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

Abstract

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.

A Rare Presentation of Idiopathic Unilateral Hypertrophic Olivary Degeneration

“…HOD diagnosis also requires the T2 hyperintensity to be T1 non-enhancing, as enhancement can represent other etiologies such as inflammation or neoplasm [ 7 ]. Other MRI sequences may become more relevant to identifying HOD in the future if quantitative approaches can be developed, but a small study involving a direct comparison between the current T2 hyperintensity methodology, proton density, and DWI-based approaches showed the best results in identifying HOD via detection of T2 hyperintensity [ 11 ]. The current literature on HOD is limited and is largely confined to case reports, case studies, and research studies limited to patient numbers in the low hundreds [ 12 ].…”

Post-traumatic hypertrophic olivary degeneration associated with Holmes tremor: clinical-imaging correlation

“…La DOH como condición clínica de baja prevalencia, es más frecuente en adultos de género masculino, dentro de las principales causas destacan el ataque cerebrovascular (ACV), el TCE, los tóxicos y las neoplasias, entidades la cuales generan lesiones parciales entre las conexiones de los componentes del TGM (excluyendo lesiones del tracto olivodentado pues estas conllevan a atrofia cerebelosa), causando degeneración transináptica e interrupción de la entrada aferente al núcleo olivar inferior, generando pérdida de la inhibición dentro del circuito y subsecuentemente hipertrofia nuclear prolongada, que a largo plazo culmina en atrofia nuclear, todo lo anterior es correlacionable con la etiología postraumática de la DOH descrita en el presente caso y se relaciona con los hallazgos de revisiones y series de casos establecidos en literatura [10][11][12][13][14] , quienes en conjunto describen como criterios diagnósticos la correlación clínico imagenológica, como se describirá a continuación.…”

“…En cuanto a los signos de neuroimagen característicos de DOH, hasta el momento no se han descrito consensos definitivos de Gold Standard diagnóstico 13,15 , por lo que la mayoría de los autores proponen la RMC como parte del arsenal para definir los criterios radiológicos, que usualmente se definen como un patrón de daño imagenológico unilateral e ipsilateral a la noxa causal ubicada predominantemente en el tronco encefálico en secuencias T2, específicamente en el recorrido del tracto tegmental central del TGM, con aumento de la hiperintensidad olivar inferior en T2 o FLAIR , producto de la Hipertrofia nuclear que suele revelarse 4 a 6 meses después de la instauración del agente etiológico 8,12,14,[16][17][18] .Varios de estos aspectos anteriormente mencionados en la literatura, se acoplan al caso en descripción, puesto que la resonancia magnética craneal del paciente mostró disrupción del TGM, dado por la asociación de una lesión hipointensa mesencefálica en T2 de tipo hemorrágica ipsilateralmente distanciada del núcleo olivar inferior hiperintenso afectado por DOH, en la misma secuencia imagenológica.…”