Cortical laminar necrosis in brain infarcts: serial MRI

High-signal cortical lesions are observed on T1-weighted images in cases of brain infarct. Histological examination has demonstrated these to be "cortical laminar necrosis", without haemorrhage or calcification. We report serial MRI in this condition in 12 patients with brain infarcts. We looked at high-signal lesions on T1-weighted images, chronological changes in signal intensity and contrast enhancement. High-signal cortical lesions began to appear about 2 weeks after the ictus, were prominent at 1-2 months, then became less evident, but occasionally remained for up to 1.5 years. They gave high signal or were isointense on T2-weighted images and did not give low signal at any stage. Contrast enhancement of these lesions was prominent at 1-2 months, and less apparent from 3 months, but was seen up to 5 months.     

Cortical laminar necrosis in brain infarcts: chronological changes on MRI

We studied the MRI characteristics of cortical laminar necrosis in ischaemic stroke. We reviewed 13 patients with cortical laminar high signal on T1-weighted images to analyse the chronological changes in signal intensity and contrast enhancement. High-density cortical lesions began to appear on T1-weighted images about 2 weeks after the ictus. At 1–2 months they were prominent. They began to fade from 3 months but could be seen up to 11 months. These cortical lesions showed isointensity or high intensity on T2-weighted images and did not show low intensity at any stage. Contrast enhancement of the laminar lesions was prominent at 1–2 months and became less apparent from 3 months, but could be seen up to 8 months. Received: 14 May 1996 Accepted: 6 September 1996     

Serial MR observation of cortical laminar necrosis caused by brain infarction

To examine the chronological changes characteristic of cortical laminar necrosis caused by brain infarction, 16 patients were repeatedly examined using T1-, T2-weighted spin-echo, T2^*-weighted gradient echo, fluid attenuated inversion recovery (FLAIR) images, and contrast enhanced T1-weighted images at 1.0 or 1.5 T. High intensity cortical lesions were visible on the T1-weighted images from 2 weeks after ictus and became prominent at 1 to 3 months, then became less apparent, but occasionally remained at high intensity for 2 years. High intensity cortical lesions on FLAIR images became prominent from 1 month, and then became less prominent from 1 year, but occasionally remained at high intensity for 2 years. Subcortical lesions did not display high intensity on T1-weighted images at any stage. On FLAIR images, subcortical lesions initially showed slightly high intensity and then low intensity from 6 months due to encephalomalacia. Cortical lesions showed prominent contrast enhancement from 2 weeks to 3 months, but subcortical lesions were prominent from 2 weeks only up to 1 month. T2*-weighted images disclosed haemosiderin in 3 of 7 patients, but there was no correlation with cortical short T1 lesions. Cortical laminar necrosis showed characteristic chronological signal changes on T1-weighted images and FLAIR images. Cortical short T1 lesions were found not to be caused by haemorrhagic infarction. Received: 27 March 1998 Accepted: 23 July 1998     

MR imaging of intracerebral hematomas: sequential changes of signal intensities on a 0.2T permanent magnetic system

We performed 67 examinations in 27 patients with intracerebral hemorrhage on a 0.2T permanent magnet system. MR appearance of the hematomas on T-1 weighted and T-2 weighted images (T1WIs, T2WIs) was carefully evaluated according to the chronological course of the lesions after the ictus. The signal intensity of each hematoma was classified into four stages in terms of the degradation process of hemoglobin. Four hematomas examined within 24 hours after the ictus (ultra-acute stage) appeared slightly hypointense or isointense relative to the normal brain tissue on T1WIs and markedly hyperintense on T2WIs. Three of those lesions became partially or totally hypointense on T2WIs at the acute stage (one to three days after the ictus), though all appeared in general isointense on T1WIs. The hematomas at the subacute stage (four days to two weeks after the ictus) were hyperintense on both T1WIs and T2WIs. At the chronic stage (more than two weeks after the ictus) the signal pattern of hematomas became variable: hyperintense on both T1WIs and T2WIs early at this stage; hypointense on T1WIs but mostly hyperintense on T2WIs latter. The results indicate the clinical feasibility of a low tesla system for MR evaluation of intracerebral hematomas.     

CT contrast enhancement in cerebral infarction.

Computed tomography was used to study 100 patients with ischemic cerebral infarcts. All cases were documented by autopsy, radionuclide imaging, cerebral angiography, or clinical course. Vascular distribution of infarcts was varied and included infarcts of cerebral hemispheres, basal ganglia, and cerebellum. Distinct patterns of enhancement are seen following administration of intravenous contrast material: predominantly peripheral, central, homogeneous, or heterogeneous. Enhancement of the infarcted area usually occurs 1-4 weeks after the onset of clinical symptoms, but was seen as early as the first day or as late as several months after the onset of symptoms. Infarcts showing contrast enhancement may or may not revert to a nonenhanced pattern on follow-up examination for several months. Lesions demonstrating contrast enhancement in cerebrovascular disease may at times be indistinguishable from tumor. Contrast enhancement was the only manifestation of infarction in some instances, and an infarcted area may be completely missed if a postcontrast examination is not performed.     

常染色体显性遗传性脑动脉病伴皮层下梗死和白质脑病的颅脑MRI表现

目的 提高对常染色体显性遗传性脑动脉病伴皮层下梗死和白质脑病(CADASIL)的颅脑MRI表现的认识.方法 对一家系2代5例患者进行头颅常规MR和MR血管成像(MRA)检查.对经Notch3基因检查或皮肤组织活检超微病理检查确诊的3例和经MRI与临床诊断的1例CADASIL的MRI资料进行分析.结果 MR检查的5例中4例CADASIL均获得明确诊断,1例排除诊断.4例CADASIL均见两侧颞叶、额叶和顶叶大致对称性皮层下与侧脑室旁白质病灶,呈长T1、长T2信号,但枕叶累及甚少且皮层不受累;O'Sullivan征阳性4例,皮层下腔隙性损害(SLLs)征阳性2例;3例半卵圆中心可见多发圆形或卵圆形囊性梗死即"黑洞",4例均见多发圆点状血管周间隙即"胡椒罐盖"样征象;4例全部显示胼胝体单发或多发斑片状显著长T1、长T2信号,其中2例伴萎缩;内囊前肢与外囊均受累,呈"人"字征;基底节和脑干可见单发或多发陈旧性腔隙性梗死灶;1例伴右侧小脑小片状梗死灶;4例全部有轻度至中度的脑干、小脑和大脑萎缩;MRA颅内Ⅰ-Ⅲ级较大动脉均未见明显异常.结论 CADASIL的颅脑MRI表现具有一定的特征性,可为CADASIL的初诊和筛选提供重要依据.     

MRI in Japanese encephalitis

We document the MRI features in seven patients with Japanese encephalitis. MRI was carried out on a 1.5 T system within 10–60 days of onset. In all the patients MRI revealed bilateral thalamic lesions, haemorrhagic in five. Signal changes were present in the cerebrum in four patients, the midbrain and cerebellum in three each, the pons in two and the basal ganglia in one. The lesions were haemorrhagic in three of the four patients with lesions in the cortex, two of the three with lesions in the midbrain and cerebellum, but the pontine lesions were haemorrhagic in both patients. Spinal cord involvement was seen in one of the three patients who underwent MRI. In two patients MRI was repeated 3 years after the onset, showing marked reduction in abnormal signal; and all the lesions gave low signal on both T1- and T2-weighted images. Bilateral thalamic involvement, especially haemorrhagic, may be considered characteristic of Japanese encephalitis, especially in endemic areas. Received: 2 January 1996 Accepted: 2 February 1996     

MR contrast enhancement in brainstem and deep cerebral infarction.

MR imaging with IV administration of gadopentetate dimeglumine was performed in 89 patients with 100 clinically and radiologically documented brainstem or deep cerebral (basal ganglia/internal capsule) infarctions to determine the patterns and time course of contrast enhancement. By location, there were 61 deep cerebral, eight midbrain, 23 pontine, and eight medullary infarctions. The age of the infarctions ranged from 1 day to 3 1/2 years, with 22% of the patients scanned within 4 days and 43% scanned within 2 weeks of clinical ictus. Abnormalities on T2-weighted images were encountered in every case. Mass effect was seen in 10 infarctions, most commonly noted between days 2 and 6, but persisting to day 20 in a single case. Parenchymal contrast enhancement was seen in 43 cases, occurring predominately between days 2 and 80. By postinfarction day 3 only half the strokes enhanced, although all did after day 6. Intravascular enhancement within the vertebral or basilar arteries was noted in five cases; all were brainstem infarctions imaged during the first week following ictus. Meningeal enhancement adjacent to the infarction was not seen in any case. Our results indicate that MR contrast enhancement of brainstem and deep cerebral infarctions typically occurs over a period from about 3 days to 3 months following ictus. Lack of both parenchymal and intravascular enhancement is thus to be expected for several days after a brainstem or deep cerebral infarction.     

Cerebral aspergillosis: comparison of radiological and neuropathologic findings in patients with bone marrow transplantation

Thirty-six lesions in six patients who died from cerebral Aspergillus infection after bone marrow transplantation (BMT) were studied with regard to signal intensity, contrast enhancement, size, and location. The diagnosis was confirmed in all cases by autopsy. Retrospective correlation of histopathological and radiological findings was possible for 14 lesions. Most of the lesions (22/36) had isointense to low signal intensity on T2-weighted images (T2WI). Histopathologically, hemorrhagic necrosis was determined in three of them. Areas of high signal intensity on T1-weighted images (T1WI) were related to gross hemorrhage. Two infarctions showed intravascular accumulation of fungal hyphae with secondary thrombosis of the vessel. The remaining 12 lesions had high signal intensity on T2WI and low on T1WI. Histopathologically, four were infectious and four were unspecific demyelinated lesions. In conclusion, cerebral aspergillosis typically presented with large lesions showing isointense to low signal intensity on T2WI that could have areas of high signal on T1WI. Contrast enhancement was only visible in 15 lesions, and the predominant locations were the subcortical white matter, the cerebellum, and the basal ganglia. Small lesions with high signal on T2WI and low signal on T1WI could not necessarily be related to Aspergillus infection.     

MR imaging of Wallerian degeneration in the brainstem: temporal relationships

Degeneration of the myelin sheath and axon distal to the most proximal site of axonal interruption secondary to axonal disease has been called wallerian degeneration. On MR imaging, wallerian degeneration of the pyramidal tract can be observed as an abnormal signal intensity, showing prolonged T1 and T2 relaxation times that correspond to the corticospinal tract, with or without shrinkage of the ipsilateral cerebral peduncle and pons. Review of MR studies in 150 cases of supratentorial cerebrovascular accidents showed abnormal signal alterations in the ipsilateral brainstem in 33 of the cases. Abnormal intensity in the ipsilateral brainstem was seen as early as 5 weeks after the supratentorial ictus and was fully evident after 10 weeks in all 33 cases. Signal alterations were strongest at about 3-6 months when compared with alterations seen at 10 weeks or even 10 months after the ictus. Shrinkage of the ipsilateral brainstem appeared as early as 8 months and was demonstrated in all cases 13 months after the ictus. MR seems to be the most effective technique for early detection of wallerian degeneration and may provide insight into its pathophysiological and chemical changes.     

脑脂肪栓塞的MRI及CT诊断

目的 总结脑脂肪栓塞(CFE)的临床及MRI及CT的影像特点。方法 分析3例急性CFE的临床表现、影像特点。结果 (1)3例均为长骨骨折，在外伤后或骨折固定、复位数小时后突发精神状态改变。(2)醒状昏迷是主要临床表现。(3)3例患者MRI能明确显示病灶，1例CT显示了病灶。(4)MRI、CT显示脑内病灶均呈基本对称性分布，为边缘模糊的点、片状长T1、长T2信号，CT呈低密度。病灶均累及脑干、分水岭区脑白质、基底节区、胼胝体压部。2例病灶累及小脑。(5)1例患者发病康复治疗3个月后MRI复查示脑内病灶完全消失。结论 急性脑脂肪栓塞的临床及MRI、CT影像改变具有特征性，MRI在病灶显示上优于CT。     

广州管圆线虫病中枢神经系统受侵的磁共振影像研究

目的：研究中枢神经系统广州管圆线虫病的磁共振影像表现。方法：５例经实验室检查和临床治疗证实的广州管圆线虫病患者共做头部及颈腰部ＭＲＩ检查１７例次。ＭＲＩ扫描仪为０．５Ｔ超导装置。在ＭＲＩ不同序列上观察脑、脊髓、脑脊膜和神经根有无病变及其分布、形态及信号表现,通过随访ＭＲＩ检查,分析病变出现及消散、好转情况。结果：５例患者ＭＲＩ显示脑膜脑炎３例,脑炎１例,脊髓脊膜炎１例。具体病变部位及表现如下：（１）脑实质累４例,脊髓１例。这些病变呈弥漫或散在分布,在Ｔ１ＷＩ上呈稍低或等信号,在Ｔ２ＷＩ和对应层面液体衰减反转恢复序列（ＦＬＡＩＲ）图像上呈高信号,注射钆喷替酸葡甲铵（Gd-DTPA）后病变中央可见圆形或卵圆形强化灶,最大直径１０mm。有时可见粗细不等的长条形强化,长达１４mm。强化灶周围可有小范围的低信号水肿区。（２）脑脊膜受累４例,其中包括室管膜及神经根受累各１例。注射Gd-DTPA后表现为软脑膜或（和）室管膜呈线条形或结节状强化及神经根强化。（３）轻度脑室扩张２例。追踪动态观察提示,发病后第５～８周是颅内病变最明显的时期,病变从发现至消退至少需要８周时间。结论：中枢神经系统广州管圆线虫病的ＭＲＩ表现多种多样。脑脊髓内多发长条形或结节状强化和软脑膜强化是本病主要的ＭＲＩ表现。     

甲基丙二酸尿症及丙酸尿症的颅脑MRI研究

目的:探讨甲基丙二酸尿症及丙酸尿症的颅脑MRI表现。方法:对16例甲基丙二酸尿症和丙酸尿症的婴幼患儿的临床资料及颅脑MRI进行分析总结。结果:16例中男10例,女6例,发病年龄为出生后～2岁。治疗前行头颅MRI检查8例,表现为脑萎缩5例,其中3例伴脑白质减少,另2例伴双侧基底节信号异常,表现为T1FLAIR稍低、T2FLAIR高信号、DWI高信号;头颅CT检查1例,表现为交通性脑积水。通过治疗后随访MRI7例,表现为MRI和DWI阴性1例,双侧基底节持续T1FLAIR稍低、T2FLAIR高信号、DWI稍高信号1例,内囊前后肢及脑干T1FLAIR低信号1例;余4例中,MRI表现好转2例,呈进行性改变2例。结论:甲基丙二酸尿症和丙酸尿症的MRI表现缺乏特异性,主要为不同程度的脑萎缩、髓鞘化延迟和基底节的异常信号,特别是苍白球。MRI的异常改变可通过合理治疗而有所改善,然而长期的异常影像学改变则预示着神经系统呈不可逆的、进行性的损害。     

Hyperintense basal ganglia on T1-weighted MR images in a patient with central nervous system lupus and chorea.

We describe a patient with central nervous system lupus and choreatic movements in whom both basal ganglia showed high signal intensity on T1-weighted MR images, while the signal on T2-weighted images remained low. Within 8 months after onset, the choreatic movements had disappeared, with a corresponding decrease in the hyperintense T1 signal. The emergence of the choreatic movement disorder in this patient might have been related to the T1 hyperintensity of the basal ganglia, which, in turn, might have resulted from a vascular insult associated with central nervous system lupus.     

Long-term MR imaging course of neurodegenerative Langerhans cell histiocytosis

BACKGROUND AND PURPOSE: MR imaging signal intensity abnormalities in the cerebellum, the pons, and the basal ganglia, compatible with a neurodegenerative process (ND) were reported in up to 10% of patients with Langerhans cell histiocytosis (LCH). Although the imaging features of ND-LCH have been extensively described, the temporal course of ND-LCH has not been assessed as of yet. The purpose of this study was to describe the long-term course of MR imaging signal intensity abnormalities in ND-LCH on T1- and T2-weighted images. MATERIALS AND METHODS: In this retrospective study, 9 patients with ND-LCH with an observation time of at least 5 years were included. Three or more MR imaging studies per patient, performed in 3-year intervals (+/-11 months), were reviewed. Signal intensity abnormalities on T1- and T2-weighted images in the cerebellum, the pons, and basal ganglia were scored for their signal intensity quality and their extension. In addition, the severity of cerebellar atrophy was scored. RESULTS: The signal intensity alterations were not resolved in any of the patients. Instead, a progression of the signal intensity alterations either in the cerebellum or basal ganglia was observed in all of the patients but did not correlate with a clinical deterioration. Overt and severe neurologic symptoms were reported in only 2 patients in whom some form of atrophy was noted. CONCLUSIONS: ND-LCH appears to be a slowly progressive process. The increase of signal intensity abnormalities in the cerebellum and basal ganglia does not correlate with neurologic deterioration. MR imaging appears to be a sensitive technique to detect and monitor radiologic ND-LCH.     

老年人皮质下动脉硬化性脑病的病理学基础和CT,MRI对照研究

本文就２６例皮质下动脉硬化性脑病患者的ＣＴ、ＭＲＩ检查结合病理学基础进行了分析。ＭＲＩ检查，当ＴＲ＝２０００ｍｓｅｅ，ＴＥ＝３０、６０ｍｓｅｃ时，皮质动脉硬化性脑病损害均为明显的高信号，Ｔ１加权像为低信号。ＣＴ像为低密度改变。Ｔ２加权像上半卵圆中心的白质表现为不均匀弥漫的高信号区，可累及基底节、丘脑、脑干及小脑的白质，并有不同程度的侧脑室扩大、脑室边缘呈斑片状改变可有脑萎缩。病理学特征是弥漫不完全     

Profound asphyxia in the premature infant: imaging findings.

PURPOSETo investigate imaging findings in premature infants who had profound asphyxia.METHODSCT (three patients), MR (three patients), and ultrasonography (four patients) studies of five patients who had profound asphyxia before the postconceptional age of 32 weeks were retrospectively reviewed. The patients ranged from 1 day to 4 months old at the time of the imaging studies. An autopsy report was available in one patient. The results were compared with reports in the literature of patients with similar injuries at similar ages.RESULTSAbnormalities of the thalami and basal ganglia were present in all infants examined with CT or MR. CT showed low attenuation in the basal ganglia and high attenuation (blood or calcium) in the thalami; thalamic cavitation and low attenuation of the upper brain stem were present in one infant. MR showed T1 and T2 shortening in the thalami in all patients. Variable MR changes were noted in the basal ganglia, ranging from diminished size with normal signal intensity to T1 and T2 shortening with normal size and complete cavitation. T1 and T2 shortening were seen in the dorsal brain stem in one patient. Sonography showed transient or persistent hyperechogenicity in the thalami in three patients and cavitation of the thalami in one patient. Damage to the perirolandic cortex was not present in any patient.CONCLUSIONProfound asphyxia before 32 weeks gestational age shows consistent injury to the thalami, basal ganglia, and brain stem that can be detected by all three imaging modalities. The pattern of injury seems to differ from that of partial asphyxia in premature infants and of profound asphyxia in term infants.     

Evolution of high-intensity basal ganglia lesions on T1-weighted MR in neurofibromatosis type 1.

PURPOSETo characterize the temporal evolution of the foci of T1 shortening in basal ganglia lesions in patients with neurofibromatosis type 1 (NF-1).METHODSA retrospective review of MR images of 37 patients with NF-1 revealed 8 patients in whom regions of T1 shortening were noted in the basal ganglia. We reviewed sequential images obtained in these selected patients with special attention to chronological changes in the foci of T1 shortening and their relationship to changes on T2-weighted images.RESULTSRegions of short T1 in the globus pallidus were observed in 8 patients. In 2 of 3 patients in whom foci of T1 shortening were not identified on the initial imaging study, T1 shortening developed and T2 prolongation diminished after an initial increase. In the third patient, T1 and T2 prolongation appeared simultaneously. Sequential scans in the other 5 patients, in whom areas of increased signal intensity in the globus pallidus were present on both T1-weighted and T2-weighted images on the initial MR examination, showed a diminution in the size of the region of T2 prolongation in 2 patients, an increase in the size of the region of T2 prolongation in 1 patient, a mixed pattern of change in the size of the region of T2 prolongation in 1 patient, and no change in the region of T2 prolongation in 1 patient. During the periods of these T2 changes, the areas of T1 shortening showed no significant interval change.CONCLUSIONThe foci of prolonged T2 relaxation in the basal ganglia appear to evolve in a manner similar to the foci of T2 prolongation in the white matter of the posterior fossa. However, the corresponding foci of short T1 in the basal ganglia may evolve with a different time course. In some patients, the foci of short T1 develop at a later time than the T2 prolongation and progress; these foci of short T1 do not appear to regress over periods as long as 90 months. Possible causes of the T1 shortening are remyelination and calcification.     

MRI in neuro-Behçet's disease

Our purpose was to characterise specific MRI findings and to determine their value in neuro-Behçet's disease. We examined 17 patients (14 men, 3 women) with neuro-Behçet's disease using T1- and T2-weighted spin-echo images and contrast-enhanced images at 0.5 T. There were 13 patients (76.5 %) who had single or multiple lesions. Most of these were in the basal ganglia, brain stem or deep white matter region, giving high signal on T2-weighted images and isointense or low signal on T1-weighted images. In 3 cases (17.6 %) there was linear high signal along the posterior limb of the internal capsule on T2-weighted images. This was considered as a potential differentiating feature of neuro-Behçet's disease. Contrast-enhancement was seen in 17 lesions in 7 patients.     

Neuropsychiatric systemic lupus erythematosus: correlation of brain MR imaging, CT, and SPECT

Systemic lupus erythematosus (SLE) patients frequently present with neuropsychiatric symptoms. We conducted an imaging study with magnetic resonance (MR) imaging, computed tomography (CT), and single photon emission CT (SPECT) in 23 patients with SLE, 13 with major neuropsychiatric symptoms (NPSLE) and 10 without (non-NPSLE). The most frequent brain imaging findings were seen with MR imaging and were more prevalent in NPSLE: high signal intensity focal white matter lesions, infarcts in the cortex and pons, and basal ganglia lesions.