cerebellum

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Related to Cerebellar peduncle: cerebral peduncle, middle cerebellar peduncle
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Progression of pathological changes in the middle cerebellar peduncle by diffusion tensor imaging correlates with lesser motor gains after pontine infarction.
The MRI showed atrophy of pons, cerebellum and middle cerebellar peduncles with cruciform hyperintense signals in pons (hot cross bun sign).
1,2] JS is an autosomal recessive neurodevelopmental disorder, characterized by molar tooth malformation, a complex brainstem malformation that reflects aplasia and marked hypoplasia of cerebellar vermis, thickened and elongated superior cerebellar peduncles, and deepened interpeduncular fossa that is apparent on axial magnetic resonance imaging (MRI) at the midbrain-hindbrain junction.
Akhlaghi H, Corben L, Georgiou-Karistianis N, Bradshaw J, Storey E, Delatycki MB, Egan GF Superior cerebellar peduncle atrophy in Friedreich's ataxia correlates with disease symptoms.
Likewise, it also has the capability to bleed spontaneously as manifested in our case by hyperdensity in the region of the inferior right cerebellar peduncle on the initial head CT.
Fifth patient with cerebellar signs, showed abnormal high intensity in both inferior cerebellar peduncle.
2), and showed T2 signal change in the brainstem, cerebellar peduncles and cerebellum associated with variable enhancement on contrasted T1-weighted images.
1) This appearance is a result of absence or hypoplasia of the cerebellar vermis, lack of normal dorsal decussation and consequent enlargement of the superior cerebellar peduncles which follow a more horizontal course as they extend perpendicularly to the brainstem between the midbrain and the cerebellum.
Two patients had balance problems which were likely due to involvement of inferior cerebellar peduncles as there was no cerebellar lesion.
A magnetic resonance imaging (MRI) scan revealed T2 hypointense lesion involving right side of tegmentum of pons with extension to superior cerebellar peduncle and vermis with postcontrast enhancement and perilesional oedema (Figure 1).
A third MRI scanning was performed 12 days later, which demonstrated hyperintense lesions on T2W, T1W, FLAIR and diffusion weighted images spreading over the basal ganglia, pons, cerebellum, medulla oblongata and middle cerebellar peduncle (Figure 2).
The lesion in the right cerebellar peduncle extending to the right cerebellar hemisphere was hypo on the T1WI and hyperintense on the T2W/FLAIR images (Figures 2 and 3).
Surgical resection of all or most of the tumor is possible in most cases unless it has spread to the 4th ventricle or cerebellar peduncle.
1-4) While hypertrophic olivary degeneration can occur with any focal lesion that involves the dentato-rubro-olivary pathway, it is typically associated with lesions that involve the superior cerebellar peduncle (dentatorubral tract), the dentate nucleus, or the central tegmental tract.
Small linear hyperintense foci are observed along the anterior and posterior aspects of the medulla oblongata and along the superior and inferior aspects of the left middle cerebellar peduncle.