A case of combat-related scorpion envenomation in Afghanistan

We report a case of scorpion envenomation occurring during combat in Tagab district, province of Kapisa, Afghanistan. A French soldier was stung by a yellow scorpion (suspected Androctonus australis) and sustained systemic envenomation with hemodynamic and neurological manifestations. We discuss the clinical features, prevention, and management of a scorpion sting.     

Thrombotic thrombocytopenic purpura: MRI demonstration of persistent small cerebral infarcts after clinical recovery

Abnormalities in the brain of patients with thrombotic thrombocytopenic purpura (TTP) are infrequent on MRI, often reversible and mainly limited to symptomatic stages of the disease. We report a case in which high-resolution MRI demonstrated multiple persistent small cortical infarcts after clinical remission. High-resolution MRI investigations may detect clinically latent but permanent brain damage, and complement clinical judgement in guiding therapeutic decisions. Received: 24 September 1999 Accepted: 20 October 1999     

Remote regional cerebral blood flow consequences of focused infarcts of the medulla, pons and cerebellum.

The aim of this study was to evaluate regional and remote diaschisis of inferior brain stem or cerebellar infarcts in 25 patients presenting with relatively limited lesions. Patients presented with medullary, pontine or cerebellar infarction. METHODS: Lesions were evaluated on MRI (0.5 T). Regional cerebral blood flow (rCBF) was assessed by means of SPECT, after injection of 9rmTc-hexamethyl propyleneamine oxime (HMPAO) and, when possible, inhalation of 133Xe in the same session. For each method, asymmetry indices (Als), comparing contralateral to ipsilateral rCBF values, were calculated in four areas of each cerebral hemisphere and in the cerebellum and later compared with values obtained in healthy subjects (P = 0.05). RESULTS: Higher rCBF values were observed in the contralateral cerebellum in 2 of 7 patients with selective lateral medullary lesions, and cerebellar Als were significantly increased. When a cerebellar infarct was associated with a lateral medullary lesion, the cerebellar and contralateral hemispheric asymmetries were more severe. Unilateral paramedian pontine infarcts had more frequent consequences on the cerebellum (2 of 3 cases), with rCBF or tracer uptake being reduced in the ipsilateral or the contralateral lobe. Inverse cerebral hemispheric asymmetry could then be observed. Bilateral pontine lesions were difficult to evaluate. Using 99mTc-HMPAO, discrete cerebellar asymmetry was observed in 3 of 6 cases. Pure cerebellar infarcts in the posterior inferior cerebellar artery territory were always associated with a severe ipsilateral flow drop in the cerebellum, and contralateral hemispheric diaschisis was frequent (3 of 4 patients), predominating in the frontotemporal cortex and subcortical structures. This was also more obvious using 99mTC-HMPAO than 133Xe. Variance analysis showed that hemispheric diaschisis was more severe in mixed brain stem and cerebellar infarcts than in pure cerebellar or brain stem lesions. Furthermore, cerebellar and hemispheric AI values were not correlated with measurements of clinical deficits, disability or handicap. CONCLUSION: Unilateral and limited inferior brain stem lesions can have ipsi- or contralateral consequences on the cerebellum and cerebral hemispheres rCBF. These remote effects are related to lesions of the main pathways joining these structures, resulting in deactivation and, in some cases, overactivation. Contrary to what has been suggested, consequences on cerebral hemispheres are more severe in mixed cerebellar and brain stem infarcts than in pure cerebellar lesions.     

Scorpion-sting induced unilateral pulmonary edema

Unilateral presentation of pulmonary edema, though well documented in the medical literature, is an uncommon entity. Pulmonary edema due to scorpion sting is common but its unilateral presentation is rare. We report a case of unilateral pulmonary edema following a one-hour onset of scorpion envenoming. The patient was symptomatically treated at the intensive care unit and discharged the following day in a good condition to the medical ward. Medical and interventional causes of unilateral pulmonary edema are discussed in this paper along with the pathophysiology of bilateral and unilateral pulmonary edema caused by scorpion envenomation.     

Imaging findings in intracranial aspergillosis

RATIONALE AND OBJECTIVES: The authors' purpose was to elucidate the various computed tomographic (CT) and magnetic resonance (MR) imaging findings in intracranial aspergillosis. MATERIALS AND METHODS: Retrospective analysis of cranial imaging findings was performed in eight proved cases of central nervous system aspergillosis. The patients ranged in age from 17 to 75 years. Four patients were immunocompromised, and four were immunocompetent. CT was performed in all eight patients, and MR imaging in five. RESULTS: Six patients (75%) had multiple lesions seen on the imaging studies, with a total of 27 focal brain lesions demonstrated. The lesions were most commonly seen in the cerebral hemispheres (n = 21), with lesser involvement of the basal ganglia (n = 2) and the posterior fossa (n = 4). Seven lesions were hemorrhagic on CT and/or MR images. There was a correlation between lesion size and hemorrhage, with hemorrhage more likely in larger lesions (>15 mm). At pathologic examination, foci of hemorrhage were noted within both infarcts and abscesses. Enhancement was noted in five lesions, four of which were confirmed abscesses. Contrast enhancement of the lesions was vague and week in immunocompromised patients but solid and strong in immunocompetent patients. There were 18 lesions without hemorrhage or enhancement; they were either infarcts or abscesses at pathologic examination. Some of these small nonhemorrhagic nonenhancing brain lesions in the subcortical white matter mimicked lacunar infarcts. CONCLUSION: Typical imaging findings of intracranial aspergillosis include multifocal lesions involving the cerebral hemispheres, with hemorrhage in approximately 25% of lesions. Lesional contrast enhancement tends to be stronger in immunocompetent hosts.     

Brain MRI Findings of Carbon Disulfide Poisoning

Objective

To evaluate the findings of brain MRI in patients with carbon disulfide poisoning.

Materials and Methods

Ninety-one patients who had suffered carbon disulfide poisoning [male:female=87:4; age, 32-74 (mean 53.3) years] were included in this study. To determine the extent of white matter hyperintensity (Grade 0-V) and lacunar infarction, T2-weighted MR imaging of the brain was performed.

Results

T2-weighted images depicted white matter hyperintensity in 70 patients (76.9%) and lacunar infarcts in 27 (29.7%).

Conclusion

In these patients, the prevalent findings at T2-weighted MR imaging of the brain were white matter hyperintensity and lacunar infarcts. Disturbance of the cardiovascular system by carbon disulfide might account for these results.     

颈动脉狭窄与眩晕症状的初步分析

目的 探讨眩晕与颈动脉狭窄之间的联系。方法 17例经手术或DSA证实的颈动脉重度狭窄病例。临床表现为大脑半球供血不足症状10例，反复发作性眩晕7例，其中4例眩晕为惟一或主要临床症状，手术解除狭窄后症状消失或减轻。17例均首先行颈部血管多普勒超声(DUS)，然后行颈部血管磁共振血流成像(MRA)及头部CT或MRI检查，其中10例同时行头部血管MRA，5例行DSA检查。测量颈动脉狭窄程度，评价颅内动脉及Willis环。结果 临床表现为大脑半球供血不足症状者，狭窄同侧腔隙性脑梗死3例，同侧多发性脑梗死2例，两侧多发梗死灶3例，狭窄对侧皮层梗死1例，未见异常1例。狭窄侧后交通动脉(PCOA)未见显示5例，显示细小1例。反复发作性眩晕者，狭窄同侧腔隙性脑梗死2例，对侧皮层梗死1例，未见异常4例。狭窄侧PCOA显示2例，PCOA粗大1例；狭窄侧未显示PCOA，而大脑后动脉增粗1例。结论 对以眩晕为惟一或主要症状的颈动脉重度狭窄者，应重视同时行头部血管MRA以评价Willis环及颅内动脉，并测量流速，适时解除颈动脉狭窄有利于消除或减轻此类病人的眩晕。     

颈动脉狭窄与眩晕

目的探讨眩晕与颈动脉狭窄之间的联系。方法17例经手术或DSA证实的颈动脉重度狭窄病例。临床表现为大脑半球供血不足症状10例,反复发作性眩晕7例,其中4例眩晕为惟一或主要临床症状,手术解除狭窄后症状消失或减轻。17例均首先行颈部血管多普勒超声(DUS),然后行颈部血管磁共振血流成像(MRA)及头部CT或MRI检查,其中10例同时行头部血管MRA,5例行DSA检查。测量颈动脉狭窄程度,评价颅内动脉及Willis环。结果临床表现为大脑半球供血不足症状者,狭窄同侧腔隙性脑梗死3例,同侧多发性脑梗死2例,两侧多发梗死灶3例,狭窄对侧皮层梗死1例,未见异常1例。狭窄侧后交通动脉(PCOA)未见显示5例,显示细小1例。反复发作性眩晕者,狭窄同侧腔隙性脑梗死2例,对侧皮层梗死1例,未见异常4例。狭窄侧PCOA显示2例,PCOA粗大1例;狭窄侧未显示PCOA,而大脑后动脉增粗1例。结论对以眩晕为惟一或主要症状的颈动脉重度狭窄者,应重视同时行头部血管MRA以评价Willis环及颅内动脉,并测量流速,适时解除颈动脉狭窄有利于消除或减轻此类病人的眩晕。     

Xenon CT cerebral blood flow in patients with head injury: influence of pulmonary trauma on the input function

The noninvasive xenon-enhanced CT (Xe CT) cerebral blood flow (CBF) method has been used in patients with severe traumatic brain injury (TBI) to identify the blood-flow thresholds for the development of irreversible ischaemia or infarction following severe TBI. Quantitative regional CBF (rCBF) estimates are based on the assumption of identity between the end-tidal xenon concentration curve, used as the input function, and the arterial xenon concentration curve, being the true input function to the brain. Accordingly, rCBF data addressing the issue of ischaemia should be viewed in relation to possible deviations between the end-tidal and arterial xenon concentration curves. To evaluate this possible source of error, we studied five patients with severe TBI (Glasgow coma score ≤ 7) who also had pulmonary trauma. CBF was studied with the Xe CT CBF method and flow rates were determined by fitting the Kety equation to each CT voxel using either the end-tidal or the arterial xenon curve as input function. In all patients rCBF estimates were lower using the end-tidal xenon curve than with the arterial xenon curve; the mean underestimation was 20.3 % in gray metter and 17.3 % in white matter. The deviation between the end-tidal and arterial xenon concentration curves should be considered as a source of error when defining critical flow values according to the flow thresholds of tissue viability Received: 1 June 1999/Accepted: 23 July 1999     

An MRI analysis of brain-stem and cerebellar lesions and olivary hypertrophy

We describe the relations between primary brain stem or cerebellar infarct or haemorrhage and secondary inferior olivary pseudohypertrophy (OPH). We identified 17 patients (43.6%) among 39 with brain stem or cerebellar vascular disease who had MRI follow-up more than 3 months after their ictus, with OPH. The primary lesions in the 22 cases without OPH were 11 haemorrhages, including 8 medial cerebellar and 3 brain stem lesions, and 11 infarcts: 4 brain stem lesions without accompanying cerebellar involvement, 2 cerebellar infarcts with brain stem extension, and 5 cerebellar lesions without a brain stem infarct. The causative lesion in the 17 patients with OPH included 5 brain stem and 7 cerebellar haemorrhages and 5 brain stem infarcts; no cerebellar infarcts without brain stem involvement were found to cause OPH. Primary involvement of the tegmentum of the brain stem was closely related to secondary OPH, but we could not characterise MRI differences in the cerebellar lesions between the patients with or without OPH.     

Serial diffusion-weighted imaging in MELAS

Clinical features of mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes (MELAS) resemble those of cerebral infarcts, but the pathogenesis of infarct-like lesions is not fully understood. To characterise these infarct-like lesions, we studied two patients with MELAS using diffusion-weighted (DWI) MRI before and after stroke-like episodes and measured the apparent diffusion coefficient (ADC) in the new infarct-like lesions. These gave high signal on DWI and had much higher ADC than normal-appearing regions. The ADC remained high even 30 days after a stroke-like episode then decreased in lesions, with or without abnormality as shown by conventional MRI. We speculate that early elevation of ADC in the acute or subacute phase reflects vasogenic rather than cytotoxic edema. The ADC of the lesions, which disappeared almost completely with clinical improvement, returned to normal levels, which may reflect tissue recovery without severe damage. To our knowledge, this is the first study of DWI in MELAS. Received: 13 September 1999/Accepted: 7 January 2000     

Atrophy of the corpus callosum correlates with white matter lesions in patients with cerebral ischaemia

Many studies of white matter high signal (WMHS) on T2-weighted MRI have disclosed that it is related to cerebral ischaemia and to brain atrophy. Atrophy of the corpus callosum (CC) has also been studied in relation to ischaemia. Our objective was to test the hypothesis that CC atrophy could be due to ischaemia. We therefore assessed CC, WMHS and brain atrophy in patients with risk factors without strokes (the risk factor group) and in those with infarcts (the infarct group), to investigate the relationships between these factors. We studied 30 patients in the infarct group, 14 in the risk factor group, and 29 normal subjects. Using axial T1-weighted MRI, cortical atrophy and ventricular enlargement (brain atrophy) were visually rated. Using axial T2-weighted MRI, WMHS was assessed in three categories: periventricular symmetrical, periventricular asymmetrical and subcortical. Using the mid-sagittal T1-weighted image, the CC was measured in its anterior, posterior, midanterior and midposterior portions. In the normal group, no correlations were noted between parameters. In the infarct group, there were significant correlations between CC and brain atrophy, and between CC atrophy and WMHS. After removing the effects of age, gender and brain atrophy, significant correlations were noted between some CC measures and subcortical WMHS. In the risk factor group, there were significant correlations between CC and brain atrophy and between CC atrophy and WMHS. After allowance for age, gender and brain atrophy, significant correlations between some CC measures and periventricular WMHS remained. The hypothesis that CC atrophy could be due to cerebral ischaemia was supported by other analyses. Namely, for correlations between the extent of infarcts and partial CC atrophy in patients with anterior middle cerebral artery (MCA) and with posterior MCA infarcts, there were significant correlations between the extent of infarct and midanterior CC atrophy in the former, and posterior CC atrophy in the latter. Our findings could indicate that CC atrophy is associated with cerebral ischaemia. Received: 5 December 1998/Accepted: 6 November 1999     

Role of subvoxel free fluid on diffusion parameters in brain tissue with cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy and its correlation with physical disability: histogram analysis of standard and fluid-attenuated MR diffusion

BACKGROUND AND PURPOSE: Subcortical signal intensity abnormalities and lacunar infarcts are the radiologic hallmark of cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy. MR diffusion studies reveal abnormalities in lesions and also within normal appearing white matter. To further characterize the underlying pathologic abnormality, we evaluated the role of subvoxel free fluid in brain with cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy on diffusion parameters and physical disability and analyzed the interrelation between diffusion variables and nonlacunar T2 lesion load. METHODS: Mean diffusivity maps from fluid-attenuated and standard diffusion images of 13 patients with cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy and seven age-matched control participants were compared by means of histogram analysis for three tissue compartments (whole brain parenchyma, normal appearing brain tissue, and nonlacunar lesions) by using a semiautomated region growing algorithm to define whole brain parenchyma and lesions on fluid-attenuated images. RESULTS: In both patients and control participants, the average mean diffusivity of whole brain parenchyma was lower on fluid-attenuated than on standard images (P <.001). Average mean diffusivity and peak location for all compartments were significantly elevated in patients (P <.001) and higher for lesions than for normal appearing brain tissue on both types of images (P <.001). The difference between standard and fluid-attenuated average mean diffusivity of normal appearing brain tissue, reflecting the subvoxel free fluid content, was elevated in patients (P <.05) and correlated closely with the Rankin score (Spearman's rank correlation coefficient = 0.889, P <.001). Average mean diffusivity of whole brain parenchyma and normal appearing brain tissue correlated strongly with the nonlacunar T2 lesion load (Pearson's correlation coefficient = 0.743-0.928, P <.005). CONCLUSION: This study shows that standard diffusion measurements are contaminated by free fluid partial volume effects for patients with cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy and for control participants. It also provides evidence of a clinical significance of increased subvoxel free fluid in normal appearing brain with cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy, which may be more important than either global atrophy, increased diffusivity or, T2 lesion load.     

2个CADASIL患者的弥散张量成像与20例正常人的比较

目的　分析2例CADASIL患者的MR特点及弥散张量指标的变化。方法　收集2例通过病理和基因检查确诊为CA DASIL的先证者的临床资料,对其进行常规MR扫描和弥散张量成像,将弥散张量成像的指标与20例正常志愿者的指标进行比较。结果　2例CADASIL患者的MR主要表现为双侧额顶叶白质内多发腔梗、脱髓鞘改变和双侧颞叶前部白质脱髓鞘。1例患者双侧外囊、内囊后肢、胼胝体膝部和压部的部分各向异性(FA)值均小于正常组的平均值减去2倍标准差,另1例患者左侧外囊的FA值小于对照组的平均值减去2倍标准差。结论　常规MR表现和弥散张量成像指标的测量均反映了CADASIL患者中存在严重的白质病变。     

Distribution territories and causative mechanisms of ischemic stroke

Ischemic stroke prognosis, risk of recurrence, clinical assessment, and treatment decisions are influenced by stroke subtype (anatomic distribution and causative mechanism of infarction). Stroke subtype diagnosis is better achieved in the early phase of acute ischemia with the use of multimodal MR imaging. The pattern of brain lesions as shown by brain MR imaging can be classified according to a modified Oxfordshire method, based on the anatomic distribution of the infarcts into six groups: (1) total anterior circulation infarcts, (2) partial anterior circulation infarcts, (3) posterior circulation infarcts, (4) watershed infarcts, (5) centrum ovale infarcts, and (6) lacunar infarcts. The subtype of stroke according to its causative mechanism is based on the TOAST method, which classifies stroke into five major etiologic groups: (1) large-vessel atherosclerotic disease, (2) small-vessel atherosclerotic disease, (3) cardioembolic source, (4) other determined etiologies, and (5) undetermined or multiple possible etiologies. The different MR imaging patterns of acute ischemic brain lesions visualized using diffusion-weighted imaging and the pattern of vessel involvement demonstrated with MR angiography are essential factors that can suggest the most likely causative mechanism of infarction. This information may have an impact on decisions regarding therapy and the performance of additional diagnostic tests.     

Identification, segmentation, and image property study of acute infarcts in diffusion-weighted images by using a probabilistic neural network and adaptive Gaussian mixture model

RATIONALE AND OBJECTIVES: Accurate identification of infarcted regions of the brain is critical in management of stroke patients. An efficient and fast method for identification and segmentation of infarcts in the diffusion-weighted images (DWI) is proposed. MATERIALS AND METHODS: Thirteen stroke patients were studied. DWI scans were acquired with a slice thickness of 5 mm. We have used a probabilistic neural network for selecting infarct slices and an adaptive (two-level) Gaussian mixture model for segmentation of the infarcts. Statistical analysis, such as identification of distribution, first-order statistics calculation, and receiver operating characteristic curve analysis, was performed. RESULTS: The average dice index is about 0.6, and average sensitivity and specificity are about 81% and 99%, respectively. The value of sensitivity and dice index are influenced by the number of false positives and false negatives. Because artifacts and infarcts have similar imaging characteristics, it is difficult to completely eliminate the artifacts. The accuracy of localization is nearly 100% as there were only two false-positive and three false-negative slices of all 381 slices. The algorithm takes about 1 minute in the Matlab computing environment to process a volume. CONCLUSION: A method to localize and segment the acute brain infarcts is proposed. The method aids the clinician in reducing the time needed to localize and segment the infarcts. The speed of localization and segmentation can be enhanced further by implementing the algorithm in VC++ and using fast algorithms for selection of Gaussian mixture model parameters.     

Detectability and detection rate of acute cerebral hemisphere infarcts on CT and diffusion-weighted MRI

Our purpose was to compare the detectability and detection rate of acute ischaemic cerebral hemisphere infarcts on CT and diffusion-weighted MRI (DWI). We investigated 32 consecutive patients with acute hemisphere stroke with unenhanced CT and DWI within 6 h of stroke onset. The interval between CT and DWI ranged from 15 to 180 min (mean 60 min). Infarct detectability on CT and DWI was determined by comparing the initial CT, DWI and later reference images in a consensus reading of five independent examiners. The “true” detection rate was assessed by analysing all single readings. Two patients had intracerebral haematomas on DWI and CT and were excluded. There were 27 patients with ischaemic infarcts; all were visible on DWI and proven by follow-up. DWI was negative in three patients without a final diagnosis of infarct (100 % sensitivity, 100 % specificity, χ² = 30, P < 0.0001). Ischaemic infarcts were visible on 15 and not seen on 12 CT studies (55 % sensitivity, 100 %specificity, χ² = 1.48, P = 0.224). With regard to the single readings (30 examinations × 5 examiners = 150 readings), 63 CT readings were true positive and 72 false negative (sensitivity 47 %, specificity 86 %, χ² = 2.88, P = 0.089). Of the DWI readings 128 were true positive and 7 false negative (sensitivity 95 %, specificity 87 %, χ² = 70.67, P < 0.0001). Interobserver agreement was substantial for CT (ϰ = 0.72, 95 % confidence interval, 0.6–0.84) and DWI (ϰ = 0.82, 95 % confidence interval, 0.46–1). Taken together, detectability and detection rate of acute (< 6 h) hemisphere infarcts are significantly higher with DWI than with CT. Received: 14 December 1999/Accepted: 15 February 2000     

Xenon contrast-enhanced CT imaging of supratentorial hypoperfusion in patients with brain stem infarction

BACKGROUND AND PURPOSE: The characteristics of hypoperfusion in the supratentorial region of patients with brain stem infarction are unclear. We investigated the relationships between the presence of hypoperfusion and the location, number, and size of the infarcts with xenon contrast-enhanced CT. METHODS: One hundred five patients with brain stem infarction detected by MR imaging underwent xenon contrast-enhanced CT to measure the regional CBF (rCBF) in the frontal, temporal, parietal, and occipital regions and in the putamen and thalamus. A decrease of more than 10% from the mean rCBF value for normal individuals was considered to indicate hypoperfusion. RESULTS: Thirty-six patients had supratentorial hypoperfusion. The mean rCBF values (measured in mL/100 g/minute) were as follows: frontal region, 36.2 +/- 5.1 (-14.8%, n = 28); parietal region, 42.3 +/- 4.7 (-19.1%, n = 29); temporal region, 41.5 +/- 2.8 (-12.6%, n = 12); and thalamus, 50.1 +/- 3.2 (-19.6%, n = 7). Supratentorial hypoperfusion was associated with pontine infarction in 33 patients (upper pons in 15, middle pons in 18, and lower pons in seven), midbrain infarction in two, and medulla infarction in one. Twenty-three patients had infarcts that were larger than 5 mm, and 11 had infarcts that were 2 to 5 mm. Only two had infarcts that were smaller than 2 mm. Seven patients each had one infarct, 13 each had two, and 16 each had three. CONCLUSION: Supratentorial hypoperfusion was associated with larger infarcts, with more infarcts, and with pontine infarction.     

Computer-aided diagnosis scheme for detection of lacunar infarcts on MR images

RATIONALE AND OBJECTIVES: The detection and management of asymptomatic lacunar infarcts on magnetic resonance (MR) images are important tasks for radiologists to ensure the prevention of severe cerebral infarctions. However, accurate identification of the lacunar infarcts on MR images is a difficult task for the radiologists. Therefore the purpose of this study was to develop a computer-aided diagnosis scheme for the detection of lacunar infarcts to assist radiologists' interpretation as a "second opinion." MATERIALS AND METHODS: Our database comprised 1,143 T1- and 1,143 T2-weighted images obtained from 132 patients. The locations of the lacunar infarcts were determined by experienced neuroradiologists. We first segmented the cerebral region in a T1-weighted image by using a region growing technique for restricting the search area of lacunar infarcts. For identifying the initial lacunar infarcts candidates, a top-hat transform and multiple-phase binarization were then applied to the T2-weighted image within the segmented cerebral region. For eliminating the false positives (FPs), we determined 12 features--the locations x and y, signal intensity differences in the T1- and T2-weighted images, nodular components from a scale of 1 to 4, and nodular and linear components from a scale of 1 to 4. The nodular components and the linear components were obtained using a filter bank technique. The rule-based schemes and a support vector machine with 12 features were applied to the regions of the initial candidates for distinguishing between lacunar infarcts and FPs. RESULTS: Our computerized scheme was evaluated by using a holdout method. The sensitivity of the detection of lacunar infarcts was 96.8% (90/93) with 0.76 FP per image. CONCLUSIONS: Our computerized scheme would be useful in assisting radiologists for identifying lacunar infarcts in MR images.     

Hemodynamically caused cerebral infarctions. Clinical importance of infarct pattern and angiomorphology

Summary Classification of brain infarcts based on the location, size and shape of parenchymal damage alone can be difficult and misleading. This is particularly true in subcortical infarctions and infarcts in so-called watershed areas between neighboring territories of the main hemispheric arteries. Pathogenetic mechanisms, signs and symptoms, lesion patterns in CT and MRI are discussed as well as angiomorphological conditions. Hemodynamically induced low-flow infarcts are rare and show typical, but not pathognomic lesion patterns on CT and MRI. Characteristic subcortical chainlike and confluent lesions are located in the supra- and paraventricular white matter, representing the core of a hemodynamically induced infarction. Definite diagnosis of low-flow infarcts requires information on the underlying complex vascular compromise of the extra- and intracranial arterial circulation. A noncompetent circle of Willis is the main predisposing condition in hemispheric low-flow infarcts even in severe occlusive disease of the internal carotid arteries.