Tuberous sclerosis: Evaluation of intracraneal lesions
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1 Tuberous sclerosis: Evaluation of intracraneal lesions Poster No.: C-3394 Congress: ECR 2010 Type: Educational Exhibit Topic: Neuro - Your latest results Authors: J. R. Docampo, M. Cabrini, C. Morales, C. Bruno; Buenos Aires/ AR Keywords: cortical tubers, subependymal hamartomas, giant-cell astrocytoma Keywords: Neuroradiology brain, Neuroradiology peripheral nerve, Neuroradiology spine DOI: /ecr2010/C-3394 Any information contained in this pdf file is automatically generated from digital material submitted to EPOS by third parties in the form of scientific presentations. References to any names, marks, products, or services of third parties or hypertext links to thirdparty sites or information are provided solely as a convenience to you and do not in any way constitute or imply ECR's endorsement, sponsorship or recommendation of the third party, information, product or service. ECR is not responsible for the content of these pages and does not make any representations regarding the content or accuracy of material in this file. As per copyright regulations, any unauthorised use of the material or parts thereof as well as commercial reproduction or multiple distribution by any traditional or electronically based reproduction/publication method ist strictly prohibited. You agree to defend, indemnify, and hold ECR harmless from and against any and all claims, damages, costs, and expenses, including attorneys' fees, arising from or related to your use of these pages. Please note: Links to movies, ppt slideshows and any other multimedia files are not available in the pdf version of presentations. Page 1 of 29
2 Learning objectives To show our imaging findings of intracranial lesions found in patients with Tuberous Sclerosis (TS) who were evaluated with MRI and/or CT. To show their typical imaging features. Page 2 of 29
3 Background Tuberous sclerosis is a neurocutaneous disease characterized by the clinical triad of mental retardation, seizures and skin lesions. Characteristic brain lesions can be diagnosed with MRI and CT. Twenty-seven patients with a clinical diagnosis of TS (20 MRI images, 2 CT scans, and 5 with both methods) were examined (age range, 2 months to 28 years). There were 15 male and 12 female patients. A 0.5 and 1.5 Tesla MRI Scanners and axial/helical CT scanners were used. One patient was evaluated with spectroscopy and diffusion. Monovoxel magnetic resonance spectroscopy was performed applying PRESS sequences, echo times of 25ms and 144ms. The protocol used on MRI consisted in SE axial T1- and T2-weighted sequences, FLAIR and GRE sequences (TK: 7mm / GAP: 0.5mm). In studies requested with paramagnetic contrast agents, T1-FSE sequences were added in the 3 post-contrast planes. Sixteen patients required paramagnetic contrast agents, with an administered dose of 0.2ml/kg body weight. Twenty-three patients underwent general anesthesia for the performance of the study. Page 3 of 29
4 Imaging findings OR Procedure details In 26 cases, the examinations showed subependymal hamartomas, cortical tubers in 26 patients, white matter lesions in 3 cases, sulcal expansion in 3 patients, 2 parenchymal cysts, giant-cell astrocytoma in 1 case, ventricular expansion in 1 patient and one patient with a space-occupying lesion in posterior fossa. Fig.: Table 1: Patients with tuberous sclerosis. SH: subependymal hamartomas; GCA: giant cell astrocytoma; CoT: cortical tubers; PC: parenchymatous cysts; WML: Page 4 of 29
5 white matter lesions; CL: cerebellous; VSD: ventricular system dilation; CSW: widened convexity sulci. References: Neuro MR, Fundacion Cientifica del Sur - Buenos Aires/AR Fig.: Graph 1: Frequency of intracranial findings in patients with tuberous sclerosis. References: Neuro MR, Fundacion Cientifica del Sur - Buenos Aires/AR Subependymal nodules These are hamartomas which histologically contain giant cells with features of neurons and astrocytes. In our case history, subependymal nodules were the most frequent finding, identified in 26 patients. The imaging appearance of subependymal hamartomas on CT scan and MRI varies with age of patient (1). On CT scan, subependymal hamartomas are isodense with respect to the white matter; in older patients they may become calcified (Picture 1 on page 10) and may be identified as hyperdense (2). Page 5 of 29
6 Nodules calcify progressively during the first two decades of life; a calcified nodule (1) is hardly found in patients under 1 year of age. We found calcified subependymal hamartomas in 4 patients under 1 year of age (Picture 2 on page 10). On MRI, subependymal nodules in newborns are slightly hyperintense on T1 with respect to the white matter (Picture 3 on page 11) and of heterogeneous intensity on T2; this is due to the hypomyelination of the white matter. As myelination occurs, nodules become isointense on T1 and T2 with respect to it (Picture 4 on page 12). If they calcify, they are markedly hypointense on gradient echo sequences (2). Post-contrast paramagnetic identification varies, absence of enhancement being more (2) frequent. In our study, 12 of the 16 patients evaluated with paramagnetic contrast agents showed enhancement of subependymal hamartomas (Pictures 5 on page 13 and 6 on page 14). Subependymal astrocytomas These are histologically benign tumors formed by giant cells which present features of astrocytes and neurons. In our case history, a subependymal astrocytoma was identified in 1 patient. Their typical location is near Monro's holes. Subependymal astrocytomas may cause obstructive hydrocephaly (2). Occurrence age is between 8 and 18 years. Their diagnosis and follow-up are important, because if they grow and produce obstructive hydrocephaly, they may require neurosurgery. On CT and MRI, subependymal astrocytomas are bigger than subependymal hamartomas; they are usually enhanced by paramagnetic contrast agents (Picture (2) 7 on page 15), they may calcify and present bleeding. Differential diagnosis with subependymal hamartomas is determined by the "evolutional control", since subependymal astrocytomas grow whereas hamartomas do not (1). Cortical tubers These are benign hamartomatous lesions, which rarely become malignant. They may be single or multiple. In our study, 26 patients presented with cortical tubers. The frontal lobes are the most frequent site, followed by the parietal, occipital and temporal lobes in decreasing order (2). Page 6 of 29
7 Histologically they are composed of bizarre giant cells, dense fibrillar gliosis and disorganized myelin bands. On CT scan, in newborns and unweaned babies, hamartomas are hyperdense (Picture 8 on page 16) and the sulci where they are located are usually widened. Throughout the years they become hypodense (Picture 9 on page 16) calcify. (1). Cortical tubers may also On MRI, at the beginning of life cortical tubers are slightly hyperintense on T1-weighted sequences with respect to the white matter, and hypointense on T2. As the encephalus myelinates, tubers become iso-hypointense on T1 and hyperintense on T2 (Picture 10 on page 17). FLAIR sequence has an enhanced sensitivity in the diagnosis of cortical tubers in children as well as in adults (Picture 11 on page 18). Cortical tubers are identified as hyperintense images of diffuse limits at the site where the lesions are located (1). When tubers calcify, they are identified as hypointense on gradient echo sequences and slightly hyperintense on T1 (2). Some authors divide cortical tubers into 2 types: "gyral core" and "sulcal island". Gyral core is a hyperintense lesion on T2 and hypointense on T1 (Picture 12 on page 18) which is located in the center of an expanded (widened) circumvolution, the cortex of which is of normal thickness (3, 4). Sulcal island is a lesion where the subcortical white matter is hyperintense on T2 and iso-hypointense on T1 (Picture 13 on page 19), and involves two adjacent circumvolutions; the cortex is of conserved thickness (3, 4). Parenchymatous cysts These lesions are usually located at any site, although they are mostly found in the periventricular white matter (2). In our study, 2 patients were reported with intraparenchymatous cysts. On CT scann, they are identified as round hypodense images. On MRI, they are hyperintense images on T2, and hypointense on T1 and FLAIR (Picture 14 on page 20). White matter lesions Page 7 of 29
8 These lesions are formed by giant cells. These cells are 5 to 10 times larger than astrocytes. Giant cells have features of neurons and of glial cells (2). In our study, they have been reported in 3 patients. These lesions present different appearances; they can be linear, cuneiform, or form a conglomerate. The usual appearance is the linear pattern, from the cortex to the periventricular region (2). On CT scan, they are usually slightly hypodense, and they may also calcify (Picture 15 on page 21). On MRI, they are identified as hyperintense images on T2. They are rarely enhanced with postcontrast agents (2). Cerebellous lesions (1) These lesions are identical to cortical tubers. They are present in 10% of patients. In our study, we only found one patient with a tuber located at the bottom of the fourth ventricle, calcified (hypointense on gradient echo), which is faintly enhanced with paramagnetic postcontrast agents (Picture 16 on page 22). They are difficult to diagnose with CT scan due to the great number of artifacts that the method has in the posterior fossa; therefore, the study of choice to identify them is MRI. Magnetic resonance diffusion and spectroscopy One patient underwent diffusion-weighted MR imaging, which confirmed that subependymal hamartomas and cortical tubers are isointense with respect to the white (5) matter on DWI. In the apparent diffusion coefficient (ADC), subependymal hamartomas are discreetly hypointense and cortical tubers are slightly hyperintense (Picture 17 on page 23). In the short echo time spectroscopy, a decrease in N-acetylaspartate (NAA) was confirmed, and a slight increase in myoinositol at the level of the cortical tubers (Picture 18 on page 24and 19 on page 25). On the long echo time PRESS sequence, a slight (6) increase in NAA was confirmed. Subependymal hamartomas cannot be evaluated by spectroscopy due to their periventricular location, since the cephaloraquideal liquid alters the spectrum. Page 8 of 29
9 Page 9 of 29
10 Images for this section: Fig. 0: CT scan of a one-year-old male patient, where hyperdense nodullary images are identified, calcified, of subependymal location, compatible with subependymal hamartomas and cortical hypodense images compatible with adolescents. Page 10 of 29
11 Fig. 0: CT scan of a 2-month-old male patient who had seizures in his first month of life. Hyperdense subependymal nodules are shown (arrows) slightly calcified (subependymal hamartomas). Page 11 of 29
12 Fig. 0: MRI on axial T1-weighted sequences of a 5-year-old male patient, who presents with hyperintense subependymal nodules located in both lateral ventricles (arrows). Page 12 of 29
13 Fig. 0: MRI on axial T1-weighted sequences (A) and axial T2 (B) of a female patient, who presents with isointense subependymal hamartomas on T1 and T2 with respect to the white matter (arrows). Page 13 of 29
14 Fig. 0: MRI on axial T1 without contrast agent (A) and with gadolinium (B) of a 2-yearold male patient, who presents with a subependymal nodule, enhanced with postcontrast agents (arrow). Page 14 of 29
15 Fig. 0: A subependymal nodule of significant size is identified, located on the wall of the left lateral ventricle (arrows), hypointense on T2 (A), isointense on T1 (B) and which is significantly enhanced with paramagnetic postcontrast agents (C), compatible with subependymal hamartoma. Fig. 0: On this MRI of a 7-year-old female patient, an intraventricular, ovoid, voluminous mass is observed, which produces hydrocephaly as it occludes Monro's holes; this mass Page 15 of 29
16 is hyperintense on T2 (A), isointense on T1 (B) and is significantly enhanced after the administration of paramagnetic contrast agents (C). This image is compatible with a subependymal giant cell astrocytoma. Fig. 0: CT scan of a 2-month-old male patient, where cortical hyperdense images are identified, compatible with cortical tubers (arrows). Page 16 of 29
17 Fig. 0: CT scan of a 1-year-old male patient, which shows cortical hypodense images, compatible with cortical tubers (arrows). Page 17 of 29
18 Fig. 0: MRI of a 2-year-old female patient, who presents with multiple hyperintense images on T2 (A), and hypointense on T1 (B), compatible with cortical tubers (arrows). Fig. 0: MRI of a 2-year-old male patient which shows, on FLAIR sequence, multiple hyperintense cortical images (arrows). Page 18 of 29
19 Fig. 0: MRI of a 7-year-old female patient. On the coronal T2-weighted sequence a hyperintense lesion is shown, located in the center of an expanded circumvolution (arrows), labeled "gyral core". Page 19 of 29
20 Fig. 0: MRI of a 2-year-old male patient. A lesion in the subcortical white matter is identified, hyperintense on axial T2-weighted sequence, which involves two adjacent circumvolutions (arrows), labeled "sulcal island". Page 20 of 29
21 Fig. 0: MRI of an 8-year-old female patient, which presents a hyperintense image on T2 (A) and hypointense on T1 and FLAIR (B and C), round, adjacent to the occipital prolongation of the right lateral ventricle (arrows)."parenchymatous cysts". Page 21 of 29
22 Fig. 0: CT scan and MRI of a 2-year-old male patient who presents with a lesion in the white matter corresponding to the left external capsule (arrows), calcified, identified as hyperdense on CT scan (A), hypointense on T2 (B) and hyperintense on T1 (C). Page 22 of 29
23 Fig. 0: MRI of a 16-year-old male patient who presents with a hypointense image on gradient-echo at the bottom of the fourth ventricle (A), which is enhanced with paramagnetic contrast agents (B), compatible with cerebellous calcified hamartoma (arrows). Page 23 of 29
24 Fig. 0: Axial T2-sequence (A) of a 1-year-old male patient, who presents with subependymal hamartomas in both lateral ventricules (white arrows), and cortical tubers (circle). In the diffusion, in DWI (B) subependymal hamartomas are isointense with respect to the white matter (arrows). In ADC (C), subependymal hamartomas are slightly hypointense with respect to the white matter (arrows) and the cortical tubers are hyperintense (circle). Page 24 of 29
25 Fig. 0: continued: The same patient underwent a spectroscopy applying monovoxel technique with PRESS sequences, echo time 25ms. corresponds to the normal side. Page 25 of 29
26 Fig. 0: continued. Spectroscopy applying monovoxel technique with PRESS sequences, echo time 25ms. Corresponds to the evaluation of the cortical tuber, where a decrease in the NAA peak is observed, and an increase in the myoinositol peak. Page 26 of 29
27 Conclusion In our study, subependymal hamartomas were the most frequent intracranial lesion (imaging feature) found in 26 patients with clinical diagnosis of TS, followed by cortical tubers in 26 cases. Giant-cell astrocytoma was found in 1 case, and was associated to ventricular expansion. Spectroscopy showed a decrease in NAA. Page 27 of 29
28 Personal Information Dr. Docampo Jorge Neurorradiologo. Fundación Cientifica del Sur (Lomas de Zamora. Bs As. Argentina). Jefe de servicio de resonancia magnética del H.I.G.A Pedro Fiorito. Bs As. Argentina. Page 28 of 29
29 References (1) Barkovich AJ. Facomatosis. En: Barkovich AJ. Neuroimagenología pediátrica. Madrid: Marbán 2001; 6: (2) Hart B, Depper M, Clericuzio C. Síndromes neurocutáneos. En: Orrison WW, ed. Neurorradiología. Madrid: Harcourt 2001; 2(51): (3) Nixon JR, Houser OW, Gómez MR, Okazaki H. Cerebral tuberous sclerosis: MR imaging. Radiology 1989;170: (4) Takanashi J, Sugita K, Fujii K, Niimi H. MR evaluation of tuberous sclerosis: increased sensitivity with fluid-attenuated inversion recovery and relation to severity of seizures and mental retardation. AJNR 1995;16: (5) Makki M, Chugani D, Janisse J, Chugani H. Characteristics of abnormal diffusivity in normal-appearing white matter investigated with diffusion tensor MR imaging in tuberous sclerosis complex. AJNR 2007; 28: (6) Mukonoweshuro W, Wilkinson I and Griffiths P. Proton MR spectroscopy of cortical tubers in adults with tuberous sclerosis complex. AJNR 2001; 22: Page 29 of 29
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