Rev Esp Med Nucl Imagen Mol. 2014;33(6):397–398
Interesting image
Crossed cerebellar diaschisis in cerebral toxoplasmosis demonstrated on 18 F-FDG PET/CT Diásquisis cerebelosa cruzada en toxoplasmosis cerebral diagnosticada por 18 F-FDG PET/TAC K.K. Agarwal a , M. Tripathi a,∗ , S. Karunanithi a , C.J. Das b , V. Suri c , A. Nalwa c a
Department of Nuclear Medicine and PET, All India Institute of Medical Sciences, New Delhi, India Department of Radiology, All India Institute of Medical Sciences, New Delhi, India c Department of Pathology, All India Institute of Medical Sciences, New Delhi, India b
a r t i c l e
i n f o
Article history: Received 22 March 2014 Accepted 17 April 2014 Available online 17 July 2014
A 44-year-old male presented with a one month history of right sided hemiparesis. Patient had undergone renal transplant one year back due to diabetic nephropathy. He underwent a MRI which revealed ring enhancing lesions in both cerebral hemispheres with a possibility of cerebral toxoplasmosis. As his toxoplasma serology was positive, patient was put on anti-toxoplasma regimen. However the patient continued to have neurological deficits for which
it was decided to biopsy the lesion and 18 F-Flurodeoxyglucose (18 F-FDG) Positron Emission Tomography/Computed Tomography (PET/CT) was requested to rule out cerebral lymphoma. 18 F-FDG PET/CT of the brain revealed reduced 18 F-FDG uptake in a large hypodense lesion in the right basifrontal region and in the left gangliocapsular region along with generalized reduced tracer uptake in the left frontal, parietal and temporal cortices and left basal
Fig. 1. PET/CT demonstrating reduced 18 F-FDG uptake in a large hypodense lesion in the right basifrontal region (surrounded by a ring of increased activity) and in the left gangliocapsular region (A and B, arrows) along with generalized reduced tracer uptake in the left frontal, parietal and temporal cortices and left basal ganglia (A and B). Additionally, the right cerebellum showed reduced FDG uptake without any morphologic abnormality on CT (C and D). Hypometabolism in left cerebral and right cerebellum regions were well appreciated in the 18 F-FDG maximum intensity projection PET image (E). MRI confirmed the ring enhancing lesions (F, arrows) in the right basifrontal region and left gangliocapsular region. Axial T2 image at the level of Pons revealed normal signal intensity of cerebellum with focal hyper intensity in left half of Pons (G).
∗ Corresponding author. E-mail addresses: madhu [email protected], [email protected] (M. Tripathi). http://dx.doi.org/10.1016/j.remn.2014.04.007 2253-654X/© 2014 Elsevier España, S.L.U. and SEMNIM. All rights reserved.
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K.K. Agarwal et al. / Rev Esp Med Nucl Imagen Mol. 2014;33(6):397–398
Fig. 2. Excisional biopsy of the right basifrontal lesion showed perivascular inflammatory cell infiltrate comprising of sheets of foamy macrophages and lymphocytes. Surrounding brain parenchyma showed reactive gliosis (HE 200×) (A). Immunohistochemical staining for Toxoplasma antibody was performed, which demonstrated intravascular multiple cysts of toxoplasmosis (IHC 400×) (B).
ganglia. Additionally, the right cerebellum showed reduced FDG uptake without any morphologic abnormality on CT. Hypometabolism in left cerebral and right cerebellum regions were well appreciated in the 18 F-FDG maximum intensity projection PET image (Fig. 1A–E). A review of his MRI confirmed the ring enhancing lesions in the right basifrontal region and left gangliocapsular region with marked surrounding edema compressing the white matter tracts, left lateral and third ventricles causing contralateral midline shift on the axial T2W MR image of the brain at the level of lateral ventricles. Axial T2 image at the level of Pons revealed normal signal intensity of cerebellum with focal hyper intensity in left half of Pons (Fig. 1F and G). Excisional biopsy of the right basifrontal lesion was performed and the immunohistochemical staining for Toxoplasma antibody demonstrated intravascular multiple cysts of toxoplasmosis (IHC 400×) (Fig. 2). Crossed cerebellar diaschisis (CCD) is a depression of neuronal metabolism and activity manifested as reduced blood flow and metabolism in the cerebellar hemisphere contralateral to a supratentorial involvement and is believed to be caused by an interruption of corticopontocerebeller tracts.1 CCD has been identified on perfusion SPECT and 18 F-FDG PET/CT imaging in patients with ganglio-capsular infarcts, brain tumor, Alzheimer’s disease, Wada test in epilepsy, and progressive supranuclear palsy. In acute brain disorders, limitation of the excitatory output from an injured brain region reduces physiological activity in connecting brain regions remote from the lesion site – a process called deafferentiation.
This is manifested as decreased cerebral blood flow or glucose metabolism.2 CCD is characterized by secondary hypoperfusion/hypometabolism due to neuronal deactivation.3 This case demonstrates CCD in cerebral toxoplasmosis because of a predominant lesion involving the left ganglio-capsular region resulting in corticopontocerebellar deafferentiation and hypometabolism in the right cerebellar hemisphere. Acknowledgements We acknowledge ‘Human Brain Tissue Repository for Neurobiological studies, Department of Neuropathology, National Institute of Mental Health and Neuroscience, Bangalore – 560029’ for carrying out immunohistochemical staining and confirming the diagnosis of Toxoplasma Encephalitis for the material received from AIIMS, New Delhi. References 1. Gold L, Lauritzen M. Neuronal deactivation explains decreased cerebellar blood flow in response to focal cortical ischemia or suppressed neocortical function. Proc Natl Acad Sci USA. 2002;99:7699–704. 2. Ito H, Kanno I, Shimosegawa E, Tamura H, Okane K, Hatazawa J. Hemodynamic changes during neural deactivation in human brain: a positron emission tomography study of crossed cerebellar diaschisis. Ann Nucl Med. 2002;16:249–54. 3. Garg G, Tripathi M, D’Souza MM, Sharma R. Crossed cerebellar diaschisis demonstrated by (18)F-FDG-PET/CT. Hell J Nucl Med. 2009;12:171–2.
Interesting image
Crossed cerebellar diaschisis in cerebral toxoplasmosis demonstrated on 18 F-FDG PET/CT Diásquisis cerebelosa cruzada en toxoplasmosis cerebral diagnosticada por 18 F-FDG PET/TAC K.K. Agarwal a , M. Tripathi a,∗ , S. Karunanithi a , C.J. Das b , V. Suri c , A. Nalwa c a
Department of Nuclear Medicine and PET, All India Institute of Medical Sciences, New Delhi, India Department of Radiology, All India Institute of Medical Sciences, New Delhi, India c Department of Pathology, All India Institute of Medical Sciences, New Delhi, India b
a r t i c l e
i n f o
Article history: Received 22 March 2014 Accepted 17 April 2014 Available online 17 July 2014
A 44-year-old male presented with a one month history of right sided hemiparesis. Patient had undergone renal transplant one year back due to diabetic nephropathy. He underwent a MRI which revealed ring enhancing lesions in both cerebral hemispheres with a possibility of cerebral toxoplasmosis. As his toxoplasma serology was positive, patient was put on anti-toxoplasma regimen. However the patient continued to have neurological deficits for which
it was decided to biopsy the lesion and 18 F-Flurodeoxyglucose (18 F-FDG) Positron Emission Tomography/Computed Tomography (PET/CT) was requested to rule out cerebral lymphoma. 18 F-FDG PET/CT of the brain revealed reduced 18 F-FDG uptake in a large hypodense lesion in the right basifrontal region and in the left gangliocapsular region along with generalized reduced tracer uptake in the left frontal, parietal and temporal cortices and left basal
Fig. 1. PET/CT demonstrating reduced 18 F-FDG uptake in a large hypodense lesion in the right basifrontal region (surrounded by a ring of increased activity) and in the left gangliocapsular region (A and B, arrows) along with generalized reduced tracer uptake in the left frontal, parietal and temporal cortices and left basal ganglia (A and B). Additionally, the right cerebellum showed reduced FDG uptake without any morphologic abnormality on CT (C and D). Hypometabolism in left cerebral and right cerebellum regions were well appreciated in the 18 F-FDG maximum intensity projection PET image (E). MRI confirmed the ring enhancing lesions (F, arrows) in the right basifrontal region and left gangliocapsular region. Axial T2 image at the level of Pons revealed normal signal intensity of cerebellum with focal hyper intensity in left half of Pons (G).
∗ Corresponding author. E-mail addresses: madhu [email protected], [email protected] (M. Tripathi). http://dx.doi.org/10.1016/j.remn.2014.04.007 2253-654X/© 2014 Elsevier España, S.L.U. and SEMNIM. All rights reserved.
398
K.K. Agarwal et al. / Rev Esp Med Nucl Imagen Mol. 2014;33(6):397–398
Fig. 2. Excisional biopsy of the right basifrontal lesion showed perivascular inflammatory cell infiltrate comprising of sheets of foamy macrophages and lymphocytes. Surrounding brain parenchyma showed reactive gliosis (HE 200×) (A). Immunohistochemical staining for Toxoplasma antibody was performed, which demonstrated intravascular multiple cysts of toxoplasmosis (IHC 400×) (B).
ganglia. Additionally, the right cerebellum showed reduced FDG uptake without any morphologic abnormality on CT. Hypometabolism in left cerebral and right cerebellum regions were well appreciated in the 18 F-FDG maximum intensity projection PET image (Fig. 1A–E). A review of his MRI confirmed the ring enhancing lesions in the right basifrontal region and left gangliocapsular region with marked surrounding edema compressing the white matter tracts, left lateral and third ventricles causing contralateral midline shift on the axial T2W MR image of the brain at the level of lateral ventricles. Axial T2 image at the level of Pons revealed normal signal intensity of cerebellum with focal hyper intensity in left half of Pons (Fig. 1F and G). Excisional biopsy of the right basifrontal lesion was performed and the immunohistochemical staining for Toxoplasma antibody demonstrated intravascular multiple cysts of toxoplasmosis (IHC 400×) (Fig. 2). Crossed cerebellar diaschisis (CCD) is a depression of neuronal metabolism and activity manifested as reduced blood flow and metabolism in the cerebellar hemisphere contralateral to a supratentorial involvement and is believed to be caused by an interruption of corticopontocerebeller tracts.1 CCD has been identified on perfusion SPECT and 18 F-FDG PET/CT imaging in patients with ganglio-capsular infarcts, brain tumor, Alzheimer’s disease, Wada test in epilepsy, and progressive supranuclear palsy. In acute brain disorders, limitation of the excitatory output from an injured brain region reduces physiological activity in connecting brain regions remote from the lesion site – a process called deafferentiation.
This is manifested as decreased cerebral blood flow or glucose metabolism.2 CCD is characterized by secondary hypoperfusion/hypometabolism due to neuronal deactivation.3 This case demonstrates CCD in cerebral toxoplasmosis because of a predominant lesion involving the left ganglio-capsular region resulting in corticopontocerebellar deafferentiation and hypometabolism in the right cerebellar hemisphere. Acknowledgements We acknowledge ‘Human Brain Tissue Repository for Neurobiological studies, Department of Neuropathology, National Institute of Mental Health and Neuroscience, Bangalore – 560029’ for carrying out immunohistochemical staining and confirming the diagnosis of Toxoplasma Encephalitis for the material received from AIIMS, New Delhi. References 1. Gold L, Lauritzen M. Neuronal deactivation explains decreased cerebellar blood flow in response to focal cortical ischemia or suppressed neocortical function. Proc Natl Acad Sci USA. 2002;99:7699–704. 2. Ito H, Kanno I, Shimosegawa E, Tamura H, Okane K, Hatazawa J. Hemodynamic changes during neural deactivation in human brain: a positron emission tomography study of crossed cerebellar diaschisis. Ann Nucl Med. 2002;16:249–54. 3. Garg G, Tripathi M, D’Souza MM, Sharma R. Crossed cerebellar diaschisis demonstrated by (18)F-FDG-PET/CT. Hell J Nucl Med. 2009;12:171–2.
