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Wallerian degeneration of the bilateral middle cerebellar peduncles
Journal of the Neurological Sciences 349 (2015) 256–257
Contents lists available at ScienceDirect
Journal of the Neurological Sciences journal homepage: www.elsevier.com/locate/jns
Letter to the Editor Wallerian degeneration of the bilateral middle cerebellar peduncles Keywords: Wallerian degeneration Stroke Middle cerebellar peduncles
A 61 year old male presented with right sided weakness and was diagnosed with acute left paramedian pontine infarction (Fig. 1 A, B) secondary to occlusion of the perforating pontine branches of the basilar artery, and was started on antiplatelet therapy and high dose of statin. Follow-up brain Magnetic Resonance Imaging (MRI) after 6 weeks demonstrated bilateral symmetrical hyperintensity in middle cerebellar peduncles on T2-weighted image (Fig. 1 C). Development of symmetrical hyperintensity in the middle cerebellar peduncles following basis pontis infarction or hemorrhage is consistent with Wallerian degeneration of pontocerebellar fibers, and should not be confused with additional infarctions. As these fibers cross the midline at the basis pontis, this phenomenon develops bilaterally, even if the initial pontine lesion is unilateral [1]. Wallerian degeneration of pontocerebellar tracts can also occur after pontine hemorrhage and central pontine myelinolysis. Bilateral symmetric involvement of cerebellar peduncles is not limited to Wallerian degeneration and has been reported in several other neurological disorders, including Wilson's disease, hepatic encephalopathy, extrapontine myelinolysis and toluene abuse. Mild diffuse abnormal signal intensity in bilateral
A
B
middle cerebellar peduncles has been also reported in neurodegenerative diseases such as multiple system atrophy and spinocerebellar degeneration. Bilateral middle cerebellar peduncle lesions are also found in bilateral anterior inferior cerebellar territory infarction, encephalitis and gliomas of the brainstem; however, the involvement is usually asymmetric in these entities [2]. Male carriers of the fragile X premutation who develop progressive intention tremor and ataxia accompanied by progressive cognitive and behavioral difficulties can also demonstrate bilateral symmetric signal abnormality in cerebellar peduncles [3]; however there is usually additional signal abnormality in the cerebellum, inferior and lateral to cerebellar nuclei, in this condition. In conclusion, neurologists should be familiar with Wallerian degeneration of bilateral middle cerebellar peduncles in the setting of acute pontine infarction to avoid misdiagnosis as additional infarctions.
Sources of funding None.
Disclosure statement Authors have no relevant financial interest to disclose. Acknowledgments None.
C
Fig. 1. Initial brain MRI demonstrates T2 prolongation (A) and restricted diffusion (B) in left paramedian pons consistent with acute infarction. Follow up MRI after 6 weeks demonstrates symmetric axial T2 hyperintensity in bilateral middle cerebellar peduncles (C).
http://dx.doi.org/10.1016/j.jns.2014.12.044 0022-510X/© 2015 Elsevier B.V. All rights reserved.
Letter to the Editor
References [1] Uchino A, Sawada A, Takase Y, Kudo S. Symmetrical lesions of the middle cerebellar peduncle: MR imaging and differential diagnosis. Magn Reson Med Sci 2004;3: 133–40. [2] De Simone T, Regna-Gladin C, Carriero MR, Farina L, Savoiardo M. Wallerian degeneration of the pontocerebellar fibers. AJNR Am J Neuroradiol 2005;26: 1062–5. [3] Brunberg JA, Jacquemont S, Hagerman RJ, Berry-Kravis EM, Grigsby J, Leehey MA, et al. Fragile X premutation carriers: characteristic MR imaging findings of adult male patients with progressive cerebellar and cognitive dysfunction. AJNR Am J Neuroradiol 2002;23:1757–66.
Seyed Ali Nabavizadeh Department of Radiology, Hospital of the University of Pennsylvania, Philadelphia, PA, United States
257
Ashkan Mowla Department of Neurology, State University of New York at Buffalo, Buffalo, NY, United States Corresponding author at: Department of Neurology, Gates Vascular Institute, School of Medicine and Biomedical Sciences, State University of New York (SUNY) at Buffalo, 100 High Street, Buffalo, NY 14203, United States. Tel.: +1 716 859 7540; fax: +1 716 859 2430. E-mail address: [email protected]. Alexander C. Mamourian Department of Radiology, Hospital of the University of Pennsylvania, Philadelphia, PA, United States 25 October 2014
Contents lists available at ScienceDirect
Journal of the Neurological Sciences journal homepage: www.elsevier.com/locate/jns
Letter to the Editor Wallerian degeneration of the bilateral middle cerebellar peduncles Keywords: Wallerian degeneration Stroke Middle cerebellar peduncles
A 61 year old male presented with right sided weakness and was diagnosed with acute left paramedian pontine infarction (Fig. 1 A, B) secondary to occlusion of the perforating pontine branches of the basilar artery, and was started on antiplatelet therapy and high dose of statin. Follow-up brain Magnetic Resonance Imaging (MRI) after 6 weeks demonstrated bilateral symmetrical hyperintensity in middle cerebellar peduncles on T2-weighted image (Fig. 1 C). Development of symmetrical hyperintensity in the middle cerebellar peduncles following basis pontis infarction or hemorrhage is consistent with Wallerian degeneration of pontocerebellar fibers, and should not be confused with additional infarctions. As these fibers cross the midline at the basis pontis, this phenomenon develops bilaterally, even if the initial pontine lesion is unilateral [1]. Wallerian degeneration of pontocerebellar tracts can also occur after pontine hemorrhage and central pontine myelinolysis. Bilateral symmetric involvement of cerebellar peduncles is not limited to Wallerian degeneration and has been reported in several other neurological disorders, including Wilson's disease, hepatic encephalopathy, extrapontine myelinolysis and toluene abuse. Mild diffuse abnormal signal intensity in bilateral
A
B
middle cerebellar peduncles has been also reported in neurodegenerative diseases such as multiple system atrophy and spinocerebellar degeneration. Bilateral middle cerebellar peduncle lesions are also found in bilateral anterior inferior cerebellar territory infarction, encephalitis and gliomas of the brainstem; however, the involvement is usually asymmetric in these entities [2]. Male carriers of the fragile X premutation who develop progressive intention tremor and ataxia accompanied by progressive cognitive and behavioral difficulties can also demonstrate bilateral symmetric signal abnormality in cerebellar peduncles [3]; however there is usually additional signal abnormality in the cerebellum, inferior and lateral to cerebellar nuclei, in this condition. In conclusion, neurologists should be familiar with Wallerian degeneration of bilateral middle cerebellar peduncles in the setting of acute pontine infarction to avoid misdiagnosis as additional infarctions.
Sources of funding None.
Disclosure statement Authors have no relevant financial interest to disclose. Acknowledgments None.
C
Fig. 1. Initial brain MRI demonstrates T2 prolongation (A) and restricted diffusion (B) in left paramedian pons consistent with acute infarction. Follow up MRI after 6 weeks demonstrates symmetric axial T2 hyperintensity in bilateral middle cerebellar peduncles (C).
http://dx.doi.org/10.1016/j.jns.2014.12.044 0022-510X/© 2015 Elsevier B.V. All rights reserved.
Letter to the Editor
References [1] Uchino A, Sawada A, Takase Y, Kudo S. Symmetrical lesions of the middle cerebellar peduncle: MR imaging and differential diagnosis. Magn Reson Med Sci 2004;3: 133–40. [2] De Simone T, Regna-Gladin C, Carriero MR, Farina L, Savoiardo M. Wallerian degeneration of the pontocerebellar fibers. AJNR Am J Neuroradiol 2005;26: 1062–5. [3] Brunberg JA, Jacquemont S, Hagerman RJ, Berry-Kravis EM, Grigsby J, Leehey MA, et al. Fragile X premutation carriers: characteristic MR imaging findings of adult male patients with progressive cerebellar and cognitive dysfunction. AJNR Am J Neuroradiol 2002;23:1757–66.
Seyed Ali Nabavizadeh Department of Radiology, Hospital of the University of Pennsylvania, Philadelphia, PA, United States
257
Ashkan Mowla Department of Neurology, State University of New York at Buffalo, Buffalo, NY, United States Corresponding author at: Department of Neurology, Gates Vascular Institute, School of Medicine and Biomedical Sciences, State University of New York (SUNY) at Buffalo, 100 High Street, Buffalo, NY 14203, United States. Tel.: +1 716 859 7540; fax: +1 716 859 2430. E-mail address: [email protected]. Alexander C. Mamourian Department of Radiology, Hospital of the University of Pennsylvania, Philadelphia, PA, United States 25 October 2014