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@@ -189,15 +197,24 @@
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@@ -214,30 +231,27 @@
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@@ -256,26 +270,40 @@
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344781fd-34ab-4335-bb66-19706f7d2d68
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## References
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||||
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# Selected References
|
||||
|
||||
1. [Koh DM et al: Cross-sectional imaging of nodal metastases in the abdomen and pelvis. Abdom Imaging. 31(6):632-43, 2006](http://www.ncbi.nlm.nih.gov/pubmed/?term=16897278%5Bpmid%5D)
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1. [Lucey BC et al: Mesenteric lymph nodes: detection and significance on MDCT. AJR Am J Roentgenol. 184(1):41-4, 2005](http://www.ncbi.nlm.nih.gov/pubmed/?term=15615948%5Bpmid%5D)
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46575243-9eec-43e0-9955-dd51cd5f49b4
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## References
|
||||
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# Selected References
|
||||
|
||||
1. [Draghi F et al: Abdominal wall sonography: a pictorial review. J Ultrasound. 23(3):265-78, 2020](http://www.ncbi.nlm.nih.gov/pubmed/?term=32125676%5Bpmid%5D)
|
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@@ -353,6 +351,52 @@ breadcrumbs:
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3aec74c8-de53-4430-a00a-d8165ad210c7
|
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|
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## References
|
||||
|
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# Selected References
|
||||
|
||||
1. [Carvalho K et al: Acute disseminated encephalomyelitis (ADEM) associated with mosquito-borne diseases: Chikungunya virus X yellow fever immunization. Rev Soc Bras Med Trop. 53:e20190160, 2020](http://www.ncbi.nlm.nih.gov/pubmed/?term=31994659%5Bpmid%5D)
|
||||
1. [Molero-Senosiain M et al: Neuro-ophthalmological manifestations as complication of an infection with Mycoplasma pneumoniae and subsequent development of disseminated acute encephalitis. Arch Soc Esp Oftalmol. 95(5(:254-8, 2020](http://www.ncbi.nlm.nih.gov/pubmed/?term=32147128%5Bpmid%5D)
|
||||
1. [Stokes Brackett AC et al: Multiphasic acute disseminated encephalomyelitis and differential with early onset multiple sclerosis. Intractable Rare Dis Res. 9(1):61-3, 2020](http://www.ncbi.nlm.nih.gov/pubmed/?term=32201679%5Bpmid%5D)
|
||||
1. [Baumann M et al: MRI of the first event in pediatric acquired demyelinating syndromes with antibodies to myelin oligodendrocyte glycoprotein. J Neurol. 265(4):845-55, 2018](http://www.ncbi.nlm.nih.gov/pubmed/?term=29423614%5Bpmid%5D)
|
||||
1. [Aubert-Broche B et al: Monophasic demyelination reduces brain growth in children. Neurology. 88(18):1744-50, 2017](http://www.ncbi.nlm.nih.gov/pubmed/?term=28381515%5Bpmid%5D)
|
||||
1. [Bester M et al: Neuroimaging of multiple sclerosis, acute disseminated encephalomyelitis, and other demyelinating diseases. Semin Roentgenol. 49(1):76-85, 2014](http://www.ncbi.nlm.nih.gov/pubmed/?term=24342677%5Bpmid%5D)
|
||||
1. [Longoni G et al: White matter changes in paediatric multiple sclerosis and monophasic demyelinating disorders. Brain. 140(5):1300-15, 2017](http://www.ncbi.nlm.nih.gov/pubmed/?term=28334875%5Bpmid%5D)
|
||||
1. [Koelman DLH et al: Acute disseminated encephalomyelitis: prognostic value of early follow-up brain MRI. J Neurol. 264(8):1754-62, 2017](http://www.ncbi.nlm.nih.gov/pubmed/?term=28695361%5Bpmid%5D)
|
||||
1. [Marziali S et al: Acute disseminated encephalomyelitis following Campylobacter jejuni gastroenteritis: Case report and review of the literature. Neuroradiol J. 30(1):65-70, 2017](http://www.ncbi.nlm.nih.gov/pubmed/?term=27888275%5Bpmid%5D)
|
||||
1. [Kanekar S et al: A pattern approach to focal white matter hyperintensities on magnetic resonance imaging. Radiol Clin North Am. 52(2):241-61, 2014](http://www.ncbi.nlm.nih.gov/pubmed/?term=24582339%5Bpmid%5D)
|
||||
1. [Daida K et al: Cytomegalovirus-associated encephalomyelitis in an immunocompetent adult: a two-stage attack of direct viral and delayed immune-mediated invasions. case report. BMC Neurol. 16(1):223, 2016](http://www.ncbi.nlm.nih.gov/pubmed/?term=27855658%5Bpmid%5D)
|
||||
1. [Pohl D et al: Acute disseminated encephalomyelitis: updates on an inflammatory CNS syndrome. Neurology. 87(9 Suppl 2):S38-45, 2016](http://www.ncbi.nlm.nih.gov/pubmed/?term=27572859%5Bpmid%5D)
|
||||
1. [Yuan JL et al: Acute Disseminated Encephalomyelitis following Vaccination against Hepatitis B in a Child: A Case Report and Literature Review. Case Rep Neurol Med. 2016:2401809, 2016](http://www.ncbi.nlm.nih.gov/pubmed/?term=27478662%5Bpmid%5D)
|
||||
1. [Baumann M et al: Clinical and neuroradiological differences of paediatric acute disseminating encephalomyelitis with and without antibodies to the myelin oligodendrocyte glycoprotein. J Neurol Neurosurg Psychiatry. 86(3):265-72, 2015](http://www.ncbi.nlm.nih.gov/pubmed/?term=25121570%5Bpmid%5D)
|
||||
1. [Karussis D: The diagnosis of multiple sclerosis and the various related demyelinating syndromes: a critical review. J Autoimmun. 48-49:134-42, 2014](http://www.ncbi.nlm.nih.gov/pubmed/?term=24524923%5Bpmid%5D)
|
||||
1. [Mariotto S et al: Clinical spectrum and IgG subclass analysis of anti-myelin oligodendrocyte glycoprotein antibody-associated syndromes: a multicenter study. J Neurol. 264(12):2420-30, 2017](http://www.ncbi.nlm.nih.gov/pubmed/?term=29063242%5Bpmid%5D)
|
||||
1. [Nakamura Y et al: Anti-MOG antibody-positive ADEM following infectious mononucleosis due to a primary EBV infection: a case report. BMC Neurol. 17(1):76, 2017](http://www.ncbi.nlm.nih.gov/pubmed/?term=28420330%5Bpmid%5D)
|
||||
1. [Tenembaum SN: Acute disseminated encephalomyelitis. Handb Clin Neurol. 112:1253-62, 2013](http://www.ncbi.nlm.nih.gov/pubmed/?term=23622336%5Bpmid%5D)
|
||||
1. [Wingerchuk DM et al: Acute disseminated encephalomyelitis, transverse myelitis, and neuromyelitis optica. Continuum (Minneap Minn). 19(4 Multiple Sclerosis):944-67, 2013](http://www.ncbi.nlm.nih.gov/pubmed/?term=23917095%5Bpmid%5D)
|
||||
1. [Callen DJ et al: Role of MRI in the differentiation of ADEM from MS in children. Neurology. 72(11):968-73, 2009](http://www.ncbi.nlm.nih.gov/pubmed/?term=19038851%5Bpmid%5D)
|
||||
1. [Noorbakhsh F et al: Acute disseminated encephalomyelitis: clinical and pathogenesis features. Neurol Clin. 26(3):759-80, ix, 2008](http://www.ncbi.nlm.nih.gov/pubmed/?term=18657725%5Bpmid%5D)
|
||||
1. [Rossi A: Imaging of acute disseminated encephalomyelitis. Neuroimaging Clin N Am. 18(1):149-61; ix, 2008](http://www.ncbi.nlm.nih.gov/pubmed/?term=18319160%5Bpmid%5D)
|
||||
1. [Tenembaum S et al: Acute disseminated encephalomyelitis. Neurology. 68(16 Suppl 2):S23-36, 2007](http://www.ncbi.nlm.nih.gov/pubmed/?term=17438235%5Bpmid%5D)
|
||||
1. [Menge T et al: Acute disseminated encephalomyelitis: an update. Arch Neurol. 62(11):1673-80, 2005](http://www.ncbi.nlm.nih.gov/pubmed/?term=16286539%5Bpmid%5D)
|
||||
1. [Yeh EA et al: Detection of coronavirus in the central nervous system of a child with acute disseminated encephalomyelitis. Pediatrics. 113(1 Pt 1):e73-6, 2004](http://www.ncbi.nlm.nih.gov/pubmed/?term=14702500%5Bpmid%5D)
|
||||
1. [Dale RC: Acute disseminated encephalomyelitis. Semin Pediatr Infect Dis. 14(2):90-5, 2003](http://www.ncbi.nlm.nih.gov/pubmed/?term=12881796%5Bpmid%5D)
|
||||
1. [Garg RK: Acute disseminated encephalomyelitis. Postgrad Med J. 79(927):11-17, 2003](http://www.ncbi.nlm.nih.gov/pubmed/?term=12566545%5Bpmid%5D)
|
||||
1. [Idrissova ZhR et al: Acute disseminated encephalomyelitis in children: clinical features and HLA-DR linkage. Eur J Neurol. 10(5):537-46, 2003](http://www.ncbi.nlm.nih.gov/pubmed/?term=12940836%5Bpmid%5D)
|
||||
1. [Okamoto K et al: MR features of diseases involving bilateral middle cerebellar peduncles. AJNR Am J Neuroradiol. 24(10):1946-54, 2003](http://www.ncbi.nlm.nih.gov/pubmed/?term=14625215%5Bpmid%5D)
|
||||
1. [Sener RN: Neuro-Behcet's disease: diffusion MR imaging and proton MR spectroscopy. AJNR Am J Neuroradiol. 24(8):1612-4, 2003](http://www.ncbi.nlm.nih.gov/pubmed/?term=13679280%5Bpmid%5D)
|
||||
1. [Stonehouse M et al: Acute disseminated encephalomyelitis: recognition in the hands of general paediatricians. Arch Dis Child. 88(2):122-4, 2003](http://www.ncbi.nlm.nih.gov/pubmed/?term=12538312%5Bpmid%5D)
|
||||
1. [Inglese M et al: Magnetization transfer and diffusion tensor MR imaging of acute disseminated encephalomyelitis. AJNR Am J Neuroradiol. 23(2):267-72, 2002](http://www.ncbi.nlm.nih.gov/pubmed/?term=11847052%5Bpmid%5D)
|
||||
1. [Murthy JM: Acute disseminated encephalomyelitis. Neurol India. 50(3):238-43, 2002](http://www.ncbi.nlm.nih.gov/pubmed/?term=12391446%5Bpmid%5D)
|
||||
1. [Tenembaum S et al: Acute disseminated encephalomyelitis: a long-term follow-up study of 84 pediatric patients. Neurology. 59(8):1224-31, 2002](http://www.ncbi.nlm.nih.gov/pubmed/?term=12391351%5Bpmid%5D)
|
||||
1. [Bizzi A et al: Quantitative proton MR spectroscopic imaging in acute disseminated encephalomyelitis. AJNR Am J Neuroradiol. 22(6):1125-30, 2001](http://www.ncbi.nlm.nih.gov/pubmed/?term=11415908%5Bpmid%5D)
|
||||
1. [Honkaniemi J et al: Delayed MR imaging changes in acute disseminated encephalomyelitis. AJNR Am J Neuroradiol. 22(6):1117-24, 2001](http://www.ncbi.nlm.nih.gov/pubmed/?term=11415907%5Bpmid%5D)
|
||||
1. [Straussberg R et al: Improvement of atypical acute disseminated encephalomyelitis with steroids and intravenous immunoglobulins. Pediatr Neurol. 24(2):139-43, 2001](http://www.ncbi.nlm.nih.gov/pubmed/?term=11275464%5Bpmid%5D)
|
||||
1. [Dale RC et al: Acute disseminated encephalomyelitis, multiphasic disseminated encephalomyelitis and multiple sclerosis in children. Brain. 123 Pt 12:2407-22, 2000](http://www.ncbi.nlm.nih.gov/pubmed/?term=11099444%5Bpmid%5D)
|
||||
1. [Rust RS: Multiple sclerosis, acute disseminated encephalomyelitis, and related conditions. Semin Pediatr Neurol. 7(2):66-90, 2000](http://www.ncbi.nlm.nih.gov/pubmed/?term=10914409%5Bpmid%5D)
|
||||
1. [Schaefer PW et al: Diffusion-weighted MR imaging of the brain. Radiology. 217(2):331-45, 2000](http://www.ncbi.nlm.nih.gov/pubmed/?term=11058626%5Bpmid%5D)
|
||||
1. [Kocer N et al: CNS involvement in neuro-Behcet syndrome: an MR study. AJNR Am J Neuroradiol. 20(6):1015-24, 1999](http://www.ncbi.nlm.nih.gov/pubmed/?term=10445437%5Bpmid%5D)
|
||||
|
||||
|
||||
## Images
|
||||
|
||||
@@ -365,7 +409,7 @@ breadcrumbs:
|
||||
|
||||
*Axial FLAIR MR shows peripheral, confluent areas of hyperintensity predominantly involving the subcortical white matter (WM) in this child with ADEM. The bilateral but asymmetric pattern is typical of ADEM.*
|
||||
|
||||
|
||||
|
||||
*Axial FLAIR MR shows peripheral, confluent areas of hyperintensity predominantly involving the subcortical white matter (WM) in this child with ADEM. The bilateral but asymmetric pattern is typical of ADEM.*
|
||||
|
||||
|
||||
|
||||
@@ -32,15 +32,13 @@ breadcrumbs:
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||||
category: "Brain"
|
||||
documentVersionId: "05d076c7-6110-4f03-952a-c22726d85e4d"
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imageCount: 12
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isComparable: true
|
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isInCompareCart: false
|
||||
lastUpdated: "08/05/20"
|
||||
pageDescription: "AHLE"
|
||||
pageKeywords: "Brain, Diagnosis, Pathology-Based Diagnoses, Infectious, Inflammatory, and Demyelinating Disease, Inflammatory and Demyelinating Disease, AHLE"
|
||||
pageTitle: "AHLE | STATdx"
|
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enhancedTitle: "AHLE"
|
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type: "DX"
|
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references: true
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breadcrumbs:
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@@ -249,6 +247,17 @@ breadcrumbs:
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||||
8f325204-5ce7-4da8-b816-cb545fa5b054
|
||||
|
||||
## References
|
||||
|
||||
# Selected References
|
||||
|
||||
1. [Mondia MWL et al: Acute hemorrhagic leukoencephalitis of Weston Hurst secondary to herpes encephalitis presenting as status epilepticus: a case report and review of literature. J Clin Neurosci. 67:265-70, 2019](http://www.ncbi.nlm.nih.gov/pubmed/?term=31239199%5Bpmid%5D)
|
||||
1. [Yae Y et al: Fulminant acute disseminated encephalomyelitis in children. Brain Dev. 41(4):373-7, 2019](http://www.ncbi.nlm.nih.gov/pubmed/?term=30522797%5Bpmid%5D)
|
||||
1. [Bonduelle T et al: Weston-Hurst syndrome with acute hemorrhagic cerebellitis. Clin Neurol Neurosurg. 173:118-9, 2018](http://www.ncbi.nlm.nih.gov/pubmed/?term=30121019%5Bpmid%5D)
|
||||
1. [Fanou EM et al: Critical illness-associated cerebral microbleeds. Stroke. 48(4):1085-7, 2017](http://www.ncbi.nlm.nih.gov/pubmed/?term=28235962%5Bpmid%5D)
|
||||
1. [Nabi S et al: Weston-Hurst syndrome: a rare fulminant form of acute disseminated encephalomyelitis (ADEM). BMJ Case Rep. 2016, 2016](http://www.ncbi.nlm.nih.gov/pubmed/?term=27797801%5Bpmid%5D)
|
||||
1. [Jeganathan N et al: Acute hemorrhagic leukoencephalopathy associated with influenza A (H1N1) virus. Neurocrit Care. 19(2):218-21, 2013](http://www.ncbi.nlm.nih.gov/pubmed/?term=23943349%5Bpmid%5D)
|
||||
|
||||
|
||||
## Images
|
||||
|
||||
@@ -261,7 +270,7 @@ breadcrumbs:
|
||||
|
||||
*Close-up view of autopsied brain in a patient with acute hemorrhagic leukoencephalitis (AHLE) shows innumerable tiny microbleeds in the subcortical and deep white matter (WM) <img src='/img/arrows/BO.png'/> and corpus callosum <img src='/img/arrows/BS.png'/>. Note the overlying cortex is almost completely spared <img src='/img/arrows/BC.png'/>. (Courtesy E. Rushing, MD.)*
|
||||
|
||||
|
||||
|
||||
*Close-up view of autopsied brain in a patient with acute hemorrhagic leukoencephalitis (AHLE) shows innumerable tiny microbleeds in the subcortical and deep white matter (WM) <img src='/img/arrows/BO.png'/> and corpus callosum <img src='/img/arrows/BS.png'/>. Note the overlying cortex is almost completely spared <img src='/img/arrows/BC.png'/>. (Courtesy E. Rushing, MD.)*
|
||||
|
||||
|
||||
|
||||
@@ -32,15 +32,13 @@ breadcrumbs:
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category: "Brain"
|
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documentVersionId: "cc8c3891-88b7-44bb-9e2a-3a321d092f4c"
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isComparable: true
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isInCompareCart: false
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lastUpdated: "08/05/20"
|
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pageDescription: "Autoimmune Encephalitis"
|
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pageKeywords: "Brain, Diagnosis, Pathology-Based Diagnoses, Infectious, Inflammatory, and Demyelinating Disease, Inflammatory and Demyelinating Disease, Autoimmune Encephalitis"
|
||||
pageTitle: "Autoimmune Encephalitis | STATdx"
|
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enhancedTitle: "Autoimmune Encephalitis"
|
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type: "DX"
|
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references: true
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breadcrumbs:
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|
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@@ -354,39 +352,123 @@ breadcrumbs:
|
||||
|
||||
89d11c00-03ef-4d5a-aea9-2d9c2669fa58
|
||||
|
||||
## References
|
||||
|
||||
# Selected References
|
||||
|
||||
1. [Iorio R et al: Clinical characteristics and outcome of patients with autoimmune encephalitis: clues for paraneoplastic etiology. Eur J Neurol. ePub, 2020](http://www.ncbi.nlm.nih.gov/pubmed/?term=32412135%5Bpmid%5D)
|
||||
1. [Mongay-Ochoa N et al: Anti-Hu-associated paraneoplastic syndromes triggered by immune-checkpoint inhibitor treatment. J Neurol. ePub, 2020](http://www.ncbi.nlm.nih.gov/pubmed/?term=32451614%5Bpmid%5D)
|
||||
1. [Vogrig A et al: Central nervous system complications associated with immune checkpoint inhibitors. J Neurol Neurosurg Psychiatry. ePub, 2020](http://www.ncbi.nlm.nih.gov/pubmed/?term=32312871%5Bpmid%5D)
|
||||
1. [Bradshaw MJ et al: An overview of autoimmune and paraneoplastic encephalitides. Semin Neurol. 38(3):330-43, 2018](http://www.ncbi.nlm.nih.gov/pubmed/?term=30011413%5Bpmid%5D)
|
||||
1. [Long JM et al: Autoimmune dementia. Semin Neurol. 38(3):303-15, 2018](http://www.ncbi.nlm.nih.gov/pubmed/?term=30011411%5Bpmid%5D)
|
||||
1. [Kelley BP et al: Autoimmune encephalitis: pathophysiology and imaging review of an overlooked diagnosis. AJNR Am J Neuroradiol. 38(6):1070-8, 2017](http://www.ncbi.nlm.nih.gov/pubmed/?term=28183838%5Bpmid%5D)
|
||||
1. [da Rocha AJ et al: Recognizing Autoimmune-Mediated Encephalitis in the Differential Diagnosis of Limbic Disorders. AJNR Am J Neuroradiol. 36(12):2196-205, 2015](http://www.ncbi.nlm.nih.gov/pubmed/?term=26381566%5Bpmid%5D)
|
||||
1. [Höftberger R et al: Encephalitis and AMPA receptor antibodies: novel findings in a case series of 22 patients. Neurology. 84(24):2403-12, 2015](http://www.ncbi.nlm.nih.gov/pubmed/?term=25979696%5Bpmid%5D)
|
||||
1. [Thomas AC et al: Autoimmune limbic encephalitis detected on FDG brain scan performed for the evaluation of dementia. Clin Nucl Med. 40(4):358-9, 2015](http://www.ncbi.nlm.nih.gov/pubmed/?term=25608163%5Bpmid%5D)
|
||||
1. [Zekeridou A et al: Treatment and outcome of children and adolescents with N-methyl-D-aspartate receptor encephalitis. J Neurol. 262(8):1859-66, 2015](http://www.ncbi.nlm.nih.gov/pubmed/?term=25987208%5Bpmid%5D)
|
||||
1. [Kotsenas AL et al: MRI findings in autoimmune voltage-gated potassium channel complex encephalitis with seizures: one potential etiology for mesial temporal sclerosis. AJNR Am J Neuroradiol. 35(1):84-9, 2014](http://www.ncbi.nlm.nih.gov/pubmed/?term=23868165%5Bpmid%5D)
|
||||
1. [Masangkay N et al: Brain 18F-FDG-PET characteristics in patients with paraneoplastic neurological syndrome and its correlation with clinical and MRI findings. Nucl Med Commun. 35(10):1038-46, 2014](http://www.ncbi.nlm.nih.gov/pubmed/?term=25023997%5Bpmid%5D)
|
||||
1. [Sarria-Estrada S et al: Neuroimaging in status epilepticus secondary to paraneoplastic autoimmune encephalitis. Clin Radiol. 69(8):795-803, 2014](http://www.ncbi.nlm.nih.gov/pubmed/?term=24824979%5Bpmid%5D)
|
||||
1. [Baumgartner A et al: Cerebral FDG-PET and MRI findings in autoimmune limbic encephalitis: correlation with autoantibody types. J Neurol. 260(11):2744-53, 2013](http://www.ncbi.nlm.nih.gov/pubmed/?term=23900756%5Bpmid%5D)
|
||||
1. [Aye MM et al: CD8 positive T-cell infiltration in the dentate nucleus of paraneoplastic cerebellar degeneration. J Neuroimmunol. 208(1-2):136-40, 2009](http://www.ncbi.nlm.nih.gov/pubmed/?term=19217169%5Bpmid%5D)
|
||||
1. [Berger JR et al: A brainstem paraneoplastic syndrome associated with prostate cancer. J Neurol Neurosurg Psychiatry. 80(8):934-5, 2009](http://www.ncbi.nlm.nih.gov/pubmed/?term=19608787%5Bpmid%5D)
|
||||
1. [Damek DM: Cerebral edema, altered mental status, seizures, acute stroke, leptomeningeal metastases, and paraneoplastic syndrome. Emerg Med Clin North Am. 27(2):209-29, 2009](http://www.ncbi.nlm.nih.gov/pubmed/?term=19447307%5Bpmid%5D)
|
||||
1. [Honnorat J et al: Onco-neural antibodies and tumour type determine survival and neurological symptoms in paraneoplastic neurological syndromes with Hu or CV2/CRMP5 antibodies. J Neurol Neurosurg Psychiatry. 80(4):412-6, 2009](http://www.ncbi.nlm.nih.gov/pubmed/?term=18931014%5Bpmid%5D)
|
||||
1. [Jaster JH: Reversible autoimmune encephalopathy spectrum. Arch Neurol. 66(7):916, 2009](http://www.ncbi.nlm.nih.gov/pubmed/?term=19597101%5Bpmid%5D)
|
||||
1. [Khan NL et al: Histopathology of VGKC antibody-associated limbic encephalitis. Neurology. 72(19):1703-5, 2009](http://www.ncbi.nlm.nih.gov/pubmed/?term=19433746%5Bpmid%5D)
|
||||
1. [Kröll-Seger J et al: Non-paraneoplastic limbic encephalitis associated with antibodies to potassium channels leading to bilateral hippocampal sclerosis in a pre-pubertal girl. Epileptic Disord. 11(1):54-9, 2009](http://www.ncbi.nlm.nih.gov/pubmed/?term=19251579%5Bpmid%5D)
|
||||
1. [McKeon A et al: Reversible extralimbic paraneoplastic encephalopathies with large abnormalities on magnetic resonance images. Arch Neurol. 66(2):268-71, 2009](http://www.ncbi.nlm.nih.gov/pubmed/?term=19204167%5Bpmid%5D)
|
||||
1. [Modoni A et al: Successful treatment of acute autoimmune limbic encephalitis with negative VGKC and NMDAR antibodies. Cogn Behav Neurol. 22(1):63-6, 2009](http://www.ncbi.nlm.nih.gov/pubmed/?term=19372772%5Bpmid%5D)
|
||||
1. [Saiz A et al: Anti-Hu-associated brainstem encephalitis. J Neurol Neurosurg Psychiatry. 80(4):404-7, 2009](http://www.ncbi.nlm.nih.gov/pubmed/?term=19015226%5Bpmid%5D)
|
||||
1. [Uribe-Uribe NO et al: Paraneoplastic sensory neuropathy associated with small cell carcinoma of the gallbladder. Ann Diagn Pathol. 13(2):124-6, 2009](http://www.ncbi.nlm.nih.gov/pubmed/?term=19302962%5Bpmid%5D)
|
||||
1. [Anderson NE et al: Limbic encephalitis - a review. J Clin Neurosci. 15(9):961-71, 2008](http://www.ncbi.nlm.nih.gov/pubmed/?term=18411052%5Bpmid%5D)
|
||||
1. [Basu S et al: Role of FDG-PET in the clinical management of paraneoplastic neurological syndrome: detection of the underlying malignancy and the brain PET-MRI correlates. Mol Imaging Biol. 10(3):131-7, 2008](http://www.ncbi.nlm.nih.gov/pubmed/?term=18297363%5Bpmid%5D)
|
||||
1. [Blaes F et al: Autoantibodies in childhood opsoclonus-myoclonus syndrome. J Neuroimmunol. 201-202:221-6, 2008](http://www.ncbi.nlm.nih.gov/pubmed/?term=18687475%5Bpmid%5D)
|
||||
1. [Corapcioglu F et al: Response to rituximab and prednisolone for opsoclonus-myoclonus-ataxia syndrome in a child with ganglioneuroblastoma. Pediatr Hematol Oncol. 25(8):756-61, 2008](http://www.ncbi.nlm.nih.gov/pubmed/?term=19065442%5Bpmid%5D)
|
||||
1. [Dalakas MC: Invited article: inhibition of B cell functions: implications for neurology. Neurology. 70(23):2252-60, 2008](http://www.ncbi.nlm.nih.gov/pubmed/?term=18519875%5Bpmid%5D)
|
||||
1. [Eker A et al: Testicular teratoma and anti-N-methyl-D-aspartate receptor-associated encephalitis. J Neurol Neurosurg Psychiatry. 79(9):1082-3, 2008](http://www.ncbi.nlm.nih.gov/pubmed/?term=18708569%5Bpmid%5D)
|
||||
1. [Fitzpatrick AS et al: Opsoclonus-myoclonus syndrome associated with benign ovarian teratoma. Neurology. 70(15):1292-3, 2008](http://www.ncbi.nlm.nih.gov/pubmed/?term=18391162%5Bpmid%5D)
|
||||
1. [Geschwind MD et al: Voltage-gated potassium channel autoimmunity mimicking creutzfeldt-jakob disease. Arch Neurol. 65(10):1341-6, 2008](http://www.ncbi.nlm.nih.gov/pubmed/?term=18852349%5Bpmid%5D)
|
||||
1. [Hassan KA et al: Long-term survival in paraneoplastic opsoclonus-myoclonus syndrome associated with small cell lung cancer. J Neuroophthalmol. 28(1):27-30, 2008](http://www.ncbi.nlm.nih.gov/pubmed/?term=18347455%5Bpmid%5D)
|
||||
1. [Jarius S et al: Relative frequency of VGKC and 'classical' paraneoplastic antibodies in patients with limbic encephalitis. J Neurol. 255(7):1100-1, 2008](http://www.ncbi.nlm.nih.gov/pubmed/?term=18574619%5Bpmid%5D)
|
||||
1. [Johnson V et al: Immune mediated neurologic dysfunction as a paraneoplastic syndrome in renal cell carcinoma. J Neurooncol. 90(3):279-81, 2008](http://www.ncbi.nlm.nih.gov/pubmed/?term=18726185%5Bpmid%5D)
|
||||
1. [Ko MW et al: Neuro-ophthalmologic manifestations of paraneoplastic syndromes. J Neuroophthalmol. 28(1):58-68, 2008](http://www.ncbi.nlm.nih.gov/pubmed/?term=18347462%5Bpmid%5D)
|
||||
1. [Musunuru K et al: Paraneoplastic opsoclonus-myoclonus ataxia associated with non-small-cell lung carcinoma. J Neurooncol. 90(2):213-6, 2008](http://www.ncbi.nlm.nih.gov/pubmed/?term=18618225%5Bpmid%5D)
|
||||
1. [Novillo-López ME et al: Treatment-responsive subacute limbic encephalitis and NMDA receptor antibodies in a man. Neurology. 70(9):728-9, 2008](http://www.ncbi.nlm.nih.gov/pubmed/?term=18299525%5Bpmid%5D)
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||||
1. [Pellkofer HL et al: Lambert-eaton myasthenic syndrome differential reactivity of tumor versus non-tumor patients to subunits of the voltage-gated calcium channel. J Neuroimmunol. 204(1-2):136-9, 2008](http://www.ncbi.nlm.nih.gov/pubmed/?term=18809213%5Bpmid%5D)
|
||||
1. [Sabater L et al: SOX1 antibodies are markers of paraneoplastic Lambert-Eaton myasthenic syndrome. Neurology. 70(12):924-8, 2008](http://www.ncbi.nlm.nih.gov/pubmed/?term=18032743%5Bpmid%5D)
|
||||
1. [Sekiguchi Y et al: Potassium channel antibody-associated encephalitis with hypothalamic lesions and intestinal pseudo-obstruction. J Neurol Sci. 269(1-2):176-9, 2008](http://www.ncbi.nlm.nih.gov/pubmed/?term=18378260%5Bpmid%5D)
|
||||
1. [Tan KM et al: Clinical spectrum of voltage-gated potassium channel autoimmunity. Neurology. 70(20):1883-90, 2008](http://www.ncbi.nlm.nih.gov/pubmed/?term=18474843%5Bpmid%5D)
|
||||
1. [Darnell RB et al: Paraneoplastic syndromes affecting the nervous system. Semin Oncol. 33(3):270-98, 2006](http://www.ncbi.nlm.nih.gov/pubmed/?term=16769417%5Bpmid%5D)
|
||||
1. [Dropcho EJ: Update on paraneoplastic syndromes. Curr Opin Neurol. 18(3):331-6, 2005](http://www.ncbi.nlm.nih.gov/pubmed/?term=15891421%5Bpmid%5D)
|
||||
1. [Dadparvar S et al: Paraneoplastic encephalitis associated with cystic teratoma is detected by fluorodeoxyglucose positron emission tomography with negative magnetic resonance image findings. Clin Nucl Med. 28(11):893-6, 2003](http://www.ncbi.nlm.nih.gov/pubmed/?term=14578703%5Bpmid%5D)
|
||||
1. [Messori A et al: Resolution of limbic encephalitis with detection and treatment of lung cancer: clinical-radiological correlation. Eur J Radiol. 45(1): 78-80, 2003](http://www.ncbi.nlm.nih.gov/pubmed/?term=12499067%5Bpmid%5D)
|
||||
1. [Barnett M et al: Paraneoplastic brain stem encephalitis in a woman with anti-Ma2 antibody. J Neurol Neurosurg Psychiatry. 70(2):222-5, 2001](http://www.ncbi.nlm.nih.gov/pubmed/?term=11160472%5Bpmid%5D)
|
||||
1. [Gultekin SH et al: Paraneoplastic limbic encephalitis: neurological symptoms, immunological findings and tumour association in 50 patients. Brain. 123 ( Pt 7):1481-94, 2000](http://www.ncbi.nlm.nih.gov/pubmed/?term=10869059%5Bpmid%5D)
|
||||
1. [Dalmau J et al: Paraneoplastic neurologic syndromes: pathogenesis and physiopathology. Brain Pathol. 9(2):275-84, 1999](http://www.ncbi.nlm.nih.gov/pubmed/?term=10219745%5Bpmid%5D)
|
||||
1. [Scaravilli F et al: The neuropathology of paraneoplastic syndromes. Brain Pathol. 9(2):251-60, 1999](http://www.ncbi.nlm.nih.gov/pubmed/?term=10219743%5Bpmid%5D)
|
||||
1. [Voltz R et al: A serologic marker of paraneoplastic limbic and brain-stem encephalitis in patients with testicular cancer. N Engl J Med. 340(23): 1788-95, 1999](http://www.ncbi.nlm.nih.gov/pubmed/?term=10362822%5Bpmid%5D)
|
||||
|
||||
|
||||
## Images
|
||||
|
||||
|
||||
### Selected Images
|
||||
|
||||
|
||||
*Axial FLAIR MR shows abnormal hyperintensity in the bilateral medial temporal lobes <img src='/img/arrows/CS.png'/>, characteristic of limbic encephalitis (LE), the most common paraneoplastic syndrome. Bilateral involvement is typical of limbic encephalitis.*
|
||||
|
||||
|
||||
*Axial FLAIR MR shows abnormal hyperintensity in the bilateral medial temporal lobes <img src='/img/arrows/CS.png'/>, characteristic of limbic encephalitis (LE), the most common paraneoplastic syndrome. Bilateral involvement is typical of limbic encephalitis.*
|
||||
|
||||
|
||||
|
||||
*Axial FLAIR MR shows abnormal hyperintensity in the bilateral medial temporal lobes <img src='/img/arrows/CS.png'/>, characteristic of limbic encephalitis (LE), the most common paraneoplastic syndrome. Bilateral involvement is typical of limbic encephalitis.*
|
||||
|
||||
|
||||
*Axial T1 C+ MR in the same patient shows no significant enhancement in the medial temporal lobes. Enhancement is often present in limbic encephalitis. The patient's symptoms often improve after treatment of the primary tumor.*
|
||||
|
||||
|
||||
*Axial T1 C+ MR in the same patient shows no significant enhancement in the medial temporal lobes. Enhancement is often present in limbic encephalitis. The patient's symptoms often improve after treatment of the primary tumor.*
|
||||
|
||||
|
||||
*Axial FLAIR MR in a 61 year old with multiple myeloma who presented with seizures shows abnormal hyperintensity <img src='/img/arrows/CS.png'/> in the cortex and subcortical white matter of the temporal lobes.*
|
||||
|
||||
|
||||
*Axial FLAIR MR in a 61 year old with multiple myeloma who presented with seizures shows abnormal hyperintensity <img src='/img/arrows/CS.png'/> in the cortex and subcortical white matter of the temporal lobes.*
|
||||
|
||||
|
||||
*Axial T1 C+ FS MR in the same patient shows no enhancement. Differential considerations include autoimmune encephalitis (AE), acute demyelinating encephalomyelitis (ADEM), viral encephalitis, and vasculitis in this case. AE related to GABAr was diagnosed by CSF and serum markers.*
|
||||
|
||||
|
||||
*Axial T1 C+ FS MR in the same patient shows no enhancement. Differential considerations include autoimmune encephalitis (AE), acute demyelinating encephalomyelitis (ADEM), viral encephalitis, and vasculitis in this case. AE related to GABAr was diagnosed by CSF and serum markers.*
|
||||
|
||||
|
||||
*Axial FLAIR MR in a 71 year old with altered mental status shows abnormal hyperintensity in the left temporal lobe <img src='/img/arrows/CS.png'/>. Differential considerations include infectious, inflammatory, and neoplastic etiologies. GAD65 AE was diagnosed at brain biopsy.*
|
||||
|
||||
|
||||
*Axial FLAIR MR in a 71 year old with altered mental status shows abnormal hyperintensity in the left temporal lobe <img src='/img/arrows/CS.png'/>. Differential considerations include infectious, inflammatory, and neoplastic etiologies. GAD65 AE was diagnosed at brain biopsy.*
|
||||
|
||||
|
||||
*Axial FLAIR MR shows hyperintensity in the medial temporal lobes <img src='/img/arrows/CS.png'/> in this patient with subacute dementia and voltage-gated potassium channel (VGKC) autoimmunity. VGKC may occur with or without a primary neoplasm and may have an LE pattern.*
|
||||
|
||||
|
||||
*Axial FLAIR MR shows hyperintensity in the medial temporal lobes <img src='/img/arrows/CS.png'/> in this patient with subacute dementia and voltage-gated potassium channel (VGKC) autoimmunity. VGKC may occur with or without a primary neoplasm and may have an LE pattern.*
|
||||
|
||||
|
||||
*Axial T2 MR shows midbrain hyperintensity <img src='/img/arrows/CS.png'/> related to brainstem encephalitis, which is characterized by hyperintensity in the midbrain, pons, cerebellar peduncle, and basal ganglia.*
|
||||
|
||||
|
||||
*Axial T2 MR shows midbrain hyperintensity <img src='/img/arrows/CS.png'/> related to brainstem encephalitis, which is characterized by hyperintensity in the midbrain, pons, cerebellar peduncle, and basal ganglia.*
|
||||
|
||||
|
||||
*Axial T1 C+ MR in the same patient shows patchy enhancement of the midbrain lesions <img src='/img/arrows/CS.png'/> and the medial temporal lobe <img src='/img/arrows/CO.png'/>. This patient was diagnosed with LE with new brainstem symptoms. Multiple paraneoplastic syndromes may occur in the same patient.*
|
||||
|
||||
|
||||
*Axial T1 C+ MR in the same patient shows patchy enhancement of the midbrain lesions <img src='/img/arrows/CS.png'/> and the medial temporal lobe <img src='/img/arrows/CO.png'/>. This patient was diagnosed with LE with new brainstem symptoms. Multiple paraneoplastic syndromes may occur in the same patient.*
|
||||
|
||||
|
||||
*Axial FLAIR MR shows abnormal hyperintensity in the medial temporal lobes bilaterally, related to LE. As imaging mimics herpes encephalitis, most patients are initially treated with antiviral therapy until HSV titers are found to be negative. < 1% of cancer patients develop a paraneoplastic syndrome.*
|
||||
|
||||
|
||||
*Axial FLAIR MR shows abnormal hyperintensity in the medial temporal lobes bilaterally, related to LE. As imaging mimics herpes encephalitis, most patients are initially treated with antiviral therapy until HSV titers are found to be negative. < 1% of cancer patients develop a paraneoplastic syndrome.*
|
||||
|
||||
|
||||
+19
-3
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pageTitle: "Basal Ganglia Calcification | STATdx"
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- Cockayne syndrome
|
||||
- Long-term complications of radiation therapy for childhood brain tumors & intrathecal chemotherapy
|
||||
|
||||
## References
|
||||
|
||||
# Selected References
|
||||
|
||||
1. [de Brouwer EJ et al: Basal ganglia calcifications: no association with cognitive function. J Neuroradiol. S0150-9861(22)00066-9, 2022](http://www.ncbi.nlm.nih.gov/pubmed/?term=35134441%5Bpmid%5D)
|
||||
1. [Di Mascio D et al: Role of fetal magnetic resonance imaging in fetuses with congenital cytomegalovirus infection: a multicenter study. Ultrasound Obstet Gynecol. ePub, 2022](http://www.ncbi.nlm.nih.gov/pubmed/?term=36056700%5Bpmid%5D)
|
||||
1. [Patel J et al: Hyperkinetic choreiform movements secondary to basal ganglia calcification and underlying developmental venous anomaly. Cureus. 14(3):e22752, 2022](http://www.ncbi.nlm.nih.gov/pubmed/?term=35371891%5Bpmid%5D)
|
||||
1. [Zavatta G et al: Basal ganglia calcification is associated with local and systemic metabolic mechanisms in adult hypoparathyroidism. J Clin Endocrinol Metab. 106(7):1900-17, 2021](http://www.ncbi.nlm.nih.gov/pubmed/?term=33788935%5Bpmid%5D)
|
||||
1. [Batla A et al: Deconstructing Fahr's disease/syndrome of brain calcification in the era of new genes. Parkinsonism Relat Disord. 37:1-10, 2017](http://www.ncbi.nlm.nih.gov/pubmed/?term=28162874%5Bpmid%5D)
|
||||
1. [Levine D et al: How does imaging of congenital Zika compare with imaging of other TORCH infections? Radiology. 285(3):744-61, 2017](http://www.ncbi.nlm.nih.gov/pubmed/?term=29155634%5Bpmid%5D)
|
||||
1. [Yoshimoto K et al: Prevalence and clinicopathological features of H3.3 G34-mutant high-grade gliomas: a retrospective study of 411 consecutive glioma cases in a single institution. Brain Tumor Pathol. 34(3):103-12, 2017](http://www.ncbi.nlm.nih.gov/pubmed/?term=28447171%5Bpmid%5D)
|
||||
1. [Donzuso G et al: Extensive bilateral striopallidodentate calcinosis: a 50 years history of hypoparathyroidism presenting like a parkinsonian syndrome. J Neurol. 263(9):1876-9, 2016](http://www.ncbi.nlm.nih.gov/pubmed/?term=27485169%5Bpmid%5D)
|
||||
1. [Nunomura A: Idiopathic basal ganglia calcification (Fahr's disease) and dementia. Psychiatry Clin Neurosci. 70(3):129-30, 2016](http://www.ncbi.nlm.nih.gov/pubmed/?term=26939914%5Bpmid%5D)
|
||||
1. [Saini AG et al: Teaching neuroimages: the syndrome of cutaneous photosensitivity, growth failure, and basal ganglia calcification. Neurology. 87(6):e56-7, 2016](http://www.ncbi.nlm.nih.gov/pubmed/?term=27502967%5Bpmid%5D)
|
||||
1. [Gossner J: Basal ganglia calcifications on brain computed tomography are also common in other elderly populations. Geriatr Gerontol Int. 15(1):128, 2015](http://www.ncbi.nlm.nih.gov/pubmed/?term=25583396%5Bpmid%5D)
|
||||
1. [Ghei SK et al: MR imaging of hypoxic-ischemic injury in term neonates: pearls and pitfalls. Radiographics. 34(4):1047-61, 2014](http://www.ncbi.nlm.nih.gov/pubmed/?term=25019441%5Bpmid%5D)
|
||||
1. [Hegde AN et al: Differential diagnosis for bilateral abnormalities of the basal ganglia and thalamus. Radiographics. 31(1):5-30, 2011](http://www.ncbi.nlm.nih.gov/pubmed/?term=21257930%5Bpmid%5D)
|
||||
|
||||
|
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0f953548-b230-4137-9147-51d6ed147c6c
|
||||
|
||||
## References
|
||||
|
||||
# Selected References
|
||||
|
||||
1. [Campagnolo M et al: Sporadic hereditary neuropathies misdiagnosed as chronic inflammatory demyelinating polyradiculoneuropathy: Pitfalls and red flags. J Peripher Nerv Syst. 25(1):19-26, 2020](http://www.ncbi.nlm.nih.gov/pubmed/?term=31919945%5Bpmid%5D)
|
||||
1. [Van den Bergh PYK et al: Boundaries of chronic inflammatory demyelinating polyradiculoneuropathy. J Peripher Nerv Syst. 25(1):4-8, 2020](http://www.ncbi.nlm.nih.gov/pubmed/?term=31981273%5Bpmid%5D)
|
||||
1. [Wu F et al: MR neurography of lumbosacral nerve roots: diagnostic value in chronic inflammatory demyelinating polyradiculoneuropathy and correlation with electrophysiological parameters. Eur J Radiol. 124:108816, 2020](http://www.ncbi.nlm.nih.gov/pubmed/?term=31923808%5Bpmid%5D)
|
||||
1. [Suanprasert N et al: Polyneuropathies and chronic inflammatory demyelinating polyradiculoneuropathy in multiple sclerosis. Mult Scler Relat Disord. 30:284-90, 2019](http://www.ncbi.nlm.nih.gov/pubmed/?term=30870805%5Bpmid%5D)
|
||||
1. [Pitarokoili K et al: High-resolution nerve ultrasound and magnetic resonance neurography as complementary neuroimaging tools for chronic inflammatory demyelinating polyneuropathy. Ther Adv Neurol Disord. 11:1756286418759974, 2018](http://www.ncbi.nlm.nih.gov/pubmed/?term=29552093%5Bpmid%5D)
|
||||
1. [Ishikawa T et al: MR neurography for the evaluation of CIDP. Muscle Nerve. 55(4):483-9, 2017](http://www.ncbi.nlm.nih.gov/pubmed/?term=27500391%5Bpmid%5D)
|
||||
1. [Kronlage M et al: Large coverage MR neurography in CIDP: diagnostic accuracy and electrophysiological correlation. J Neurol. 264(7):1434-43, 2017](http://www.ncbi.nlm.nih.gov/pubmed/?term=28620719%5Bpmid%5D)
|
||||
1. [Kronlage M et al: Diffusion tensor imaging in chronic inflammatory demyelinating polyneuropathy: diagnostic accuracy and correlation with electrophysiology. Invest Radiol. 52(11):701-7, 2017](http://www.ncbi.nlm.nih.gov/pubmed/?term=28574858%5Bpmid%5D)
|
||||
1. [Said G et al: Chronic inflammatory demyelinative polyneuropathy. Handb Clin Neurol. 115:403-13, 2013](http://www.ncbi.nlm.nih.gov/pubmed/?term=23931792%5Bpmid%5D)
|
||||
1. [Mahdi-Rogers M et al: Overview of the pathogenesis and treatment of chronic inflammatory demyelinating polyneuropathy with intravenous immunoglobulins. Biologics. 4:45-9, 2010](http://www.ncbi.nlm.nih.gov/pubmed/?term=20376173%5Bpmid%5D)
|
||||
1. [Tracy JA et al: Investigations and treatment of chronic inflammatory demyelinating polyradiculoneuropathy and other inflammatory demyelinating polyneuropathies. Curr Opin Neurol. 23(3):242-8, 2010](http://www.ncbi.nlm.nih.gov/pubmed/?term=20389243%5Bpmid%5D)
|
||||
1. [Vallat JM et al: Chronic inflammatory demyelinating polyradiculoneuropathy: diagnostic and therapeutic challenges for a treatable condition. Lancet Neurol. 9(4):402-12, 2010](http://www.ncbi.nlm.nih.gov/pubmed/?term=20298964%5Bpmid%5D)
|
||||
1. [Van den Bergh PY et al: European Federation of Neurological Societies/Peripheral Nerve Society guideline on management of chronic inflammatory demyelinating polyradiculoneuropathy: report of a joint task force of the European Federation of Neurological Societies and the Peripheral Nerve Society - first revision. Eur J Neurol. 17(3):356-63, 2010](http://www.ncbi.nlm.nih.gov/pubmed/?term=20456730%5Bpmid%5D)
|
||||
1. [Brannagan TH 3rd: Current treatments of chronic immune-mediated demyelinating polyneuropathies. Muscle Nerve. 39(5):563-78, 2009](http://www.ncbi.nlm.nih.gov/pubmed/?term=19301378%5Bpmid%5D)
|
||||
1. [Laughlin RS et al: Incidence and prevalence of CIDP and the association of diabetes mellitus. Neurology. 73(1):39-45, 2009](http://www.ncbi.nlm.nih.gov/pubmed/?term=19564582%5Bpmid%5D)
|
||||
1. [Tazawa K et al: Spinal nerve root hypertrophy on MRI: clinical significance in the diagnosis of chronic inflammatory demyelinating polyradiculoneuropathy. Intern Med. 47(23):2019-24, 2008](http://www.ncbi.nlm.nih.gov/pubmed/?term=19043253%5Bpmid%5D)
|
||||
1. [Tsuchiya K et al: Demonstration of spinal cord and nerve root abnormalities by diffusion neurography. J Comput Assist Tomogr. 32(2):286-90, 2008](http://www.ncbi.nlm.nih.gov/pubmed/?term=18379319%5Bpmid%5D)
|
||||
1. [Said G: Chronic inflammatory demyelinating polyneuropathy. Neuromuscul Disord. 16(5):293-303, 2006](http://www.ncbi.nlm.nih.gov/pubmed/?term=16631367%5Bpmid%5D)
|
||||
1. [Köller H et al: Chronic inflammatory demyelinating polyneuropathy--update on pathogenesis, diagnostic criteria and therapy. Curr Opin Neurol. 18(3):273-8, 2005](http://www.ncbi.nlm.nih.gov/pubmed/?term=15891411%5Bpmid%5D)
|
||||
1. [Matsuoka N et al: Detection of cervical nerve root hypertrophy by ultrasonography in chronic inflammatory demyelinating polyradiculoneuropathy. J Neurol Sci. 219(1-2):15-21, 2004](http://www.ncbi.nlm.nih.gov/pubmed/?term=15050432%5Bpmid%5D)
|
||||
1. [Cocito D et al: Different clinical, electrophysiological and immunological features of CIDP associated with paraproteinaemia. Acta Neurol Scand. 108(4):274-80, 2003](http://www.ncbi.nlm.nih.gov/pubmed/?term=12956862%5Bpmid%5D)
|
||||
1. [Fee DB et al: Resolution of chronic inflammatory demyelinating polyneuropathy-associated central nervous system lesions after treatment with intravenous immunoglobulin. J Peripher Nerv Syst. 8(3):155-8, 2003](http://www.ncbi.nlm.nih.gov/pubmed/?term=12904236%5Bpmid%5D)
|
||||
1. [Haq RU et al: Chronic inflammatory demyelinating polyradiculoneuropathy in diabetic patients. Muscle Nerve. 27(4):465-70, 2003](http://www.ncbi.nlm.nih.gov/pubmed/?term=12661048%5Bpmid%5D)
|
||||
1. [Magda P et al: Comparison of electrodiagnostic abnormalities and criteria in a cohort of patients with chronic inflammatory demyelinating polyneuropathy. Arch Neurol. 60(12):1755-9, 2003](http://www.ncbi.nlm.nih.gov/pubmed/?term=14676052%5Bpmid%5D)
|
||||
1. [Odaka M et al: Patients with chronic inflammatory demyelinating polyneuropathy initially diagnosed as Guillain-Barre syndrome. J Neurol. 250(8):913-6, 2003](http://www.ncbi.nlm.nih.gov/pubmed/?term=12928908%5Bpmid%5D)
|
||||
1. [Oguz B et al: Diffuse spinal and intercostal nerve involvement in chronic inflammatory demyelinating polyradiculoneuropathy: MRI findings. Eur Radiol. 13 Suppl 4:L230-4, 2003](http://www.ncbi.nlm.nih.gov/pubmed/?term=15018192%5Bpmid%5D)
|
||||
1. [Press R et al: Aberrated levels of cerebrospinal fluid chemokines in Guillain-Barre syndrome and chronic inflammatory demyelinating polyradiculoneuropathy. J Clin Immunol. 23(4):259-67, 2003](http://www.ncbi.nlm.nih.gov/pubmed/?term=12959218%5Bpmid%5D)
|
||||
1. [Rodriguez-Casero MV et al: Childhood chronic inflammatory demyelinating polyneuropathy with central nervous system demyelination resembling multiple sclerosis. Neuromuscul Disord. 13(2):158-61, 2003](http://www.ncbi.nlm.nih.gov/pubmed/?term=12565914%5Bpmid%5D)
|
||||
1. [Ropper AH: Current treatments for CIDP. Neurology. 60(8 Suppl 3):S16-22, 2003](http://www.ncbi.nlm.nih.gov/pubmed/?term=12707418%5Bpmid%5D)
|
||||
1. [Saperstein DS et al: Current concepts and controversy in chronic inflammatory demyelinating polyneuropathy. Curr Neurol Neurosci Rep. 3(1):57-63, 2003](http://www.ncbi.nlm.nih.gov/pubmed/?term=12507413%5Bpmid%5D)
|
||||
1. [Toyka KV et al: The pathogenesis of CIDP: rationale for treatment with immunomodulatory agents. Neurology. 60(8 Suppl 3):S2-7, 2003](http://www.ncbi.nlm.nih.gov/pubmed/?term=12707416%5Bpmid%5D)
|
||||
1. [Costello F et al: Childhood-onset chronic inflammatory demyelinating polyradiculoneuropathy with cranial nerve involvement. J Child Neurol. 17(11):819-23, 2002](http://www.ncbi.nlm.nih.gov/pubmed/?term=12585721%5Bpmid%5D)
|
||||
1. Cros D: Peripheral Neuropathy. 1st ed. Philadelphia: Lippincott Williams & Wilkins: 432, 2001
|
||||
1. [Sabatelli M et al: Pure motor chronic inflammatory demyelinating polyneuropathy. J Neurol. 248(9):772-7, 2001](http://www.ncbi.nlm.nih.gov/pubmed/?term=11596782%5Bpmid%5D)
|
||||
1. [Saperstein DS et al: Clinical spectrum of chronic acquired demyelinating polyneuropathies. Muscle Nerve. 24(3):311-24, 2001](http://www.ncbi.nlm.nih.gov/pubmed/?term=11353415%5Bpmid%5D)
|
||||
1. [Taniguchi N et al: Sonographic detection of diffuse peripheral nerve hypertrophy in chronic inflammatory demyelinating polyradiculoneuropathy. J Clin Ultrasound. 28(9):488-91, 2000](http://www.ncbi.nlm.nih.gov/pubmed/?term=11056027%5Bpmid%5D)
|
||||
1. [Van den Bergh PY et al: Chronic demyelinating hypertrophic brachial plexus neuropathy. Muscle Nerve. 23(2):283-8, 2000](http://www.ncbi.nlm.nih.gov/pubmed/?term=10639625%5Bpmid%5D)
|
||||
1. [Duarte J et al: Hypertrophy of multiple cranial nerves and spinal roots in chronic inflammatory demyelinating neuropathy. J Neurol Neurosurg Psychiatry. 67(5):685-7, 1999](http://www.ncbi.nlm.nih.gov/pubmed/?term=10519883%5Bpmid%5D)
|
||||
1. [Midroni G et al: MRI of the cauda equina in CIDP: clinical correlations. J Neurol Sci. 170(1):36-44, 1999](http://www.ncbi.nlm.nih.gov/pubmed/?term=10540034%5Bpmid%5D)
|
||||
1. [Mizuno K et al: Chronic inflammatory demyelinating polyradiculoneuropathy with diffuse and massive peripheral nerve hypertrophy: distinctive clinical and magnetic resonance imaging features. Muscle Nerve. 21(6):805-8, 1998](http://www.ncbi.nlm.nih.gov/pubmed/?term=9585338%5Bpmid%5D)
|
||||
1. [Kuwabara S et al: Magnetic resonance imaging at the demyelinative foci in chronic inflammatory demyelinating polyneuropathy. Neurology. 48(4):874-7, 1997](http://www.ncbi.nlm.nih.gov/pubmed/?term=9109870%5Bpmid%5D)
|
||||
1. [Simmons Z et al: Chronic inflammatory demyelinating polyradiculoneuropathy in children: I. Presentation, electrodiagnostic studies, and initial clinical course, with comparison to adults. 20(12):1569-75, 1997](http://www.ncbi.nlm.nih.gov/pubmed/?term=9390670%5Bpmid%5D)
|
||||
1. [Van Es HW et al: Magnetic resonance imaging of the brachial plexus in patients with multifocal motor neuropathy. Neurology. 48(5):1218-24, 1997](http://www.ncbi.nlm.nih.gov/pubmed/?term=9153446%5Bpmid%5D)
|
||||
|
||||
|
||||
## Images
|
||||
|
||||
|
||||
### Selected Images
|
||||
|
||||
|
||||
*Sagittal T1 C+ MR of the cervical spine shows marked hypertrophy and enhancement of all exiting cervical nerve roots <img src='/img/arrows/CS.png'/>. 5 mm is considered an adequate cut-off value of cervical spinal nerve root diameter, discriminating CIDP from controls. Mean diameter of spinal nerve roots in CIDP: Cervical 6-6.8 mm; lumbosacral 7.3-10.4 mm.*
|
||||
|
||||
|
||||
*Sagittal T1 C+ MR of the cervical spine shows marked hypertrophy and enhancement of all exiting cervical nerve roots <img src='/img/arrows/CS.png'/>. 5 mm is considered an adequate cut-off value of cervical spinal nerve root diameter, discriminating CIDP from controls. Mean diameter of spinal nerve roots in CIDP: Cervical 6-6.8 mm; lumbosacral 7.3-10.4 mm.*
|
||||
|
||||
|
||||
|
||||
*Sagittal T1 C+ MR of the cervical spine shows marked hypertrophy and enhancement of all exiting cervical nerve roots <img src='/img/arrows/CS.png'/>. 5 mm is considered an adequate cut-off value of cervical spinal nerve root diameter, discriminating CIDP from controls. Mean diameter of spinal nerve roots in CIDP: Cervical 6-6.8 mm; lumbosacral 7.3-10.4 mm.*
|
||||
|
||||
|
||||
*Sagittal T2WI MR reveals enlargement and T2 hyperintensity of exiting extradural lumbosacral nerves <img src='/img/arrows/CS.png'/>. High signal of CSF should be excluded while measuring nerve root size/area in T2 MR.*
|
||||
|
||||
|
||||
*Sagittal T2WI MR reveals enlargement and T2 hyperintensity of exiting extradural lumbosacral nerves <img src='/img/arrows/CS.png'/>. High signal of CSF should be excluded while measuring nerve root size/area in T2 MR.*
|
||||
|
||||
|
||||
*Axial T1WI C+ MR depicts enlargement and abnormal enhancement of exiting extradural lumbosacral nerves <img src='/img/arrows/CS.png'/>. Blood-nerve barrier breakdown can cause contrast enhancement. Axon loss associated with demyelination is the most important factor of disability and resistance to treatment. Root hypertrophy also may cause stenosis symptoms.*
|
||||
|
||||
|
||||
*Axial T1WI C+ MR depicts enlargement and abnormal enhancement of exiting extradural lumbosacral nerves <img src='/img/arrows/CS.png'/>. Blood-nerve barrier breakdown can cause contrast enhancement. Axon loss associated with demyelination is the most important factor of disability and resistance to treatment. Root hypertrophy also may cause stenosis symptoms.*
|
||||
|
||||
|
||||
*Sagittal FLAIR MR demonstrates periventricular ovoid hyperintensities <img src='/img/arrows/CO.png'/> in a typical case of marked fusiform CIDP nerve enlargement with brain demyelination.*
|
||||
|
||||
|
||||
*Sagittal FLAIR MR demonstrates periventricular ovoid hyperintensities <img src='/img/arrows/CO.png'/> in a typical case of marked fusiform CIDP nerve enlargement with brain demyelination.*
|
||||
|
||||
|
||||
### Additional Images
|
||||
|
||||
|
||||
*Axial T1WI C+ MR shows thickening and enhancement of ventral and dorsal cauda equina nerve roots <img src='/img/arrows/WS.png'/>.*
|
||||
|
||||
|
||||
*Axial T1WI C+ MR shows thickening and enhancement of ventral and dorsal cauda equina nerve roots <img src='/img/arrows/WS.png'/>.*
|
||||
|
||||
|
||||
*Sagittal T2WI MR demonstrates diffuse thickening of the intradural cauda equina nerve roots.*
|
||||
|
||||
|
||||
*Sagittal T2WI MR demonstrates diffuse thickening of the intradural cauda equina nerve roots.*
|
||||
|
||||
|
||||
*Sagittal FLAIR MR of the brain in a CIDP patient shows a typical paraventricular demyelinating lesion <img src='/img/arrows/WS.png'/> similar to those seen in multiple sclerosis patients.*
|
||||
|
||||
|
||||
*Sagittal FLAIR MR of the brain in a CIDP patient shows a typical paraventricular demyelinating lesion <img src='/img/arrows/WS.png'/> similar to those seen in multiple sclerosis patients.*
|
||||
|
||||
|
||||
*Sagittal T2WI MR depicts enlarged lumbar nerve roots extending into extraforaminal ventral primary rami <img src='/img/arrows/WS.png'/>.*
|
||||
|
||||
|
||||
*Sagittal T2WI MR depicts enlarged lumbar nerve roots extending into extraforaminal ventral primary rami <img src='/img/arrows/WS.png'/>.*
|
||||
|
||||
|
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@@ -256,42 +254,84 @@ breadcrumbs:
|
||||
|
||||
0e17b374-1564-4020-a6e2-552480332e98
|
||||
|
||||
## References
|
||||
|
||||
# Selected References
|
||||
|
||||
1. [Li Z et al: CLIPPERS, a syndrome of lymphohistiocytic disorders. Mult Scler Relat Disord. 42:102063, 2020](http://www.ncbi.nlm.nih.gov/pubmed/?term=32234602%5Bpmid%5D)
|
||||
1. [Turnquist C et al: CLIPPERS: a case report with radiology, three serial biopsies and a literature review. Clin Neuropathol. 39(1):19-24, 2020](http://www.ncbi.nlm.nih.gov/pubmed/?term=31661071%5Bpmid%5D)
|
||||
1. [Taieb G et al: CLIPPERS and its mimics: evaluation of new criteria for the diagnosis of CLIPPERS. J Neurol Neurosurg Psychiatry. 90(9):1027-38, 2019](http://www.ncbi.nlm.nih.gov/pubmed/?term=31072955%5Bpmid%5D)
|
||||
1. [Berzero G et al: CLIPPERS mimickers: relapsing brainstem encephalitis associated with anti-MOG antibodies. Eur J Neurol. 25(2):e16-7, 2018](http://www.ncbi.nlm.nih.gov/pubmed/?term=29356261%5Bpmid%5D)
|
||||
1. [Tian D et al: Case 259: Primary central nervous system lymphomatoid granulomatosis mimicking chronic lymphocytic inflammation with pontine perivascular enhancement responsive to steroids (CLIPPERS). Radiology. 289(2):572-7, 2018](http://www.ncbi.nlm.nih.gov/pubmed/?term=30332362%5Bpmid%5D)
|
||||
1. [Tobin WO et al: Diagnostic criteria for chronic lymphocytic inflammation with pontine perivascular enhancement responsive to steroids (CLIPPERS). Brain. 140(9):2415-25, 2017](http://www.ncbi.nlm.nih.gov/pubmed/?term=29050399%5Bpmid%5D)
|
||||
1. [Taieb G et al: Punctate and curvilinear gadolinium enhancing lesions in the brain: a practical approach. Neuroradiology. 58(3):221-35, 2016](http://www.ncbi.nlm.nih.gov/pubmed/?term=26700824%5Bpmid%5D)
|
||||
1. [Gul M et al: Atypical presentation of CLIPPERS syndrome: a new entity in the differential diagnosis of central nervous system rheumatologic diseases. J Clin Rheumatol. 21(3):144-8, 2015](http://www.ncbi.nlm.nih.gov/pubmed/?term=25807094%5Bpmid%5D)
|
||||
1. [Dudesek A et al: CLIPPERS: chronic lymphocytic inflammation with pontine perivascular enhancement responsive to steroids. Review of an increasingly recognized entity within the spectrum of inflammatory central nervous system disorders. Clin Exp Immunol. 175(3):385-96, 2014](http://www.ncbi.nlm.nih.gov/pubmed/?term=24028073%5Bpmid%5D)
|
||||
1. [Pittock SJ et al: Chronic lymphocytic inflammation with pontine perivascular enhancement responsive to steroids (CLIPPERS). Brain. 133(9):2626-34, 2010](http://www.ncbi.nlm.nih.gov/pubmed/?term=20639547%5Bpmid%5D)
|
||||
|
||||
|
||||
## Images
|
||||
|
||||
|
||||
### Selected Images
|
||||
|
||||
|
||||
*Sagittal FLAIR MR in a 56-year-old woman with weight loss and a 3-week history of diplopia and disequilibrium shows confluent and punctate hyperintensities in the pons <img src='/img/arrows/WO.png'/> and medulla <img src='/img/arrows/WS.png'/>.*
|
||||
|
||||
|
||||
*Sagittal FLAIR MR in a 56-year-old woman with weight loss and a 3-week history of diplopia and disequilibrium shows confluent and punctate hyperintensities in the pons <img src='/img/arrows/WO.png'/> and medulla <img src='/img/arrows/WS.png'/>.*
|
||||
|
||||
|
||||
|
||||
*Sagittal FLAIR MR in a 56-year-old woman with weight loss and a 3-week history of diplopia and disequilibrium shows confluent and punctate hyperintensities in the pons <img src='/img/arrows/WO.png'/> and medulla <img src='/img/arrows/WS.png'/>.*
|
||||
|
||||
|
||||
*Axial T1 C+ MR in the same patient shows multiple punctate and curvilinear enhancing foci "peppering" the pons <img src='/img/arrows/WS.png'/>. Additional lesions are present in both cerebellar peduncles, vermis, and the left cerebellar hemisphere.*
|
||||
|
||||
|
||||
*Axial T1 C+ MR in the same patient shows multiple punctate and curvilinear enhancing foci "peppering" the pons <img src='/img/arrows/WS.png'/>. Additional lesions are present in both cerebellar peduncles, vermis, and the left cerebellar hemisphere.*
|
||||
|
||||
|
||||
*More cephalad T1 C+ MR scan in the same patient shows the punctate <img src='/img/arrows/WS.png'/> and curvilinear <img src='/img/arrows/WC.png'/> lesions involving the upper pons.*
|
||||
|
||||
|
||||
*More cephalad T1 C+ MR scan in the same patient shows the punctate <img src='/img/arrows/WS.png'/> and curvilinear <img src='/img/arrows/WC.png'/> lesions involving the upper pons.*
|
||||
|
||||
|
||||
*Coronal T1 C+ FS MR in the same patient shows the lesions "peppering" the pons. Note cephalad extension into the cerebral peduncles <img src='/img/arrows/WO.png'/> and inferior extension into the medulla <img src='/img/arrows/WC.png'/> and upper cervical cord <img src='/img/arrows/WS.png'/>. DSA (not shown) was negative. The lesions resolved with corticosteroids, so this is a presumed case of CLIPPERS.*
|
||||
|
||||
|
||||
*Coronal T1 C+ FS MR in the same patient shows the lesions "peppering" the pons. Note cephalad extension into the cerebral peduncles <img src='/img/arrows/WO.png'/> and inferior extension into the medulla <img src='/img/arrows/WC.png'/> and upper cervical cord <img src='/img/arrows/WS.png'/>. DSA (not shown) was negative. The lesions resolved with corticosteroids, so this is a presumed case of CLIPPERS.*
|
||||
|
||||
|
||||
### Additional Images
|
||||
|
||||
|
||||
*Sagittal FLAIR in a 52-year-old man with diplopia, dysarthria, and facial numbness shows confluent hyperintensity in the pons <img src='/img/arrows/WS.png'/>.*
|
||||
|
||||
|
||||
*Sagittal FLAIR in a 52-year-old man with diplopia, dysarthria, and facial numbness shows confluent hyperintensity in the pons <img src='/img/arrows/WS.png'/>.*
|
||||
|
||||
|
||||
*Axial T1 C+ MR shows scattered, faint, punctate enhancing foci <img src='/img/arrows/WS.png'/> as well as larger confluent, nodular <img src='/img/arrows/WO.png'/>, and partial ring-enhancing <img src='/img/arrows/WC.png'/> lesions in the pons.*
|
||||
|
||||
|
||||
*Axial T1 C+ MR shows scattered, faint, punctate enhancing foci <img src='/img/arrows/WS.png'/> as well as larger confluent, nodular <img src='/img/arrows/WO.png'/>, and partial ring-enhancing <img src='/img/arrows/WC.png'/> lesions in the pons.*
|
||||
|
||||
|
||||
*Coronal T1 C+ MR in the same patient shows large, confluent, patchy enhancing lesions <img src='/img/arrows/WS.png'/> in the pons. Differential diagnosis included lymphoma, lymphomatoid granulomatosis, vasculitis, and CLIPPERS. The patient improved on steroids.*
|
||||
|
||||
|
||||
*Coronal T1 C+ MR in the same patient shows large, confluent, patchy enhancing lesions <img src='/img/arrows/WS.png'/> in the pons. Differential diagnosis included lymphoma, lymphomatoid granulomatosis, vasculitis, and CLIPPERS. The patient improved on steroids.*
|
||||
|
||||
|
||||
*Sagittal FLAIR in the same patient obtained a year later when symptoms relapsed off steroids shows multiple punctate hyperintensities "peppering" the pons <img src='/img/arrows/WS.png'/> and medulla <img src='/img/arrows/WC.png'/>. Note extension into upper spinal cord <img src='/img/arrows/WO.png'/>.*
|
||||
|
||||
|
||||
*Sagittal FLAIR in the same patient obtained a year later when symptoms relapsed off steroids shows multiple punctate hyperintensities "peppering" the pons <img src='/img/arrows/WS.png'/> and medulla <img src='/img/arrows/WC.png'/>. Note extension into upper spinal cord <img src='/img/arrows/WO.png'/>.*
|
||||
|
||||
|
||||
*Axial T1 C + FS MR in the same patient shows small, punctate foci of enhancement <img src='/img/arrows/WS.png'/> "peppering" the pons, cerebellar peduncles.*
|
||||
|
||||
|
||||
*Axial T1 C + FS MR in the same patient shows small, punctate foci of enhancement <img src='/img/arrows/WS.png'/> "peppering" the pons, cerebellar peduncles.*
|
||||
|
||||
|
||||
@@ -28,9 +28,6 @@ breadcrumbs:
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- Long "aspect ratio" → fusiform appearance
|
||||
- Often multilobulated, bizarre
|
||||
|
||||
## References
|
||||
|
||||
# Selected References
|
||||
|
||||
1. [Kyle K et al: Contrasting cases of HIV vasculopathy associated fusiform aneurysms. Neurohospitalist. 13(1):69-73, 2023](http://www.ncbi.nlm.nih.gov/pubmed/?term=36531848%5Bpmid%5D)
|
||||
1. [Chung CY et al: Imaging intracranial aneurysms in the endovascular era: surveillance and posttreatment follow-up. Radiographics. 42(3):789-805, 2022](http://www.ncbi.nlm.nih.gov/pubmed/?term=35333634%5Bpmid%5D)
|
||||
1. [Ritchey Z et al: Stroke recurrence in children with vertebral artery dissecting aneurysm. AJNR Am J Neuroradiol. 43(6):913-8, 2022](http://www.ncbi.nlm.nih.gov/pubmed/?term=35550284%5Bpmid%5D)
|
||||
1. [Wang MX et al: Neurofibromatosis from head to toe: what the radiologist needs to know. Radiographics. 42(4):1123-44, 2022](http://www.ncbi.nlm.nih.gov/pubmed/?term=35749292%5Bpmid%5D)
|
||||
1. [Law-Ye B et al: Considerations on the relevance of cerebral fusiform aneurysms observed during HIV infection. Clin Neuroradiol. 28(3):357-65, 2018](http://www.ncbi.nlm.nih.gov/pubmed/?term=28378026%5Bpmid%5D)
|
||||
1. [Kim ST et al: Prevalence of intracranial aneurysms in patients with connective tissue diseases: a retrospective study. AJNR Am J Neuroradiol. 37(8):1422-6, 2016](http://www.ncbi.nlm.nih.gov/pubmed/?term=26992822%5Bpmid%5D)
|
||||
1. [van Oel LI et al: Reconstructive endovascular treatment of fusiform and dissecting basilar trunk aneurysms with flow diverters, stents, and coils. AJNR Am J Neuroradiol. 34(3):589-95, 2013](http://www.ncbi.nlm.nih.gov/pubmed/?term=22918431%5Bpmid%5D)
|
||||
1. [Park SH et al: Intracranial fusiform aneurysms: it's pathogenesis, clinical characteristics and managements. J Korean Neurosurg Soc. 44(3):116-23, 2008](http://www.ncbi.nlm.nih.gov/pubmed/?term=19096660%5Bpmid%5D)
|
||||
|
||||
|
||||
## Images
|
||||
|
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pageDescription: "Guillain-Barr\u00e9 Spectrum Disorders"
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5e867f2a-de7e-44dd-83cf-67453b9125d2
|
||||
|
||||
## References
|
||||
|
||||
# Selected References
|
||||
|
||||
1. [Al Othman B et al: Update: the Miller Fisher variants of Guillain-Barré syndrome. Curr Opin Ophthalmol. 30(6):462-6, 2019](http://www.ncbi.nlm.nih.gov/pubmed/?term=31567467%5Bpmid%5D)
|
||||
1. [Leonhard SE et al: Diagnosis and management of Guillain-Barré syndrome in ten steps. Nat Rev Neurol. 15(11):671-83, 2019](http://www.ncbi.nlm.nih.gov/pubmed/?term=31541214%5Bpmid%5D)
|
||||
1. [Malhotra A et al: MRI findings of optic pathway involvement in Miller Fisher syndrome in 3 pediatric patients and a review of the literature. J Clin Neurosci. 39:63-7, 2017](http://www.ncbi.nlm.nih.gov/pubmed/?term=28209311%5Bpmid%5D)
|
||||
1. [Cuneo GL et al: An atypical Bickerstaff's brainstem encephalitis with involvement of spinal cord. Neuroradiol J. 29(5):396-9, 2016](http://www.ncbi.nlm.nih.gov/pubmed/?term=27540012%5Bpmid%5D)
|
||||
1. [Tyrakowska Z et al: Relapsing-Remitting Severe Bickerstaff's Brainstem Encephalitis - Case Report and Literature Review. Pol J Radiol. 81:622-628, 2016](http://www.ncbi.nlm.nih.gov/pubmed/?term=28096906%5Bpmid%5D)
|
||||
1. [Zuccoli G et al: Redefining the Guillain-Barré spectrum in children: neuroimaging findings of cranial nerve involvement. AJNR Am J Neuroradiol. 32(4):639-42, 2011](http://www.ncbi.nlm.nih.gov/pubmed/?term=21292802%5Bpmid%5D)
|
||||
1. [Inoue N et al: MR imaging findings of spinal posterior column involvement in a case of Miller Fisher syndrome. AJNR Am J Neuroradiol. 25(4):645-8, 2004](http://www.ncbi.nlm.nih.gov/pubmed/?term=15090361%5Bpmid%5D)
|
||||
|
||||
|
||||
## Images
|
||||
|
||||
|
||||
### Selected Images
|
||||
|
||||
|
||||
*Axial T1 C+ MR of the lumbar spine in a patient with Guillain-Barré syndrome (GBS) shows the characteristic ventral cauda equina (CE) nerve root enhancement <img src='/img/arrows/CS.png'/> and slight thickening.*
|
||||
|
||||
|
||||
*Axial T1 C+ MR of the lumbar spine in a patient with Guillain-Barré syndrome (GBS) shows the characteristic ventral cauda equina (CE) nerve root enhancement <img src='/img/arrows/CS.png'/> and slight thickening.*
|
||||
|
||||
|
||||
|
||||
*Axial T1 C+ MR of the lumbar spine in a patient with Guillain-Barré syndrome (GBS) shows the characteristic ventral cauda equina (CE) nerve root enhancement <img src='/img/arrows/CS.png'/> and slight thickening.*
|
||||
|
||||
|
||||
*Sagittal T1 C+ FS MR of the lumbar spine in a patient with GBS shows CE nerve root enhancement, more intense in ventral <img src='/img/arrows/CS.png'/> than dorsal <img src='/img/arrows/CC.png'/> CE. Also note enhancement of the pial surface of the distal cord/conus <img src='/img/arrows/CO.png'/>. GBS is an immune-mediated peripheral nerves and nerve roots disorder, usually triggered by infections.*
|
||||
|
||||
|
||||
*Sagittal T1 C+ FS MR of the lumbar spine in a patient with GBS shows CE nerve root enhancement, more intense in ventral <img src='/img/arrows/CS.png'/> than dorsal <img src='/img/arrows/CC.png'/> CE. Also note enhancement of the pial surface of the distal cord/conus <img src='/img/arrows/CO.png'/>. GBS is an immune-mediated peripheral nerves and nerve roots disorder, usually triggered by infections.*
|
||||
|
||||
|
||||
*Coronal angled T1 C+ MPRAGE MR reformat in a patient with Miller Fisher syndrome (MFS) shows mild thickening and enhancement of right facial (CNVII) <img src='/img/arrows/CC.png'/> and bilateral trigeminal (CNV) <img src='/img/arrows/CS.png'/> nerves.*
|
||||
|
||||
|
||||
*Coronal angled T1 C+ MPRAGE MR reformat in a patient with Miller Fisher syndrome (MFS) shows mild thickening and enhancement of right facial (CNVII) <img src='/img/arrows/CC.png'/> and bilateral trigeminal (CNV) <img src='/img/arrows/CS.png'/> nerves.*
|
||||
|
||||
|
||||
*Axial FLAIR MR in a patient with BBE shows hyperintense signal in the pons <img src='/img/arrows/CS.png'/>, middle cerebellar peduncles <img src='/img/arrows/CC.png'/>, and cerebellum <img src='/img/arrows/CO.png'/>. Both MFS and BBE may initially show ophthalmoplegia, ataxia, and areflexia, the differentiating feature being reduced consciousness and other brainstem signs in BBE later.*
|
||||
|
||||
|
||||
*Axial FLAIR MR in a patient with BBE shows hyperintense signal in the pons <img src='/img/arrows/CS.png'/>, middle cerebellar peduncles <img src='/img/arrows/CC.png'/>, and cerebellum <img src='/img/arrows/CO.png'/>. Both MFS and BBE may initially show ophthalmoplegia, ataxia, and areflexia, the differentiating feature being reduced consciousness and other brainstem signs in BBE later.*
|
||||
|
||||
|
||||
### Additional Images
|
||||
|
||||
|
||||
*Axial FLAIR MR in a patient with Bickerstaff brainstem encephalitis (BBE) shows abnormal hyperintense signal in the pons <img src='/img/arrows/CS.png'/>. Both MFS and BBE initially present with ophthalmoplegia, ataxia and areflexia; the differentiating feature being development of brainstem dysfunction in BBE later (reduced consciousness and pyramidal tract signs).*
|
||||
|
||||
|
||||
*Axial FLAIR MR in a patient with Bickerstaff brainstem encephalitis (BBE) shows abnormal hyperintense signal in the pons <img src='/img/arrows/CS.png'/>. Both MFS and BBE initially present with ophthalmoplegia, ataxia and areflexia; the differentiating feature being development of brainstem dysfunction in BBE later (reduced consciousness and pyramidal tract signs).*
|
||||
|
||||
|
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+455
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---
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---
|
||||
# KEY FACTS
|
||||
|
||||
- ## Terminology
|
||||
|
||||
|
||||
- Inferior olivary nucleus (ION) degeneration
|
||||
- Unique type of transsynaptic neuronal degeneration
|
||||
- Olivary deafferentation thought to be source of ensuing hypertrophic olivary degeneration (HOD)
|
||||
- Usually caused by primary lesions in dentato-rubro-olivary pathway (Guillain-Mollaret triangle)
|
||||
- Triangle of Guillain-Mollaret defined by 3 anatomic structures
|
||||
- Red nucleus (RN)
|
||||
- ION ipsilateral to RN
|
||||
- Contralateral dentate nucleus (DN) of cerebellum
|
||||
- ## Imaging
|
||||
|
||||
|
||||
- ION initially hypertrophies rather than atrophies
|
||||
- 3 distinct MR stages in HOD
|
||||
- Hyperintense signal without hypertrophy of ION: Within first 6 months of ictus
|
||||
- ↑ signal + ION hypertrophy: Between 6 months & 3-4 years after ictus
|
||||
- Only ION hyperintensity: Begins when hypertrophy resolves (can persist indefinitely)
|
||||
- MR also detects primary lesion located in ipsilateral CTT, SCP or contralateral DN
|
||||
- ## Top Differential Diagnoses
|
||||
|
||||
|
||||
- Vertebrobasilar perforating artery infarct
|
||||
- Demyelination (multiple sclerosis, microvascular disease)
|
||||
- Amyotrophic lateral sclerosis
|
||||
- HIV/AIDS
|
||||
- Rhombencephalitis
|
||||
- ## Clinical Issues
|
||||
|
||||
|
||||
- Palatal myoclonus (palatal "tremor"), ocular myoclonus
|
||||
- Usually develops 10-11 months after primary lesion
|
||||
- Clinical symptoms (tremors) rarely improve
|
||||
|
||||
# TERMINOLOGY
|
||||
|
||||
- ## Abbreviations
|
||||
|
||||
|
||||
- Hypertrophic olivary degeneration (HOD)
|
||||
- ## Synonyms
|
||||
|
||||
|
||||
- Pseudohypertrophy of inferior olivary nucleus
|
||||
- ## Definitions
|
||||
|
||||
|
||||
- Transsynaptic degeneration of inferior olivary nucleus (ION), usually caused by primary lesions in dentato-rubro-olivary pathway (DROP) also called anatomic triangle of Guillain & Mollaret (GMT)
|
||||
|
||||
# IMAGING
|
||||
|
||||
- ## General Features
|
||||
|
||||
|
||||
- ### Best diagnostic clue
|
||||
|
||||
|
||||
- T2-hyperintense, nonenhancing enlargement of ION
|
||||
- ### Location
|
||||
|
||||
|
||||
- GMT is defined by 3 anatomic structures
|
||||
- Red nucleus (RN)
|
||||
- ION ipsilateral to RN
|
||||
- Contralateral dentate nucleus (DN) of cerebellum
|
||||
- Central tegmental tract (CTT or rubro-olivary pathway) connects RN to ipsilateral ION
|
||||
- Superior cerebellar peduncle (SCP, dentato-rubral tract) connects DN to contralateral RN
|
||||
- Inferior cerebellar peduncle (olivo-cerebellar pathway) connects ION to contralateral cerebellar cortex & contralateral DN
|
||||
- 4 patterns of HOD in relation to primary lesion
|
||||
- Ipsilateral HOD: Primary lesion is limited to brainstem (CTT)
|
||||
- Contralateral HOD: Primary lesion is in cerebellum (DN or SCP)
|
||||
- Bilateral HOD: Primary lesion involves midline/paramedian brainstem affecting brachium conjunctivum
|
||||
- Bilateral HOD: Primary lesion involves both unilateral brainstem & cerebellum
|
||||
- ### Size
|
||||
|
||||
|
||||
- Variable (time-dependent) size of affected ION
|
||||
- Normal in acute stage
|
||||
- ↑ (hypertrophy) from 6 months to 3-4 years
|
||||
- ↓ (atrophy) in advanced stage (> 3-4 years)
|
||||
- ### Morphology
|
||||
|
||||
|
||||
- Unique type of transsynaptic neuronal degeneration
|
||||
- ION initially hypertrophies rather than atrophies
|
||||
- ## CT Findings
|
||||
|
||||
|
||||
- ### NECT
|
||||
|
||||
|
||||
- May show acute primary injury (e.g., hemorrhage) in tegmentum
|
||||
- HOD typically not depicted on CT
|
||||
- ## MR Findings
|
||||
|
||||
|
||||
- ### T1WI
|
||||
|
||||
|
||||
- Acute phase: Normal ION
|
||||
- Shows primary lesion in brainstem (cerebellum or tegmentum)
|
||||
- After HOD ensues
|
||||
- Enlargement confined to ION, isointense to slightly hypointense to gray matter
|
||||
- Slightly ↑ olivary T1 signal also reported
|
||||
- ± residual primary lesion
|
||||
- ### T2WI
|
||||
|
||||
|
||||
- 3 distinct MR stages in HOD
|
||||
- Hyperintense signal without hypertrophy of ION: Within first 6 months of ictus
|
||||
- Both ↑ signal & hypertrophy of ION: Between 6 months & 3-4 years after ictus
|
||||
- ↑ signal only in ION: Begins when hypertrophy resolves & can persist indefinitely
|
||||
- Axial MR: Disappearance of pre- & postolivary sulci in hypertrophic stage
|
||||
- MR also detects primary lesion located in ipsilateral central tegmental tract or contralateral DN
|
||||
- Old hematomas: Low-signal areas on T2WI revealing hemosiderin deposition
|
||||
- ± ↓ size of contralateral ION with higher than normal signal intensity
|
||||
- ± mild to severe atrophic changes of cerebellar cortex contralateral to HOD
|
||||
- ### PD/intermediate
|
||||
|
||||
|
||||
- High signal intensity of ION better detected on PD images than on T2WI
|
||||
- ### FLAIR
|
||||
|
||||
|
||||
- Similar to T2WI
|
||||
- ### T1WI C+
|
||||
|
||||
|
||||
- No contrast enhancement of degenerated ION
|
||||
- DTI
|
||||
- ↑ radial diffusivity, ↑ mean diffusion & ↓ fractional anisotropy in GMT components reflecting demyelination
|
||||
- ↑ fractional anisotropy & ↑ axial diffusivity in ION reflect rearrangement of regenerating axons & shrunken neurons
|
||||
- ## Nuclear Medicine Findings
|
||||
|
||||
|
||||
- ### PET
|
||||
|
||||
|
||||
- Focal glucose hypermetabolism in medulla of patients with HOD
|
||||
- ## Imaging Recommendations
|
||||
|
||||
|
||||
- ### Best imaging tool
|
||||
|
||||
|
||||
- MR
|
||||
- ### Protocol advice
|
||||
|
||||
|
||||
- T2WI (include coronal or sagittal sections)
|
||||
|
||||
# DIFFERENTIAL DIAGNOSIS
|
||||
|
||||
- ## Other Causes of High T2 Signal Intensity in Anterior Part of Medulla
|
||||
|
||||
|
||||
- [Demyelination related to multiple sclerosis](/document/multiple-sclerosis/7892b2a2-f52a-4d7f-9858-a326f2b7ab04)
|
||||
- Tumor (astrocytoma, metastasis, lymphoma)
|
||||
- Lesions involving corticospinal tract
|
||||
- Wallerian degeneration, adrenoleukodystrophy
|
||||
- [Amyotrophic lateral sclerosis](/document/amyotrophic-lateral-sclerosis-als/23de52b7-d9bd-441c-a18c-95c8afccb470)
|
||||
- Vertebrobasilar perforating artery infarct
|
||||
- Most medullary infarctions occur in posteroinferior cerebellar artery territory & involve posterolateral medulla (e.g., vertebral artery dissection)
|
||||
- Alternatively, medullary infarcts could be related to perforating branches of anterior spinal or vertebral arteries & have paramedial location
|
||||
- Infectious/inflammatory processes
|
||||
- [Tuberculosis](/document/tuberculosis/6e389773-2150-4299-9ce2-0b83b13c2119)
|
||||
- [Sarcoidosis](/document/neurosarcoid/fef69139-0019-4be3-9bdc-e26bc3644251)
|
||||
- HIV/AIDS
|
||||
- [Rhombencephalitis](/document/miscellaneous-encephalitis/1c3c0881-4046-46a1-90fc-371941c0cf2c)
|
||||
|
||||
# PATHOLOGY
|
||||
|
||||
- ## General Features
|
||||
|
||||
|
||||
- ### Etiology
|
||||
|
||||
|
||||
- Transsynaptic degeneration caused by interruption of pathways composing GMT
|
||||
- Olivary deafferentation thought to be source of ensuing HOD
|
||||
- Primary lesions usually located in contralateral DN or ipsilateral CTT
|
||||
- Focal brainstem insults that may lead to dentato-rubral-olivary pathway interruption
|
||||
- Ischemic infarction, demyelination
|
||||
- Hemorrhage (related to hypertensive disease, occult cerebrovascular malformation, or diffuse axonal injury following severe head trauma)
|
||||
- Cavernous malformation
|
||||
- ### Associated abnormalities
|
||||
|
||||
|
||||
- Primary brainstem insult
|
||||
- Most commonly pontine hemorrhage from trauma (including surgery), hypertension, tumor, & infarction
|
||||
- Olivary enlargement: Histologically unusual vacuolar cytoplasmic degeneration → hypertrophy related in part to ↑ number of astrocytes
|
||||
- After onset of primary lesion
|
||||
- Vacuolar cytoplasmic degeneration in 6-15 months
|
||||
- Gliosis follows at 15-20 months
|
||||
- ## Staging, Grading, & Classification
|
||||
|
||||
|
||||
- 6 phases of pathologic change
|
||||
- No olivary changes within first 24 hours
|
||||
- Degeneration of olivary amiculum (white matter capsule at olive periphery) at ≥ 2-7 days
|
||||
- Olivary hypertrophy (mild enlargement with neuronal hypertrophy, no glial reaction) at 3 weeks
|
||||
- Maximal olivary enlargement (hypertrophy of neurons & astrocytes) at 8.5 months
|
||||
- Olivary pseudohypertrophy (neuronal dissolution with prevailing large gemistocytic astrocytes) after 9.5 months
|
||||
- Olivary atrophy (neuronal disappearance with olivary atrophy & prominent degeneration of amiculum olivae) after 3-5 years of primary lesion
|
||||
- ## Gross Pathologic & Surgical Features
|
||||
|
||||
|
||||
- Focal swelling of ION
|
||||
- Unilateral HOD
|
||||
- Asymmetric enlargement of anterior medulla
|
||||
- "Pallor" in contralateral DN
|
||||
- Atrophy of contralateral cerebellar cortex
|
||||
- Bilateral HOD: More difficult to observe
|
||||
- No left-right asymmetry
|
||||
- ## Microscopic Features
|
||||
|
||||
|
||||
- Changes in hypertrophic degenerated ION
|
||||
- Hypertrophic, thickened neurites
|
||||
- Vacuolation of neurons
|
||||
- Fibrillary gliosis
|
||||
- Demyelination & astrocytic proliferation of WM
|
||||
- In contralateral cerebellar cortex
|
||||
- ↓ number of Purkinje cells
|
||||
- Contralateral DN reduced in size, possibly due to
|
||||
- Iron depletion secondary to axonal iron transport block
|
||||
- Loss of cells in nucleus
|
||||
|
||||
# CLINICAL ISSUES
|
||||
|
||||
- ## Presentation
|
||||
|
||||
|
||||
- ### Most common signs/symptoms
|
||||
|
||||
|
||||
- Symptomatic palatal tremor/myoclonus
|
||||
- Rhythmic involuntary movement of soft palate, uvula, pharynx, & larynx
|
||||
- Severe myoclonus may also affect cervical muscles & diaphragm
|
||||
- ± dentato-rubral tremor (Holmes tremor)
|
||||
- 2-5 Hz rest, postural, & kinetic tremor of upper extremity
|
||||
- May occur before onset of palatal tremor
|
||||
- Symptoms of cerebellar or brainstem dysfunction
|
||||
- Associated with acute lesion within triangle of Guillain-Mollaret
|
||||
- Ocular myoclonus & nystagmus
|
||||
- ### Clinical profile
|
||||
|
||||
|
||||
- Palatal myoclonus (palatal "tremor")
|
||||
- Usually develops 10-11 months after primary lesion
|
||||
- Virtually all patients who develop palatal myoclonus after brain insult will have HOD
|
||||
- Not all HOD patients develop palatal myoclonus
|
||||
- May result from hypermetabolism of ION
|
||||
- ## Demographics
|
||||
|
||||
|
||||
- ### Age
|
||||
|
||||
|
||||
- Rare; reported in all ages, both sexes
|
||||
- ## Natural History & Prognosis
|
||||
|
||||
|
||||
- After primary brainstem injury, olivary hypertrophy typically appears in delayed fashion
|
||||
- May occur between 3 weeks to 11 months (usually within 4-6 months)
|
||||
- Maximum hypertrophy at 5-15 months
|
||||
- Olivary hypertrophy typically resolves in 10-16 months
|
||||
- Olivary hyperintensity on T2WI may persist for years after resolution of hypertrophy
|
||||
- Finally ION undergoes atrophy
|
||||
- Clinical symptoms (tremors) rarely improve
|
||||
- Self-limiting disease & can be managed by symptomatic treatment
|
||||
|
||||
# DIAGNOSTIC CHECKLIST
|
||||
|
||||
- ## Image Interpretation Pearls
|
||||
|
||||
|
||||
- Avoid misdiagnosis of tumor or multiple sclerosis
|
||||
- Bilateral & symmetrical lesions in ION argue against subacute infarct & vertebral artery dissection
|
||||
|
||||
9342df55-d4e7-4743-8a78-b03338f00dc0
|
||||
|
||||
## References
|
||||
|
||||
# Selected References
|
||||
|
||||
1. [Choi WY et al: Ocular motor and vestibular disorders in brainstem disease. J Clin Neurophysiol. 36(6):396-404, 2019](http://www.ncbi.nlm.nih.gov/pubmed/?term=31688322%5Bpmid%5D)
|
||||
1. [Ohara M et al: Olivary hypertrophy improved by steroid treatment: two case reports with unique presentations. J Neuroimmunol. 334:577003, 2019](http://www.ncbi.nlm.nih.gov/pubmed/?term=31306854%5Bpmid%5D)
|
||||
1. [Wang H et al: Hypertrophic olivary degeneration: a comprehensive review focusing on etiology. Brain Res. 1718:53-63, 2019](http://www.ncbi.nlm.nih.gov/pubmed/?term=31026459%5Bpmid%5D)
|
||||
1. [Onen MR et al: Hypertrophic olivary degeneration: neurosurgical perspective and literature review. World Neurosurg. 112:e763-71, 2018](http://www.ncbi.nlm.nih.gov/pubmed/?term=29382617%5Bpmid%5D)
|
||||
1. [Tilikete C et al: Hypertrophic olivary degeneration and palatal or oculopalatal tremor. Front Neurol. 8:302, 2017](http://www.ncbi.nlm.nih.gov/pubmed/?term=28706504%5Bpmid%5D)
|
||||
1. [Cosentino C et al: Bilateral hypertrophic olivary degeneration and Holmes tremor without palatal tremor: an unusual association. Tremor Other Hyperkinet Mov (N Y). 6:400, 2016](http://www.ncbi.nlm.nih.gov/pubmed/?term=27536461%5Bpmid%5D)
|
||||
1. [Van Eetvelde R et al: Imaging features of hypertrophic olivary degeneration. J Belg Soc Radiol. 100(1):71, 2016](http://www.ncbi.nlm.nih.gov/pubmed/?term=30151471%5Bpmid%5D)
|
||||
1. [Blanco Ulla M et al: Magnetic resonance imaging of hypertrophic olivary degeneration. Radiologia. 57(6):505-11, 2015](http://www.ncbi.nlm.nih.gov/pubmed/?term=25660593%5Bpmid%5D)
|
||||
1. [Carr CM et al: Frequency of bilateral hypertrophic olivary degeneration in a large retrospective cohort. J Neuroimaging. 25(2):289-95, 2015](http://www.ncbi.nlm.nih.gov/pubmed/?term=24716899%5Bpmid%5D)
|
||||
1. [Sen D et al: MRI and MR tractography in bilateral hypertrophic olivary degeneration. Indian J Radiol Imaging. 24(4):401-5, 2014](http://www.ncbi.nlm.nih.gov/pubmed/?term=25489133%5Bpmid%5D)
|
||||
1. [Khoyratty F et al: The dentato-rubro-olivary tract: clinical dimension of this anatomical pathway. Case Rep Otolaryngol. 2013:934386, 2013](http://www.ncbi.nlm.nih.gov/pubmed/?term=23662232%5Bpmid%5D)
|
||||
1. [Ogawa K et al: Pathological study of pseudohypertrophy of the inferior olivary nucleus. Neuropathology. 30(1):15-23, 2010](http://www.ncbi.nlm.nih.gov/pubmed/?term=19496939%5Bpmid%5D)
|
||||
1. [Lim CC et al: Images in clinical medicine. Pendular nystagmus and palatomyoclonus from hypertrophic olivary degeneration. N Engl J Med. 360(9):e12, 2009](http://www.ncbi.nlm.nih.gov/pubmed/?term=19246355%5Bpmid%5D)
|
||||
1. [Hornyak M et al: Hypertrophic olivary degeneration after surgical removal of cavernous malformations of the brain stem: report of four cases and review of the literature. Acta Neurochir (Wien). 150(2):149-56; discussion 156, 2008](http://www.ncbi.nlm.nih.gov/pubmed/?term=18166990%5Bpmid%5D)
|
||||
1. [Harter DH et al: Hypertrophic olivary degeneration after resection of a pontine cavernoma. Case illustration. J Neurosurg. 100(4):717, 2004](http://www.ncbi.nlm.nih.gov/pubmed/?term=15070130%5Bpmid%5D)
|
||||
1. [Krings T et al: Hypertrophic olivary degeneration following pontine haemorrhage: hypertensive crisis or cavernous haemangioma bleeding? J Neurol Neurosurg Psychiatry. 74(6):797-9, 2003](http://www.ncbi.nlm.nih.gov/pubmed/?term=12754356%5Bpmid%5D)
|
||||
1. [Rieder CR et al: Holmes tremor in association with bilateral hypertrophic olivary degeneration and palatal tremor: chronological considerations. Case report. Arq Neuropsiquiatr. 61(2B):473-7, 2003](http://www.ncbi.nlm.nih.gov/pubmed/?term=12894288%5Bpmid%5D)
|
||||
1. [Conceicao C et al: Hypertrophic olivary degeneration. Semiology with magnetic resonance. Acta Med Port. 14(1):107-11, 2001](http://www.ncbi.nlm.nih.gov/pubmed/?term=11321964%5Bpmid%5D)
|
||||
1. [Goyal M et al: Hypertrophic olivary degeneration: metaanalysis of the temporal evolution of MR findings. AJNR Am J Neuroradiol. 21(6):1073-7, 2000](http://www.ncbi.nlm.nih.gov/pubmed/?term=10871017%5Bpmid%5D)
|
||||
1. [Salamon-Murayama N et al: Diagnosis please. Case 17: hypertrophic olivary degeneration secondary to pontine hemorrhage. Radiology. 213(3):814-7, 1999](http://www.ncbi.nlm.nih.gov/pubmed/?term=10580959%5Bpmid%5D)
|
||||
1. [Tsui EY et al: Hypertrophic olivary degeneration following surgical excision of brainstem cavernous hemangioma: a case report. Clin Imaging. 23(4):215-7, 1999](http://www.ncbi.nlm.nih.gov/pubmed/?term=10631896%5Bpmid%5D)
|
||||
1. [Kim SJ et al: Cerebellar MR changes in patients with olivary hypertrophic degeneration. AJNR Am J Neuroradiol. 15(9):1715-9, 1994](http://www.ncbi.nlm.nih.gov/pubmed/?term=7847219%5Bpmid%5D)
|
||||
1. [Revel MP et al: MR appearance of hypertrophic olivary degeneration after contralateral cerebellar hemorrhage. AJNR Am J Neuroradiol. 12(1):71-2, 1991](http://www.ncbi.nlm.nih.gov/pubmed/?term=1899520%5Bpmid%5D)
|
||||
|
||||
|
||||
## Images
|
||||
|
||||
|
||||
### Selected Images
|
||||
|
||||
|
||||
*Axial graphic of the upper medulla shows the medullary pyramids <img src='/img/arrows/CC.png'/> on each side of the ventral median fissure. The olives <img src='/img/arrows/CO.png'/> lie just posterior to the preolivary sulci <img src='/img/arrows/CS.png'/>.*
|
||||
|
||||
|
||||
*Axial graphic of the upper medulla shows the medullary pyramids <img src='/img/arrows/CC.png'/> on each side of the ventral median fissure. The olives <img src='/img/arrows/CO.png'/> lie just posterior to the preolivary sulci <img src='/img/arrows/CS.png'/>.*
|
||||
|
||||
|
||||
*Coronal graphic of the midbrain, pons, and medulla is sectioned to depict the Guillain-Mollaret triangle (GMT). The GMT is composed of the ipsilateral inferior olivary nucleus (green), dentate nucleus (blue) of the contralateral cerebellum, and the ipsilateral red nucleus (RN, red).*
|
||||
|
||||
|
||||
*Axial T2 MR of a 40-year-old woman with brainstem glioma and secondary hypertrophic olivary degeneration (HOD) shows a heterogeneous mass lesion involving midbrain <img src='/img/arrows/CO.png'/> invading the RN <img src='/img/arrows/CS.png'/> (R > L). RN is a component of GMT.*
|
||||
|
||||
|
||||
*Axial T2 MR at the level of medulla in the same patient shows enlarged right inferior olivary nucleus with hyperintense signal <img src='/img/arrows/CC.png'/> indicating HOD. Also note normal-appearing left olivary nucleus <img src='/img/arrows/BC.png'/> and preolivary sulcus <img src='/img/arrows/BS.png'/>.*
|
||||
|
||||
|
||||
*Axial FLAIR MR of a 58-year-old woman presenting with palatal myoclonus and a history of treated CNS lymphoma shows volume loss and hyperintense signal in left dentate nucleus (DN) <img src='/img/arrows/CO.png'/> due to encephalomalacia (DN is a component of GMT).*
|
||||
|
||||
|
||||
*Axial T2 MR in the same patient at the level of medulla shows mild hypertrophy and increased signal involving bilateral inferior olivary nuclei <img src='/img/arrows/CC.png'/> indicating HOD.*
|
||||
|
||||
|
||||
*Axial T2 of a 67-year-old man with left para median pontine cavernous malformation (CM) involving central tegmental tract resulting in ipsilateral HOD shows hyperintense popcorn lesion with rim of hemosiderin in left para median pons <img src='/img/arrows/CS.png'/> due to CM.*
|
||||
|
||||
|
||||
*Axial FLAIR MR in the same patient shows enlarged left inferior olivary nucleus with hyperintense signal <img src='/img/arrows/CO.png'/> due to HOD.*
|
||||
|
||||
|
||||
*Axial T2 MR at 1 day (top left), 4 months (top right), and 7 months (bottom left) postoperative follow-up show edema in left DN <img src='/img/arrows/CS.png'/> and normal right olive <img src='/img/arrows/CO.png'/>. Note light enlargement and ↑ signal in right olive <img src='/img/arrows/CC.png'/>, progressive enlargement and ↑ signal in olive <img src='/img/arrows/WC.png'/>, and lack of enhancement in olive <img src='/img/arrows/WO.png'/> on postcontrast T1WI (bottom right).*
|
||||
|
||||
|
||||
*Axial graphic of the midbrain at the level of the hypoglossal nuclei shows the distinct wavy pattern of the olives <img src='/img/arrows/CS.png'/> corresponding to the FLAIR hyperintensity in the previous image.*
|
||||
|
||||
|
||||
### Additional Images
|
||||
|
||||
|
||||
*Axial T2WI MR demonstrates hypertrophy of both inferior olivary nuclei, which are also hyperintense <img src='/img/arrows/CS.png'/>, secondary to HOD.*
|
||||
|
||||
|
||||
*Sagittal FLAIR MR shows abnormally ↑ signal intensity in an anterior medullary area <img src='/img/arrows/CS.png'/> that corresponds to the inferior olivary nucleus.*
|
||||
|
||||
|
||||
*Axial FLAIR MR in the same patient who suffered midbrain hemorrhage (not shown) depicts bilateral hyperintense and hypertrophied inferior olivary nuclei <img src='/img/arrows/CS.png'/>.*
|
||||
|
||||
|
||||
*Axial FLAIR MR shows high signal intensity and asymmetric enlargement of right anterior medulla corresponding to the region of hypertrophic degeneration of the right inferior olivary nucleus <img src='/img/arrows/CS.png'/> .*
|
||||
|
||||
|
||||
*Axial T2WI MR in the same patient shows a right pontine infarct, the primary lesion that led to right HOD.*
|
||||
|
||||
|
||||
*Axial T2WI MR shows bilateral symmetric hypertrophy with ↑ signal intensity confined to inferior olivary nuclei, with loss of pre- and postolivary sulci <img src='/img/arrows/CS.png'/>.*
|
||||
|
||||
|
||||
*Axial T2WI MR in the same patient shows the primary midbrain lesion that caused the occurrence of bilateral HOD.*
|
||||
|
||||
|
||||
*Axial T2WI MR in a patient who developed onset of dysarthria and upper extremity dysmetria 15 months following stereotaxic XRT for midbrain arteriovenous malformation shows mixed hyper-/hypointensity in the residual vascular malformation <img src='/img/arrows/CO.png'/>.*
|
||||
|
||||
|
||||
*Axial T2WI MR in the same patient shows bilateral inferior olivary hyperintensity and hypertrophy <img src='/img/arrows/CS.png'/>.*
|
||||
|
||||
|
||||
*Axial T2WI MR (CISS) shows the normal shape of the medullary olives <img src='/img/arrows/CS.png'/>.*
|
||||
|
||||
|
||||
*Axial T2WI MR in a patient who developed palatal myoclonus ~ 6 months after resection of a midbrain CM shows hyperintensity and enlargement of both olives <img src='/img/arrows/CS.png'/>. This pattern is typical in the subacute stage of HOD, which typically appears between 6 months and 3-4 years after injury to the dentato-rubro-olivary pathway.*
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*Axial SWI MR demonstrates hemosiderin staining in the dorsal aspect of the brainstem <img src='/img/arrows/CC.png'/> in the midline and to the right due to an old hemorrhage.*
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*Axial FLAIR MR in the same patient at the level of the medulla shows mild hypertrophy with hyperintensity in the region of the right inferior olivary nucleus <img src='/img/arrows/CS.png'/>. Findings are typical for HOD caused by primary lesions in dentato-rubro-olivary pathway (anatomical GMT).*
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*Axial T2WI MR through the medulla shows that the ipsilateral olive is atrophic and hyperintense <img src='/img/arrows/CS.png'/>. This patient also has crossed cerebellar atrophy <img src='/img/arrows/CO.png'/> due to interruption of the ponto-cerebellar pathway.*
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*Axial T2WI MR in a patient who developed palatal myoclonus several months following midbrain surgery for CM. Imaging obtained 1 year later shows residual CM <img src='/img/arrows/CO.png'/>.*
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*Axial FLAIR MR in the same patient delineates the somewhat wavy appearance of the hyperintensity conforming to the configuration of the olives <img src='/img/arrows/CS.png'/>. The pyramids <img src='/img/arrows/CO.png'/> are spared, helping differentiate HOD from perforating artery infarction.*
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Reference in New Issue
Block a user