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Perfusion MRI Demonstrates Crossed-Cerebellar Diaschisis in Sickle Cell Disease
Perfusion MRI Demonstrates Crossed-Cerebellar Diaschisis in Sickle Cell Disease Ruth L. O’Gorman, PhD*†, Ata Siddiqui, MBBS*, David C. Alsop, PhD‡, and Jozef M. Jarosz, MBBS* Arterial spin labeling is a fully noninvasive magnetic resonance perfusion imaging method, ideally suited to pediatric perfusion imaging. We describe an 8-year-old boy with sickle cell disease, extensive righthemispheric cerebral infarction, and crossed-cerebellar diaschisis apparent on arterial spin labeling perfusion magnetic resonance imaging. To our knowledge, this is the first case of crossed-cerebellar diaschisis demonstrated with arterial spin labeling, highlighting the potential value of perfusion magnetic resonance imaging in the clinical evaluation and follow-up of crossed-cerebellar diaschisis, and the suitability of arterial spin labeling methods for routine perfusion imaging in pediatric patients. Ó 2010 by Elsevier Inc. All rights reserved. O’Gorman RL, Siddiqui A, Alsop DC, Jarosz JM. Perfusion MRI demonstrates crossed-cerebellar diaschisis in sickle cell disease. Pediatr Neurol 2010;42:437-440.
This method has been used in a number of clinical and research studies [1-10], and was recently implemented as part of a routine cranial magnetic resonance imaging protocol at some centers [11-13]. Arterial spin labeling perfusion magnetic resonance imaging is particularly suitable for pediatric populations because it does not involve exposure to ionizing radiation or the injection of a contrast agent. In children, the higher perfusion rates also provide a strong arterial spin labeling signal, whereas in certain adult populations, the low signal-tonoise ratio relative to other perfusion imaging techniques represents one of the main limitations of spin labeling methods. Arterial spin labeling perfusion imaging holds particular promise for the assessment and monitoring of pediatric stroke. In addition to regions of localized ischemic damage, strokes also produce hypoperfusion in distant areas, resulting from an interruption of the afferent/efferent fiber pathways providing excitation to those regions. This phenomenon of diaschisis may be evident both contralateral and ipsilateral to the area of primary stroke, depending on the morphology of the affected fibers and the age at the time of cerebral insult [14], but is most often observed in the contralateral cerebellar hemisphere, resulting from the alteration of excitatory or inhibitory inputs through the corticopontocerebellar fibers. Although crossed-cerebellar diaschisis is typically reported in the context of large hemispheric infarcts, it has also arisen from small white-matter strokes [15,16], migraine [17], encephalitis [18], tumors [19], and epilepsy [20]. Within the context of acute stroke, crossed-cerebellar diaschisis correlates positively with the volume of primary hypoperfusion, and inversely with stroke outcome, such that diaschisis in the acute stage appears to be associated with less favorable outcomes [21]. We describe a case of crossed-cerebellar diaschisis in a patient with sickle cell disease and righthemispheric infarction, as revealed through arterial spin labeling magnetic resonance perfusion imaging. Case Report
Introduction Arterial spin labeling is a fully noninvasive magnetic resonance perfusion imaging method that uses magnetically labeled arterial water as a freely diffusible endogenous tracer, enabling perfusion to be quantified from two sets of images acquired with and without previous spin labeling.
We describe an 8-year-old boy with severe right-hemispheric stroke and resulting left-sided weakness, secondary to cerebrovascular disease associated with sickle cell disease. Before the onset of stroke, the patient was neurologically normal. The initial computed tomography scans, performed acutely on days 1 and 3 at an outside institution (Fig 1), revealed an extensive area of low density in the right cerebral hemisphere involving the territory of the right middle cerebral artery. Magnetic resonance imaging on day 2 demonstrated an extensive area of cortical T2 hyperintensity
From the *Department of Neuroradiology, King’s College Hospital, London, United Kingdom; †Magnetic Resonance Zentrum, University Children’s Hospital, Zurich, Switzerland; and ‡Department of Radiology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts.
Communications should be addressed to: Dr. O’Gorman; Magnetic Resonance Zentrum, University Children’s Hospital; Steinwiesstrasse 75; Zurich CH-8032, Switzerland. E-mail: [email protected] Received October 16, 2009; accepted February 11, 2010.
Ó 2010 by Elsevier Inc. All rights reserved. doi:10.1016/j.pediatrneurol.2010.02.008 0887-8994/$—see front matter
O’Gorman et al: Perfusion MRI and Diaschisis in Sickle Cell
437
Figure 1. Acute computed tomography (day 3; left) and T2-weighted magnetic resonance imaging (day 2; right) demonstrate a large, acute, right middle cerebral artery infarct with mass effect and a midline shift. An area of old infarction is evident within the left lentiform nucleus. involving the entirety of the right middle cerebral artery territory, in addition to T2 hyperintensity of the right basal ganglia. Further cortical T2 hyperintensity was evident in the left frontal lobe in parasagittal watershed regions, and mature, small infarcts were evident in the left lentiform nucleus. Although no angiographic sequences were performed, the intracranial portion of the right internal carotid artery appeared markedly attenuated in caliber on structural magnetic resonance imaging. The patient was treated neurosurgically in the acute phase by decompressive craniotomy, and was referred to the regional neurosciences center for further imaging. Follow-up magnetic resonance imaging, performed after 4.5 months, demonstrated an extensive, established infarction involving the entirety of the right middle cerebral artery territory, including the corpus striatum, with an additional mature infarction involving the right anterior and posterior cerebral artery territories and ischemic changes in parasagittal
watershed regions and the basal ganglia on the left side (Fig 2). Regional volume loss, with sulcal dilatation and a ventricular prominence, was evident. Magnetic resonance angiography demonstrated a severe narrowing of the distal right internal carotid artery and a stenosis at the origin of the left middle cerebral artery, with flow in the right anterior and middle cerebral arteries originating in the anterior communicating artery. Arterial spin-labeled perfusion images were acquired with a 1.5-T GE Twin Speed HD.x Magnetic Resonance Imaging Scanner (General Electric Medical Systems, Milwaukee, WI), using a pseudocontinuous labeling scheme with a threedimensional, interleaved, spiral, fast spin-echo readout [22]. Sixty-four axial slices were collected, with a repetition time of 5.5 seconds and an echo time of 25 ms, a slice thickness of 3 mm, a field of view of 24 cm, and an acquisition matrix of 64 64. The arterial spin labeling perfusion images revealed an extensive area of hypoperfusion corresponding to the area of primary
Figure 2. Follow-up T2-weighted magnetic resonance imaging (left) and corresponding arterial spin labeling images after 4.5 months (right) demonstrate the expected evolution of the large, established right middle cerebral artery infarct, with a corresponding perfusion deficit.
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Figure 3. Follow-up axial T2-weighted (left) and corresponding arterial spin labeling perfusion (right) magnetic resonance images indicate a relatively normal cerebellum on structural imaging, other than a very subtle fissural prominence on the left, but a clearly obvious perfusion defect within the left cerebellar hemisphere, in keeping with the phenomenon of crossed-cerebellar diaschisis.
infarction, with a corresponding decrease in perfusion in the left cerebellum, consistent with crossed-cerebellar diaschisis (Fig 3). Mild left cerebellar hemispheric volume loss was observed, but the degree of perfusion abnormality appeared slightly out of keeping with the severity of volume loss. Moderate recovery was evident during clinical follow-up, and the patient could walk independently with the aid of a foot orthosis, although persistent left hemiparesis, particularly distal to the wrist, and left homonymous hemianopia were observed. Initially left-handed, the patient now manifested signs of right-handedness. No cerebellar signs were obvious. Cognitively there was some disinhibition, but no other major concerns. The patient subsequently underwent an uneventful encephalo-dural-arterial-synangiosis procedure on the left side, and has suffered no further strokes.
Discussion Crossed-cerebellar diaschisis is thought to arise from reductions in the afferent inputs to crossing corticopontocerebellar fibers, resulting in functional deactivation and decreased perfusion in the cerebellar hemisphere contralateral to the primary site of hypoperfusion. The severity of crossed-cerebellar diaschisis appears to represent a possible marker for recovery and outcome, and has also proven responsive to treatment [16,21]. To date, most cases of crossed-cerebellar diaschisis were reported using single-photon emission computed tomography and positron emission tomography, but one study examined the incidence of crossed-cerebellar diaschisis in a series of stroke patients with dynamic susceptibility contrast perfusion magnetic resonance imaging [23]. Like dynamic susceptibility contrast magnetic resonance imaging, arterial spin labeling is advantageous because it does not involve exposure to ionizing radiation, can be acquired with a relatively high spatial resolution, and can be applied in conjunction with structural, diffusion-weighted, and angiographic magnetic resonance imaging, enabling
a more extensive evaluation of tissue morphology and function within a single scanning session. Moreover, arterial spin labeling does not require an injection of intravenous gadolinium, making it fully noninvasive and ideally suited to pediatric populations and groups of patients with impaired renal function. Arterial spin labeling perfusion magnetic resonance imaging may represent a potentially valuable tool for investigating the clinical and prognostic significance of crossed-cerebellar diaschisis and for further elucidating the relationship between diaschisis and recovery. References [1] Detre JA, Samuels OB, Alsop DC, et al. Hemodynamic assessment using arterial spin labeled magnetic resonance imaging. Stroke 1999;30:276. [2] Detre JA, Alsop DC, Vives LR, Maccotta L, Teener JW, Raps EC. Noninvasive MRI evaluation of cerebral blood flow in cerebrovascular disease. Neurology 1998;50:633-41. [3] O’Gorman RL, Mehta MA, Asherson P, et al. Increased cerebral perfusion in adult attention deficit hyperactivity disorder is normalised by stimulant treatment: A non-invasive MRI pilot study. Neuroimage 2008;42:36-41. [4] Oguz KK, Golay X, Pizzini FB, et al. Sickle cell disease: Continuous arterial spin-labeling perfusion MR imaging in children. Radiology 2003;227:567-74. [5] Rashid W, Parkes LM, Ingle GT, et al. Abnormalities of cerebral perfusion in multiple sclerosis. J Neurol Neurosurg Psychiatry 2004;75: 1288-93. [6] Wang Z, Fernandez-Seara M, Alsop DC, et al. Assessment of functional development in normal infant brain using arterial spin labeled perfusion MRI. Neuroimage 2008;39:973-8. [7] Wolf RL, Alsop DC, French JA, et al. Detection of mesial temporal lobe hypoperfusion in patients with temporal lobe epilepsy using multislice arterial spin labeled perfusion MRI. Epilepsia 1999;40:249. [8] Wolf RL, Wang JJ, Wang SM, et al. Grading of CNS neoplasms using continuous arterial spin labeled perfusion MR imaging at 3 Tesla. J Magn Reson Imag 2005;22:475-82.
O’Gorman et al: Perfusion MRI and Diaschisis in Sickle Cell
439
[9] Chalela JA, Alsop DC, Gonzalez-Atavales JB, Maldjian JA, Kasner SE, Detre JA. Magnetic resonance perfusion imaging in acute ischemic stroke using continuous arterial spin labeling. Stroke 2000;31:680-7. [10] Wang J, Licht DJ. Pediatric perfusion MR imaging using arterial spin labeling. Neuroimag Clin North Am 2006;16:149-67. [11] Deibler AR, Pollock JM, Kraft RA, Tan H, Burdette JH, Maldjian JA. Arterial spin-labeling in routine clinical practice, part 3: Hyperperfusion patterns. AJNR 2008;29:1428-35. [12] Deibler AR, Pollock JM, Kraft RA, Tan H, Burdette JH, Maldjian JA. Arterial spin-labeling in routine clinical practice, part 1: Technique and artifacts. AJNR 2008;29:1228-34. [13] Deibler AR, Pollock JM, Kraft RA, Tan H, Burdette JH, Maldjian JA. Arterial spin-labeling in routine clinical practice, part 2: Hypoperfusion patterns. AJNR 2008;29:1235-41. [14] Chakravarty A. MR evaluation of crossed and uncrossed cerebral-cerebellar diaschisis. Acta Neurol Scand 2003;108:60-5. [15] Flint AC, Naley MC, Wright CB. Ataxic hemiparesis from strategic frontal white matter infarction with crossed cerebellar diaschisis. Stroke 2006;37:E1-2. [16] Lai MH, Wang TY, Chang CC, Li TY, Chang ST. Cerebellar diaschisis and contralateral thalamus hyperperfusion in a stroke patient with complex regional pain syndrome. J Clin Neurosci 2008;15:1166-8.
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[17] Dodick DW, Roarke MC. Crossed cerebellar diaschisis during migraine with prolonged aura: A possible mechanism for cerebellar infarctions. Cephalagia 2007;28:83-6. [18] Thajeb P, Shih BF, Wu MC. Crossed cerebellar diaschisis in herpes simplex encephalitis. Eur J Radiol 2001;38:55-8. [19] Otte A, Roelcke U, von Ammon K, et al. Crossed cerebellar diaschisis and brain tumor biochemistry studied with positron emission tomography, F-18 fluorodeoxyglucose and C-11 methionine. J Neurol Sci 1998; 156:73-7. [20] Mewasingh LD, Christiaens F, Aeby A, Christophe C, Dan B. Crossed cerebellar diaschisis secondary to refractory frontal seizures in childhood. Seizure 2002;11:489-93. [21] Sobesky J, Thiel A, Ghaemi M, et al. Crossed cerebellar diaschisis in acute human stroke: A PET study of serial changes and response to supratentorial reperfusion. J Cereb Blood Flow Metab 2005; 25:1685-91. [22] Dai W, Garcia D, de Bazelaire C, Alsop DC. Continuous flowdriven inversion for arterial spin labeling using pulsed radio frequency and gradient fields. Magn Reson Med 2008;60:1488-97. [23] Lin DDM, Kleinman JT, Wityk RJ, et al. Crossed cerebellar diaschisis in acute stroke detected by dynamic susceptibility contrast MR perfusion imaging. AJNR 2009;30:710-5.
This method has been used in a number of clinical and research studies [1-10], and was recently implemented as part of a routine cranial magnetic resonance imaging protocol at some centers [11-13]. Arterial spin labeling perfusion magnetic resonance imaging is particularly suitable for pediatric populations because it does not involve exposure to ionizing radiation or the injection of a contrast agent. In children, the higher perfusion rates also provide a strong arterial spin labeling signal, whereas in certain adult populations, the low signal-tonoise ratio relative to other perfusion imaging techniques represents one of the main limitations of spin labeling methods. Arterial spin labeling perfusion imaging holds particular promise for the assessment and monitoring of pediatric stroke. In addition to regions of localized ischemic damage, strokes also produce hypoperfusion in distant areas, resulting from an interruption of the afferent/efferent fiber pathways providing excitation to those regions. This phenomenon of diaschisis may be evident both contralateral and ipsilateral to the area of primary stroke, depending on the morphology of the affected fibers and the age at the time of cerebral insult [14], but is most often observed in the contralateral cerebellar hemisphere, resulting from the alteration of excitatory or inhibitory inputs through the corticopontocerebellar fibers. Although crossed-cerebellar diaschisis is typically reported in the context of large hemispheric infarcts, it has also arisen from small white-matter strokes [15,16], migraine [17], encephalitis [18], tumors [19], and epilepsy [20]. Within the context of acute stroke, crossed-cerebellar diaschisis correlates positively with the volume of primary hypoperfusion, and inversely with stroke outcome, such that diaschisis in the acute stage appears to be associated with less favorable outcomes [21]. We describe a case of crossed-cerebellar diaschisis in a patient with sickle cell disease and righthemispheric infarction, as revealed through arterial spin labeling magnetic resonance perfusion imaging. Case Report
Introduction Arterial spin labeling is a fully noninvasive magnetic resonance perfusion imaging method that uses magnetically labeled arterial water as a freely diffusible endogenous tracer, enabling perfusion to be quantified from two sets of images acquired with and without previous spin labeling.
We describe an 8-year-old boy with severe right-hemispheric stroke and resulting left-sided weakness, secondary to cerebrovascular disease associated with sickle cell disease. Before the onset of stroke, the patient was neurologically normal. The initial computed tomography scans, performed acutely on days 1 and 3 at an outside institution (Fig 1), revealed an extensive area of low density in the right cerebral hemisphere involving the territory of the right middle cerebral artery. Magnetic resonance imaging on day 2 demonstrated an extensive area of cortical T2 hyperintensity
From the *Department of Neuroradiology, King’s College Hospital, London, United Kingdom; †Magnetic Resonance Zentrum, University Children’s Hospital, Zurich, Switzerland; and ‡Department of Radiology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts.
Communications should be addressed to: Dr. O’Gorman; Magnetic Resonance Zentrum, University Children’s Hospital; Steinwiesstrasse 75; Zurich CH-8032, Switzerland. E-mail: [email protected] Received October 16, 2009; accepted February 11, 2010.
Ó 2010 by Elsevier Inc. All rights reserved. doi:10.1016/j.pediatrneurol.2010.02.008 0887-8994/$—see front matter
O’Gorman et al: Perfusion MRI and Diaschisis in Sickle Cell
437
Figure 1. Acute computed tomography (day 3; left) and T2-weighted magnetic resonance imaging (day 2; right) demonstrate a large, acute, right middle cerebral artery infarct with mass effect and a midline shift. An area of old infarction is evident within the left lentiform nucleus. involving the entirety of the right middle cerebral artery territory, in addition to T2 hyperintensity of the right basal ganglia. Further cortical T2 hyperintensity was evident in the left frontal lobe in parasagittal watershed regions, and mature, small infarcts were evident in the left lentiform nucleus. Although no angiographic sequences were performed, the intracranial portion of the right internal carotid artery appeared markedly attenuated in caliber on structural magnetic resonance imaging. The patient was treated neurosurgically in the acute phase by decompressive craniotomy, and was referred to the regional neurosciences center for further imaging. Follow-up magnetic resonance imaging, performed after 4.5 months, demonstrated an extensive, established infarction involving the entirety of the right middle cerebral artery territory, including the corpus striatum, with an additional mature infarction involving the right anterior and posterior cerebral artery territories and ischemic changes in parasagittal
watershed regions and the basal ganglia on the left side (Fig 2). Regional volume loss, with sulcal dilatation and a ventricular prominence, was evident. Magnetic resonance angiography demonstrated a severe narrowing of the distal right internal carotid artery and a stenosis at the origin of the left middle cerebral artery, with flow in the right anterior and middle cerebral arteries originating in the anterior communicating artery. Arterial spin-labeled perfusion images were acquired with a 1.5-T GE Twin Speed HD.x Magnetic Resonance Imaging Scanner (General Electric Medical Systems, Milwaukee, WI), using a pseudocontinuous labeling scheme with a threedimensional, interleaved, spiral, fast spin-echo readout [22]. Sixty-four axial slices were collected, with a repetition time of 5.5 seconds and an echo time of 25 ms, a slice thickness of 3 mm, a field of view of 24 cm, and an acquisition matrix of 64 64. The arterial spin labeling perfusion images revealed an extensive area of hypoperfusion corresponding to the area of primary
Figure 2. Follow-up T2-weighted magnetic resonance imaging (left) and corresponding arterial spin labeling images after 4.5 months (right) demonstrate the expected evolution of the large, established right middle cerebral artery infarct, with a corresponding perfusion deficit.
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Figure 3. Follow-up axial T2-weighted (left) and corresponding arterial spin labeling perfusion (right) magnetic resonance images indicate a relatively normal cerebellum on structural imaging, other than a very subtle fissural prominence on the left, but a clearly obvious perfusion defect within the left cerebellar hemisphere, in keeping with the phenomenon of crossed-cerebellar diaschisis.
infarction, with a corresponding decrease in perfusion in the left cerebellum, consistent with crossed-cerebellar diaschisis (Fig 3). Mild left cerebellar hemispheric volume loss was observed, but the degree of perfusion abnormality appeared slightly out of keeping with the severity of volume loss. Moderate recovery was evident during clinical follow-up, and the patient could walk independently with the aid of a foot orthosis, although persistent left hemiparesis, particularly distal to the wrist, and left homonymous hemianopia were observed. Initially left-handed, the patient now manifested signs of right-handedness. No cerebellar signs were obvious. Cognitively there was some disinhibition, but no other major concerns. The patient subsequently underwent an uneventful encephalo-dural-arterial-synangiosis procedure on the left side, and has suffered no further strokes.
Discussion Crossed-cerebellar diaschisis is thought to arise from reductions in the afferent inputs to crossing corticopontocerebellar fibers, resulting in functional deactivation and decreased perfusion in the cerebellar hemisphere contralateral to the primary site of hypoperfusion. The severity of crossed-cerebellar diaschisis appears to represent a possible marker for recovery and outcome, and has also proven responsive to treatment [16,21]. To date, most cases of crossed-cerebellar diaschisis were reported using single-photon emission computed tomography and positron emission tomography, but one study examined the incidence of crossed-cerebellar diaschisis in a series of stroke patients with dynamic susceptibility contrast perfusion magnetic resonance imaging [23]. Like dynamic susceptibility contrast magnetic resonance imaging, arterial spin labeling is advantageous because it does not involve exposure to ionizing radiation, can be acquired with a relatively high spatial resolution, and can be applied in conjunction with structural, diffusion-weighted, and angiographic magnetic resonance imaging, enabling
a more extensive evaluation of tissue morphology and function within a single scanning session. Moreover, arterial spin labeling does not require an injection of intravenous gadolinium, making it fully noninvasive and ideally suited to pediatric populations and groups of patients with impaired renal function. Arterial spin labeling perfusion magnetic resonance imaging may represent a potentially valuable tool for investigating the clinical and prognostic significance of crossed-cerebellar diaschisis and for further elucidating the relationship between diaschisis and recovery. References [1] Detre JA, Samuels OB, Alsop DC, et al. Hemodynamic assessment using arterial spin labeled magnetic resonance imaging. Stroke 1999;30:276. [2] Detre JA, Alsop DC, Vives LR, Maccotta L, Teener JW, Raps EC. Noninvasive MRI evaluation of cerebral blood flow in cerebrovascular disease. Neurology 1998;50:633-41. [3] O’Gorman RL, Mehta MA, Asherson P, et al. Increased cerebral perfusion in adult attention deficit hyperactivity disorder is normalised by stimulant treatment: A non-invasive MRI pilot study. Neuroimage 2008;42:36-41. [4] Oguz KK, Golay X, Pizzini FB, et al. Sickle cell disease: Continuous arterial spin-labeling perfusion MR imaging in children. Radiology 2003;227:567-74. [5] Rashid W, Parkes LM, Ingle GT, et al. Abnormalities of cerebral perfusion in multiple sclerosis. J Neurol Neurosurg Psychiatry 2004;75: 1288-93. [6] Wang Z, Fernandez-Seara M, Alsop DC, et al. Assessment of functional development in normal infant brain using arterial spin labeled perfusion MRI. Neuroimage 2008;39:973-8. [7] Wolf RL, Alsop DC, French JA, et al. Detection of mesial temporal lobe hypoperfusion in patients with temporal lobe epilepsy using multislice arterial spin labeled perfusion MRI. Epilepsia 1999;40:249. [8] Wolf RL, Wang JJ, Wang SM, et al. Grading of CNS neoplasms using continuous arterial spin labeled perfusion MR imaging at 3 Tesla. J Magn Reson Imag 2005;22:475-82.
O’Gorman et al: Perfusion MRI and Diaschisis in Sickle Cell
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[9] Chalela JA, Alsop DC, Gonzalez-Atavales JB, Maldjian JA, Kasner SE, Detre JA. Magnetic resonance perfusion imaging in acute ischemic stroke using continuous arterial spin labeling. Stroke 2000;31:680-7. [10] Wang J, Licht DJ. Pediatric perfusion MR imaging using arterial spin labeling. Neuroimag Clin North Am 2006;16:149-67. [11] Deibler AR, Pollock JM, Kraft RA, Tan H, Burdette JH, Maldjian JA. Arterial spin-labeling in routine clinical practice, part 3: Hyperperfusion patterns. AJNR 2008;29:1428-35. [12] Deibler AR, Pollock JM, Kraft RA, Tan H, Burdette JH, Maldjian JA. Arterial spin-labeling in routine clinical practice, part 1: Technique and artifacts. AJNR 2008;29:1228-34. [13] Deibler AR, Pollock JM, Kraft RA, Tan H, Burdette JH, Maldjian JA. Arterial spin-labeling in routine clinical practice, part 2: Hypoperfusion patterns. AJNR 2008;29:1235-41. [14] Chakravarty A. MR evaluation of crossed and uncrossed cerebral-cerebellar diaschisis. Acta Neurol Scand 2003;108:60-5. [15] Flint AC, Naley MC, Wright CB. Ataxic hemiparesis from strategic frontal white matter infarction with crossed cerebellar diaschisis. Stroke 2006;37:E1-2. [16] Lai MH, Wang TY, Chang CC, Li TY, Chang ST. Cerebellar diaschisis and contralateral thalamus hyperperfusion in a stroke patient with complex regional pain syndrome. J Clin Neurosci 2008;15:1166-8.
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[17] Dodick DW, Roarke MC. Crossed cerebellar diaschisis during migraine with prolonged aura: A possible mechanism for cerebellar infarctions. Cephalagia 2007;28:83-6. [18] Thajeb P, Shih BF, Wu MC. Crossed cerebellar diaschisis in herpes simplex encephalitis. Eur J Radiol 2001;38:55-8. [19] Otte A, Roelcke U, von Ammon K, et al. Crossed cerebellar diaschisis and brain tumor biochemistry studied with positron emission tomography, F-18 fluorodeoxyglucose and C-11 methionine. J Neurol Sci 1998; 156:73-7. [20] Mewasingh LD, Christiaens F, Aeby A, Christophe C, Dan B. Crossed cerebellar diaschisis secondary to refractory frontal seizures in childhood. Seizure 2002;11:489-93. [21] Sobesky J, Thiel A, Ghaemi M, et al. Crossed cerebellar diaschisis in acute human stroke: A PET study of serial changes and response to supratentorial reperfusion. J Cereb Blood Flow Metab 2005; 25:1685-91. [22] Dai W, Garcia D, de Bazelaire C, Alsop DC. Continuous flowdriven inversion for arterial spin labeling using pulsed radio frequency and gradient fields. Magn Reson Med 2008;60:1488-97. [23] Lin DDM, Kleinman JT, Wityk RJ, et al. Crossed cerebellar diaschisis in acute stroke detected by dynamic susceptibility contrast MR perfusion imaging. AJNR 2009;30:710-5.