-D-glucose in 11 ambulatory non-obese DM patients and in 11 age and sex matched healthy subjects. All subjects underwent a glucose tolerance test with plasma insulin determinations. The expansion of CTG triplet repeats was analyzed in patients with the probe cDNA25 after EcoRI digestion. As compared to controls, in DM patients, the CMRGlu was significantly decreased (26.26 +/- 5.05 vs. 33.43 +/- 2.18, mumol/100 g/min, P = 0.004), and after oral glucose loading, plasma insulin levels were significantly higher and plasma glucose levels remained unchanged (respectively, F = 11.21, P = 0.004 and F = 0.20, P = 0.66). Subsequently, the glucose/insulin ratio was significantly lower in DM patients (F = 6.25, P = 0.02). The length of the expansion of the CTG repeats correlated negatively with the CMRGlu (r2 = 0.63, P = 0.003) and positively with the area under the curve for insulin changes over time after oral glucose (r2 = 0.49, P = 0.016). We conclude that, in DM patients, the brain metabolism of glucose is impaired in a repeat dependent manner.

Patent foramen ovale and its embolic implications.

This study investigates the usefulness of the echocardiographic characteristics of patent foramen ovale (PFO) in the stratification of stroke recurrence risk in patients with acute ischemic cerebral disease. Shunting at rest and a highly mobile fossa ovalis membrane are more frequently detected in stroke patients with PFO as the only identifiable cause of embolism. For PFO patients with both rest patency and membrane mobility > 6.5 mm, the risk of stroke/transient ischemic attack recurrence was 7.6% (95% CI, 0-18.0) at 12 months and 12.5% (95% CI, 0-26.1) at 24 months (p = 0.05). The association of both rest patency and high membrane mobility seems to identify those stroke patients with PFO at higher risk for further brain embolism.

Role of transthoracic and transesophageal echocardiography in predicting embolic events in patients with active infective endocarditis involving native cardiac valves.

Some studies describe an increased risk for emboli in infective endocarditis patients with large (>10 mm) and mobile vegetations. Other studies fail to demonstrate the above relation. Most studies have been performed using transthoracic echocardiography or with a monoplane transesophageal approach. The present study examines whether distinctive characteristics of vegetative lesions detected by transthoracic and multiplane transesophageal echocardiography are predictive of embolic risk. We reviewed both transthoracic and transesophageal echocardiograms of 57 patients with diagnosis of acute infective endocarditis and no documented or suspected previous embolic events. We evaluated site, length, width, mobility, and echodensity of vegetations. Twenty-five patients (44%) had embolic events. No statistical differences in age, sex distribution, location of endocarditis, or offending pathogens between embolic (n = 25) and nonembolic (n = 32) patients were found. There were no differences in any of the echo characteristics of vegetations detected by transthoracic and transesophageal approach in embolic and nonembolic groups. Thus, transthoracic and transesophageal characteristics of vegetations are not helpful in defining embolic risk in patients with infective endocarditis.

Relationship between vascular enhancement, cerebral hemodynamics, and MR angiography in cases of acute stroke.

BACKGROUND AND PURPOSE: The use of MR angiography and contrast-enhanced T1-weighted MR imaging in cases of acute cerebral ischemia may be helpful in the evaluation of middle cerebral artery (MCA) occlusion and leptomeningeal collaterals, respectively. The aim of our work was to investigate the relationship between MCA occlusion, T1-weighted vascular contrast enhancement, hemodynamic alterations, and tissue damage in cases of acute ischemic stroke. METHODS: We studied the MCA territory in 15 patients with acute ischemic stroke within 8 hr of symptom onset. The first MR imaging study (<8 hr after onset) comprised diffusion-weighted imaging, MR angiography, perfusion-weighted imaging, and contrast-enhanced T1-weighted MR imaging sequences. Follow-up MR imaging, performed 1 week later, consisted of MR angiography and T2-weighted fluid-attenuated inversion recovery MR imaging. RESULTS: Early MR angiography showed MCA stem occlusion in nine of 15 patients. Patients with MCA occlusion had significantly larger areas of abnormality on early diffusion-weighted images, significantly larger areas of altered hemodynamics, larger final lesion volumes, and poorer clinical outcome. Among the nine patients with MCA stem occlusion, vascular enhancement was marked in seven and absent in two who had complete MCA infarcts and poor clinical outcome. Among patients with MCA patency, vascular enhancement was marked in only one, mild in four, and absent in one. Patients with marked vascular enhancement had significantly larger regions of altered hemodynamics and significantly higher asymmetries in both regional cerebral blood volume and mean transit time because of increased values in the affected hemisphere. CONCLUSION: Among patients with stroke with MCA occlusion, marked vascular enhancement and increased blood volume indicate efficient leptomeningeal collaterals and compensatory hemodynamic mechanisms.

Fast spin-echo and fast fluid-attenuated inversion-recovery versus conventional spin-echo sequences for MR quantification of multiple sclerosis lesions.

PURPOSE: To compare fast spin-echo (FSE) and fast fluid-attenuated inversion recovery (FLAIR) sequences with conventional spin-echo (CSE) MR imaging in the quantification of the number and volume of multiple sclerosis lesions. METHODS: In 30 patients with relapsing-remitting multiple sclerosis, we calculated the total number and volume of lesions detected with each of the three sequences using a semiautomated program. RESULTS: On CSE sequences, we calculated a total of 2,583 lesions with a global volume of 836.3 cm3. With FSE sequences, we observed a 16% relative reduction in the number of lesions detected and a 25% relative reduction in global volume as compared with CSE. With fast FLAIR sequences, we detected a significantly lower number and volume of infratentorial lesions, whereas at the cortical/subcortical level the lesions were both more numerous and bulkier than on CSE sequences. Finally, we observed a higher lesion/white matter contrast, a significant reduction in time required for the quantification of lesion load, and a very low interobserver variability in favor of fast FLAIR sequences. CONCLUSION: Despite its limitations in the detection of infratentorial lesions, the fast FLAIR sequence in conjunction with a semiautomated quantification program provides a reliable means to evaluate the total lesion burden in patients with MS.