Case Report Magnetic Resonance Characteristics and Susceptibility Weighted Imaging of the Brain in Gadolinium Encephalopathy Dejan Samardzic, MD, Krishnamoorthy Thamburaj, MD From the Department of Radiology, Penn State Milton S Hershey Medical Center, Penn State College of Medicine, Hershey, PA 17033.
ABSTRACT BACKGROUND AND PURPOSE
To report the brain imaging features on magnetic resonance imaging (MRI) in inadvertent intrathecal gadolinium administration.
Keywords: Intrathecal gadolinium, susceptibility weighted imaging, subarachnoid hemorrhage, gadolinium encephalopathy.
METHODS
A 67-year-old female with gadolinium encephalopathy from inadvertent high dose intrathecal gadolinium administration during an epidural steroid injection was studied with multisequence 3T MRI.
Acceptance: Received March 24, 2013, and in revised form May 16, 2013. Accepted for publication June 30, 2013.
RESULTS
Correspondence: Address correspondence to Krishnamoorthy Thamburaj M.D., Director of MRI Neuroradiology, Penn State Milton S Hershey Medical Center, Penn State College of Medicine, Hershey. Email: [email protected].
T1-weighted imaging shows pseudo-T2 appearance with diffusion of gadolinium into the brain parenchyma, olivary bodies, and membranous labyrinth. Nulling of cerebrospinal fluid (CSF) signal is absent on fluid attenuation recovery (FLAIR). Susceptibility-weighted imaging (SWI) demonstrates features similar to subarachnoid hemorrhage. CT may demonstrate a pseudo-cerebral edema pattern given the high attenuation characteristics of gadolinium. CONCLUSION
J Neuroimaging 2015;25:136-139. DOI: 10.1111/jon.12067
Intrathecal gadolinium demonstrates characteristic imaging features on MRI of the brain and may mimic subarachnoid hemorrhage on susceptibility-weighted imaging. Identifying high dose gadolinium within the CSF spaces on MRI is essential to avoid diagnostic and therapeutic errors.
Introduction Despite being less radiopaque than iodinated contrast, gadolinium is an attractive alternative for needle guidance during epidural spine procedures.1, 2 Given the relatively higher dose of gadolinium used for this purpose compared to myelograhy and cisternography, where .5 mL have been safely used, there is a potential risk of inadvertent injection of high doses of gadolinium into the thecal space. This can result in neurotoxicity and has been coined gadolinium encephalopathy.3, 4 Lack of awareness of imaging findings in this setting may lead to misdiagnosis on MRI and CT. Here, we present a case of gadolinium induced encephalopathy from large-dose intrathecal gadolinium injection and discuss the MRI imaging characteristics on susceptibility weighted imaging and other MRI sequences.
Case Report A 67-year-old female allergic to iodinated contrast presented to an outside pain management clinic for epidural steroid injection for low back pain. Gadolinium contrast agent was used for needle localization during the fluoroscopically guided injection. According to the procedure note, after injection of 4 mL of gadodiamide (OMNISCAN, 287 mg of gadolinium/mL)
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on the right L5-S1 interspace, the gadolinium flow pattern was suggestive of intrathecal flow. A left approach subsequently demonstrated epidural flow and a 6 mL mixture consisting of 2 mL of triamcinolone (40 mg/cc) and 4 mL of saline was injected. There were no immediate complications, and the patient was discharged after a short observation period. Approximately 3 hours after the procedure, the patient started having nausea, dyspnea, and subjective chills. She presented to an outside emergency department disoriented to place and time but without focal deficits, including no visual, auditory, or cerebellar symptoms. A noncontrast CT of the head was performed and officially interpreted as diffuse cerebral edema with uncal herniation (Fig 1). The patient was transferred to our facility at this time. Upon arrival to our facility the patient was awake but confused and disoriented to place and time. A noncontrast MRI of the brain with SWI demonstrated hyperintense signal within the sulci, cisterns, membranous labyrinth, and orbits on T1 sequence and susceptibility signals on SWI indicative of a large amount of gadolinium in the CSF spaces (Fig 1 & 2). There was no evidence of edema or herniation as was suggested on initial CT.
◦ 2013 by the American Society of Neuroimaging C
Fig 1. (A) Unenhanced CT head obtained 13 hours prior to MRI demonstrates cerebral swelling with no evidence of hemorrhage. (B) mIP image from SWI demonstrates susceptibility signal loss in the sulci and cisterns (arrows) mimicking subarachnoid hemorrhage. (C) T2-weighted TSE contrast is unaffected (D) T1 FLASH sequence demonstrates bright signals in CSF spaces from gadolinium. Note the pseudo-T2 appearance. (E) FLAIR sequence with fat saturation fails to demonstrate inversion and nulling of CSF signal due to intrathecal gadolinium. Image is almost identical to T2 TSE except for suppression of scalp fat. (F) T1 MPRAGE demonstrates bright CSF signal from gadolinium. Note the bright signal of the white matter predominantly in the frontal lobes and subcortical white matter of the insula, consistent with gadolinium in the parenchyma. (G) T1 FLASH weighted image at the level of medulla demonstrates increased signals in the bilateral inferior olivary nuclei. (H) T1 weighted fat saturated SE image demonstrates bright signals in the bilateral membranous labyrinth and the internal auditory canals.
Fig 2. (A) Axial T2 TSE image of the brain demonstrates hyperintense signal in the vitreous globes. (B) Note the inversion of vitreous T2 signal in the corresponding FLAIR image. Gadolinium in the perioptic CSF space (arrow) results in hyperintense signal secondary to absence of inversion. (C) Axial T1 FLASH at the same level demonstrates hypointense signals in the vitreous spaces typical of T1 sequence. Hyperintense signal in the perioptic CSF space is due to the presence of gadolinium (arrow). There is no gadolinium in the vitreous space. An electroencephalogram confirmed encephalopathy without any epileptiform activity. The patient received four doses of dexamethasone (4 mg IV q6 hours) prophylactically at the recommendation of the Neurology service. Infectious workup remained negative, and the patient’s mental status improved over the course of the next 2 days. She was discharged in good medical and neurological condition with discharge diagnosis of gadolinium-induced encephalopathy.
Discussion In patients allergic to iodinated contrast material, gadolinium is commonly used for needle localization during image guided
epidural injections for back and radicular pain. This can potentially lead to inadvertent intrathecal injection of high dose gadolinium. Doses ranging .5-1.0 mL (.18-.36 µmol/g brain tissue) of gadolinium can be safely administered in MR cisternography to evaluate CSF leaks and other conditions.5–7 During epidural steroid injections, potentially higher dose of gadolinium may be delivered into the intrathecal space resulting in gadolinium induced encephalopathy and peculiar MR imaging findings. Our patient received 4 mL of gadodiamide, equivalent to 1.4 µmol/g brain tissue assuming an average brain weight of 1400 g. Free water such as CSF has both long T1WI and T2WI relaxation times, and normally appears hypointense on T1WI
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and hyperintense on T2WI. With the presence of gadolinium as in our case, T1 is preferentially shortened leading to hyperintense CSF on T1WI (Fig 1D). Gadolinium also alters the inversion properties of CSF leading to absence of nulling of CSF on FLAIR (Fig 1E). Depending on the dose of gadolinium injected and time of imaging, FLAIR can appear identical to T2 as in our case.8 An interesting finding is that diffusion of gadolinium seems to be limited by the insertion of the optic nerve sheath to the sclera, with no evidence of gadolinium in the vitreous space (Fig 2). Despite the orbital involvement, our patient did not experience any visual symptoms during her admission. The pattern of intraparenchymal enhancement in our patient was a gradual decrease in signal intensity from the periphery towards the ventricles, suggestive of diffusion across the pial surface from the subarachnoid space (Fig 1F). Progressive enhancement of brain parenchyma on MR imaging was first demonstrated in rabbit brains after intrathecal administration of 75-100 µmol of gadopentetate dimeglumine.9 The authors suggested that there is no barrier between the CSF and the brain in regards to gadolinium, which can freely diffuse into the brain parenchyma. This parenchymal enhancement was shown to take up to 6 hours in animal models and 4-30 hours in humans.5, 9 Similar intraparenchymal enhancement on T1 images was seen in other cases of gadolinium encephalopathy.8, 10 The Virchow-Robbin perivascular spaces have also been postulated as a possible entry site for gadolinium.9 The gradual drop in signal towards the center of the field of view may at least in part be also related to inhomogeneous signal intensity inherently observed with phased array coil technology. Areas of focally increased gadolinium uptake were also noted in the olivary bodies on T1WI. These consist of the superior olivary nuclei, believed to function in spatial localization of sound, and inferior olivary nuclei, which function in motor coordination (Fig 1G). The significance of this finding is uncertain as our patient had no symptoms of ataxia or hearing related symptoms at presentation or during her admission. Despite the lack of labyrinthine symptoms such as tinnitus, hearing difficulties, and vertigo on initial presentation, gadolinium was also seen within the membranous labyrinth. The mode of entry into the labyrinthine fluid, whether by direct diffusion or along the vestibulocochlear nerve filaments, endolymphatic sac or a combination of these routes, is uncertain. Similar preferentially deep gray matter topographic distribution was seen in prior animal studies.11, 12 Gadolinium in the CSF causes susceptibility changes, particularly in the cisterns and sulci. This can be mistaken for subarachnoid hemorrhage on SWI which combines phase and magnitude data to create images highly sensitive for paramagnetic substances, specifically hemorrhage.13 These data can be further processed into minimum intensity projection (mIP) images to enhance visualization of blood products and calcification. The use of SWI combined with filtered phase images is replacing gradient echo imaging in the detection of intracranial hemorrhage and is routinely used at our institution. We observed extensive hypointense signal in the sulci and cisterns in our patient on SWI (Fig 1B), however given the rapid clini-
138
cal improvement and lack of hemorrhage on CT, SWI findings are most likely due to gadolinium in the CSF. To our knowledge, these findings have not been described in the literature to date. Similarly confounding findings were present in terms of the reported cerebral edema on CT scan. The sulcal effacement noted on the noncontrast CT obtained at the outside facility was not evident on the MRI obtained approximately 13 hours after the CT. The CT findings represent pseudocerebral edema due to isoattenuating gadolinium contrast in the CSF.
Conclusion Identifying the imaging characteristics of high dose gadolinium within the CSF spaces on MRI is essential to avoid diagnostic and therapeutic errors. T1-weighted images may have a pseudoT2 appearance with diffusion of gadolinium into the gray and white matter, olivary bodies, and membranous labyrinth. CSF may fail to suppress on FLAIR imaging. Susceptibility weighted imaging may demonstrate features similar to subarachnoid hemorrhage. CT may demonstrate a pseudo-cerebral edema pattern given the high attenuation characteristics of gadolinium. When the pertinent clinical history is not initially known as in our case, attention to MR sequence parameters and the vitreous globe signals, which will stay hypointense and true to their normal T1 imaging pattern, may help distinguish technical errors in image acquisition from true gadolinium in the CSF. An awareness of these imaging characteristics is paramount to avoid potentially needless medical or surgical intervention. Limitations of our case report include lack of serum and CSF gadolinium correlations with imaging and follow-up.
References 1. Safriel Y, Ali M, Hayt M, et al. Gadolinium use in spine procedures for patients with allergy to iodinated contrast-experience of 127 procedures. AJNR Am J Neuroradiol 2006;27:1194-1197. 2. Shetty SK, Nelson EN, Lawrimore TM, et al. Use of gadolinium chelate to confirm epidural needle placement in patients with an iodinated contrast reaction. Skeletal Radiol 2007;36:301-307. 3. Maramattom BV, Manno EM, Wijdicks EFM, et al. Gadolinium encephalopathy in a patient with renal failure. Neurology 2005;64:1276-1278. 4. Arlt S, Cepek L, Rustenbeck HH, et al. Gadolinium encephalopathy due to accidental intrathecal administration of gadopentetate dimeglumine. J Neurol 2007;254:810-812. 5. Zeng Q, Xiong L, Jinkins JR, et al. Intrathecal gadoliniumenhanced MR myelography and cisternography: a pilot study in human patients. AJR Am J Roentgenol 1999;173:1109-1115. 6. Tali ET, Ercan N, Krumina G, et al. Intrathecal gadolinium (gadopentetate dimeglumine) enhanced magnetic resonance myelography and cisternography: results of a multicenter study. Invest Radiol 2002;37:152-159. 7. Algin O, Turkbey B. Intrathecal gadolinium-enhanced MR cisternography: a comprehensive review. AJNR Am J Neuroradiol 2013;34:14-22. 8. Li L, Gao FQ, Zhang B, et al. Overdosage of intrathecal gadolinium and neurological response. Clin Radiol 2008;63:1063-1068. 9. Jinkins JR, Williams RF, Xiong L. Evaluation of gadopentetate dimeglumine magnetic resonance cisternography in an animal model: preliminary report. Invest Radiol 1999;34:156-159.
Journal of Neuroimaging Vol 25 No 1 January/February 2015
10. Kapoor R, Liu J, Devasenapathy A, et al. Gadolinium encephalopathy after intrathecal gadolinium injection. Pain Physician 2010;13:E321-E326. 11. Ray DE, Cavanagh JB, Nolan CC, et al. Neurotoxic effects of gadopentetate dimeglumine: behavioral disturbance and morphology after intracerebroventricular injection in rats. AJNR Am J Neuroradiol 1996;17:365-373.
12. Ray DE, Holton JL, Nolan CC, et al. Neurotoxic potential of gadodiamide after injection into the lateral cerebral ventricle of rats. AJNR Am J Neuroradiol 1998;19:14551462. 13. Haacke EM, Mittal S, Wu Z, et al. Susceptibility-weighted imaging: technical aspects and clinical applications, part 1. AJNR Am J Neuroradiol 2009;30:19-30.
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ABSTRACT BACKGROUND AND PURPOSE
To report the brain imaging features on magnetic resonance imaging (MRI) in inadvertent intrathecal gadolinium administration.
Keywords: Intrathecal gadolinium, susceptibility weighted imaging, subarachnoid hemorrhage, gadolinium encephalopathy.
METHODS
A 67-year-old female with gadolinium encephalopathy from inadvertent high dose intrathecal gadolinium administration during an epidural steroid injection was studied with multisequence 3T MRI.
Acceptance: Received March 24, 2013, and in revised form May 16, 2013. Accepted for publication June 30, 2013.
RESULTS
Correspondence: Address correspondence to Krishnamoorthy Thamburaj M.D., Director of MRI Neuroradiology, Penn State Milton S Hershey Medical Center, Penn State College of Medicine, Hershey. Email: [email protected].
T1-weighted imaging shows pseudo-T2 appearance with diffusion of gadolinium into the brain parenchyma, olivary bodies, and membranous labyrinth. Nulling of cerebrospinal fluid (CSF) signal is absent on fluid attenuation recovery (FLAIR). Susceptibility-weighted imaging (SWI) demonstrates features similar to subarachnoid hemorrhage. CT may demonstrate a pseudo-cerebral edema pattern given the high attenuation characteristics of gadolinium. CONCLUSION
J Neuroimaging 2015;25:136-139. DOI: 10.1111/jon.12067
Intrathecal gadolinium demonstrates characteristic imaging features on MRI of the brain and may mimic subarachnoid hemorrhage on susceptibility-weighted imaging. Identifying high dose gadolinium within the CSF spaces on MRI is essential to avoid diagnostic and therapeutic errors.
Introduction Despite being less radiopaque than iodinated contrast, gadolinium is an attractive alternative for needle guidance during epidural spine procedures.1, 2 Given the relatively higher dose of gadolinium used for this purpose compared to myelograhy and cisternography, where .5 mL have been safely used, there is a potential risk of inadvertent injection of high doses of gadolinium into the thecal space. This can result in neurotoxicity and has been coined gadolinium encephalopathy.3, 4 Lack of awareness of imaging findings in this setting may lead to misdiagnosis on MRI and CT. Here, we present a case of gadolinium induced encephalopathy from large-dose intrathecal gadolinium injection and discuss the MRI imaging characteristics on susceptibility weighted imaging and other MRI sequences.
Case Report A 67-year-old female allergic to iodinated contrast presented to an outside pain management clinic for epidural steroid injection for low back pain. Gadolinium contrast agent was used for needle localization during the fluoroscopically guided injection. According to the procedure note, after injection of 4 mL of gadodiamide (OMNISCAN, 287 mg of gadolinium/mL)
136
Copyright
on the right L5-S1 interspace, the gadolinium flow pattern was suggestive of intrathecal flow. A left approach subsequently demonstrated epidural flow and a 6 mL mixture consisting of 2 mL of triamcinolone (40 mg/cc) and 4 mL of saline was injected. There were no immediate complications, and the patient was discharged after a short observation period. Approximately 3 hours after the procedure, the patient started having nausea, dyspnea, and subjective chills. She presented to an outside emergency department disoriented to place and time but without focal deficits, including no visual, auditory, or cerebellar symptoms. A noncontrast CT of the head was performed and officially interpreted as diffuse cerebral edema with uncal herniation (Fig 1). The patient was transferred to our facility at this time. Upon arrival to our facility the patient was awake but confused and disoriented to place and time. A noncontrast MRI of the brain with SWI demonstrated hyperintense signal within the sulci, cisterns, membranous labyrinth, and orbits on T1 sequence and susceptibility signals on SWI indicative of a large amount of gadolinium in the CSF spaces (Fig 1 & 2). There was no evidence of edema or herniation as was suggested on initial CT.
◦ 2013 by the American Society of Neuroimaging C
Fig 1. (A) Unenhanced CT head obtained 13 hours prior to MRI demonstrates cerebral swelling with no evidence of hemorrhage. (B) mIP image from SWI demonstrates susceptibility signal loss in the sulci and cisterns (arrows) mimicking subarachnoid hemorrhage. (C) T2-weighted TSE contrast is unaffected (D) T1 FLASH sequence demonstrates bright signals in CSF spaces from gadolinium. Note the pseudo-T2 appearance. (E) FLAIR sequence with fat saturation fails to demonstrate inversion and nulling of CSF signal due to intrathecal gadolinium. Image is almost identical to T2 TSE except for suppression of scalp fat. (F) T1 MPRAGE demonstrates bright CSF signal from gadolinium. Note the bright signal of the white matter predominantly in the frontal lobes and subcortical white matter of the insula, consistent with gadolinium in the parenchyma. (G) T1 FLASH weighted image at the level of medulla demonstrates increased signals in the bilateral inferior olivary nuclei. (H) T1 weighted fat saturated SE image demonstrates bright signals in the bilateral membranous labyrinth and the internal auditory canals.
Fig 2. (A) Axial T2 TSE image of the brain demonstrates hyperintense signal in the vitreous globes. (B) Note the inversion of vitreous T2 signal in the corresponding FLAIR image. Gadolinium in the perioptic CSF space (arrow) results in hyperintense signal secondary to absence of inversion. (C) Axial T1 FLASH at the same level demonstrates hypointense signals in the vitreous spaces typical of T1 sequence. Hyperintense signal in the perioptic CSF space is due to the presence of gadolinium (arrow). There is no gadolinium in the vitreous space. An electroencephalogram confirmed encephalopathy without any epileptiform activity. The patient received four doses of dexamethasone (4 mg IV q6 hours) prophylactically at the recommendation of the Neurology service. Infectious workup remained negative, and the patient’s mental status improved over the course of the next 2 days. She was discharged in good medical and neurological condition with discharge diagnosis of gadolinium-induced encephalopathy.
Discussion In patients allergic to iodinated contrast material, gadolinium is commonly used for needle localization during image guided
epidural injections for back and radicular pain. This can potentially lead to inadvertent intrathecal injection of high dose gadolinium. Doses ranging .5-1.0 mL (.18-.36 µmol/g brain tissue) of gadolinium can be safely administered in MR cisternography to evaluate CSF leaks and other conditions.5–7 During epidural steroid injections, potentially higher dose of gadolinium may be delivered into the intrathecal space resulting in gadolinium induced encephalopathy and peculiar MR imaging findings. Our patient received 4 mL of gadodiamide, equivalent to 1.4 µmol/g brain tissue assuming an average brain weight of 1400 g. Free water such as CSF has both long T1WI and T2WI relaxation times, and normally appears hypointense on T1WI
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and hyperintense on T2WI. With the presence of gadolinium as in our case, T1 is preferentially shortened leading to hyperintense CSF on T1WI (Fig 1D). Gadolinium also alters the inversion properties of CSF leading to absence of nulling of CSF on FLAIR (Fig 1E). Depending on the dose of gadolinium injected and time of imaging, FLAIR can appear identical to T2 as in our case.8 An interesting finding is that diffusion of gadolinium seems to be limited by the insertion of the optic nerve sheath to the sclera, with no evidence of gadolinium in the vitreous space (Fig 2). Despite the orbital involvement, our patient did not experience any visual symptoms during her admission. The pattern of intraparenchymal enhancement in our patient was a gradual decrease in signal intensity from the periphery towards the ventricles, suggestive of diffusion across the pial surface from the subarachnoid space (Fig 1F). Progressive enhancement of brain parenchyma on MR imaging was first demonstrated in rabbit brains after intrathecal administration of 75-100 µmol of gadopentetate dimeglumine.9 The authors suggested that there is no barrier between the CSF and the brain in regards to gadolinium, which can freely diffuse into the brain parenchyma. This parenchymal enhancement was shown to take up to 6 hours in animal models and 4-30 hours in humans.5, 9 Similar intraparenchymal enhancement on T1 images was seen in other cases of gadolinium encephalopathy.8, 10 The Virchow-Robbin perivascular spaces have also been postulated as a possible entry site for gadolinium.9 The gradual drop in signal towards the center of the field of view may at least in part be also related to inhomogeneous signal intensity inherently observed with phased array coil technology. Areas of focally increased gadolinium uptake were also noted in the olivary bodies on T1WI. These consist of the superior olivary nuclei, believed to function in spatial localization of sound, and inferior olivary nuclei, which function in motor coordination (Fig 1G). The significance of this finding is uncertain as our patient had no symptoms of ataxia or hearing related symptoms at presentation or during her admission. Despite the lack of labyrinthine symptoms such as tinnitus, hearing difficulties, and vertigo on initial presentation, gadolinium was also seen within the membranous labyrinth. The mode of entry into the labyrinthine fluid, whether by direct diffusion or along the vestibulocochlear nerve filaments, endolymphatic sac or a combination of these routes, is uncertain. Similar preferentially deep gray matter topographic distribution was seen in prior animal studies.11, 12 Gadolinium in the CSF causes susceptibility changes, particularly in the cisterns and sulci. This can be mistaken for subarachnoid hemorrhage on SWI which combines phase and magnitude data to create images highly sensitive for paramagnetic substances, specifically hemorrhage.13 These data can be further processed into minimum intensity projection (mIP) images to enhance visualization of blood products and calcification. The use of SWI combined with filtered phase images is replacing gradient echo imaging in the detection of intracranial hemorrhage and is routinely used at our institution. We observed extensive hypointense signal in the sulci and cisterns in our patient on SWI (Fig 1B), however given the rapid clini-
138
cal improvement and lack of hemorrhage on CT, SWI findings are most likely due to gadolinium in the CSF. To our knowledge, these findings have not been described in the literature to date. Similarly confounding findings were present in terms of the reported cerebral edema on CT scan. The sulcal effacement noted on the noncontrast CT obtained at the outside facility was not evident on the MRI obtained approximately 13 hours after the CT. The CT findings represent pseudocerebral edema due to isoattenuating gadolinium contrast in the CSF.
Conclusion Identifying the imaging characteristics of high dose gadolinium within the CSF spaces on MRI is essential to avoid diagnostic and therapeutic errors. T1-weighted images may have a pseudoT2 appearance with diffusion of gadolinium into the gray and white matter, olivary bodies, and membranous labyrinth. CSF may fail to suppress on FLAIR imaging. Susceptibility weighted imaging may demonstrate features similar to subarachnoid hemorrhage. CT may demonstrate a pseudo-cerebral edema pattern given the high attenuation characteristics of gadolinium. When the pertinent clinical history is not initially known as in our case, attention to MR sequence parameters and the vitreous globe signals, which will stay hypointense and true to their normal T1 imaging pattern, may help distinguish technical errors in image acquisition from true gadolinium in the CSF. An awareness of these imaging characteristics is paramount to avoid potentially needless medical or surgical intervention. Limitations of our case report include lack of serum and CSF gadolinium correlations with imaging and follow-up.
References 1. Safriel Y, Ali M, Hayt M, et al. Gadolinium use in spine procedures for patients with allergy to iodinated contrast-experience of 127 procedures. AJNR Am J Neuroradiol 2006;27:1194-1197. 2. Shetty SK, Nelson EN, Lawrimore TM, et al. Use of gadolinium chelate to confirm epidural needle placement in patients with an iodinated contrast reaction. Skeletal Radiol 2007;36:301-307. 3. Maramattom BV, Manno EM, Wijdicks EFM, et al. Gadolinium encephalopathy in a patient with renal failure. Neurology 2005;64:1276-1278. 4. Arlt S, Cepek L, Rustenbeck HH, et al. Gadolinium encephalopathy due to accidental intrathecal administration of gadopentetate dimeglumine. J Neurol 2007;254:810-812. 5. Zeng Q, Xiong L, Jinkins JR, et al. Intrathecal gadoliniumenhanced MR myelography and cisternography: a pilot study in human patients. AJR Am J Roentgenol 1999;173:1109-1115. 6. Tali ET, Ercan N, Krumina G, et al. Intrathecal gadolinium (gadopentetate dimeglumine) enhanced magnetic resonance myelography and cisternography: results of a multicenter study. Invest Radiol 2002;37:152-159. 7. Algin O, Turkbey B. Intrathecal gadolinium-enhanced MR cisternography: a comprehensive review. AJNR Am J Neuroradiol 2013;34:14-22. 8. Li L, Gao FQ, Zhang B, et al. Overdosage of intrathecal gadolinium and neurological response. Clin Radiol 2008;63:1063-1068. 9. Jinkins JR, Williams RF, Xiong L. Evaluation of gadopentetate dimeglumine magnetic resonance cisternography in an animal model: preliminary report. Invest Radiol 1999;34:156-159.
Journal of Neuroimaging Vol 25 No 1 January/February 2015
10. Kapoor R, Liu J, Devasenapathy A, et al. Gadolinium encephalopathy after intrathecal gadolinium injection. Pain Physician 2010;13:E321-E326. 11. Ray DE, Cavanagh JB, Nolan CC, et al. Neurotoxic effects of gadopentetate dimeglumine: behavioral disturbance and morphology after intracerebroventricular injection in rats. AJNR Am J Neuroradiol 1996;17:365-373.
12. Ray DE, Holton JL, Nolan CC, et al. Neurotoxic potential of gadodiamide after injection into the lateral cerebral ventricle of rats. AJNR Am J Neuroradiol 1998;19:14551462. 13. Haacke EM, Mittal S, Wu Z, et al. Susceptibility-weighted imaging: technical aspects and clinical applications, part 1. AJNR Am J Neuroradiol 2009;30:19-30.
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