Brain Imaging with MRI and CT: Part 2

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(BQ) Continued part 1, part 2 of the document Brain Imaging with MRI and CT presents the following contents: Abnormalities without significant mass effect, primarily extra axial focal space occupying lesions, primarily intra axial masses, intracranial calcifications.

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Nội dung Text: Brain Imaging with MRI and CT: Part 2

SECTION 4 Abnormalities Without Signiﬁcant Mass Effect Cases Other Relevant Cases 19 Lissencephaly A. Primarily Non-Enhancing Mariasavina Severino 97 Dural Venous Sinus Thrombosis 20 Herpes Simplex Encephalitis Giulio Zuccoli Zoran Rumboldt and Mauricio Castillo 98 Dural Arteriovenous Fistula 21 Limbic Encephalitis Matthew Omojola and Zoran Rumboldt Mauricio Castillo 99 Subarachnoid Hemorrhage Matthew Omojola B. Primarily Enhancing 100 Laminar Necrosis 118 Neurosarcoidosis Matthew Omojola Zoran Rumboldt 101 Neurocutaneous Melanosis 119 Meningeal Carcinomatosis Majda Thurnher Alessandro Cianfoni 102 Superficial Siderosis 120 Meningitis (Infectious) Mauricio Castillo Mauricio Castillo 103 Polymicrogyria 121 Perineural Tumor Spread Maria Vittoria Spampinato Zoran Rumboldt 104 Seizure-Related Changes (Peri-Ictal MRI Abnormalities) 122 Moyamoya Mauricio Castillo Maria Vittoria Spampinato 105 Embolic Infarcts 123 Central Nervous System Vasculitis Benjamin Huang Giulio Zuccoli 106 Focal Cortical Dysplasia 124 Subacute Infarct Zoran Rumboldt and Maria Gisele Matheus Benjamin Huang and Zoran Rumboldt 107 Tuberous Sclerosis 125 Active Multiple Sclerosis Maria Gisele Matheus Mariasavina Severino 108 Dysembroplastic Neuroepithelial Tumor (DNT, DNET) 126 Capillary Telangiectasia Giovanni Morana Alessandro Cianfoni 109 Nonketotic Hyperglycemia With Hemichorea–Hemiballismus 127 Developmental Venous Anomaly Zoran Rumboldt Giulio Zuccoli 110 Hyperdensity following Endovascular Intervention 128 Immune Reconstitution Inflammatory Syndrome (IRIS) Zoran Rumboldt and Benjamin Huang Zoran Rumboldt 111 Early (Hyperacute) Infarct 129 Ventriculitis Benjamin Huang Zoran Rumboldt and Majda Thurnher 112 Acute Disemminated Encephalomyelitis (ADEM) Benjamin Huang Other Relevant Cases 113 Susac Syndrome 30 X-linked Adrenoleukodystrophy Mauricio Castillo Mariasavina Severino 114 Diffuse Axonal Injury 33 Alexander Disease Majda Thurnher Mariasavina Severino 115 Multiple Sclerosis 37 Spontaneous Intracranial Hypotension Matthew Omojola and Zoran Rumboldt Maria Vittoria Spampinato 116 Progressive Multifocal Leukoencephalopathy (PML) 86 Sturge–Weber Syndrome Zoran Rumboldt Maria Gisele Matheus 117 Nodular Heterotopia Maria Gisele Matheus
SECTION 4A Abnormalities Without Signiﬁcant Mass Effect: Primarily Non-Enhancing A B C Figure 1. Non-enhanced axial CT image (A) shows hyperdensity in the superior sagittal sinus (arrow). Sagittal T1WI (B) reveals increased signal within the sinus (arrows). Corresponding (slightly tilted anteriorly) post-contrast T1WI (C) shows lack of normal enhancement (arrows) within the sinus. Compare to normal enhancing vein of Galen and straight sinus (arrowheads). A B C Figure 2. Enhanced axial CT image (A) shows a ﬁlling defect (arrows) in the superior sagittal sinus. Sagittal T1WI (B) shows increased intensity of the anterior superior sagittal sinus (arrows). Compare to normal posterior aspect of the sinus (arrowheads). Peripheral enhancement around the sinus ﬁlling defect (arrow) is seen on coronal post-contrast T1WI (C). Figure 3. Non-enhanced axial CT image (A) shows hyperdensity of the right sigmoid sinus (arrow). Posterior right oblique MIP from post-contrast MRV (B) demonstrates absence of the right transverse and sigmoid sinuses as well as the internal jugular vein. Note normal left transverse sinus (small arrowhead), sigmoid sinus (large arrowhead), and internal jugular vein (arrow). A B 200
Dural Venous Sinus Thrombosis CASE 97 GIULIO ZUCCOLI Specific Imaging Findings Congenital Hypoplasia/Atresia Increased density in the occluded sinus leading to a “cord • unilateral transverse sinus, variant anatomy of the torcular sign” is the classic imaging finding of dural venous sinus herophili thrombosis (DVST) on unenhanced CT images. However, a • focal areas of narrowing may be indistinguishable high variability in the degree of thrombus density is respon- Prominent Arachnoid Granulations (Pacchioni’s sible for a low sensitivity of this sign. Thus, evaluation with Granulations) (130) CT angiogram, MR and MRV may be required to confirm the • typically round or ovoid filling defect of CSF density/intensity diagnosis. The “empty delta” sign consisting of a triangular • transverse and superior sagittal sinus locations are typical area of enhancement with a relatively low-density center is seen in 25–30% of cases on contrast-enhanced CT scans. On Background MRI, acute thrombus is T1 isointense, T2 and T2* hypoin- DVST is a rare cause of stroke affecting all age groups and tense. Of note, this T2 hypointensity may mimic normal flow- accounting for 1–2% of strokes in adults. While age distribution void. Peripheral enhancement is seen around the acute is uniform in men, a peak incidence is reported in women aged hypointense clot corresponding to the empty delta CT sign. 20–35 years which may be related to pregnancy and use of Subacute thrombus becomes T1 and T2 hyperintense. Chronic contraceptives. DVST should always be considered in the differ- thrombus is most commonly T1 isointense and T2 hyperin- ential diagnosis in patients with severe headache, focal neuro- tense. DWI/ADC signal of the thrombus is variable, as is the logical deficits, idiopathic intracranial hypertension and degree of enhancement in organized thrombus. Visible ser- intracranial hemorrhage. Many causative conditions have been piginous intrathrombus flow-voids on T2WI, corresponding described in DVST including infections, trauma, hypercoagulable areas of flow signal on TOF-MRV, and brightly enhancing states, hyperhomocysteinemia, hematologic disorders, collageno- channels on post-contrast MRV are present in most cases of pathies, inflammatory bowel diseases, use of medications, and chronic partial recanalization. Thrombosis shows no flow- intracranial hypotension. Thrombosis most frequently affects the related signal on phase contrast MRV, and absent to dimin- superior sagittal sinus. However, multiple locations, particularly ished enhancement on post contrast MRV and CTV. Engorged in the contiguous transverse and sigmoid sinuses, are found in collateral veins may be present, primarily in the chronic phase. as many as 90% of patients. Focal brain abnormalities have TOF-MRV of a subacute T1 bright clot may potentially mis- been found in as many as 57% of patients. Bleeding represents represent sinus patency. a non-negligible complication of thrombolytic therapy, poten- tially affecting patients’ outcome. Pertinent Clinical Information DVST has a large spectrum of clinical manifestations as it may references present with headache, seizure, papilledema, altered mental 1. Leach JL, Fortuna RB, Jones BV, Gaskill-Shipley MF. Imaging of status, and focal neurological deficit including cranial nerve pal- cerebral venous thrombosis: current techniques, spectrum of findings, sies. Unilateral headache is more common than diffuse headache. and diagnostic pitfalls. Radiographics 2006;26(Suppl 1):S19–41. However, pain location is not associated with the site of throm- 2. Meckel S, Reisinger C, Bremerich J, et al. Cerebral venous thrombosis: bosis. Affected patients may initially show subarachnoid hemor- diagnostic accuracy of combined, dynamic and static, contrast-enhanced rhage sparing the basal cisterns. 4D MR venography. AJNR 2010;31:527–35. Differential Diagnosis 3. Leach JL, Wolujewicz M, Strub WM. Partially recanalized chronic dural sinus thrombosis: findings on MR imaging, time-of-flight MR Normal Dural Venous Sinuses venography, and contrast-enhanced MR venography. AJNR • blood in venous sinuses is usually slightly hyperdense; espe- 2007;28:782–9. cially in newborns, physiologic polycythemia in combination 4. Oppenheim C, Domingo V, Gauvrit JY, et al. Subarachnoid with unmyelinated brain makes the dural sinuses appear hemorrhage as the initial presentation of dural sinus thrombosis. AJNR hyperdense 2005;26:614–7. Acute Subdural Hematoma (133) 5. Dentali F, Squizzato A, Gianni M, et al. Safety of thrombolysis in • blood along the entire tentorium of the cerebellum, not limited cerebral venous thrombosis. A systematic review of the literature. Thromb to the periphery Haemost 2010;104:1055–62. 201 Brain Imaging with MRI and CT, ed. Zoran Rumboldt et al. Published by Cambridge University Press. © Cambridge University Press 2012.
SECTION 4A Abnormalities Without Signiﬁcant Mass Effect: Primarily Non-Enhancing A B C Figure 1. Axial T2WI (A) shows large tortuous basal veins of Rosenthal (arrows) and vessels within the right temporo-occipital sulci (arrowheads). Slightly more cephalad (B) a large vein of Galen (black arrow), tortuous sulcal signal voids (arrowhead) and large subgaleal veins (white arrow) are seen. Post-contrast T1WI (C) shows enhancement of leptomeningeal vessels on the right and bilateral medullary veins (arrows). A C Figure 2. Contrast-enhanced MRV reveals multiple small curvilinear structures (arrows) B D on the left. Left transverse and sigmoid sinuses show areas of narrowing and Figure 3. 3D TOF MRA source images (A, B) show multiple high-intensity structures occlusion. Normal right transverse and (arrowheads) adjacent to left jugular bulb (arrows) with extension into the bulb. At a more sigmoid sinuses (arrowheads). cephalad level (C, D) bright linear structures (arrowheads) are adjacent and extending into the left sigmoid sinus (arrow). Note mild hyperintensity of left sigmoid sinus and jugular bulb. Figure 4. Axial post-contrast T1WI (A) shows enhancing prominent venous structures (arrows) and adjacent hypointense edema in the subcortical white matter. Corresponding FLAIR image (B) more clearly shows the hyperintensity of edema (arrows) caused by venous hypertension. A B 202
Dural Arteriovenous Fistula CASE 98 MA T T H E W O M O JO L A A N D Z O R A N R U M B O L D T Specific Imaging Findings Venous Thrombosis (97) Dural arteriovenous fistula (DAVF) may not be visualized on • presence of intraluminal clot routine CT or MRI images. MRI findings of larger or high-flow • may lead to DAVF DAVFs include: multiple extra axial linear or tortuous flow-voids on T2WI, either at the base of the brain, around the tentorial Background incisura, in the basal cisterns, or in the sulci along the convexity, DAVF is thought to represent acquired pachymeningeal connec- which are even better visualized with susceptibility-weighted tion between arteries and veins without an intervening nidus. imaging (SWI). Major deep and superficial draining veins may The true incidence is not known, but has been reported to be enlarged. Large tortuous signal voids may be present in the represent about 10–15% of all intracranial vascular malforma- scalp of the affected side. Post-contrast images may show prom- tions. Common locations are tentorial, parasellar, along the inent tortuous vessels within the sulci indicating retrograde cor- transverse sinuses and falx. Dural sinus thrombosis and trauma tical venous drainage. Large deep medullary (white matter) veins are considered responsible for development of these lesions. and white matter T2 hyperintensity are indicative of venous DAVF may occur and occlude spontaneously. There are various hypertension. Perfusion studies show increased relative cerebral classification methods of DAVF based upon the venous outflow blood volume (rCBV) in all of these patients. CT demonstrates pattern and associated outflow restrictions, which might influence complications, primarily subarachnoid, subdural, parenchymal, the clinical presentation and treatment outcomes. Retrograde flow or occasionally intraventricular hemorrhages. MRA or CTA in the into cortical veins results in deep venous engorgement, leading high-flow DAVF often show enlarged tortuous arterial and to venous hypertension, which in turn leads to ischemia and venous structures. Findings of high intensity structures adjacent hemorrhage. to the sinus wall on 3D TOF MRA appear to be diagnostic of Recent developments in rapid 4D contrast-enhanced MR angi- DAVF. MRV confirms enlarged venous structures and may show ography technique are very promising and it may eventually evidence of venous sinus thrombosis or occlusion. DSA demon- obviate the need for diagnostic catheter angiography. strates the exact fistula site, is very useful for treatment planning and offers endovascular treatment options. references Pertinent Clinical Information 1. Kwon BJ, Han MH, Kang HS, Chang KH. MR imaging findings of DAVFS occur in adults, more commonly females. They may intracranial dural arteriovenous fistulas: relations with venous drainage be clinically silent and incidentally found at imaging. Pulsatile patterns. AJNR 2005;26:2500–7. tinnitus, audible bruit, headache, cognitive impairment, seizures, 2. Noguchi K, Melhem ER, Kanazawa T, et al. Intracranial dural cranial nerve palsies and focal neurologic deficit may all occur in arteriovenous fistulas: evaluation with combined 3D time-of-flight patients with DAVF. Lesions located in the cavernous sinus region MR angiography and MR digital subtraction angiography. AJR present with ophthalmoplegia, eye pain, orbital congestion or fea- 2004;182:183–90. tures of carotid cavernous fistula. Development of venous hyper- 3. Meckel S, Maier M, San Millan Ruiz D, et al. MR angiography of tension frequently leads to progressive dementia. Acute symptoms dural arteriovenous fistulas: diagnosis and follow-up after treatment may be due to intracranial hemorrhages, which occur in DAVFs using a time-resolved 3D contrast-enhanced technique. AJNR with retrograde cortical flow. Therefore, the presence of retrograde 2007;28:877–84. cortical flow represents a clear indication for treatment of these 4. Nishimura S, Hirai T, Sasao A, et al. Evaluation of dural arteriovenous lesions. fistulas with 4D contrast-enhanced MR angiography at 3T. AJNR 2010;31:80–5. Differential Diagnosis 5. Noguchi K, Kuwayama N, Kubo M, et al. Intracranial dural Arteriovenous Malformation (AVM) (182) arteriovenous fistula with retrograde cortical venous drainage: use of • usually parenchymal in location with a focal nidus (“bag of susceptibility-weighted imaging in combination with dynamic worms”) best seen on T2-weighted images susceptibility contrast imaging. AJNR 2010;31:1903–10. 203 Brain Imaging with MRI and CT, ed. Zoran Rumboldt et al. Published by Cambridge University Press. © Cambridge University Press 2012.
SECTION 4A Abnormalities Without Signiﬁcant Mass Effect: Primarily Non-Enhancing A B C Figure 1. Non-enhanced CT (A) shows hyperdensity throughout basal cisterns extending into sylvian (arrows) and interhemispheric (arrowhead) ﬁssures. A more cephalad CT (B) shows subtle sulcal iso- to hyperdensity (arrowheads). Midsagittal T1WI (C) reveals isodense material within the cisterns (arrows). Figure 2. Non-enhanced CT (A) shows hyperintensity within the right sylvian ﬁssure (arrow) and layering in the lateral ventricle (arrowhead). CT along the convexity (B) shows subtle sulcal hyperintensities (arrow), better seen (arrow) on corresponding FLAIR image (C). B A C 3 A B 4 Figure 5. Axial FLAIR image (A) shows subtle hyperintensity of the CSF-containing spaces Figures 3 and 4. Non-enhanced CT images along the brain surface (arrow) and within ventricles (arrowhead). Corresponding in two patients show perimesencephalic hypointensity is not well appreciated on T2*WI (B). hemorrhage (arrows), limited to basal cisterns. 204
Subarachnoid Hemorrhage CASE 99 MA T T H E W O M O JO L A Specific Imaging Findings Meningitis (120) On CT, subarachnoid hemorrhage (SAH) characteristically pre- • high protein content of CSF may be indistinguishable from sents as hyperdense material filling the basal cisterns and/or SAH on FLAIR fissures and cortical sulci. The density and extent depend on the • not CT hyperdense, no signal loss on T2* images volume of blood. If sufficiently diluted by the CSF, a small SAH Collateral Leptomeningeal Vessels in Arterial Occlusions may not be seen on CT. Dilution and redistribution may lead to (Moyamoya) (122) intraventricular extension and the hyperdensity gradually fades • vascular structures can usually be identified away. Diluted SAH can appear as effacement of the cortical sulci. • uncommon in basal cisterns Traumatic SAH may be associated with other injuries such as parenchymal and extra-axial hematomas. The most common Cortical Vein Thrombosis (181) cause of nontraumatic SAH is aneurysmal rupture, usually pre- • localized sulcal CT hyperdensity and T2* hypointensity corres- senting with diffuse SAH, while a filling defect within the hyper- ponding to cortical vein dense clot may indicate the aneurysm location. An associated • adjacent parenchymal infarct and/or hemorrhage may be parenchymal hematoma may also be present. Nonaneurysmal present SAH (NASAH) is most commonly perimesencephalic, located almost exclusively in the basal cisterns with possible minimal Background extension into the interhemispheric and sylvian fissures. Other The most common cause of nontraumatic SAH is by far rupture types of NASAH tend to be located along the convexity – apart of intracranial aneurysm (about 85% of cases). Mortality of from trauma, vasculitis, cortical vein thrombosis, Moyamoya, aneurysmal SAH is very high at about 30–40% with permanent and cerebral amyloid angiopathy may present this way. On neurological deficit in another third of patients. Recent advances MRI, SAH is best seen with FLAIR sequence, which is more in diagnosis and treatment appear to have somewhat mitigated sensitive than CT. T2*WI tend to show hypointensity, but this the morbidity and mortality of SAH. CT is diagnostic in about is variable. Hyperacute SAH (within the first few hours), similar 100% of patients within the first 12 h of a major SAH. About 10% to hyperacute hematoma, is extremely T2 hyperintense, brighter of SAH may not be detectable after 24 h. A negative CT scan in than the CSF; it becomes hypointense in the acute phase. T1 the appropriate clinical setting should be followed by a lumbar signal varies but is always hyperintense compared to the CSF. puncture. CTA has become the main technique for detection of Leptomeningeal enhancement may be present. In patients with aneurysms. DSA offers both diagnostic confirmation and endo- nontraumatic SAH and either the perimesencephalic pattern or vascular embolization treatment. Around 8–10% of patients have no blood on CT, negative CTA is reliable in ruling out aneurysms. NASAH, most commonly perimesencephalic, which has excellent DSA is indicated for diffuse SAH with negative CTA. prognosis. Pertinent Clinical Information references Acute nontraumatic SAH typically presents with a sudden onset 1. Agid R, Andersson T, Almqvist H, et al. Negative CT angiography “thunderclap” headache described as “the worst headache ever”. findings in patients with spontaneous subarachnoid hemorrhage: Prodromal or sentinel headache is reported by many patients. when is digital subtraction angiography still needed? AJNR Nausea and vomiting are common, photophobia and neck stiff- 2010;31:696–705. ness may be present. Hydrocephalus and vasospasm are the main 2. Brinjikji W, Kallmes DF, White JB, et al. Inter and intra observer complications of SAH. The presence of three or more separate agreement in CT characterization of non aneurysmal perimesencephalic areas of SAH in traumatized patients is a poor prognostic subarachnoid hemorrhage. AJNR 2010;31:1103–5. indicator. 3. van Asch CJJ, van der Schaaf IC, Rinkel GJE. Acute hydrocephalus and cerebral perfusion after aneurysmal subarachnoid hemorrhage. AJNR Differential Diagnosis 2010;31:67–70. Diffuse Brain Edema 4. Cuvinciuc V, Viguier A, Calviere L, et al. Isolated acute nontraumatic • diffuse hypodensity of the brain with loss of differentiation cortical subarachnoid hemorrhage. AJNR 2010;31:1355–62. between gray and white matter 5. Boesiger BM, Shiber JR. Subarachnoid hemorrhage diagnosis by • cerebellum usually spared, appears relatively hyperdense computed tomography and lumbar puncture: are fifth generation CT • fading SAH may resemble cerebral edema due to effacement of scanners better at identifying subarachnoid hemorrhage? J Emerg Med cortical sulci 2005;29:23–7. 205 Brain Imaging with MRI and CT, ed. Zoran Rumboldt et al. Published by Cambridge University Press. © Cambridge University Press 2012.
SECTION 4A Abnormalities Without Signiﬁcant Mass Effect: Primarily Non-Enhancing A B C Figure 1. Axial non-enhanced CT image (A) a few days following gunshot injury in a young man shows subtle gyral high-density areas (arrows). Further follow-up CT (B) demonstrates extensive gyral hyperdensity (arrows) in the right hemisphere. Sagittal non-contrast T1WI (C) reveals gyral hyperintense signal along the parafalcine right parietal cortex (arrows). Figure 2. Non-enhanced axial CT image (A) in a patient with sequelae of a remote severe untreated posterior reversible encephalopathy syndrome (PRES) shows bilateral predominantly posterior hypodense areas of encephalomalacia (arrows) with focal gyral cortical hyperdensities (arrowheads). Bright cortical lesions (arrowheads) are more conspicuous on a non-contrast T1WI at a similar level (B). A more superior T1WI (C) reveals a prominent left frontal cortical hyperintensity (arrow), which is further accentuated on the corresponding FLAIR image (D). Note bilateral areas of gliosis (arrowheads), with low T1 signal and hyperintensity on FLAIR image. A B C D 206
Laminar Necrosis CASE 100 MA T T H E W O M O JO L A Specific Imaging Findings Cortical Calcifications/Mineralization (188, 189, 191) Acute to subacute laminar necrosis (LN) on CT cannot be • may be permanent on follow-up differentiated from brain swelling/edema and often occurs in • may be indistinguishable on CT and T2*-weighted MRI (calci- the setting of hypoxic–ischemic changes and other lesions that fication and mineralization have been demonstrated in LN) lead to cerebral edema/swelling. Follow-up CT shows resolution Background of edema with possible local volume loss. Chronic LN demon- strates cortical hyperdensity in the affected gyri. MRI of LN in The cortical and deep gray matter is hypermetabolic and as the acute to subacute setting shows reduced diffusion of the such is more susceptible to ischemia or anoxia than the white involved cortical regions, frequently with T2 hyperintensity matter, with the cortical layer 3 being the most vulnerable. LN and effacement of the sulci. Subcortical U fibers are usually is a manifestation of selective vulnerability of the gray matter affected by the edema. There is no evidence of blood products and may therefore occur in the absence of white matter on T2*-weighted images. Associated deep gray matter changes changes. However, severe hypoxic–ischemic changes tend to may be present depending on the cause of the LN. Gyral also affect the white matter and result in associated encepha- enhancement on post-contrast T1WI may occur, usually in the lomalacia. Histologically, LN has been described as pan necro- subacute stage. Chronic LN is classically visualized as T1 hyper- sis with fat-laden macrophages. Presence of mineralization intense gyri with surrounding volume loss. The hyperintensity such as calcification with traces of iron has also been demon- may be even more prominent on FLAIR images while diffusion strated. Acute LN changes could be missed at imaging: brain imaging is unremarkable. Cortical hypointensity is present on swelling may mask the changes on CT while improper T2* images in some cases. Findings of LN start fading away on windowing on MR may produce a ‘superscan’ that may ini- long follow-up studies. Encephalomalacia and gliosis of the tially be mistaken for a normal study. Recently described find- adjacent or other areas of the brain may be present, depending ings on susceptibility-weighted imaging (SWI) are absence of on the underlying etiology. blood products in a large proportion of pediatric patients, while dotted or laminar hemorrhages are found in a minority of cases. LN in a setting of hypoxic–ischemic encephalopathy, Specific Clinical Information especially in adults, shows linear gyral and basal ganglia LN tends to occur in the setting of hypoxic–ischemic encephal- hypointensities. opathy from any cause, infarction, and hypoglycemia. It is seen with seizures, posterior reversible encephalopathy syndrome references (PRES), mitochondrial disorders, osmotic myelinolysis, CNS 1. Niwa T, Aida N, Shishikura A, et al. Susceptibility weighted imaging lupus, and brain injury. Extensive changes have a poor prognosis findings of cortical laminar necrosis in pediatric patients. AJNR and tend to be associated with death or vegetative state. 2008;29:1795–8. 2. Kesavadas C, Santhosh K, Thomas B, et al. Signal changes in cortical laminar necrosis – evidence from susceptibility-weighted magnetic Differential Diagnosis resonance imaging. Neuroradiology 2009;51:293–8. Cortical Hemorrhage (178, 179, 181) 3. Siskas N, Lefkopoulos A, Ioannidis I, et al. Cortical laminar necrosis in • usually focal and mass-like brain infarcts: serial MRI. Neuroradiology 2003;45:283–8. • signal loss on T2* MRI 4. McKinney AM, Teksam M, Felice R, et al. Diffusion-weighted imaging in the setting of diffuse cortical laminar necrosis and hypoxic–ischemic Hemorrhagic Conversion of Infarct encephalopathy. AJNR 2004;25:1659–65. • usually associated with larger acute infarction 5. Takahashi S, Higano S, Ishii K, et al. Hypoxic brain damage: cortical • not limited to the gray matter laminar necrosis and delayed changes in white matter at sequential MR • signal loss on T2* MRI imaging. Radiology 1993;189:449–56. 207 Brain Imaging with MRI and CT, ed. Zoran Rumboldt et al. Published by Cambridge University Press. © Cambridge University Press 2012.
SECTION 4A Abnormalities Without Signiﬁcant Mass Effect: Primarily Non-Enhancing Figure 1. Axial T1WI (A) in a child with seizures shows hyperintense abnormality (arrow) in the left amygdala, without signiﬁcant mass effect or perifocal edema. T2WI (B) at a similar level fails to reveal any abnormal signal in the left amygdala (arrow). A B Figure 2. Sagittal T1WI (A) in a neonate shows hyperintense areas in the cerebellum (arrowheads) and supratentorial brain (arrow). Axial IR T1WI (B) also shows the cerebellar lesions (arrowheads), without mass effect. T2WI (C) shows a subtle left thalamic hypointensity (arrow). IR T1WI (D) reveals corresponding hyperintensity (arrow). Follow-up IR T1WI at a similar level a year later (E) shows interval white matter myelination with decreased conspicuity of the left thalamic lesion (arrow). A B C D E 208
Neurocutaneous Melanosis CASE 101 MA J D A T HU RNH E R Specific Imaging Findings Subarachnoid Hemorrhage (99) Neurocutaneous melanosis (NCM) appears to involve the brain • sulcal hyperintensity on FLAIR images is usually more focal in specific locations; most commonly, melanocytic lesions are and not diffuse detected in the anterior temporal lobe (amygdala) and cerebel- • typically sudden onset of symptoms lum, followed by the pons and medulla oblongata. Round or oval Moyamoya (122) shaped lesions are best seen on T1-weighted images as areas of • prominent flow-voids within the subarachnoid spaces high signal intensity (due to melanin). The lesions are T2 iso- or • parenchymal T1 hyperintensities only if associated with infarct hypointense and do not enhance with contrast. The T1 hyper- and/or hemorrhage intensity is more conspicuous within the first months of life, before the myelination appears complete on T1-weighted images. Background In patients with leptomeningeal involvement FLAIR images show Primary melanocytic lesions of the CNS arise from melanocytes sulcal/leptomeningeal hyperintensity and enhancement of the located within the leptomeninges, and this group includes dif- thickened leptomeninges is seen on post-contrast images, espe- fuse melanocytosis and meningeal melanomatosis, melanocy- cially prominent along the basal cistern, tentorium, brainstem, toma, and malignant melanoma. NCM or Touraine syndrome inferior vermis and folia of the cerebellar hemispheres. NCM is a rare, noninherited congenital phakomatosis characterized by lesions are slightly hyperdense on CT; very high density may the presence of congenital melanocytic nevi and a benign or suggest associated hemorrhage. Echogenic foci may be seen on malignant pigmented cell tumor of the leptomeninges. Giant neonatal head ultrasound exam. cutaneous melanocytic nevi (GCMN) and leptomeningeal mel- anocytosis (LM) are caused by proliferation of melanin-produ- cing cells. Intra-axial benign or malignant melanotic brain Pertinent Clinical Information lesions are found in approximately 50% of individuals with NCM typically presents early in childhood. Neurological mani- NCM. The overall risk for malignant transformation of nevi is festations of NCM are most commonly related to increased 12%. Symptomatic patients generally have very poor prognosis. intracranial pressure, communicating hydrocephalus (due to the NCM may be associated with other neurocutaneous syndromes leptomeningeal melanocytic tumors) and epilepsy. Cranial nerve such as Sturge–Weber or von Recklinghausen disease. Features palsies are frequently associated. The risk for NCM is high in of Dandy–Walker complex are also present in some cases. NCM children with large congenital melanocytic nevi, in particular is considered to follow from neurulation disorders, which could those over the trunk and neck with multiple satellite lesions. account for the associated developmental malformations. The criteria for diagnosing NCM are: (a) large or numerous Although NCM is seen almost exclusively in children with pigmented nevi in association with leptomeningeal melanosis, congenital nevi, rare cases with or without dermatologic lesions (b) no evidence of malignant transformation of the cutaneous have been described in young adults, in the third and fourth lesions, and (c) no malignant melanoma in other organs. decades of life. Differential Diagnosis references Metastatic Melanoma (180) 1. Hayashi M, Maeda M, Maji T, et al. Diffuse leptomeningeal • intracerebral metastases show perifocal edema and/or necrosis hyperintensity on fluid-attenuated inversion recovery MR images in • leptomeningeal enhancement is usually nodular neurocutaneous melanosis. AJNR 2004;25:138–41. 2. Barkovich AJ, Frieden IJ, Williams ML. MR of neurocutaneous Meningeal Carcinomatosis (119) melanosis. AJNR 1994;15:859–67. • typically focal linear and/or nodular leptomeningeal contrast 3. Smith AB, Rushing EJ, Smirniotopoulos JG. Pigmented lesions of the enhancement central nervous system: radiologic–pathologic correlation. Radiographics • additional parenchymal enhancing lesions are frequently 2009;29:1503–24. present 4. Sutton BJ, Tatter SB, Stanton CA, Mott RT. Leptomeningeal Infectious and Inflammatory Meningeal Processes melanocytosis in an adult male without large congenital nevi: a rare (118, 120, 160) and atypical case of neurocutaneous melanosis. Clin Neuropathol • enhancing meningeal and intraparenchymal enhancing lesions 2011;30:178–82. are T1 hypo- to isointense 5. Marnet D, Vinchon M, Mostofi K, et al. Neurocutaneous melanosis • associated hydrocephalus, abscess, and/or empyema may be and the Dandy–Walker complex: an uncommon but not so insignificant present association. Childs Nerv Syst 2009;25:1533–9. 209 Brain Imaging with MRI and CT, ed. Zoran Rumboldt et al. Published by Cambridge University Press. © Cambridge University Press 2012.
SECTION 4A Abnormalities Without Signiﬁcant Mass Effect: Primarily Non-Enhancing Figure 1. Axial non-enhanced CT image (A) in a patient with progressive sensorineural hearing loss shows only atrophy of the cerebellum (arrows). Axial T2WI at a similar level (B) reveals very dark regions (arrows) that are lining the surface of the superior vermis and adjacent cerebellar hemispheres (white arrows) as well as the pons (black arrow). A B Figure 2. Axial FSE T2WI with fat suppression (A) in another patient shows linear areas of very low signal in the superior vermis (white arrowheads) and along the pons (black arrowheads). Corresponding GRE T2*WI (B) demonstrates a marked loss of signal intensity along the superior cerebellum and the brainstem. A B Figure 3. Axial T2WI reveals dark lining (arrows) along the midbrain Figure 4. Axial T2*WI in a young child with history of germinal matrix surface. A more subtle dark lining is present along the mesial temporal hemorrhage shows hypointensity along the surface of the brainstem lobes and vermis (arrowheads). and cerebellum (arrows). 210
Superﬁcial Siderosis CASE 102 MAURICIO CASTILLO Specific Imaging Findings Background MRI using T2-weighted sequences is the imaging method of SS refers to deposition of chronic blood products, particularly choice, particularly with gradient-recalled echo T2* techniques. hemosiderin, in the pia and subpial regions of the brain and Susceptibility effects induced by superficial siderosis (SS) are spinal cord. Repeat bouts of hemorrhage are needed for SS to more obvious at 3.0 T than at 1.5 T. A black line follows the occur. Chronic exposure of brain cells (particularly microglia contour of the cerebellum, medulla, pons, and midbrain and to and oligodendrocytes) to hemosiderin leads to their production a lesser extent the supratentorial regions such as the temporal of ferritin, which worsens the process. The cells that are more lobes (particularly the sylvian and interhemispheric fissures). The prone to produce ferritin are found in the cerebellum (Bergman cisternal portions of the cranial nerves may also appear dark. glia), explaining why SS occurs there with a higher frequency The surface of the spinal cord can also show SS. The cerebellum and severity. The causes of SS are multiple and may include commonly shows atrophy particularly in its vermis and the repeated hemorrhages from amyloidosis, cavernomas, tumors anterior aspects of the hemispheres. The cerebral hemispheres (ependymoma, meningioma, oligodendroglioma, pineocy- may also be atrophic. Occasionally, dystrophic calcifications toma), dural AV fistulae, aneurysms, AVMs, repeated trauma develop in areas of chronic SS, which is better seen on CT. (boxing, use of jackhammer), dural tears, post-operative (post- Contrast enhancement may rarely occur. The most important hemispherectomy, chronic suboccipital subdural hematoma), role of imaging is to look for the underlying cause of SS. If the encephalocele, intracranial hypotension, anticoagulation, and brain study does not reveal obvious causes the next step is spinal nerve root avulsions. The end result is neuronal loss, gliosis MRI. If all MRI studies are non-conclusive a myelogram and and demyelination. Schwann cells are particularly prone to post-myelogram CT may be done to identify causes of CSF damage, which explains frequent sensorineural hearing loss in leak in spinal axis. Occasionally cerebral and spinal angiography these patients. There is no specific treatment of SS and the may be used as the last resort in attempting to find out the reason use of chelating drugs is unclear with reports of deferiprone, a for SS. lipid-soluble iron chelator, leading to improvement of symp- toms. Treatment should be guided towards the underlying Pertinent Clinical Information disease (if identified) that resulted in SS. Because the cochlea Classically, SS presents in adults with progressive gait ataxia and is spared, implantation may improve hearing loss in some other cerebellar abnormalities as well as sensorineural hearing individuals. loss and other cranial nerve deficits. Pyramidal signs and loss of bladder control are observed in a small number of patients and at references the end of the disease, dementia will develop in about 25% of 1. Kumar N. Neuroimaging in superficial siderosis: an in-depth look. patients. SS should be excluded in all patients with signs of AJNR 2010;31:5–14. cerebellar degeneration. CSF analysis may reveal xanthochromia, 2. Linn J, Herms J, Dichgans M, et al. Subarachnoid hemosiderosis and high iron concentrations, red blood cells and increased proteins. superficial cortical hemosiderosis in cerebral amyloid angiopathy. AJNR The peripheral nervous system is not affected but involvement of 2008;29:184–6. spinal nerve roots may give rise to conflicting clinical symptoms. 3. Hsu WC, Loevner LA, Forman MS, Thaler ER. Superficial siderosis of the CNS associated with multiple cavernous malformations. AJNR Differential Diagnosis 1999;20:1245–8. Leptomeningeal Seeding with Inflammatory, Infectious 4. Kakeda S, Korogi Y, Ohnari N, et al. Superficial siderosis associated and Neoplastic Processes (118, 119, 120, 135) with a chronic subdural hematoma: T2-weighted MR imaging at 3T. • prominent contrast enhancement Acad Radiol 2010;17:871–6. • T2 hypointensity is rare 5. Levy M, Llinas RH. Pilot safety trial of deferiprone in 10 subjects with • possible nodularity superficial siderosis. Stroke 2012;43:120–4. 211 Brain Imaging with MRI and CT, ed. Zoran Rumboldt et al. Published by Cambridge University Press. © Cambridge University Press 2012.
SECTION 4A Abnormalities Without Signiﬁcant Mass Effect: Primarily Non-Enhancing A B Figure 1. Sagittal (A) and reconstructed axial (B) T1WIs from a 3D acquisition in a Figure 2. Coronal IR T1WI shows irregular 3-year-old patient with intractable seizures show a focal area of irregular cortical thickening thickened cortex (arrow) along a deep left along the right posterior perisylvian region (arrows). sylvian ﬁssure. There is an adjacent anomalous enlarged vein (arrowhead). A B C Figure 3. Axial IR T1WI (A) demonstrates thickened and irregular cortex of the left frontal and parietal lobes with absent or rudimentary cortical sulci (arrows). Note adjacent large venous structure (arrowhead). A more cephalad image (B) shows corrugated appearance of the affected cortex (arrowheads) and reduced sulci. Coronal IR T1WI (C) demonstrates indentation of the brain (arrowhead) in the region of abnormal cortex. Figure 4. Non-enhanced axial CT image (A) in a 4-month-old child with infantile spasms reveals diffuse abnormal thickening of the cortical ribbon (arrowheads), reduced sulcation, and indistinct gray-white matter junction. Corresponding T2WI (B) shows diffuse bilateral thickening of the cortex with the appearance of cortical palisades. A B 212
Polymicrogyria CASE 103 MARIA VITTORIA SPAMPINATO Specific Imaging Findings Focal Cortical Dysplasia (FCD) (106) Polymicrogyria is characterized by an irregular cortical surface, • focal small lesion, frequently at the bottom of a sulcus apparent thickening of the cortex, “stippled” gray–white matter • high T2 signal of the cortex and/or underlying white matter is junction, and a greater than expected number of abnormally commonly present small gyri, usually without T2 signal abnormality in the myelin- • blurring of the gray–white matter junction in Type I ated brain. High-resolution images reveal that the cortical ribbon • tapered linear extension of T2 hyperintensity towards the ven- itself is thin, and the apparent thickening results from juxtapos- tricle (transmantle sign) may be present in Type II ition of the small folds. The perisylvian cortex is the site most Dysembryoplastic Neuroepithelial Tumor (DNET) (108) commonly affected by polymicrogyria; however, any region of the • multicystic “bubbly” lesion cortical mantle can be involved. Cortical involvement can be • typically sharply demarcated and wedge-shaped extending restricted to a single focus or it can affect extended areas, as seen toward the ventricle in cases of uni- or bilateral, symmetrical or asymmetrical, diffuse polymicrogyria. The imaging appearances of polymicrogyric Low-Grade Glioma (Oligodendroglioma) (161) cortex can be heterogeneous, ranging from multiple abnormal • gray and white matter involvement small gyri to a relatively smooth cortical surface and an overall • presence of mass effect coarse appearance. Diffuse coarse polymicrogyria can have the • T2 hyperintensity appearance of cortical palisades. The sulcation pattern is aber- Background rant, without a recognizable pattern. Sulci may be shallow or deeply indent the parenchyma. Polymicrogyria may be associated Polymicrogyria is one of the most common malformations of with schizencephaly, corpus callosum dysgenesis, cerebellar hypo- cortical development. It is caused by disturbance of the late plasia, periventricular and subcortical heterotopias. An imaging neuronal migration or early cortical organization. The deep protocol including volumetric T1-weighted images with thin neuronal layers do not develop normally, leading to overfolding sections (< 1.5 mm) and reconstruction in the three orthogonal and abnormal lamination of the cortex. As a result, the polymi- planes is optimal for evaluation of these abnormalities. crogyric cortex is either four-layered or unlayered. The develop- ment of these irregular undulations occurs as early as 18 Pertinent Clinical Information gestational weeks, before the first primary sulci form at mid- gestation. Because it is a primary cortical disorder, both connect- Clinical manifestations and the age of presentation vary ivity and gyration/sulcation of these regions are very abnormal. depending on the location of the malformation, the extent of In addition, the overlying meninges are thickened and may dem- cortical involvement (focal, multifocal, diffuse, unilateral, or onstrate vascular proliferation of unclear etiology. Causes of bilateral), and the presence or absence of associated anomalies. polymicrogyria include congenital infection (especially cyto- Patients affected by unilateral or bilateral diffuse polymicrogyria megalovirus infection), mutations of one or multiple genes, and present with moderate or severe intellectual impairment, mixed in-utero ischemia. It can also occur with several chromosomal seizure types, and motor dysfunction. Individual clinical features deletion and duplication syndromes (Aicardi, DiGeorge, and include hemiparesis or tetraparesis, speech disturbance, dyslexia, Delleman syndromes, among others). and developmental delay. Neurological and development abnor- malities can precede the onset of seizures. Coexistent anomalies references include dysmorphic facial features, hand, foot, skin, palate, and 1. Barkovich AJ. Current concepts of polymicrogyria. Neuroradiology cardiac abnormalities. 2010;52:479–87. Differential Diagnosis 2. Leventer RJ, Jansen A, Pilz DT, et al. Clinical and imaging heterogeneity of polymicrogyria: a study of 328 patients. Brain Classic Lissencephaly (19) 2010;133:1415–27. • abnormally thickened cortex (10–15 mm) 3. Chang B, Walsh CA, Apse K, Bodell A. Polymicrogyria overview. In: • smooth brain surface with areas of agyria and pachygyria Pagon RA, Bird TD, Dolan CR, Stephens K, eds. GeneReviews [Internet]. • shallow sylvian fissures Seattle (WA): University of Washington, Seattle; 1993–2005 Apr 18 Cobblestone Complex (92) [updated 2007 Aug 06]. • mixed cortical malformation with areas of polymicrogyria, 4. Raybaud C, Widjaja E. Development and dysgenesis of the cerebral agyria and pachygyria cortex: malformations of cortical development. Neuroimaging Clin N Am • hydrocephalus, hypoplastic brain stem and cerebellum, dysplas- 2011;21:483–543. tic corpus callosum 5. Hehr U, Schuierer G. Genetic assessment of cortical malformations. • with congenital muscular dystrophies Neuropediatrics 2011;42:43–50. 213 Brain Imaging with MRI and CT, ed. Zoran Rumboldt et al. Published by Cambridge University Press. © Cambridge University Press 2012.
SECTION 4A Abnormalities Without Signiﬁcant Mass Effect: Primarily Non-Enhancing Figure 1. Coronal FLAIR image (A) shows swollen and bright left amygdala (arrow). Axial DWI (B) shows corresponding high signal intensity (arrow). A B Figure 2. Coronal T2WI (A) in another patient after seizures shows a bright and somewhat expanded left hippocampus (arrow). Figure 3. ADC map shows a focal low signal (arrow) in the splenium of corpus callosum. A B C Figure 4. Axial T2WI (A) at the convexities shows high signal in the left posterior frontal lobe (arrow) involving gray and white matter, which corresponded to the epileptogenic focus on EEG. Matching FLAIR image (B) conﬁrms ﬁndings and shows that the cortex is slightly swollen. Follow-up FLAIR image 2 months later (C) shows complete resolution of abnormalities. 214
Seizure-Related Changes (Peri-Ictal MRI CASE 104 Abnormalities) MAURICIO CASTILLO Specific Imaging Findings • may be indistinguishable with follow-up needed, tumors that The cortex involved is expanded and bright on T2 and FLAIR produce seizures may also induce cortical edema sequences. DWI shows high signal and on ADC maps values may • MR spectroscopy shows high choline levels be normal to slightly low. Mesial temporal lobes are typically Focal Cortical Dysplasia (106) affected but other parts of the brain may also be involved. Con- • MR spectroscopy and ADC values are normal trast enhancement is rare but has been described. Findings gen- • does not change over time erally disappear from 2 weeks to 2 months after the ictus and the affected regions return to normal or become atrophic. MR spec- Global Anoxia (13) troscopy may show normal choline, low n-acetyl aspartate (NAA) • clinical history is typically suggestive of anoxic injury and lactate. Lactate tends to disappear within the first few days Background after the ictus. PET studies show increased fluoro-deoxyglucose uptake in corresponding sites. The abnormality may be localized Seizure-induced abnormalities, also known as (transient) in the splenium of the corpus callosum, also showing reduced peri-ictal MRI abnormalities, tend to affect the cortex acutely, diffusion. Occasionally the white matter can be diffusely affected, particularly the hippocampi. The hippocampi may be affected by with T2 hyperintensity and reduced diffusion in a pattern similar the seizures directly or as a result of seizure activity elsewhere or to diffuse anoxia. In these patients, MR spectroscopy may show high fever. The abnormalities are due to vasogenic, cytotoxic, or high glutamine and glutamate and low NAA. Patients with per- excitotoxic edema or a combination of any of these three pro- sistent low NAA after the first week have worse prognosis. This cesses. These underlying mechanisms probably include increased syndrome is called acute encephalopathy with biphasic seizures blood flow due to increased activity. This increased blood flow is and late reduced diffusion (AESD). unable to compensate the high regional metabolism and the end result is hypoxia, hypercarbia, lactic acidosis and vasodilation. Pertinent Clinical Information Increased permeability may also play a role. Similar findings have been produced in experimental models of kainic acid-induced Most patients have prolonged seizures which may be partial or partial status epilepticus. As the condition progresses, the generalized. The imaging findings are seen in the first 3 days that sodium–potassium pump fails and there is secondary intracellu- follow the seizure episode and thereafter tend to slowly normal- lar accumulation of calcium which may induce cell death. ize. Patients tend to be children, but these MRI findings may be seen at any age. These imaging abnormalities tend to correspond references with sites of electroencephalographic ictal activity and increased 1. Kim J-A, Chung JI, Yoon PH, et al. Transient MR signal changes in radionuclide uptake on PET studies. Patients with AESD have a patients with generalized tonicoclonic seizure or status epilepticus: typical clinical course: a prolonged (> 30 min duration) usually periictal diffusion-weighted imaging. AJNR 2001;22:1149–60. febrile seizure followed by secondary seizures (generally clusters 2. Cox JE, Mathews VP, Santos CC, Elster AD. Seizure-induced transient of partial complex ones) a few days later and encephalopathy. hippocampal abnormalities on MR: correlation with positron emission Infection and associated pathologic changes are considered tomography and electroencephalography. AJNR 1995;16:1736–8. responsible for AESD. 3. Castillo M, Smith JK, Kwock L. Proton MR spectroscopy in patients Differential Diagnosis with acute temporal lobe seizures. AJNR 2001;22:152–7. 4. Takanashi J, Tada H, Terada H, Barkovich AJ. Excitotoxicity in acute Herpes Encephalitis (20) encephalopathy with biphasic seizures and late reduced diffusion. • no previous seizures, acute onset AJNR 2009;30:132–5. • fever or viral-like illness, positive CSF 5. Gu¨rtler S, Ebner A, Tuxhorn I, et al. Transient lesion in the splenium Gliomas (165, 166) of the corpus callosum and antiepileptic drug withdrawal. Neurology • may enhance and contain calcifications 2005;65:1032–6. 215 Brain Imaging with MRI and CT, ed. Zoran Rumboldt et al. Published by Cambridge University Press. © Cambridge University Press 2012.
SECTION 4A Abnormalities Without Signiﬁcant Mass Effect: Primarily Non-Enhancing A B C Figure 1. Axial DWI (A) and FLAIR image (B) through the level of the centrum semiovale show multiple small foci of cortical and subcortical hyperintensity (arrowheads) in the frontal and parietal lobes. Axial image from a neck CTA (C) demonstrates a ﬁlling defect (arrow) in the right common carotid artery consistent with a nonocclusive thrombus. Figure 2. Axial CT image (A) in a patient with atrial ﬁbrillation shows hypodense infarcts in the left occipital lobe (black arrow), thalamus (white arrow), and anterior limb of the internal capsule (arrowheads). DWI (B) at a higher level reveals many additional lesions (arrowheads) in bilateral cerebral hemispheres. Note involvement of multiple vascular territories and varying size of the lesions. A B Figure 3. Axial DWIs (A) in another patient shows multiple bilateral small bright areas. Corresponding ADC map (B) demonstrates low signal (arrowheads) of the lesions, consistent with reduced diffusion and representing acute infarcts. Again note involvement of multiple vascular territories and varying size of the lesions. A B 216
Embolic Infarcts CASE 105 BENJAMIN HUANG Specific Imaging Findings • MRA frequently shows multifocal stenoses in large and Embolic infarcts may be isolated or multiple and vary in size medium vessel vasculitis depending on the size of the dislodged thrombus. Small acute • scattered areas of pial enhancement may be found embolic infarcts are extremely difficult to detect prospectively on • may present with subarachnoid hemorrhage CT or conventional MR sequences, particularly in patients with Small Vessel (Lacunar) Infarct pre-existing chronic ischemic lesions. The infarcts are hypodense • a single lesion usually located in deep gray matter, internal on CT and T2 hyperintense, with little or no mass effect when capsule, pons, or corona radiata small. Diffusion MRI is the most sensitive technique for early • may be indistinguishable from an isolated embolic infaction detection of infarcts, which are bright on trace DWI and dark on ADC maps, consistent with reduced diffusion. The infarcts are Septic Emboli typically located peripherally in the cortex or subcortical white • often subcortical in location matter of the cerebral hemispheres, but involvement of deep • (rim) enhancement is commonly present early on (acute phase) structures such as the basal ganglia and centrum semiovale is Fat Emboli not uncommon, as well as location along “watershed” areas • usually history of a long bone fracture; petechial rash and between vascular territories. Most embolic infarcts occur in the respiratory distress present middle cerebral artery territory due to preferential blood flow • “starfield pattern” of innumerable punctate lesions predomin- through the MCA. The presence of multiple infarctions involving antly in the “watershed” distribution more than one major arterial territory is highly suggestive of embolic etiology. Bilaterality and/or involvement of anterior Background and posterior circulations suggests a cardiac or aortic source, while multiple infarcts of differing ages suggest ongoing emboli- Most ischemic cerebral infarcts are due to local thrombosis or zation. Like with other infarcts, enhancement may occur in the thromboembolism, while a small minority has hemodynamic subacute period. etiology. Thrombotic infarction occurs when thrombosis of an atherosclerotic or otherwise diseased vessel causes luminal occlu- Pertinent Clinical Information sion, while embolic infarcts are caused by thrombus dislodge- Signs and symptoms of embolic infarcts vary depending upon ment and distal migration from an upstream location, the most the size, number, and location, and can also be asymptomatic. common being carotid bifurcation and the heart. In patients with Patients may present with a history of repeated transient ischemic TIAs, early diffusion MRI abnormalities may be reversible and attacks (TIAs) and 21–67% of patients presenting with TIA have only evident during the first two days. This is presumably due to focal signal abnormalities on DWI imaging in the acute setting; autolysis of clot and vessel recanalization. Diffusion MRI has also additional ischemic events occur in around 15% of these cases. been used for the detection of frequently clinically silent embolic Further evaluation of the heart and extracranial vessels is manda- events associated with vascular and cardiac surgery as well as with tory, as an underlying cardiac or vascular abnormality will be diagnostic and interventional endovascular procedures. detected in roughly 78% of these patients. Approximately one- quarter of patients presenting with classical “lacunar stroke” references syndromes (dysarthria–clumsy hand syndrome, pure motor 1. Kunst MM, Schaefer PW. Ischemic stroke. Radiol Clin North Am stroke, pure sensory stroke, etc.) and normal CT scan show 2011;49:1–26. embolic stroke patterns with multiple lesions on DWI, indicating 2. Wessels T, Rottger C, Jauss M, et al. Identification of embolic stroke that the diagnosis of lacunar infarcts with clinical and CT find- patterns by diffusion-weighted MRI in clinically defined lacunar ings is inaccurate. stroke syndromes. Stroke 2005;36:757–61. Differential Diagnosis 3. Moustafa RR, Izquierdo-Garcia D, Jones PS, et al. Watershed infarcts in transient ischemic attack/minor stroke with > or = 50% carotid Hemodynamic (Hypoperfusion) Infarctions stenosis: hemodynamic or embolic? Stroke 2010;41:1410–6. • infarcts are located in the watershed regions between vascular 4. Purroy F, Montaner J, Rovira A, et al. Higher risk of further vascular territories events among transient ischemic attack patients with diffusion-weighted • may be indistinguishable from embolic infarcts imaging acute ischemic lesions. Stroke 2004;35:2313–9. CNS Vasculitis (123) 5. Ryu CW, Lee DH, Kim TK, et al. Cerebral fat embolism: • can involve gray matter, subcortical white matter or deep white diffusion-weighted magnetic resonance imaging findings. Acta Radiol matter 2005;46:528–33. 217 Brain Imaging with MRI and CT, ed. Zoran Rumboldt et al. Published by Cambridge University Press. © Cambridge University Press 2012.
SECTION 4A Abnormalities Without Signiﬁcant Mass Effect: Primarily Non-Enhancing A B C Figure 1. Axial T2WI (A) in a 4-year-old patient with intractable seizures shows a subtle left frontal subcortical hyperintensity (arrow). Coronal FLAIR image (B) also shows the subcortical hyperintensity (arrow). Coronal IR T1WI (C) reveals a slightly larger area of the subcortical decreased signal with blurring of the gray matter–white matter junction (arrow). Figure 2. Axial T2WI (A) in a 35-year-old patient with epilepsy shows a slightly thickened gyrus with hyperintense cortex (arrow). There is a funnel-shaped extension of the abnormal high signal (arrowhead) from the cortex to the ventricular surface. Corresponding FLAIR image (B) better depicts the swollen hyperintense gyrus (arrow) and radial extension of the abnormal signal (arrowhead). A B A B Figure 3. Coronal FLAIR image (A) reveals a subtle hyperintense cortical thickening Figure 4. Axial FLAIR shows abnormal left (arrow) as well as extension of the abnormal signal (arrowhead) toward the ventricle. hemisphere with prominent occipital A more posterior FLAIR image (B) shows an additional similar lesion (arrowhead). hyperintensity (arrows). 218