Bilateral Hypertrophic Olivary Degeneration Following Brainstem Insult: A Retrospective Review and Examination of Causative Pathology

Zhu

et al. 2023

Preprint

Hypertrophic olivary degeneration (HOD) is a transsynaptic degeneration characterized by the disruption of dentato-rubro-olivary tract, a region also known as the Guillain-Mollaret triangle (GMT), which often occurs because of posterior fossa or brainstem lesions. Infratentorial cerebrovascular diseases (ICVD) has been linked to HOD in previous studies. The underlying mechanism of ICVD patients developed HOD, however, remains undetermined. In this study, we analyzed clinical features of 334 patients with ICVD and the results showed that brainstem hemorrhage was most likely to develop HOD (43.5%) among four types of ICVD. In addition, multivariate regression analysis revealed that PSP-RS was an independent risk factor (OR = 6.69, 95% CI: 1.58–28.32) for ICVD-HOD, and the presence of HOD was obviously higher in PSP-RS patients complicated by ICVD (43.5%) than that in PSP-RS patients uncomplicated by ICVD (4.2%). Furthermore, DTI study showed that the PSP-RS, HOD, PSP-RS with HOD, and PSP-RS with ICVD-HOD groups displayed the impaired microstructural integrity of the GMT compared to iPD and HCs groups. Moreover, some DTI parameters of the GMT showed correlation with the Progressive Supranuclear Palsy Rating Scale (PSPRS) score in PSP-RS patients. Taken together, our study demonstrated that PSP-RS was an independent etiological factor for ICVD-HOD which might due to impaired microstructural integrity of the GMT. More importantly, these findings suggest that PSP-RS patients should aim for the prevention of ICVD to reduce the occurrence of HOD.

Section: Discussionmentioning

confidence: 99%

Progressive Supranuclear Palsy drives the Infratentorial Cerebrovascular Diseases-associated Hypertrophic Olivary Degeneration

Zhu

et al. 2023

Preprint

“…Although there are reports of HOD without visible causative lesions on MRI ( 36 ), the correlation of HOD development with preceding lesions in the GMT is undoubtedly proven, and for a circumscribed lesion within the GMT, the side of HOD occurrence is well–predictable ( 2 , 10 ). While the actual etiology of the underlying index lesion seems to be non-relevant ( 18 , 26 , 37 , 38 ), our study focused on stroke patients, because this allowed for both a precise localization of the index lesion on MRI and a precise determination of the index lesion onset. Nevertheless, it is yet unknown how frequently a lesion within the GMT causes a HOD and to what extent the anatomical structures in the GMT must be affected.…”

Section: Discussionmentioning

confidence: 99%

Qualitative and quantitative detectability of hypertrophic olivary degeneration in T2, FLAIR, PD, and DTI: A prospective MRI study

et al. 2022

Purpose:Hypertrophic olivary degeneration (HOD) is a pathology of the inferior olivary nucleus (ION) that occurs after injuries to the Guillain-Mollaret triangle (GMT). Lacking a diagnostic gold standard, diagnosis is usually based on T2 or FLAIR imaging and expert rating. To facilitate precise HOD diagnosis in future studies, we assessed the reliability of this rater-based approach and explored alternative, quantitative analysis.MethodsPatients who had suffered strokes in the GMT and a matched control group prospectively underwent an MRI examination including T2, FLAIR, and proton density (PD). Diffusion tensor imaging (DTI) was additionally performed in the patient group. The presence of HOD was assessed on FLAIR, T2, and PD separately by 3 blinded reviewers. Employing an easily reproducible segmentation approach, relative differences in intensity, fractional anisotropy (FA), and mean diffusivity (MD) between both IONs were calculated.ResultsIn total, 15 patients were included in this study. The interrater reliability was best for FLAIR, followed by T2 and PD (Fleiss κ = 0.87 / 0.77 / 0.65). The 3 raters diagnosed HOD in 38–46% (FLAIR), 40–47% (T2), and 53–67% (PD) of patients. False-positive findings in the control group were less frequent in T2 than in PD and FLAIR (2.2% / 8.9% / 6.7%). In 53% of patients, the intensity difference between both IONs on PD was significantly increased in comparison with the control group. These patients also showed significantly decreased FA and increased MD.ConclusionWhile the rater-based approach yielded the best performance on T2 imaging, a quantitative, more sensitive HOD diagnosis based on ION intensities in PD and DTI imaging seems possible.

“…8) [41]. However, many case reports of metronidazole encephalopathy reported synchronous involvement of the red nucleus and dentate nucleus [41], which are components of the Guillain-Mollaret triangle [42]. In addition, there may be bilateral T2 intensities in the dentate nucleus in HE related to methyl bromide poisoning, enteroviral encephalomyelitis, and maple syrup urine disease [43][44][45].…”

Section: Deep Gray Matter and Connectivitymentioning

confidence: 99%

Hepatic encephalopathy on magnetic resonance imaging and its uncertain differential diagnoses: a narrative review

Lim

Hahm

Lee

2023

JYMS

Hepatic encephalopathy (HE) is a severe neuropsychiatric abnormality in patients with either acute or chronic liver failure. Typical brain magnetic resonance imaging findings of HE are bilateral basal ganglia high signal intensities due to manganese deposition in chronic liver disease and hyperintensity in T2, fluid-attenuated inversion recovery, or diffusion-weighted imaging (DWI) with hemispheric white matter changes including the corticospinal tract. Low values on apparent diffusion coefficient mapping of the affected area on DWI, indicating cytotoxic edema, can be observed in acute HE. However, neuropsychological impairment in HE ranges from mild deficits in psychomotor abilities affecting quality of life to stupor or coma with higher grades of hepatic dysfunction. In particular, the long-lasting compensatory mechanisms for the altered metabolism in chronic liver disease make HE imaging results variable. Therefore, the clinical relevance of imaging findings is uncertain and differentiating HE from other metabolic diseases can be difficult. The recent introduction of concepts such as "acute-on-chronic liver failure (ACLF)," a new clinical entity, has led to a change in the clinical view of HE. Accordingly, there is a need to establish a corresponding concept in the field of neuroimaging diagnosis. Herein, we review HE from a historical and etiological perspective to increase understanding of brain imaging and help establish an imaging approach for advanced new concepts such as ACLF. The purpose of this manuscript is to provide an understanding of HE by reviewing neuroimaging findings based on pathological and clinical concepts of HE, thereby assisting in neuroimaging interpretation.