|Year : 2017 | Volume
| Issue : 2 | Page : 61-72
Intracranial T1 Weighted Hyperintense Lesions
Neetika Gupta1, Aishwarya Gulati1, Arif Mirza1, Vaibhav Gulati2, Parveen Gulati1
1 MRI Division, Dr Gulati Imaging Institute, J-16 Hauz Khas Enclave, New Delhi, India
2 Maulana Azad Medical College, Bahadur, Shah Zafar Marg, New Delhi, India
|Date of Web Publication||28-Jun-2017|
MRI Division, Dr Gulati Imaging Institute, J-16, Hauz Khas Enclave, New Delhi 110016
Source of Support: None, Conflict of Interest: None
Most of the intracranial pathologies appear hypointense on T1-weighted images. However, there are some intracranial substances and pathological lesions that appear hyperintense on T1-weighted images. This article aims to highlight the various cranial lesions showing hyperintense signal on T1-weighted images. Various substances which are responsible for the intrinsically high signal intensity observed in intracranial lesions at T1-weighted magnetic resonance imaging such as methemoglobin, melanin, lipid, various minerals, and other will be enumerated, and how these signal changes can lead to more specific diagnoses will be discussed.
Keywords: Lipid, manganes, melanin, T1 hyperintense
|How to cite this article:|
Gupta N, Gulati A, Mirza A, Gulati V, Gulati P. Intracranial T1 Weighted Hyperintense Lesions. MAMC J Med Sci 2017;3:61-72
|How to cite this URL:|
Gupta N, Gulati A, Mirza A, Gulati V, Gulati P. Intracranial T1 Weighted Hyperintense Lesions. MAMC J Med Sci [serial online] 2017 [cited 2019 Oct 22];3:61-72. Available from: http://www.mamcjms.in/text.asp?2017/3/2/61/209025
| Background|| |
Substances with shorter T1 relaxation times appear hyperintense on T1-weighted imaging [Table 1]. The specific effect of T1 weighting on the imaging appearance of a substance depends on the repetition time, echo time, proton density, and magnetic field strength. T1 (or spin-lattice) relaxation is the process by which protons return to their normal equilibrium magnetization in a static magnetic field after radiofrequency pulse excitation. Protons exchange excess energy with the magnetic “lattice” of neighboring molecules in their return to the equilibrium state. The value of T1 is a measure of the time that is required for spins to return to 63% of their baseline magnetization and is primarily determined by the size of molecule to which spins are bound. Macromolecules such as proteins are subject to greater inertial forces in a magnetic field and, hence, have short T1 times, smaller molecules such as unbound water equilibrate rapidly and have long T1 times. On T1W images, tissues with large T1 have hypointense signal and tissues with short T1 have hyperintense signal.,
| Lesions with Hemorrhagic Components|| |
Magnetic resonance imaging (MRI) appearances of hemorrhages and lesions containing blood products largely depend on the age of the blood. Both intracellular methemoglobin (early subacute phase hemorrhage, 3–7 days after onset [Figure 1]) and extracellular methemoglobin (late subacute phase hemorrhage, from 8 days to 1 month after onset) produce T1 shortening effects and, therefore, have intrinsically high signal intensity on T1-weighted images. This short T1 of methemoglobin is attributed to paramagnetic dipole–dipole interactions.
|Figure 1: Axial T2 (a), T1 (b) showing a parenchymal hemorrhagic lesion with subacute hemorrhage showing hyperintense signal on T1 images in the right temporal lobe. Coronal FLAIR image (c) shows loss of flow void in the transverse sinus and MR venography (d) showing transverse and sigmoid sinus thrombosis with multiple collaterals – Venous infarct in right temporal lobe|
Click here to view
| Cavernous Malformations|| |
These are uncommon congenital or acquired vascular anomalies that occur in approximately 0.5% of the general population. These may be asymptomatic or patients may present with seizures or neurologic deficits depending upon the location and size of the lesion. MRI appearance is highly characteristic and classic features seen at T2- and T2*-weighted images include a lesion with a popcorn ball-like appearance and a low signal intensity rim due to hemosiderin deposition [Figure 2]. Subacute hemorrhage and degraded blood products within the lesion form a halo of signal hyperintensity around the lesion on T1-weighted images, a useful finding for differentiating cavernous malformations from hemorrhagic tumors and other intracranial hemorrhages.,
|Figure 2: Axial T1(a) & gradient echo (b) images showing a Cavernous angioma in the right temporal lobe seen as a reticulated core of high and low signal intensities surrounded by a hypointense rim of hemosiderin on axial T1 images and area of markedly lowintense signal with central focal areas of hyperintense signal on GE images|
Click here to view
| Arteriovenous Malformations|| |
The most common symptomatic cerebral vascular malformations, may occur sporadically, congenitally or in association with a history of trauma. They are most commonly located in the supratentorial location (80–90%). Arteriovenous malformations (AVMs) contain multiple tightly packed tortuous tubular flow void structures on T1- and T2-weighted images secondary to patent arteries with high blood flow and do not contain brain tissue within the nidus of lesion. The signal-intensity characteristics of AVMs depend on the presence of various components. Areas of T1 shortening may be detected secondary to thrombosis, hemorrhage, or calcification. They are not usually associated with mass effect, except in the case of a recent hemorrhage or venous occlusion.,
| Intracranial Aneurysms|| |
Aneurysms are the most common reasons for nontraumatic subarachnoid hemorrhage, which may cause areas of T1 shortening during the subacute phase of subarachnoid bleeding. The aneurysms depending on their shape may be saccular, fusiform, or blister-like structures. Larger saccular aneurysms greater than 25 mm in diameter are referred to as giant aneurysms and lumina of giant saccular aneurysms may be at least partially occupied by a thrombus that often has a lamellar or concentric appearance. The layers of intermediate- and high signal intensity on T1 are caused by thrombi of different ages.,
| Cerebral Venous Thrombosis|| |
Cerebral venous sinus thrombosis is a not so uncommon condition that usually manifests with a headache. The appearance of venous thrombosis at MRI varies, depending mainly on the age of the thrombus at presentation. A subacute thrombus often has high signal intensity on T1-weighted images; the signal intensity on T2-weighted images is more variable but is also usually high [Figure 3]. Gradient-recalled echo sequences are particularly sensitive to the susceptibility effects of paramagnetic blood breakdown products in venous thrombi, which produce blooming artifacts on images. Magnetic resonance (MR) venography is effective for depicting the extent of venous occlusion and collateral vessel formation.
|Figure 3: Sagittal T1 weighted image showing hyper-intense signal of the thrombus replacing the low-signal of flowing blood in the superior sagittal sinus – Superior sagittal sinus thrombosis|
Click here to view
| Brain Infarcts|| |
Brain infarcts usually result from vascular occlusive diseases involving arteries or (very rarely) veins. The MRI appearance of cerebral infarcts depends mainly on the age of infarct at the time of examination. T1-hyperintense areas may be seen starting from the second day of infarct until the end of second month due to associated area of hemorrhage secondary to the dissolution of an embolus allowing a reperfusion hemorrhage or due to anticoagulant treatment. Multifocal hemorrhagic infarcts suggest an embolic source. Venous pathologies, such as dural sinus thrombosis, should also be considered as the underlying reason of hemorrhagic cerebral infarction.,
| Lipid-containing Lesions|| |
High signal intensity on T1-weighted MRI is a result of short T1 relaxation time of hydrogen nuclei within lipid molecules. Frequency-selective fat suppression and short inversion time inversion-recovery sequences are routinely used at MRI to eliminate this high signal intensity and to differentiate various T1 hyperintense lesions from fat. The difference in the precession frequencies of protons in lipid and protons in water also results in a chemical shift artifact at fat–water interfaces, which is also a useful property in diagnostic MRI.
T1 hyperintense lesions due to increased fat content include: lipomas, dermoid cysts, and various lipid-containing tumors (mainly teratomas and other fat containing lesions).
| Lipomas|| |
Intracranial lipomas are uncommon congenital malformations that arise from the abnormal differentiation of persistent primitive meninx that is ectodermal in origin in the brain. The common locations for lipomas are as pericallosal (25–50%) [Figure 4] and [Figure 5], sylvian fissure, quadrigeminal cistern, interpeduncular cistern, cerebellopontine angle cistern, cerebellomedullary cistern, chiasmatic-suprasellar cistern, and choroid plexus of the atrium. The pericallosal region lipomas are morphologically of two types: tubulonodular and curvilinear. Lipomas in the sylvian fissure are strongly associated with seizure activity. Lipomas are characteristically hyperintense masses on T1- and less hyperintense masses on T2-weighted sequences with decreased signal intensity on fat suppressed sequences on MRI.,,
|Figure 4: Sagittal T1 (a) and T2 FATSAT (b) and Axial T1 (c) and T2 weighted (d) image showing a thin band of hyperintense signal on T1 weighted images around the splenium with lesion showing suppression on FATSAT sequences – Peri callosal lipoma|
Click here to view
|Figure 5: Axial T2 (a), T1 (c) and coronal T2 (b) and T1 FATSAT (d) images showing a well defined lesion (arrow) in the right infero medial temporal region extending towards Meckel’s cave showing hyperintense signal on T1 as well as T2 weighted images with suppression on FATSAT images suggestive of a lipoma|
Click here to view
| Teratomas|| |
These are true neoplasms that usually contain tissue derived from all three germ cell layers, but they also can arise from a single germ cell layer if cellular differentiation is disturbed. Most intracranial teratomas are benign; however, mature, immature, and malignant variants exist. Teratomas are the most common congenital intracranial tumor and are usually diagnosed prenatally. Intracranial teratomas are most frequently found in the cerebral hemispheres and pineal gland. At MRI, they typically manifest as multiloculated cystic lesions that contain calcifications and fat appearing hyperintense on T1 [Figure 6].,
|Figure 6: Sagittal pre (a) & post (b) contrast T1, coronal T2 (c) FATSAT and post contrast (d) FATSAT images showing a complex hetrogenous sellar suprasellar mass with fatty and soft tissue component – Terato dermoid|
Click here to view
| Dermoid Cysts|| |
Dermoid cysts, accounting for approximately 0.3% of all intracranial tumors, are rare, benign, congenital ectodermal inclusion cysts, that commonly occur at the midline in the sellar and parasellar compartments, fourth ventricle, and vermis. At MRI, dermoid cysts typically show high signal intensity on T1-weighted images, variable signal intensity on T2-weighted images, and lack of enhancement on contrast-enhanced images. Dermoid cyst rupture is a rare complication that can cause severe chemical meningitis and sensory or motor hemi syndrome. This complication manifests as scattered high-signal-intensity foci within the ventricles or subarachnoid spaces at T1-weighted MRI [Figure 7]. MR spectroscopy discloses mobile lipid peaks at 0.9 and 1.3 ppm.,
|Figure 7: Sagittal T1 (a), axial T2FATSAT (b), coronal T2 (c) and T1 (d) WI showing a suprasellar mass with mixed areas of hyperintense signal on T1 weighted images getting suppressed on FATSAT images and areas of iso with lowintense signal on all sequences - dermoid|
Click here to view
| Lipomatous Meningioma|| |
Meningeomas are the most common intracranial extra-axial tumors, commonly located in parasagittal area, convexity, sphenoid ridge, parasellar area, posterior fossa, optic nerve sheath, and intraventricular region. They are usually isointense with cortical gray matter on all MRI sequences with a prominent gadolinium enhancement. Lipomatous meningiomas are relatively rare, benign tumors that are characterized either by an admixture of mature adipocytes and meningioma or the production of lipids by neoplastic meningothelial cells assuming a lipoblast-like appearance. The signal intensity of lipomatous meningiomas is heterogeneous, but hyperintense components are detected on both T1- and T2-weighted images secondary to the presence of lipid.,
| Lipomatous Ependymomas|| |
Ependymoma are glial cell tumors with lipomatous differentiation being a rare variant of ependymoma in which tumor cells contain lipid droplets. Many lipomatous ependymomas show hyperintense signal on T1-weighted images. Lipomatous ependymomas tend to occur in the pediatric population and are slow growing.,
| Protein-containing Lesions|| |
High signal intensity in certain lesions on T1-weighted images can be attributed to their protein content and the hydration layer effect. In addition, macromolecular docking decreases T1 by slowing the mean motional state of the proteins. Both T1 and T2 relaxation times are dependent on the amount of free water, protein content, and viscosity within these lesions.
| Colloid Cysts|| |
Colloid cysts have a characteristic location, exclusively arising from the inferior aspect of the septum pellucidum and protrude into the anterior portion of the third ventricle between columns of the fornix. About two-thirds of colloid cysts show high signal intensity at T1-weighted MRI [Figure 8] and most exhibit low signal intensity at T2-weighted imaging. Colloid cysts that show low signal intensity at T1-weighted imaging and high signal intensity at T2-weighted imaging have a tendency to enlarge rapidly.,,
|Figure 8: Axial T2 (a), T1 (b) weighted, sagittal T1 (c)-weighted and coronal fluid-attenuated inversion recovery (d) images showing a round area of increased signal intensity on T1 images with suppression of signal on T2 images in the anterosuperior portion of the third ventricle at foramen of Monro – colloid cyst|
Click here to view
| Rathke Cleft Cyst|| |
These are benign remnants of the Rathke cleft that may be located in the sellar compartment, the suprasellar compartment, or both. About half of Rathke cleft cysts show hyperintense signal at T1-weighted imaging. The lesions also frequently appear hyperintense at T2-weighted imaging. Small intracystic nodules with high signal intensity at T1-weighted imaging and low signal intensity at T2-weighted imaging are present in approximately 45% of cases and are considered a characteristic feature of Rathke cleft cysts. Peripheral enhancement is sometimes noted at MRI which shows correlation between the presence of peripheral enhancement and an increased risk of recurrence after surgical resection.,
| Ectopic Posterior Pituitary Gland|| |
This is a rare congenital malformation of the hypothalamus that is associated with hypoplasia or absence of the pituitary stalk and resultant dwarfism due to growth hormone deficiency. This condition may be associated with septo-optic dysplasia and periventricular heterotopias. The ectopic posterior pituitary lobe is most commonly located along the median eminence in the floor of the third ventricle. Signal hyperintensity in the posterior aspect of the pituitary gland on T1-weighted images is related to the paramagnetic effect of the vasopressin–neurophysin-II–copeptin complex.,
| Craniopharyngioma|| |
Craniopharyngiomas are benign neoplasms derived from epithelial rests in the Rathke pouch. The main histopathologic subtypes are papillary, adamantinomatous, and mixed craniopharyngiomas. An estimated 90% of craniopharyngiomas contain calcifications. The T1 hyperintensity observed in the cystic components of craniopharyngiomas is attributable to the presence of protein, cholesterol granules, and methemoglobin [Figure 9]. The cystic portions of craniopharyngiomas also frequently display T2 hyperintensity and rim-like enhancement on contrast-enhanced T1-weighted images.,
|Figure 9: Sagittal T1 (a), Coronal T2 (b) & T1 (c) and axial FATSAT (d) images showing a complex mass in the supra region with areas of hyperintense signal on T1 images representing high cholesterol/lipid rich, the fat/lipid component showing suppression on FATSAT images – Craniopharyngioma. Note is made of post operative changes in the right temporal region with subdural effusion in the temporo parietal region|
Click here to view
| Atypical/White Epidermoid Cyst|| |
Epidermoid cysts are extra-axial off-midline nonneoplastic lesions with congenital or acquired origins that are filled with desquamated cells and keratinaceous debris. The prepontine and cerebellopontine angle cisterns and suprasellar and parasellar areas are common sites for epidermoid cysts. They are well circumscribed, spheroid, or multilobulated cystic lesions. They frequently have signal intensities similar to that of cerebrospinal fluid on MRI. Very rarely, epidermoid cysts demonstrate short T1 and T2 values resembling dermoid cysts due to viscous liquid components containing relatively high concentrations of protein and causing high signal intensity on T1-weighted scans also known as white epidermoid. The lack of contrast enhancement is characteristic of epidermoid cysts.,,
| Mineral-containing Lesions|| |
Calcium and Other Minerals
Calcifications may exhibit high signal on T1-weighted images, if they contain diamagnetic calcium salts that together with paramagnetic cations such as ferrum and manganesecause shortening of T1 relaxation time. In brain tissue, signal hyperintensity increases in the presence of calcium concentrations of 30% or less by weight. Excessive intracerebral calcium deposition may accompany endocrine disorders such as: hypo- or hyperparathyroidism, hypothyroidism or inflammatory processes such as toxoplasmosis, cytomegalus, or rubella infections.,,
| Fahr’s Syndrome|| |
Also known as bilateral striato-pallido-dentate calcinosisis, a rare neurodegenerative disorder characterized by bilateral, symmetrical deposition of calcium (and other mineral compounds such as zinc, aluminum, ferrous, and magnesium) in the basal ganglia, thalamus, dentate nuclei of the cerebellum, and in the subcortical white matter appearing hyperintense on T1 in the absence of disturbances in calcium–phosphorus metabolism.,,
| Cockayne Syndrome|| |
Cockayne syndrome is an autosomal recessive defect in DNA repair. Typical imaging findings include cerebral atrophy, white matter hypomyelination, and extensive calcifications within but not limited to the bilateral lentiform and dentate nuclei. These calcifications may exhibit high signal intensity at T1-weighted and low signal intensity at T2-weighted imaging.
| Neurodegeneration with Brain Iron Accumulation|| |
Neurodegeneration with iron accumulation in the brain occurs in various disorders that result in the accumulation of iron within the globus pallidus and substantia nigra. This condition manifests clinically as progressive extrapyramidal and pyramidal dysfunction. At T1-weighted MRI, the bilateral globus pallidus may sometimes appear hyperintense [Figure 10]. However, at T2-weighted MRI, bilateral symmetric foci of signal hyperintensity in the globus pallidus are surrounded by a low-signal-intensity border, producing a characteristic “eye-of-the-tiger” appearance.,
|Figure 10: T1 weighted axial (a) image showing hyperintensity in globus pallidus and T2 weighted coronal (b) image of the same patient showing focal central hyperintensity with hypointensity in periphery due to magnetic susceptibility effect of Iron – Eye of the tiger sign in a patient of Hallerverdon Spatz|
Click here to view
| Hepatic Encephalopathy/Acquired Hepatocerebral Disorder|| |
Acquired hepatocerebral degeneration is a rare, nonhereditary neurologic syndrome that occurs in patients with chronic liver disease characterized by mental status changes and motor dysfunction in patients with underlying liver disease. At MRI, hepatic encephalopathy characteristically manifests as bilateral regions of signal hyperintensity in the lentiform nucleus and substantia nigra on T1-weighted images [Figure 11]. These regions of abnormally high signal intensity at T1-weighted imaging are related to the accumulation of manganese. Manganese is also responsible for symmetrical increase of signal in the hypothalamus and anterior pituitary on T1-weighted images [Figure 12]. After liver transplantation the cerebral T1-hyperintensity may return to normal.
|Figure 11: Axial T1 weighted images (a–d) in a patient of hepatic encephalopathy showing hyperintense signal in globus pallidus and substantia nigra reflecting manganese deposits|
Click here to view
|Figure 12: T1-weighted axial images (a&b) reveal high signal intensity in the heads of both caudate nuclei, putamina and dentate nucleI in a patient of Primary hypermagnesimia|
Click here to view
| Wilson Disease|| |
Wilson disease is a rare autosomal recessive condition caused by mutations in the ATP7B gene with resultant abnormal copper metabolism and accumulation. Signal hyperintensity at T1-weighted imaging in patients with Wilson disease is most commonly found in the bilateral basal ganglia and ventrolateral thalami. The precise distribution of the signal abnormality correlates with clinical symptoms. Regression of the signal abnormality at T1-weighted MRI correlates with response to treatment. T2-weighted sequences are also helpful, particularly with findings of signal hyperintensity in the midbrain combined with sparing of the superior colliculus, red nucleus, and portions of the substantia nigra; this combination of findings produces the “face of the giant panda” appearance on axial T2-weighted MRI.,
| Melanin-containing Lesions|| |
High signal intensity on T1-weighted images of melanin-containing lesions is because of the paramagnetic effects of stable free radicals in which melanin binds to chelated metal ions, forming metallomelanin. Furthermore, the signal intensity of metallomelanin on T1-weighted images was found to increase with an increasing iron concentration.,
| Metastatic Melanoma|| |
Approximately 40% of patients with malignant melanoma have intracranial metastases, appearing hyperintense on T1-weighted images and hypointense on T2-weighted images. However, amelanotic metastatic melanoma tends to exhibit signal that is either isointense or hypointense to that in normal tissue on T1-weighted images.
| Primary Diffuse Meningeal Melanomatosis|| |
It is an extremely rare and aggressive form of primary intracranial melanoma. The lesions in primary diffuse meningeal melanomatosis display intermediate or high signal intensity on T1-weighted MRI. In all cases, a careful search must be made to rule out an occult extracranial primary melanoma.,
| Neurocutaneous Melanosis|| |
An uncommon congenital condition characterized by multiple giant or hairy pigmented nevi and melanin-containing leptomeningeal lesions without evidence of extracranial melanoma. Melanoma arises from the leptomeningeal lesions in 40 to 60% of cases of neurocutaneous melanosis. The intracranial lesions have a predilection for the anterior temporal lobes and cerebellum. The lesions in neurocutaneous melanosis typically appear hyperintense on T1-weighted images and hypointense on T2-weighted images because of the characteristic effects of melanin.
| Miscellaneous|| |
Cortical Laminar Necrosis
It is a sequel of a global hypoxic ischemic event or less commonly, an effect of immunosuppressive therapy or chemotherapy affecting the third layer of the cortex, which is particularly susceptible to depletion of oxygen and glucose. At MRI, a characteristic series of changes are seen: high-signal-intensity cortical lesions appear on T1-weighted images about 2 weeks after the inciting event and become increasingly conspicuous at 1 to 2 months after the event, along with maximum contrast enhancement. T1 signal hyperintensity usually fades after 2 years, whereas parenchymal atrophy progresses. The high-signal-intensity features seen on T1-weighted images may be related to mineralization, protein denaturation, or lipid. However, methemoglobin does not appear to contribute to this signal hyperintensity.,
These are benign masses composed of proteinaceous debris and cholesterol crystals from blood breakdown secondary to obstruction and consequent chronic inflammatory foreign-body reaction. These lesions commonly occur within the petrous apex, but occasionally arise in the mastoid segment, middle ear, and orbitofrontal region.,
Chronic Phase of Multiple Sclerosis
One of the most common demyelinating diseases with plaque lesions having usually low-to-intermediate signal intensity on T1-weighted images and high signal intensity on T2-weighted images with or without gadolinium enhancement depending on the activity of disease. However, chronic plaque lesions of multiple sclerosis may be characterized by peripheral T1 shortening possibly related to the accumulation of myelin degradation products.,,
Neurofibromatosis Type I
This is the most common neurocutaneous syndrome with an autosomal-dominant transmission. Multiple focal areas of high signal intensity are present in the basal ganglia (most commonly globuspallidi), thalami, hippocampal gyri, and brainstem. They are thought to represent hamartomas, spongiotic, or vacuolar changes of myelin with usually high signal on T2-weighted images and intermediate to slightly high signal on T1-weighted images. This may be due to an admixture of areas of myelin breakdown and remyelination of initially destroyed myelin and probable association of microcalcifications. They may show spontaneous regression over time by serial MRI.,
To summarize, there are certain substances and cranial pathological lesions that appear hyperintense on T1-weighted images. The common substances responsible for the high signal intensity on T1-weighted images include methemoglobin, melanin, lipid, various minerals, and others. This can help in better characterization of the lesion.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Jacobs MA, Ibrahim TS, Ouwerkerk R. MR imaging: brief overview and emerging applications. Radiographics 2007;27:1213-29.
Bitar R, Leung G, Perng R, Tadros S, Moody AR, Sarrazin J et al.
MR pulse sequences: what every radiologist wants to know but is afraid to ask. Radiographics 2006;26:513-37.
Bradley WG Jr. MR appearance of hemorrhage in the brain. Radiology 1993;189:15-26.
Zabramski JM, Wascher TM, Spetzler RF, Johnson B, Golfinos J, Drayer BP et al.
The natural history of familial cavernous malformations: results of an ongoing study. J Neurosurg 1994;80:422-32.
Yun TJ, Na DG, Kwon BJ, Rho HG, Park SH, Suh YL et al.
A T1 hyperintense perilesional signal aids in the differentiation of a cavernous angioma from other hemorrhagic masses. AJNR Am J Neuroradiol 2008;29:494-500.
Barkovich AJ, Atlas SW. Magnetic resonance imaging of intracranial hemorrhage. Radiol Clin North Am 1988;26:801-20.
Warren DJ, Hoggard N, Walton L, Radatz MW, Kemeny AA, Forster DM et al.
Cerebral arteriovenous malformations: comparison of novel magnetic resonance angiographic techniques and conventional catheter angiography. Neurosurgery 2001;48:973-82.
Kivisaari RP, Salonen O, Servo A, Autti T, Hernesniemi J, Ohman J. MR imaging after aneurysmal subarachnoid hemorrhage and surgery: a long-term follow-up study. Am J Neuroradiol 2001;22:1143-8.
Katayama Y, Tsubokawa T, Miyazaki S, Furuichi M, Hirayama T, Himi K. Growth of totally thrombosed giant aneurysm within the posterior cranial fossa. Diagnostic and therapeutic considerations. Neuroradiology 1991;33:168-70.
Isensee C, Reul J, Thron A. Magnetic resonance imaging of thrombosed dural sinuses. Stroke 1994;25:29-34.
Serrano Ponz M, Ara Callizo JR, Fayed Miquel N, Alarcia Alejos R, Latorre Jimencz AM. Hypoxic encephalopathy and cortical laminar necrosis. Rev Neurol 2001;32:843-7.
Komiyama M, Nishikawa M, Yasui T. Cortical laminar necrosis in brain infarcts: chronological changes on MRI. Neuroradiology 1997;39:474-9.
Warakaulle DR, Anslow P. Differential diagnosis of intracranial lesions with high signal on T1 or low signal on T2-weighted MRI. Clin Radiol 2003;58:922-33.
Jabot G, Stoquart-Elsankari S, Saliou G, Toussaint P, Deramond H, Lehmann P. Intracranial lipomas: clinical appearances on neuroimaging and clinical significance. J Neurol 2009;256:851-5.
Yildiz H, Hakyemez B, Koroglu M, Yesildag A, Baykal B. Intracranial lipomas: importance of localization. Neuroradiology 2006;48:1-7.
Bakshi R, Shaikh ZA, Kamran S, Kinkel PR. MRI findings in 32 consecutive lipomas using conventional and advanced sequences. J Neuroimaging 1999;9:134-40.
Smirniotopoulos JG, Chiechi MV. Teratomas, dermoids, and epidermoids of the head and neck. Radiographics 1995;15:1437-55.
Isaacs H Jr. Perinatal brain tumors: a review of 250 cases. Pediatr Neurol 2002;27:249-61.
Liu JK, Gottfried ON, Salzman KL, Schmidt RH, Couldwell WT. Ruptured intracranial dermoid cysts: clinical, radiographic, and surgical features. Neurosurgery 2008;62:377-84.
Osborn AG, Preece MT. Intracranial cysts: radiologic-pathologic correlation and imaging approach. Radiology 2006;239:650-64.
LeRoux P, Hope A, Lofton S, Harris AB. Lipomatous meningioma: an uncommon tumor with distinct radiographic findings. Surg Neurol 1989;32:360-5.
Jesionek-Kupnicka D, Liberski PP, Kordek R, Kolasa P, Alwasiak J. Metaplastic meningioma with lipomatous changes. Folia Neuropathol 1997;35:187-90.
Ruchoux MM, Kepes JJ, Dhellemmes P, Hamon M, Maurage CA, Lecomte M et al.
Lipomatous differentiation in ependymomas: a report of three cases and comparison with similar changes reported in other central nervous system neoplasms of neuroectodermal origin. Am J SurgPathol 1998;22:338-46.
Chang WE, Finn LS. MR appearance of lipomatous ependymoma in a 5-year-old boy. AJR Am J Roentgenol 2001;177:1475-8.
Fullerton GD, Finnie MF, Hunter KE, Ord VA, Cameron IL. The influence of macromolecular polymerization of spin-lattice relaxation of aqueous solutions. Magn Reson Imaging 1987;5:353-70.
Cakirer S, Karaarslan E, Arslan A. Spontaneously T1-hyperintense lesions of the brain on MRI: a pictorial review. Curr Probl Diagn Radiol 2003;32:194-217.
Armao D, Castillo M, Chen H, Kwock L. Colloid cyst of the third ventricle: imaging-pathologic correlation. AJNR Am J Neuroradiol 2000;21:1470-7.
Sumida M, Uozumi T, Mukada K, Arita K, Kurisu K, Eguchi K. Rathke cleft cysts: correlation of enhanced MR and surgical findings. AJNR Am J Neuroradiol 1994;15:525-32.
Binning MJ, Gottfried ON, Osborn AG, Couldwell WT. Rathke cleft cyst intracystic nodule: a characteristic magnetic resonance imaging finding. J Neurosurg 2005;103:837-40.
Mitchell LA, Thomas PQ, Zacharin MR, Scheffer IE. Ectopic posterior pituitary lobe and periventricular heterotopia: cerebral malformations with the same underlying mechanism? AJNR Am J Neuroradiol 2002;23:1475-81.
Kurokawa H, Fujisawa I, Nakano Y, Kimura H, Akagi K, Ikeda K et al.
Posterior lobe of the pituitary gland: correlation between signal intensity on T1-weighted MR images and vasopressin concentration. Radiology 1998;207:79-83.
Prabhu VC, Brown HG. The pathogenesis of craniopharyngiomas. Childs Nerv Syst 2005;21:622-7.
Ahmadi J, Destian S, Apuzzo ML, Segall HD, Zee CS. Cystic fluid in craniopharyngiomas: MR imaging and quantitative analysis. Radiology 1992;182:783-5.
Loevner LA. Imaging features of posterior fossa neoplasms in children and adults. Semin Roentgenol 1999;34:84-101.
Ochi M, Hayashi K, Hayashi T, Morikawa M, Ogino A, Hashmi R et al.
Unusual CT and MR appearance of an epidermoid tumor of the cerebellopontine angle. Am J Neuroradiol 1998;19:1113-5.
Ikushima I, Korogi Y, Hirai T, Sugahara T, Shigematsu Y, Komohara Y et al.
MR of epidermoids with a variety of pulse sequences. Am J Neuroradiol 1997;18:1359-63.
Warakaulle DR, Anslow P. Differential diagnosis of intracranial lesions with high signal on T1 or low signal on T2-weighted MRI. Clin Radiol 2003;58:922-33.
Ginat DT, Meyers SP. Intracranial lesions with high signal intensity on T1-weighted MR: differential diagnosis. Radiographics 2012;32:499-516.
Acou M, Vanslembrouck J, Deblaere K, Bauters W, Achten E. Fahr disease. JBR-BTR 2008;91:19.
Koob M, Laugel V, Durand M, Fothergill H, Dalloz C, Sauvanaud F et al.
Neuroimaging in Cockayne syndrome. AJNR Am J Neuroradiol 2010;31:1623-30.
Sener RN. Pantothenate kinase-associated neurodegeneration: MR imaging, proton MR spectroscopy, and diffusion MR imaging findings. AJNR Am J Neuroradiol 2003;24:1690-3.
Hayflick SJ, Hartman M, Coryell J, Gitschier J, Rowley H. Brain MRI in neurodegeneration with brain iron accumulation with and without PANK2 mutations. AJNR Am J Neuroradiol 2006;27:1230-3.
Rovira A, Alonso J, Córdoba J. MR imaging findings in hepatic encephalopathy. AJNR Am J Neuroradiol 2008;29:1612-21.
Kim TJ, Kim IO, Kim WS, Cheon JE, Moon SG, Kwon JW et al.
MR imaging of the brain in Wilson disease of childhood: findings before and after treatment with clinical correlation. AJNR Am J Neuroradiol 2006;27:1373-8.
Thapa R, Ghosh A. ‘Face of the giant panda’ sign in Wilson disease. Pediatr Radiol 2008;38:1355.
Isiklar I, Leeds NE, Fuller GN, Kumar AJ. Intracranial metastatic melanoma: correlation between MR imaging characteristics and melanin content. AJR Am J Roentgenol 1995;165:1503-12.
Enochs WS, Petherick P, Bogdanova A, Mohr U, Weissleder R. Paramagnetic metal scavenging by melanin: MR imaging. Radiology 1997;204:417-23.
Escott EJ. A variety of appearances of malignant melanoma in the head: a review. Radiographics 2001;21:625-39.
Liubinas SV, Maartens N, Drummond KJ. Primary melanocytic neoplasms of the central nervous system. J Clin Neurosci 2010;17:1227-32.
Smith AB, Rushing EJ, Smirniotopoulos JG. Pigmented lesions of the central nervous system: radiologic–pathologic correlation. Radiographics 2009;29:1503-24.
Siskas N, Lefkopoulos A, Ioannidis I, Charitandi A, Dimitriadis AS. Cortical laminar necrosis in brain infarcts: serial MRI. Neuroradiology 2003;45:283-8.
Niwa T, Aida N, Shishikura A, Fujita K, Inoue T. Susceptibility-weighted imaging findings of cortical laminar necrosis in pediatric patients. AJNR Am J Neuroradiol 2008;29:1795-8.
Royer MC, Pensak ML. Cholesterol granulomas. Curr Opin Otolaryngol Head Neck Surg 2007;15:319-22.
Chapman PR, Shah R, Curé JK, Bag AK. Petrous apex lesions: pictorial review. AJR Am J Roentgenol 2011;196(3 Suppl):WS26–37.
Wallace CJ, Seland TP, Fong TC. Multiple sclerosis: the impact of MR imaging. Am J Roentgenol 1992;158:849-57.
Lucchinetti C, Bruck W, Noseworthy J. Multiple sclerosis: recent developments in neuropathology, pathogenesis, magnetic resonance imaging studies and treatment. Curr Opin Neurol 2001;14:259-69.
Nyul LG, Udupa JK. MR image analysis in multiple sclerosis. Neuroimaging Clin North Am 2000;10:799-816.
Raininko R, Thelin L, Eeg-Olofsson XX. Non-neoplastic brain abnormalities on MRI in children and adolescents with neurofibromatosis type 1. Neuropediatrics 2001;32:225-30.
DeBella K, Poskitt K, Szudek J, Friedman JM. Use of “unidentified bright objects” on MRI for diagnosis of neurofibromatosis 1 in children. Neurology 2000;54:1646-50.
[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7], [Figure 8], [Figure 9], [Figure 10], [Figure 11], [Figure 12]