If the lesion is located in the tegmentum of the brainstem and involves the CTT, the degeneration occurs to the olive ipsilateral to the side of haemorrhage.

    If the lesion is located in a cerebellar hemisphere and involves the dentate nucleus, the olivary degeneration will be contralateral due to the decussation of the dentato-rubral fibers. If the lesion is located in the brainstem and involves the superior cerebellar peduncles at the level of decussation, the degeneration will occur bilaterally.

    The microscopic changes underlying HOD are characterized by hypertrophy of degenerated neurons followed by hypertrophy of astrocytes. The presence of proliferation of glial cells (gliosis) is controversial. No change is seen on MRI images or on pathologic specimens within a week after the onset of ictus. A hyperintense olive is demonstrable on PD/T2 weighted images 3 weeks after, corresponding to the pathological stage of neuronal hypertrophy. Maximum hypertrophy of the olive is seen 5-15 months after the onset of ictus and corresponds to an associated neuronal and glial hypertrophy.

    Because of projections from the inferior olivary nucleus to the contralateral cerebellum via the inferior cerebellar peduncle (Fig1), contralateral cerebellar changes are associated with the HOD. These changes are characterized by atrophy and increased signal on PD/T2 weighted images of the dentate nucleus and atrophy of the cerebellar cortex.

Fig5 MR images obtained in a patient with brainstem cavernous haemangioma and left HOD. (A) Axial PD-weighted image shows hyposignal suggesting hemosiderin deposits in the left tegmentum of the pons and increased signal at the level of the right dentate nucleus. (B) Coronal T1-weighted image shows prominence of the right cerebellar cortical sulci.

     HOD is known to be accompanied by palatal myoclonus, a recurrent dysrythmic contraction of the soft palate. An hyperintense hypertrophic olivary nucleus, associated with a brainstem tegmental or cerebellar lesion, should not be mistaken for a primary medullary lesion, like an infarct, a neoplasm or a plaque of demyelinating disease.