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2015, Practical neurology
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9 pages
1 file
Cerebral cortical lesions develop in many disorders including vascular diseases, metabolic disorders, inflammatory diseases, tumours, infections and genetic disorders. In some diseases, the cortical involvement is typical and sometimes isolated, while in others the cortical lesions occur only occasionally (often alongside other typical extra-cortical lesions). In this review, we discuss mainly the MRI characteristics of cortical lesions encountered in different disorders. From a radiological perspective, identifying the origin of a cortical lesion depends on the exact localisation of signal changes, the presence of extra-cortical lesions, the signal changes on different MRI sequences and the evolution of the radiological abnormalities over time. These must be interpreted in light of the history and clinical state of the patient, and other radiological and non-radiological examinations.
F1000posters, 2011
MR data analysis Cortical Lesions. All CLs were identified on DIR images. CLs were defined as those focal hyperintensities entirely or partly located in the cortical GM, in accordance to recently published consensus recommendations 7. Lesion Volumes. T2 hyperintense white matter (WM) lesions were identified on PD/T 2-W images, employing a segmentation technique based on user-supervised local thresholding. Brain Volumes. Normalized volumes of brain (NBV) and cortex (NCV) were measured on T 1-W images by using the software SIENAX, part of FSL. Statistical analysis Comparisons between RIS subjects with and without CLs were performed with Mann-Whitney test. Correlations of CLs with MRI features were done through Spearman coefficient. A p-value <0.05 was considered for statistical significance.
Cerebrovascular Diseases, 2002
Magnetic resonance imaging (MRI) is very sensitive for the detection of white matter lesions (WML), which occur even in normal ageing. Intrinsic WML should be separated from physiological changes in the ageing brain, such as periventricular caps and bands, and from dilated Virchow-Robin spaces. Genuine WML are best seen with T2-weighted sequences such as long TR dual-echo spinecho or FLAIR (fluid-attenuated inversion recovery); the latter has the advantage of easily separating WML from CSF-like lesions. Abnormal T2 signal in MRI is not specific, and can accompany any change in tissue composition. In the work-up of WML in small vessel disease, magnetic resonance angiography can be used to rule out (concomitant) large vessel disease, and diffusionweighted MRI to identify new ischaemic lesions (amidst pre-existing old WML). The differential diagnosis of WML includes hereditary leukodystrophies and acquired disorders. The leukodystrophies that can present in adult age include metachromatic leukodystrophy, globoid cell leukodystrophy, adrenomyeloneuropathy, mitochondrial disorders, vanishing white matter, and cerebrotendinous xanthomatosis. These metabolic disorders typically present with symmetrical abnormalities that can be very diffuse, often with involvement of brainstem and cerebellum. Only the mitochondrial disorders tend to be more asymmetric and frequently involve the grey matter preferentially. Among the acquired white matter disorders, hypoxic-ischaemic causes are by far the most prevalent and without further clinical clues there is no need to even consider the next most common disorder, i.e. multiple sclerosis (MS). Among the nonischaemic disorders, MS is far more common than vasculitis, infection, intoxication and trauma. While vasculitis can mimic small vessel disease, MS has distinctive features with preferential involvement of the subcortical U-fibres, the corpus callosum, temporal lobes and the brainstem/cerebellum. Spinal cord lesions are very common in MS, but do not occur in normal ageing nor in small vessel disease.
The Neuroradiology Journal, 2009
Medicine, 2016
To date, it remains largely unknown whether there is in radiologically isolated syndrome (RIS) brain damage beyond visible T2 white matter lesions. We used single-voxel proton magnetic resonance spectroscopy and diffusion tensor imaging (3 T MRI) to analyze normal-appearing brain tissue regions in 18 RIS patients and 18 matched healthy controls. T2-hyperintense lesion volumes and structural brain volumes were also measured. The absolute metabolite concentrations and ratios of total N-acetylaspartate+Nacetylaspartyl glutamate (NAA), choline-containing compounds, myoinositol, and glutamine-glutamate complex to creatine were calculated. Spectral analysis was performed by LCModel. Voxelwise morphometry analysis was performed to localize regions of brain tissue showing significant changes of fractional anisotropy or mean diffusivity. Compared with healthy controls, RIS patients did not show any significant differences in either the absolute concentration of NAA or NAA/Cr ratio in mid-parietal gray matter. A trend toward lower NAA concentrations (-3.35%) was observed among RIS patients with high risk for conversion to multiple sclerosis. No differences in the other metabolites or their ratios were observed. RIS patients showed lower fractional anisotropy only in clusters overlapping lesional areas, namely in the cingulate gyrus bilaterally and the frontal lobe subgyral bilaterally (P < 0.001). Normalized brain and cortical volumes were significantly lower in RIS patients than in controls (P = 0.01 and P = 0.03, respectively). Our results suggest that in RIS, global brain and cortical atrophy are not primarily driven by significant occult microstructural normal appearing brain damage. Longitudinal MRI studies are needed to better understand the pathological processes underlying this novel entity. Abbreviations: Cho = choline-containing compounds, CIS = clinically isolated syndrome, Cr = creatine, DTI = diffusion tensor imaging, Glx = glutamine-glutamate complex, 1H-MRS = proton magnetic resonance spectroscopy, MS = multiple sclerosis, MI = myo-inositol, MRI = magnetic resonance imaging, NAA = N-acetylaspartate+N-acetylaspartyl glutamate, PRESS = point resolved spin echo, RIS = radiologically isolated syndrome, SD = standard deviation.
Medicine, 2016
The unanticipated magnetic resonance imaging (MRI) detection in the brain of asymptomatic subjects of white matter lesions suggestive of multiple sclerosis has recently been named as radiologically isolated syndrome (RIS). The pathophysiological processes of RIS remain largely unknown and questions as to whether gray matter alterations actually occur in this entity are yet to be investigated in more detail. By means of a 3 T multimodal MRI approach, we searched for cortical and deep gray matter changes in a cohort of RIS patients. Seventeen RIS patients, 17 clinically isolated syndrome (CIS) patients (median disease duration from symptom onset ¼ 12 months), and 17 healthy controls underwent MRI and neuropsychological testing. Normalized deep gray matter volumes and regional cortical thickness were assessed using FreeSurfer. SIENAX was used to obtain normalized global and cortical brain volumes. Voxelwise morphometry analysis was performed by using SPM8 software to localize regions of brain tissue showing significant changes of fractional anisotropy or mean diffusivity. Although no differences were observed between CIS and healthy controls groups, RIS patients showed significantly lower normalized cortical volume (673 AE 27.07 vs 641 AE 35.88 [cm 3 Â 10 3 , Tukey P test ¼ 0.009) and mean thalamic volume (0.0051 AE 0.4 vs 0.0046 AE 0.4 mm, P ¼ 0.014) compared with healthy controls. RIS patients also showed significant thinning in a number of cortical areas, that were primarily distributed in frontal and temporal lobes (P < 0.05, uncorrected). Strong correlations were observed between T2-white matter lesion volume and regional cortical thickness (rho spearman ranging from 0.60 to 0.80). Our data suggest that white matter lesions on T2-weighted images are not the only hallmark of RIS. Future longitudinal studies with larger samples are warranted to better clarify the effect of RIS-related white matter lesions on gray matter tissue.
Neurology, 2016
Objective: To use multimodal neuroimaging to evaluate the influence of heterogeneous underlying pathology in corticobasal syndrome (CBS) on the neuroanatomical distribution of disease. Methods: We performed a retrospective evaluation of 35 patients with CBS with T1-weighted MRI, diffusion tensor imaging, and neuropathologic, genetic, or CSF evidence of underlying pathology. Patients were assigned to 2 groups: those with evidence of Alzheimer pathology (CBS-AD) and those without Alzheimer pathology (CBS-non-AD). Group comparisons of CBS-AD and CBS-non-AD assessed clinical features, gray matter (GM) cortical thickness, and white matter (WM) fractional anisotropy. Results: CBS-AD was found in 34% (n 5 12) and CBS-non-AD in 66% (n 5 23) of CBS patients. Clinical evaluations revealed that CBS-non-AD had a higher frequency of asymmetric rigidity compared to CBS-AD, but groups otherwise did not differ in dementia severity, impairments in cognition, or rates of extrapyramidal symptoms. We found frontoparietal GM and WM disease in each group compared to healthy, demographically comparable controls, as well as multimodal neuroimaging evidence of a double dissociation: CBS-non-AD had WM disease in the corpus callosum, corticospinal tract, and superior longitudinal fasciculus relative to CBS-AD, and CBS-AD had reduced temporoparietal GM relative to CBS-non-AD, including the precuneus and posterior cingulate. Conclusions: Patients with CBS have a pathology-mediated dissociation of GM and WM disease. Multimodality neuroimaging may be useful for improving in vivo pathologic diagnosis of CBS.
BMJ, 2009
Objective-Incidental findings identified by MRI of the brain have been reported in up to18% of healthy adults, with clinically significant neuropathology in 0.5-2%. There are two smaller series of incidental findings on MRI of the brain in children. We describe the prevalence and range of incidental intracranial abnormalities identified by MRI of the brain in a large group of children screened for a clinical trial.
Neurologia i neurochirurgia polska
The differential diagnosis of cerebral ring enhancing lesions is usually challenging and involves the use of multiple paraclinical tools such as central nervous system (CNS) imaging and cerebrospinal fluid (CSF) studies [1,2]. These lesions can be the manifestation of a variety of pathologies, including infection, primary or secondary neoplastic processes and demyelinating diseases, amongst others. By using conventional magnetic resonance imaging (MRI), an accurate diagnosis of ring enhancing lesions is often difficult. Therefore, the use of novel imaging techniques plays a crucial role in fully characterizing and identifying the underlying pathology of such ring enhancing lesions. A 23-year-old man from the south of Chile was admitted to our Department of Neurology in Santiago, with a history of 2 weeks of multiple self-limiting episodes of involuntary clonic movements of his right face and arm, and one single episode of generalized tonic-clonic seizure. On admission, his vital signs and general examination were unremarkable. Initial neurological examination revealed mild right hemiparesis (MCR score 4) with symmetrical tendon reflexes and an ipsilateral up-going plantar reflex. Cranial nerves and sensory function were normal. Complete blood count, erythrocyte sedimentation rate and C-reactive protein were normal, together with negative antibody testing for HIV, Hepatitis B and C, and VDRL. CSF analysis showed 4.8 leukocytes per microliter, protein of 0.27 g/L, normal glucose levels, and a negative Gram stain and culture. The brain MRI showed one cortico-subcortical lesion in the left precentral frontal region (Fig. 1), mildly hyperintense to CSF on T1-weighted image, hyperintense on T2-weighted image and fluid-attenuated inversion recovery (FLAIR) image,
American Journal of Neuroradiology, 2009
BACKGROUND AND PURPOSE: The clinical diagnosis of corticobasal degeneration (CBD) is often difficult due to varied clinical manifestations. In 4 patients with neuropathologically confirmed CBD, characteristic imaging findings and correlations with neuropathologic features were evaluated. Furthermore, imaging findings in CBD were compared with neuropathologically confirmed progressive supranuclear palsy (PSP) for a differential diagnosis. MATERIALS AND METHODS: Four patients with neuropathologically confirmed CBD were studied. We evaluated the area of the tegmentum in the midsagittal plane, subcortical white matter (SCWM) abnormality, asymmetric cerebral atrophy, and signal-intensity abnormality in the subthalamic nuclei on MR imaging and compared them with histopathologic findings. Then, MR imaging findings in CBD were compared with those in 13 patients with PSP. RESULTS: On MR imaging, 3 patients had asymmetric cerebral atrophy extending to the central sulcus. On midsagittal sections, the mean midbrain tegmentum area was 66 mm 2 , being markedly smaller than normal, but there was no significant difference between PSP and CBD. All patients had signalintensity abnormalities of the SCWM, constituting primary degeneration neuropathologically; however, no diffuse signal-intensity abnormality in the SCWM existed in the 13 patients with PSP. In 3 patients, T1-weighted images showed symmetric high signal intensity in the subthalamic nuclei. Neuropathologically, these areas showed characteristic CBD. MR imaging signal-intensity changes also existed in 4 patients with PSP; however, subthalamic nucleus degeneration was more severe in PSP than in CBD. CONCLUSIONS: In cases with midbrain tegmentum atrophy and signal-intensity changes in the subthalamic nuclei, the differential diagnosis distinguishing CBD from PSP based on MR imaging alone was difficult. White matter lesions and asymmetric atrophy can be useful for a differential diagnosis.
Epilepsia, 2009
Neuroimaging is essential in the work-up of patients with intractable epilepsy. In pediatric patients with medically refractory epilepsy, cortical dysplasias account for a large percentage of the epileptogenic substrate. Unfortunately, these are also the most subtle lesions to identify. For this reason, there has been ongoing interest in utilizing new advanced magnetic resonance imaging (MRI) techniques to improve the ability to identify, diagnose, characterize, and delineate cortical dysplasias. Technologic gains such as multichannel coils (32 phased array and beyond) and higher field strengths (3T, 7T, and greater) coupled with newer imaging sequences such as arterial spin labeling (ASL), susceptibility weighted imaging (SWI) and diffusion tensor/spectrum imaging (DTI/DSI) are likely to increase yield. Improved MRI techniques coupled with a multimodality approach including magnetoencephalography (MEG), positron emission tomography (PET), and other techniques will increase sensitivity and specificity for identifying cortical dysplasias.
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