Reye's syndrome with cortical laminar necrosis: MRI

Serial MRI findings are described in two patients with Reye's syndrome, demonstrating diffuse cortical and white matter changes. In the acute stage, T2-weighted images showed subtle but definite laminar high signal and contrast-enhanced T1-weighted images laminar enhancement, along the entire cerebral cortexbilateraly. In the chronic stage, unenhanced T1-weighted images showed diffuse cortical laminar high signal. These characteristic MRI features seemed very similar to those of laminar cortical necrosis in hypoxic brain damage. MRI also displayed delayed white matter changes with cerebral atrophy.     

Immunohistochemical investigation of hypoxiclischemic brain damage in forensic autopsy cases

A neuropathological study of 41 forensic autopsy cases of hypoxic/ischemic brain damage has been undertaken, using immunohistochemical staining to detect the 70-kDa heat shock protein (hsp70) and the status of the glial cells. In cases surviving 2–5 h after hypoxic/ischemic injury, ischemic cell changes were seen whereas glial reactions were not apparent. In cases of longer survival, neuronal necrosis and a loss of neurons were seen, and these changes were accompanied by proliferation of glial fibrillary acidic protein (GFAP), vimentin-positive astrocytes and microglia which transformed into rod cells or lipid-laden macrophages. In cases with a history of hypoxic attacks, GFAP-positive and vimentin-negative astrocytes had proliferated in the CA3 and CA4 regions of hippocampus. The cases of severe hypoxic injury, such as an asthmatic attack and choking, showed no ischemic changes in the hippocampul neurons. On the other hand, the CA1 pyramidal cells showed neuronal necrosis in a patient suffering from tetralogy of Fallot (TOF), who survived for 2 h after a traffic accident. Therefore, it is suggested that even moderate hypoxic injury induces astrocytosis in the CA3 and CA4 regions and may affect the neuronal proteins and the metabolism, and that in cases with a history of hypoxic attacks neuronal damage may be severe even several hours after ischemic injury. The protein hsp70 expression was found in the CA2, CA3 and CA4 regions in cases of long-term survival after severe hypoxic/ischemic injury and in cases of alcoholic intake or toluene abuse just before acute death. Thus, it is suggested that the detection of hsp70 in the hippocampus indicates hypoxic/ischemic injury or other stress prior to death. In forensic practice, immunohistochemical investigation of the hsp70 and glial cell staining can be of great value for diagnosing not only hypoxic/ischemic brain damage during the process of death but also the victim's past history of hypoxic attacks.     

MRI findings of hypoxic cortical laminar necrosis in a child with hemolytic anemia crisis

We present magnetic resonance imaging findings of a 5-year-old girl who had a rapidly installing hemolytic anemia crisis induced by trimethoprim-sulfomethoxazole, resulting in cerebral anoxia leading to permanent damage. Magnetic Resonance imaging revealed cortical laminar necrosis in arterial border zones in both cerebral hemispheres, ischemic changes in subcortical white matter of left cerebral hemisphere, and in the left putamen. Although cortical laminar necrosis is a classic entity in adulthood related to conditions of energy depletions, there are few reports available in children. A wide review of the literature is also presented.     

Susceptibility-weighted imaging findings of cortical laminar necrosis in pediatric patients

BACKGROUND AND PURPOSE: MR susceptibility-weighted imaging (SWI) is a highly sensitive technique for detection of hemorrhage, but its utility in the evaluation of children with laminar necrosis is not yet known. We assessed whether cortical laminar necrosis in pediatric patients contains hemorrhage on SWI.MATERIALS AND METHODS: “Cortical laminar necrosis” was defined as a hyperintense cortical lesion on T1-weighted imaging in the subacute or chronic phase of brain damage in some foci involving the cerebral cortex and white matter such as hypoxic-ischemic incidents and encephalopathy. Medical records, CT, and MR images were retrospectively analyzed. Fifteen patients (7 boys, 8 girls; age range, 0–13 years) were included. The areas of signal-intensity loss on SWI that were considered to be hemorrhage were correlated with the laminar necrosis. CT was assessed to correlate with the presence of calcification at the location of the signal-intensity loss on SWI. To assess appearance or signal-intensity changes of hemorrhage in the laminar necrosis, follow-up SWI was performed.RESULTS: The causes of laminar necrosis included infarction in 4 patients, ischemic changes from Moyamoya disease in 2, meningoencephalitis in 2, hypoxic-ischemic encephalopathy in 2, shaken baby syndrome in 1, encephalopathy from severe infection in 1, status epilepticus in 1, citrullinemia in 1, and brain injury with posterior reversible encephalopathy syndrome in 1. T1-weighted imaging showed focal laminar necrosis in 8, multifocal laminar necrosis in 2, and diffuse laminar necrosis in 5. SWI findings correlated with laminar necrosis included the following: no hemorrhage in 13 patients (80.0%), dotted hemorrhage in 2 (13.3%), and laminar hemorrhage in 1 (6.7%). Follow-up SWI performed in 6 patients showed no additional hemorrhage.CONCLUSION: Most areas of cortical laminar necrosis in pediatric patients showed no hemorrhage on SWI.

Cortical laminar necrosis is caused by cerebral energy depletion, resulting in necrosis of particular cortical laminae.¹ On T1-weighted MR images, hyperintense lesions are seen in the cerebral cortex during the subacute or chronic stage of brain damage. Cortical laminar necrosis has been described in different conditions. In children, cortical laminar necrosis can be caused by various diseases, including hypoxic-ischemic encephalopathy, infarction, status epilepticus, Moyamoya disease, metabolic disorders, and intoxication.^1-5 Because varying brain damage leads to laminar necrosis, it is important to understand the underlying pathology and clinical outcome with imaging findings.MR susceptibility-weighted imaging (SWI) was designed to be a high-spatial-resolution 3D fast low-angle shot MR imaging technique; it is extremely sensitive to susceptibility changes and can be performed by using conventional MR imaging units.⁶ This sequence was originally designed for MR venography and involves the use of the paramagnetic property of intravenous deoxyhemoglobin. Recently, SWI has been reported to be very sensitive for the detection of extravascular blood products, and several investigators have shown that it has higher sensitivity to detect hemorrhage than conventional MR imaging.^7,8 Detection of hemorrhage is important in the diagnosis and management of a variety of intracranial diseases. Treatments such as thrombolysis and imaging follow-up interval might be affected by the presence of hemorrhage. To the best of our knowledge, the presence of hemorrhage in cortical laminar necrosis has not been well-established in pediatric patients. The purpose of this study was to identify, by using SWI, whether cortical laminar necrosis contains hemorrhage in these patients.     

新生儿低血糖脑损伤的MRI表现

目的 初步探讨新生儿低血糖脑损伤的MRI表现特征及扩散加权成像(DWI)存早期发现低血糖脑损伤中的应用价值.方法 回顾性分析12例低血糖新生儿(其中10例诊断为新生儿低血糖脑病)MRI资料,12例患儿于出生后3至10 d内进行了头部MR扫描,包括常规T1 WI、T2、WI 和DWI扫描.其中4例在第一次检杏后7至10 d后再次行MR扫描.结果 12例首次DWI检查中11例出现异常高信号,受累脑区包括双侧枕叶皮层2例、右侧枕叶皮层1例、左侧枕叶皮层及皮层下1例,双侧枕叶皮层及皮层下2例、双侧顶枕叶皮层2例、舣侧顶枕叶皮层及皮层下2例、胼胝体压部4例、双侧放射冠2例、左侧尾状核及苍白球1例、舣侧背侧丘脑1例、双侧内囊后肢1例.12例首次常规T1 WI、T2 WI中,4例T1 WI呈现异常信号,表现为受累部位皮层T1信号减低3例、受累的双枕叶皮层稍短T1信号1例;5例T2 WI见异常信号,均表现为受累部位皮层及皮层下T2信号稍增高且灰白质分界不清.4例复查中,受累枕叶局部白质软化4例,残存枕叶皮层见条状稍高T1信号2例,双侧大脑半球白质呈弥漫性脱髓鞘改变1例,胼胝体压部T2高信号消失1例,胼胝体压部仍见稍高T2信号1例.结论 在新生儿期,可能和低血糖相关的腑拟伤多发生在双侧顶、枕叶后部脑组织.早期的DWI扫描有助于低血糖脑损伤的早期发现和评估.     

Diffusion-weighted MRI in cortical ischaemia

We carried out MRI on 16 male and three female comatose patients, aged 2 days to 79 years, with suspected cortical ischaemia referred from our intensive care units. Using a head coil, and following standard imaging, including coronal fluid-attenuated inversion-recovery images, we performed diffusion-weighted imaging (DWI) using a whole-brain multislice single-shot echo-planar sequence with b 0 and 1000 s/mm²: 5-mm slices covering the whole brain, TR 7000 TE 106 ms, 128×128 pixels, field of view 250 mm, one excitation. Maps of apparent diffusion coefficients (ADC) were generated automatically. DWI showed cortical, basal ganglia and watershed-area high signal in all cases, associated with a decrease in ADC to 60– 80% of normal. DWI showed lesions not seen (40%) or underestimated (40%) on conventional T2-weighted imaging. Within 24 h of the onset of symptoms, DWI showed changes not readily detectable on T2-weighted images. The cortical high signal on DWI and the ADC changes, suggesting severe ischaemia rather than oedema, was found in areas known to be affected by cortical laminar necrosis. Extension to the brain stem and white matter was associated with a higher likelihood of death.     

Acute hepatic encephalopathy with diffuse cortical lesions

Acute hepatic encephalopathy is a poorly defined syndrome of heterogeneous aetiology. We report a 49-year-old woman with alcoholic cirrhosis and hereditary haemorrhagic telangiectasia who developed acute hepatic coma induced by severe gastrointestinal bleeding. Laboratory analysis revealed excessively elevated blood ammonia. MRI showed lesions compatible with chronic hepatic encephalopathy and widespread cortical signal change sparing the perirolandic and occipital cortex. The cortical lesions resembled those of hypoxic brain damage and were interpreted as acute toxic cortical laminar necrosis. Received: 8 May 2000 Accepted: 10 August 2000     

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.     

MRI investigation of the threshold for thermally induced blood-brain barrier disruption and brain tissue damage in the rabbit brain.

The ability of MRI-derived thermometry to predict thermally induced tissue changes in the brain was tested, and the thermal thresholds for blood-brain barrier (BBB) disruption and brain tissue damage were estimated. In addition, the ability of standard MRI to detect threshold-level effects was confirmed. These safety thresholds are being investigated to provide guidelines for clinical thermal ablation studies in the brain. MRI-monitored focused ultrasound heating was delivered to 63 locations in 26 rabbits. Tissue changes were detected in T(2)-weighted imaging and T(1)-weighted imaging (with and without contrast) and with light microscopy. The probability for tissue damage as a function of the accumulated thermal dose, the peak temperature achieved, the applied acoustic energy, and the peak acoustic power was estimated with probit regression. The discriminative abilities of these parameters were compared using the areas under the receiver operator characteristic (ROC) curves. In MRI, BBB disruption was observed in contrast-enhanced T(1)-weighted imaging shortly after the ultrasound exposures, sometimes accompanied by changes in T(2)-weighted imaging. Two days later, changes in T(2)-weighted imaging were observed, sometimes accompanied by changes in T(1)-weighted imaging. In histology, tissue damage was seen at every location where MRI changes were observed, ranging from small (diameter <1.0 mm) areas of tissue necrosis to severe vascular damage and associated hemorrhagic infarct. In one location, small (diameter: 0.8 mm) damage was not detected in MRI. The thermal dose and peak temperature thresholds were between 12.3-40.1 equivalent min at 43 degrees C and 48.0-50.8 degrees C, respectively, and values of 17.5 equivalent min at 43 degrees C and 48.4 degrees C were estimated to result in tissue damage with 50% probability. Thermal dose and peak temperature were significantly better predictors than the applied acoustic energy and peak acoustic power (P < 0.01). BBB disruption was always accompanied by tissue damage. The temperature information was better than the applied acoustic power or energy for predicting the damage than the ultrasound parameters. MRI was sensitive in detecting threshold-level damage.     

Phenylketonuria: MR imaging of the brain with clinical correlation

Fifteen patients with biochemically documented phenylketonuria (PKU) were studied with use of magnetic resonance (MR) imaging with spin-echo T2-weighted pulse sequences. The resulting images demonstrated varying degrees of symmetric high signal intensity of the white matter within the posterior cerebral hemispheres. Involvement of the anterior hemispheres was seen only in cases with severe signal intensity changes. There was no involvement of the cerebral cortex, brain stem, or cerebellum. Moreover, no anatomic structural abnormalities were observed. Mild cortical atrophy was observed in eight of the 15 patients. There was no significant correlation between the patients' IQ scores and the level of MR signal intensity changes. Although MR imaging routinely shows relatively distinct abnormalities in patients with PKU, the clinical severity of the disease does not parallel its imaging severity.     

Association of heterotopic gray matter with seizures: MR imaging. Work in progress

Heterotopic gray matter, which previously had been associated with severe congenital malformations of the brain and developmental delay, was found without these associated conditions. The authors found ten cases of heterotopic gray matter on magnetic resonance (MR) images. The lesions had a signal intensity that was isointense compared with that of gray matter on T1, spin-density, and T2-weighted images. Nine of the ten cases were associated with a seizure disorder. The tenth case, discovered during a workup for metastatic lung disease, was confirmed with pathologic studies. Heterotopic gray matter is the presence of cortical neurons in an abnormal location, which may be periventricular (nodular) or within the white matter (laminar). A knowledge of heterotopic gray matter and its association with seizures may prevent the misinterpretation of findings on MR images.     

Subcortical damage and cortical functional changes in men and women with Fabry disease: a multifaceted MR study

PURPOSE: To prospectively compare brain magnetic resonance (MR) imaging and hydrogen 1 (1H) MR spectroscopy findings and to use functional MR imaging to explore the patterns of brain activation in men and women with Fabry disease (FD). MATERIALS AND METHODS: Eight men and eight women with FD (mean age, 38.8 years +/- 13.9 [standard deviation]) with absent or mild neurologic deficit and 16 healthy control subjects (eight men and eight women; mean age, 42.7 years +/- 15.3) gave informed consent to participate in the study, which was approved by the local ethical committee. Patients and control subjects underwent MR imaging, 1H MR spectroscopy of the frontal cortex and subcortical white matter, and functional MR imaging during repetitive flexion-extension of the last four fingers of the right hand. Extent of cerebral white matter damage was rated on fluid-attenuated inversion recovery MR images by using a visual score. Areas of activation were identified by using statistical parametric mapping software and the adoption of a height threshold of P < .001 (uncorrected) and an extent threshold of P < .05 (corrected). RESULTS: Men and women with FD showed a similar distribution of cerebral white matter changes, lacunar and cortical infarcts, small hemorrhages, and vertebrobasilar dolichoectasia. No significant (P > .05) difference was observed between patients with FD and control subjects for concentration of N-acetylaspartate, creatine, and choline. During the motor task, patients showed recruitment of additional cortical areas in comparison with control subjects. Increased activation of the contralateral sensorimotor area correlated (P = .002) with extent of white matter damage. CONCLUSION: Subcortical ischemic changes in men and women with FD are similar and are associated with increased recruitment of the sensorimotor network during a simple motor task, which might limit the functional effect of the white matter small-vessel disease.     

Cortical laminar necrosis caused by immunosuppressive therapy and chemotherapy

We report three patients in whom neurologic symptoms and cortical laminar necrosis developed after immunosuppressive treatment (cyclosporin A and FK 506) and polychemotherapy (vincristine and methotrexate). Initial neuroradiologic studies showed cortical and white matter involvement. Follow-up studies showed cortical hyper-intense lesions on T1-weighted MR images, consistent with cortical laminar necrosis. The clinical and radiologic data indicate that a transient hypoxic-ischemic process could have been responsible for the encephalic lesions in these three patients.     

A fatal case of myocardial damage due to misuse of the “designer drug” MDMA

A 39-year-old woman collapsed after oral intake of 3,4-methylenedioxymethyl-amphetamine (MDMA, “ecstasy”). After ingestion of the drug, she had felt persistent discomfort in her anterior chest area, and lost consciousness for a few minutes on the following morning. She was transported to a hospital and died seven days after collapse. A serum sample obtained on admission revealed an MDMA concentration of 1.2 mg/L, but no evidence of any other drug including amphetamine, methamphetamine, or other ring-substituted amphetamines. Microscopic examination at autopsy revealed striking changes in the heart, including small foci of myocyte necrosis with a surrounding macrophage inflammatory response, foci of fibrosis, and calcification accompanied by myocyte necrosis, these changes being predominant in the right ventricle. In the liver, hepatic necrosis was observed with fatty degeneration accompanied by inflammation. Myoglobinuria was demonstrated in the kidney by immunohistochemistry. Degeneration of neurons throughout the whole brain was also evident, in addition to haemorrhagic foci in the pons and medulla. Serious bronchopneumonia was also found in the right lung. These findings provide evidence that oral intake of MDMA can result in cardiotoxicity, inducing cardiac arrhythmia and cardiovascular collapse. As a consequence of the compromised blood supply, brain necrosis may occur, followed by severe bronchopneumonia. Ingestion of MDMA could also lead to liver damage as well as myoglobinuria resulting from rhabdomyolysis. These data suggest that death in this case had been caused largely by MDMA intoxication.     

Region and tissue differences of metabolites in normally aged brain using multislice 1H magnetic resonance spectroscopic imaging.

Quantitative measurements of regional and tissue specific concentrations of brain metabolites were measured in elderly subjects using multislice proton magnetic resonance spectroscopic imaging ((1)H MRSI). Selective k-space extrapolation and an inversion-recovery sequence were used to minimize lipid contamination and linear regression was used to account for partial volume problems. The technique was applied to measure the concentrations of N-acetyl aspartate (NAA), and creatine (Cr)- and choline (Cho)-containing compounds in cortical gray and white matter, and white matter lesions of the frontal and the parietal lobe in 40 normal elderly subjects (22 females and 18 males, 56-89 years old, mean age 74 +/- 8). NAA was about 15% lower in cortical gray matter and 23% lower in white matter lesions when compared to normal white matter. Cr was 11% higher in cortical gray matter than in white matter, and also about 15% higher in the parietal cortex than in the frontal cortex. Cho was 28% lower in cortical gray matter than in white matter. Furthermore, NAA and Cr changes correlated with age. In conclusion, regional and tissue differences of brain metabolites must be considered in addition to age-related changes when interpreting (1)H MRSI data.     

Reversal sign on CT: effect of anoxic/ischemic cerebral injury in children

A retrospective study was performed to determine the clinical and pathologic features, etiology, and outcome of children with the reversal sign. The reversal sign, a striking CT finding, probably represents a diffuse, anoxic/ischemic cerebral injury. CT features of the reversal sign are diffusely decreased density of cerebral cortical gray and white matter with a decreased or lost gray/white matter interface, or reversal of the gray/white matter densities and relatively increased density of the thalami, brainstem, and cerebellum. Twenty children with the reversal sign were retrospectively analyzed. We divided the patients into three groups: (1) acute reversal, (2) intermediate group, and (3) chronic reversal. There were nine cases of trauma (seven of child abuse); nine hypoxia/anoxia incidents (birth asphyxia, drowning, status epilepticus); one bacterial meningitis; and one degenerative encephalitis. All acute- and intermediate-group patients had respiratory problems requiring ventilator support and intensive care. In five of seven patients who died, autopsy findings were consistent with anoxic/ischemic encephalopathy. Surviving patients have profound neurologic deficits with severe developmental delay. The CT reversal sign carries a poor prognosis and indicates irreversible brain damage.     

Reversal sign on CT: effect of anoxic/ischemic cerebral injury in children

A retrospective study was performed to determine the clinical and pathologic features, etiology, and outcome of children with the reversal sign. The reversal sign, a striking CT finding, probably represents a diffuse, anoxic/ischemic cerebral injury. CT features of the reversal sign are diffusely decreased density of cerebral cortical gray and white matter with a decreased or lost gray/white matter interface, or reversal of the gray/white matter densities and relatively increased density of the thalami, brainstem, and cerebellum. Twenty children with the reversal sign were retrospectively analyzed. We divided the patients into three groups: (1) acute reversal, (2) intermediate group, and (3) chronic reversal. There were nine cases of trauma (seven of child abuse); nine hypoxia/anoxia incidents (birth asphyxia, drowning, status epilepticus); one bacterial meningitis; and one degenerative encephalitis. All acute- and intermediate-group patients had respiratory problems requiring ventilator support and intensive care. In five of seven patients who died, autopsy findings were consistent with anoxic/ischemic encephalopathy. Surviving patients have profound neurologic deficits with severe developmental delay. The CT reversal sign carries a poor prognosis and indicates irreversible brain damage.     

In vivo quantitative proton MRSI study of brain development from childhood to adolescence

PURPOSE: To quantify regional variations in metabolite levels in the developing brain using quantitative proton MR spectroscopic imaging (MRSI). MATERIALS and METHODS: Fifteen healthy subjects three to 19 years old were examined by in vivo multislice proton MRSI. Concentrations of N-acetyl aspartate (NAA), total choline (Cho), total creatine (Cr), and peak area ratios were determined in selected frontal and parietal gray and white matter regions, basal ganglia, and thalamus. RESULTS: In cortical gray matter regions, the ratio of NAA/Cho increased to a maximum at 10 years and decreased thereafter (P = 0.010). In contrast, in white matter, average ratios NAA/Cho increased linearly with age (P = 0.045). In individual brain regions, age-related changes in NAA/Cho were found in the putamen (P = 0.044). No significant age-related changes in NAA, Cho, Cr, or other metabolite ratios could be determined. CONCLUSION: Consistent with recent studies using other structural and functional neuroimaging techniques, our data suggest that small but significant changes occur in regional cerebral metabolism during childhood and adolescence. Non-linear age related changes of NAA/Cho in frontal and parietal areas, resembling previously reported age related changes in rates of glucose utilization and cortical volumes, may be associated with dendritic and synaptic development and regression. Linear age-related changes of NAA/Cho in white matter are also in agreement with age-related increases in white matter volumes, and may reflect progressive increases in axonal diameter and myelination.     

Metric to quantify white matter damage on brain magnetic resonance images

Purpose

Quantitative assessment of white matter hyperintensities (WMH) on structural Magnetic Resonance Imaging (MRI) is challenging. It is important to harmonise results from different software tools considering not only the volume but also the signal intensity. Here we propose and evaluate a metric of white matter (WM) damage that addresses this need.

Methods

We obtained WMH and normal-appearing white matter (NAWM) volumes from brain structural MRI from community dwelling older individuals and stroke patients enrolled in three different studies, using two automatic methods followed by manual editing by two to four observers blind to each other. We calculated the average intensity values on brain structural fluid-attenuation inversion recovery (FLAIR) MRI for the NAWM and WMH. The white matter damage metric is calculated as the proportion of WMH in brain tissue weighted by the relative image contrast of the WMH-to-NAWM. The new metric was evaluated using tissue microstructure parameters and visual ratings of small vessel disease burden and WMH: Fazekas score for WMH burden and Prins scale for WMH change.

Results

The correlation between the WM damage metric and the visual rating scores (Spearman ρ > =0.74, p < 0.0001) was slightly stronger than between the latter and WMH volumes (Spearman ρ > =0.72, p < 0.0001). The repeatability of the WM damage metric was better than WM volume (average median difference between measurements 3.26% (IQR 2.76%) and 5.88% (IQR 5.32%) respectively). The follow-up WM damage was highly related to total Prins score even when adjusted for baseline WM damage (ANCOVA, p < 0.0001), which was not always the case for WMH volume, as total Prins was highly associated with the change in the intense WMH volume (p = 0.0079, increase of 4.42 ml per unit change in total Prins, 95%CI [1.17 7.67]), but not with the change in less-intense, subtle WMH, which determined the volumetric change.

Conclusion

The new metric is practical and simple to calculate. It is robust to variations in image processing methods and scanning protocols, and sensitive to subtle and severe white matter damage.

     

脑放射损伤的影像学研究进展

脑放射损伤发病机制主要有三种学说即血管损伤、胶质损伤和免疫反应机制,最近多数学者的研究支持血管和胶质损伤机制,血管方面的改变在晚期放射效应中起主要作用。CT和MRI对局限性脑损伤和弥漫性脑白质损伤可明确诊断。MRI的T₂加权成像(T₂WI)显示水分变化敏感性高,又不受颅底线束硬化伪影的影响,MRI发现白质病变的敏感性是CT的2~3倍。如果是脑本身肿瘤放疗后,CT和MRI区别病灶复发或放射性坏死比较困难,PET和MRS(磁共振波谱成像)在两者鉴别诊断中则初步呈现出一定的优势。行PET检查时,如为肿瘤则代谢活跃,坏死则代谢低下,但敏感性和特异性欠理想。MRS测量感兴趣区内代谢产物的量或比率有助于两者的鉴别诊断。另外,PET功能成像和MRS还可预测放疗病人较早期无症状的可逆性放射损伤,以便及时应用激素等药物治疗,避免其进一步发展为临床症状明显的不可逆性损伤。