Abstract:Wallerian degeneration (WD) is the process of demyelination and disintegration of the distal axonal segment following the interruption of the axonal integrity or damage to the neuron. We report a patient having WD of middle cerebellar peduncles due to pontine infarction caused by basilar artery thrombosis. We review the anatomy and discuss the pathogenesis of this condition.
“…[ 10 ] In this study, bilateral MCPs lesions appeared after the unilateral and isolated infarction involving the ventral pons without additional abnormalities, which is consistent with the diagnosis of WD of MCPs, owing to damage of the above-mentioned anatomical structures. In addition, it has been reported that the primary infarction often involves the basis pontis, and that paramedian pontine infarction is the most common location,[ 3 7 11 12 13 14 ] which is consistent with observations in this study. Moreover, the BA in previously reported cases was normal,[ 11 ] or exhibited atherosclerosis plaque formation,[ 12 ] severe stenosis, or occlusion.…”
Section: Discussionsupporting
confidence: 92%
“…Moreover, the BA in previously reported cases was normal,[ 11 ] or exhibited atherosclerosis plaque formation,[ 12 ] severe stenosis, or occlusion. [ 13 ] In this study, BA lesions were also nonspecific; thus, we suspect that the etiology of pons infarction might have been small vascular disease, atherosclerotic stenotic disease of the BA, or branch artery disease.…”
Section: Discussionmentioning
confidence: 82%
“…With advances in MRI, however, some studies have reported signal intensity changes in DWI or ADC maps, and not only limited to the corticospinal tracts. [ 13 15 ] De Simone et al [ 5 ] described two cases with WD of the pontocerebellar tracts, with abnormal hyperintense signals on T2WI and DWI demonstrated for 5 and 7 months after infarction. Fitzek et al [ 3 ] reported three cases with large paramedian pons infarctions, no abnormal signal of MCPs was detected on T2WI and DWI within 2 weeks after infarction, while bright hyperintensities on T2WI and moderately increased signal intensities on DWI were found after 4 months.…”
Section: Discussionmentioning
confidence: 99%
“…The aforementioned case reports suggest that conventional MRI can only reveal WD of MCPs in the subacute or chronic phases;[ 3 5 ] however, others do not support this viewpoint. [ 12 13 ] Musson et al [ 12 ] described an individual who experienced progressive stroke in the pons and underwent repeated MRI at days 4, 9, and 23 after onset due to neurological deterioration. The acute WD of bilateral MCPs was detected on the final MRI, with high-intensity signals on T2WI and DWI, and low-intensity signals on ADC maps.…”
Section: Discussionmentioning
confidence: 99%
“…The acute WD of bilateral MCPs was detected on the final MRI, with high-intensity signals on T2WI and DWI, and low-intensity signals on ADC maps. Gala et al [ 13 ] described a patient with WD of MCPs due to pontine infarction caused by BA thrombosis. The acute WD was detected on MRI 21 days after onset with signal features similar to those reported by Musson et al [ 12 ] However, control MRI performed 12 weeks later revealed persistent hyperintense signals on T2WI, mild hyperintense signals on DWI and ADC maps, and gliosis in the midbrain and ventral pons.…”
Background:Wallerian degeneration (WD) of bilateral middle cerebellar peduncles (MCPs) can occur following pontine infarction, but its characteristics have not yet been clarified because of the low incidence. Thus, the present study discussed the clinical and radiological features to improve the awareness of this disease.Methods:Clinical and radiological information from consecutive individuals diagnosed with WD of bilateral MCPs following pontine infarction in three hospitals over the past 4 years between October 2012 and October 2016 were retrospectively investigated and compared with a control group (patients with pontine infarction had no secondary WD).Results:This study involved 30 patients with WD of MCPs, with a detection rate of only 4.9%. The primary infarctions (χ2 =24.791, P = 0.001, vs. control group) were located in the paramedian pons in 21 cases (70.0%), and ventrolateral pons in nine cases (30.0%). WD of the MCPs was detected 8–24 weeks after pons infarction using conventional magnetic resonance imaging (MRI); all secondary WDs were asymptomatic and detected incidentally. All WD lesions exhibited bilateral, symmetrical, and boundary blurring on MRI. The signal features were hypointense on T1-weighted imaging, hyperintense on T2-weighted imaging and fluid-attenuated inversion recovery, and slightly hyperintense or isointense on diffusion-weighted imaging and apparent diffusion coefficient maps. Secondary brainstem atrophy was found in six (20.0%) cases. A Modified Rankin Scale score 0–2 was found in 10 (33.3%) cases and score >2 in 20 (66.7%) cases at 90 days after discharge, and the short-term prognosis was worse than that in control group (χ2 =12.814, P = 0.001).Conclusions:Despite the rarity of bilateral and symmetrical lesions of MCPs, secondary WD should be highly suspected if these lesions occur within 6 months after pontine infarction, particularly paramedian pons. Conventional MRI appears to be a relatively sensitive method for detecting WD of MCPs, which might affect the short-term prognosis.
“…[ 10 ] In this study, bilateral MCPs lesions appeared after the unilateral and isolated infarction involving the ventral pons without additional abnormalities, which is consistent with the diagnosis of WD of MCPs, owing to damage of the above-mentioned anatomical structures. In addition, it has been reported that the primary infarction often involves the basis pontis, and that paramedian pontine infarction is the most common location,[ 3 7 11 12 13 14 ] which is consistent with observations in this study. Moreover, the BA in previously reported cases was normal,[ 11 ] or exhibited atherosclerosis plaque formation,[ 12 ] severe stenosis, or occlusion.…”
Section: Discussionsupporting
confidence: 92%
“…Moreover, the BA in previously reported cases was normal,[ 11 ] or exhibited atherosclerosis plaque formation,[ 12 ] severe stenosis, or occlusion. [ 13 ] In this study, BA lesions were also nonspecific; thus, we suspect that the etiology of pons infarction might have been small vascular disease, atherosclerotic stenotic disease of the BA, or branch artery disease.…”
Section: Discussionmentioning
confidence: 82%
“…With advances in MRI, however, some studies have reported signal intensity changes in DWI or ADC maps, and not only limited to the corticospinal tracts. [ 13 15 ] De Simone et al [ 5 ] described two cases with WD of the pontocerebellar tracts, with abnormal hyperintense signals on T2WI and DWI demonstrated for 5 and 7 months after infarction. Fitzek et al [ 3 ] reported three cases with large paramedian pons infarctions, no abnormal signal of MCPs was detected on T2WI and DWI within 2 weeks after infarction, while bright hyperintensities on T2WI and moderately increased signal intensities on DWI were found after 4 months.…”
Section: Discussionmentioning
confidence: 99%
“…The aforementioned case reports suggest that conventional MRI can only reveal WD of MCPs in the subacute or chronic phases;[ 3 5 ] however, others do not support this viewpoint. [ 12 13 ] Musson et al [ 12 ] described an individual who experienced progressive stroke in the pons and underwent repeated MRI at days 4, 9, and 23 after onset due to neurological deterioration. The acute WD of bilateral MCPs was detected on the final MRI, with high-intensity signals on T2WI and DWI, and low-intensity signals on ADC maps.…”
Section: Discussionmentioning
confidence: 99%
“…The acute WD of bilateral MCPs was detected on the final MRI, with high-intensity signals on T2WI and DWI, and low-intensity signals on ADC maps. Gala et al [ 13 ] described a patient with WD of MCPs due to pontine infarction caused by BA thrombosis. The acute WD was detected on MRI 21 days after onset with signal features similar to those reported by Musson et al [ 12 ] However, control MRI performed 12 weeks later revealed persistent hyperintense signals on T2WI, mild hyperintense signals on DWI and ADC maps, and gliosis in the midbrain and ventral pons.…”
Background:Wallerian degeneration (WD) of bilateral middle cerebellar peduncles (MCPs) can occur following pontine infarction, but its characteristics have not yet been clarified because of the low incidence. Thus, the present study discussed the clinical and radiological features to improve the awareness of this disease.Methods:Clinical and radiological information from consecutive individuals diagnosed with WD of bilateral MCPs following pontine infarction in three hospitals over the past 4 years between October 2012 and October 2016 were retrospectively investigated and compared with a control group (patients with pontine infarction had no secondary WD).Results:This study involved 30 patients with WD of MCPs, with a detection rate of only 4.9%. The primary infarctions (χ2 =24.791, P = 0.001, vs. control group) were located in the paramedian pons in 21 cases (70.0%), and ventrolateral pons in nine cases (30.0%). WD of the MCPs was detected 8–24 weeks after pons infarction using conventional magnetic resonance imaging (MRI); all secondary WDs were asymptomatic and detected incidentally. All WD lesions exhibited bilateral, symmetrical, and boundary blurring on MRI. The signal features were hypointense on T1-weighted imaging, hyperintense on T2-weighted imaging and fluid-attenuated inversion recovery, and slightly hyperintense or isointense on diffusion-weighted imaging and apparent diffusion coefficient maps. Secondary brainstem atrophy was found in six (20.0%) cases. A Modified Rankin Scale score 0–2 was found in 10 (33.3%) cases and score >2 in 20 (66.7%) cases at 90 days after discharge, and the short-term prognosis was worse than that in control group (χ2 =12.814, P = 0.001).Conclusions:Despite the rarity of bilateral and symmetrical lesions of MCPs, secondary WD should be highly suspected if these lesions occur within 6 months after pontine infarction, particularly paramedian pons. Conventional MRI appears to be a relatively sensitive method for detecting WD of MCPs, which might affect the short-term prognosis.
ObjectiveWallerian degeneration (WD) of the middle cerebellar peduncles (MCPs) following pontine infarction is a rare secondary degenerative neurological condition. Due to its infrequency, there is limited research on its characteristics.MethodsThis study aims to present three cases of WD of MCPs following pontine infarction and to analyze the prognosis, clinical manifestations, and neuroimaging features by amalgamating our cases with previously reported ones.ResultsThe cohort consisted of 25 cases, comprising 18 men and 7 women aged 29 to 77 years (mean age: 66.2 years). The majority of patients (94%) exhibit risk factors for cerebrovascular disease, with hypertension being the primary risk factor. Magnetic resonance imaging (MRI) can detect WD of MCPs within a range of 21 days to 12 months following pontine infarction. This degeneration is characterized by bilateral symmetric hyperintensities on T2/FLAIR‐weighted images (WI) lesions in the MCPs. Moreover, restricted diffusion, with hyperintensity on diffusion‐weighted imaging (DWI) and low apparent diffusion coefficient (ADC) signal intensity may be observed as early as 21 days after the infarction. Upon detection of WD, it was observed that 20 patients (80%) remained asymptomatic during subsequent clinic visits, while four (16%) experienced a worsening of pre‐existing symptoms.ConclusionsThese findings underscore the importance of neurologists enhancing their understanding of this condition by gaining fresh insights into the neuroimaging characteristics, clinical manifestations, and prognosis of individuals with WD of bilateral MCPs.
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