Bilateral Wallerian degeneration of the medial cerebellar peduncles after ponto-mesencephalic infarction

doi:10.1016/S0720-048X(03)00132-3

European Journal of Radiology

Volume 49, Issue 3, March 2004, Pages 198-203

https://doi.org/10.1016/S0720-048X(03)00132-3 Get rights and content

Abstract

Three patients with acute large paramedian ponto-mesencephalic infarctions developed a bilateral retrograde degeneration of the medial cerebellar peduncles within 4 months after the insult. In an initial magnetic resonance imaging (MRI) within the first 2 weeks, the medial cerebellar peduncles showed normal intensities, but a control MRI after 4 months showed bright hyperintensities in the T2-TSE weighted images, and moderately increased signal intensities in echo planar imaging–diffusion weighted imaging were seen, possibly representing bilateral Wallerian degeneration of the cerebellar-pontine fibers.

Introduction

Wallerian degeneration of the tractus pyramidalis after lesions of the motor cortex or the brainstem is well described [1], [2], [3], [4] and independently of the kind of lesion, specific magnetic resonance imaging (MRI) signal changes develop in the corticospinal tract during the following months [5]. After peripheral and central lesions Wallerian degeneration is described such as degeneration within the optic nerves after lateral geniculate body lesion [4] or olivary degeneration after intracranial haemorrhage or trauma [6], [7], [8], [9], [10], [11]. In Wallerian degeneration myelinated fibres show a loss of the cytoplasmic circumferential bands and longitudinal columns and their associated membrane pores [12]. Macrophage recruitment for myelin removal also takes place [13]. These changes of demyelination lead to signal increase in T2-weighted images (T2w), which is also measurable by diffusion weighted imaging (DWI) [14], [15], [16], [17].

Section snippets

Patients

Three patients with acute paramedian ponto-mesencephalic brainstem infarction and consequent degeneration of the medial cerebellar peduncle were included.

CT/MRI

Computer tomography (CT) scan without application of contrast medium was performed immediately after admission of the patient to hospital. Up to three MRI were performed: the first MRI (MR0) in the first day after onset of symptoms or admission of the patient to hospital (echo planar imaging (EPI) DWI: TR/TE=4000/103 ms, with separately

General characteristics

There were three patients one men and two women (age 73, 62, 59 years) with acute ponto-mesencephalic paramedian brain stem infarctions. All three patients had initial symptoms of gait ataxia, dysarthria and contralateral hemiparesis with good improvement during the following 4–5 months. At the follow up only mild gait disturbance and slight hemiparesis was found.

MRI

In the acute phase all three patients had large paramedian ponto-mesencephalic stroke lesions covering the crossing area of the

Discussion

We describe three patients with first time acute brain stem stroke and corresponding large unilateral paramedian ponto-mesencephalic ischemic brain stem lesions. The majority of brain stem infarctions do not cross the midline [18], [19], [20]. Only in few cases, especially in basilar artery thrombosis, bilateral brain stem infarctions may occur [19], [20], [21].

Brain stem infarctions, except those due to basilary thrombosis, have a good prognosis concerning the clinical outcome [22]. Wallerian

Conclusion

Large paramedian lesions which cover the crossing zone of the medial cerebellar peduncles can lead to a bilateral Wallerian degeneration of the PCTs.

References (32)

V. Sawlani et al.
MRI demonstration of Wallerian degeneration in various intracranial lesions and its clinical implications
J. Neurol. Sci.
(1997)
T. Sakai et al.
Olivocerebellar retrograde trans-synaptic degeneration from the lateral cerebellar hemisphere to the medial inferior olivary nucleus in an infant
Brain Dev.
(1994)
W. Bruck et al.
The role of complement in myelin phagocytosis during PNS Wallerian degeneration
J. Neurol. Sci.
(1991)
J. Ono et al.
Differentiation of dys- and demyelination using diffusional anisotropy
Pediatr. Neurol.
(1997)
J. Ono et al.
Differentiation between dysmyelination and demyelination using magnetic resonance diffusional anisotropy
Brain Res.
(1995)
S. Fitzek et al.
Time course of lesion development in patients with acute brain stem infarction and correlation with NIHSS score
Eur. J. Radiol.
(2001)
P. Brodal et al.
Organization of the pontine nuclei
Neurosci. Res.
(1992)
D.W. Kang et al.
Diffusion-weighted imaging in Wallerian degeneration
J. Neurol. Sci.
(2000)
C. Pierpaoli et al.
Water diffusion changes in Wallerian degeneration and their dependence on white matter architecture
Neuroimage
(2001)
M. Nakane et al.
MR detection of secondary changes remote from ischemia: preliminary observations after occlusion of the middle cerebral artery in rats
Am. J. Neuroradiol.
(1997)

M. Koshinaga et al.

The temporal and spatial activation of microglia in fiber tracts undergoing anterograde and retrograde degeneration following spinal cord lesion

J. Neurotrauma

(1995)

J.L. Becerra et al.

MR-pathologic comparisons of Wallerian degeneration in spinal cord injury

Am. J. Neuroradiol.

(1995)

M. Savoiardo et al.

The effects of Wallerian degeneration of the optic radiations demonstrated by MRI

Neuroradiology

(1992)

T. Hanihara et al.

Hypertrophy of the inferior olivary nucleus in patients with progressive supranuclear palsy

Eur. Neurol.

(1998)

G.M. Shepherd et al.

Midbrain tremor and hypertrophic olivary degeneration after pontine hemorrhage

Mov. Disord.

(1997)

T. Yamamoto et al.

Thalamo-olivary degeneration in a patient with laryngopharyngeal dystonia

J. Neurol. Neurosurg. Psychiatry

(1995)

Cited by (22)

Imaging secondary neuronal degeneration
2022, Radiologia
La degeneración neuronal distal (DND) define el proceso de desintegración de una neurona o un circuito neuronal como consecuencia de una noxa localizada a distancia. Es un hallazgo frecuente debido al creciente número de realización de pruebas de imagen y a que refleja un desenlace común a múltiples etiologías. El objetivo de este artículo es definir los distintos tipos de daño neuronal a distancia, revisar la anatomía y función de los tractos más frecuentemente afectados e ilustrar la DND con esquemas y casos representativos de la práctica habitual.
El conocimiento de la respuesta a distancia esperable según la topografía de una lesión neuronal es crucial para evitar errores diagnósticos. La degeneración axonal y transináptica puede ser tanto anterógrada como retrógrada. Los estudios de metabolismo cerebral, las secuencias de perfusión y de difusión muestran cambios cada vez más precoces del mismo proceso con los que debemos estar familiarizados.
Distal nerve degeneration refers to the process of disintegration of a neuron or neuronal circuit as a consequence of distal damage. The end result of multiple etiologies, this finding is becoming common due to the increasing number of imaging tests done. This paper aims to define the different types of distal nerve damage, review the anatomy and function of the most commonly affected tracts, and illustrate distal nerve damage through diagrams and representative cases from routine practice.
Knowing the distant response that can be expected according to the topography of a neuronal lesion is crucial to avoid diagnostic errors. Axonal degeneration and transsynaptic degeneration can be both antegrade and retrograde. Studies of cerebral metabolism, perfusion sequences, and diffusion sequences are showing increasingly earlier changes related to the same process; radiologists need to be aware of these changes.
Clinical Application of Diffusion Tensor Imaging in Chiari Malformation Type I– Advances and Perspectives. A Systematic Review
2021, World Neurosurgery
Citation Excerpt :
Although the literature is sparse and the current data are based on single cohort studies, the authors of all studies outlined earlier suggest a specific pathology of MCPs associated with the symptomatic CMI presentation. A clinical presentation including ataxia, vertigo, dysarthria, and nystagmus might be observed not only in patients with CMI but also in individuals affected by a paramedian pontine stroke resulting in pontine nuclei injury and Wallerian degeneration of MCP fibers.41-43 Changes in DTI parameters observed in the latter entity include a decrease of AD as well as an increase of MD in MCPs and thus correspond with the findings of Eshetu et al.10 and Abeshaus et al.,18 respectively.
Diffusion tensor imaging (DTI) application in Chiari malformation type I (CMI) is still poorly defined. This study aimed to systematically review the literature and propose perspectives toward the clinical application of DTI in CMI.
PubMed and Embase were searched for English-language articles published until October 20, 2020. Clinical studies and case series, evaluating fractional anisotropy (FA), mean diffusivity (MD), axial diffusivity (AD), or radial diffusivity values in patients with CMI, were included.
Eight articles were included. Lower FA values were found at the syrinx level, which decreased with syrinx extent and intensity of symptoms, reflecting myelopathy severity. Decreased AD and MD in the middle cerebellar peduncles in symptomatic patients with CMI might explain the presence of cerebellar signs. Increased FA in various supratentorial structures positively correlated with pain severity. Worse performance in neuropsychological tests correlated with decreased FA, increased MD, and radial diffusivity, reflecting axonal degeneration. Postoperative FA decrease in the brainstem compression area reflects successful decompression. A positive correlation was found between the extent of tonsillar ectopia and increased FA, MD, and AD values, which could act as an early indicator of acute brainstem compression.
DTI might provide a valuable insight into the neurobiological foundation of symptomatic CMI presentation. The severity of white matter injury evident on DTI could serve as a reliable predictor of postoperative outcomes, therefore facilitating selection of appropriate surgical candidates. Postinterventional DTI reassessment might enable differentiation between unsuccessful surgical technique and irreversible myelopathy. The extent of tonsillar ectopia reflects the severity of microstructural brainstem injury.
Bilateral wallerian degeneration of the middle cerebellar peduncles secondary to pontine infarction: A case series
2018, Journal of the Neurological Sciences
Citation Excerpt :
In our patients, bilateral MCPs show hyperintense on T2- weighted and FLAIR images on follow-up, which are correlated to histologic and metabolic features of the third stage of WD. There is also case reports that increased signal intensities in the MCPs on DWI can persist for 4 months later after stroke [16]. In our study, a slightly restricted diffusion in the MCPs is revealed in two patients on follow-up (mean time: 3.5 months).
Wallerian degeneration (WD) of middle cerebellar peduncles (MCPs) secondary to pontine infarction is rarely reported in the literature. Our aim in this study is to characterize its clinical and neuroradiological features.
A retrospective review of 7 patients from a single institution was conducted. Only patients with pontine infarction and subsequent degeneration of the MCPs were included in the analysis. The features of clinical presentation and neuroimaging finding were summarized by our experienced neurologists.
Seven patients (5 male, 2 female), ranging in age from 50 to 77 years, satisfied the inclusion criteria. All patients had cardiovascular risk factors and hypertension was the most common one. Almost all of the patients had hemiparesis and dysarthria, and could achieved good clinical outcome. On the initial scan, hyperintense on T2- and diffusion-weighted images suggested the acute pontine infarction. On the follow-up scan, however, hyperintensities of bilateral MCPs on T2-weight and FLAIR images were apparently demonstrated in all patients. The specific lesions in the MCPs were attributed to bilateral WD of the pontocerebellar fibres secondary to pontine infarction.
WD should be taken into account when patients are initially diagnosed with paramedian pontine infarction and follow-up MRI manifest as symmetrical hyperintense in the MCPs.
Bilateral wallerian degeneration of the pontocerebellar fibers secondary to pontine stroke: A report of 4 cases
2010, Radiologia
La degeneración walleriana es una desmielinización de los axones neuronales distales por una daño proximal de cualquier etiología.
Se presentan los hallazgos de resonancia magnética en 4 pacientes con ictus de tronco y signos de degeneración walleriana de los haces pontocerebelosos. Para ello se revisan las resonancias magnéticas de 4 pacientes con lesiones pontinas en fase subaguda o crónica, y las alteraciones de señal en los pedúnculos cerebelosos medios. Los hallazgos en las secuencias potenciadas en T2 y en difusión se relacionan con el tiempo de evolución y la etiología del ictus.
Wallerian degeneration occurs after demyelination of the distal neuronal axons due to proximal damage of any type.
We present the magnetic resonance findings in four patients with brainstem stroke and signs of Wallerian degeneration in the pontocerebellar tracts.
We reviewed the magnetic resonance studies in four patients with subacute or chronic stage pontine lesions and the signal alterations at the level of the medial cerebellar peduncles. We correlated the findings in T2-weighted sequences and diffusion-weighted sequences with the time of evolution and etiology of the stroke.
Bilateral Wallerian degeneration of the middle cerebellar peduncles due to unilateral pontine infarction: A morphologic and spectroscopic study
2006, Journal of Neuroradiology
We report the case of a patient with bilateral and symmetrical T2 hyperintensities of the middle cerebellar peduncles. She had a history of left pontine infarction 8 months before. This was attributed to bilateral Wallerian degeneration.
MR Spectroscopy showed decreased N-acetyl aspartate/Creatine (NAA/Cr) ratio in the cerebellar peduncles as well as in the whole cerebellum. We hypothesize that this could reflect neuronal degeneration following a stroke.
Nous relatons le cas d’une patiente de 70 ans avec un antécédent d’accident ischémique constitué (AIC) unilatéral de la protubérance. La récupération clinique avait été complète. Une IRM cérébrale réalisée 8 mois plus tard révélait l’AIC unilatéral ainsi que des hypersignaux symétriques et bilatéraux en T2 des pédoncules cérébelleux moyens qui ont été mis sur le compte d’une dégénérescence wallérienne bilatérale.
La spectroscopie IRM a révélé une baisse du ratio N-acetyl aspartate/Creatine (NAA/Cr) dans les pédoncules cérébelleux ainsi que dans l’ensemble du cervelet. Nous émettons l’hypothèse que cela reflète la dégénérescence neuronale suivant un AIC.
Clinical analysis of two cases of spastic paraplegia caused by Wallerian degeneration in lateral corticospinal tracts after pontine infarction
2021, Chinese Journal of Neurology

View all citing articles on Scopus

View full text

Bilateral Wallerian degeneration of the medial cerebellar peduncles after ponto-mesencephalic infarction

Abstract

Introduction

Section snippets

Patients

CT/MRI

General characteristics

MRI

Discussion

Conclusion

J. Neurol. Sci.

Brain Dev.

J. Neurol. Sci.

Pediatr. Neurol.

Brain Res.

Eur. J. Radiol.

Neurosci. Res.

J. Neurol. Sci.

Neuroimage

MR detection of secondary changes remote from ischemia: preliminary observations after occlusion of the middle cerebral artery in rats

Am. J. Neuroradiol.

The temporal and spatial activation of microglia in fiber tracts undergoing anterograde and retrograde degeneration following spinal cord lesion

J. Neurotrauma

MR-pathologic comparisons of Wallerian degeneration in spinal cord injury

Am. J. Neuroradiol.

The effects of Wallerian degeneration of the optic radiations demonstrated by MRI

Neuroradiology

Hypertrophy of the inferior olivary nucleus in patients with progressive supranuclear palsy

Eur. Neurol.

Midbrain tremor and hypertrophic olivary degeneration after pontine hemorrhage

Mov. Disord.

Thalamo-olivary degeneration in a patient with laryngopharyngeal dystonia

J. Neurol. Neurosurg. Psychiatry