The Dentato-Rubro-Olivary Tract: Clinical Dimension of This Anatomical Pathway

Abstract

Symptomatic palatal tremor is potentially the result of a lesion in the triangle of Guillain-Mollaret (1931) and is associated with hypertrophic olivary degeneration (HOD) which has characteristic MR findings. The triangle is defined by dentate efferents ascending through the superior cerebellar peduncle and crossing in the decussation of the brachium conjunctivum inferior to the red nucleus, to finaliy reach the inferior olivary nucleus (ION) via the central tegmental tract. The triangle is completed by ION decussating efferents terminating on the original dentate nucleus via the inferior cerebellar peduncle. We can demonstrate the anatomy of this anatomical triangle using a clinical case of palatal tremor presenting with bilateral subjective pulsatile tinnitus along with the pathognomonic MR findings previously described. The hyperintense T2 signal in these patients may be permanent, but the hypertrophied olive normally regresses after 4 years. The temporal relationship between the evolution of the histopathology and the development of the palatal tremor remains unknown as does the natural history of the tremor. Botox injection at the level of tensor and levator veli palatini insertion have been used to treat patients with disabling tremor synchronous tinnitus. A lesion involving the triangle can have a quite varied clinical expression.

Hypertrophic Olivary Degeneration: A Neurosurgical Point of View

“…2 Lesions of the contralateral dentate nucleus, superior cerebellar peduncle, or the ipsilateral central tegmental tract can produce ipsilateral deafferentation of the inferior olivary nucleus and result in HOD. 1,2,4 HOD may occur contralateral, ipsilateral, or bilaterally. Contralateral HOD develops when the primary lesion is localized in the dentate nucleus or in the superior cerebellar peduncle.…”

“…5,[13][14][15] However, neoplastic lesions, inflammatory lesions, infectious lesions, degenerative lesions, and radiosurgery also can cause HOD. 1,4,6,[14][15][16][17][18][19] Supratentorial lesions may cause HOD indirectly by disruption of pathways that modulate olivary function. 5 Most HOD cases occur in adults.…”

“…HOD frequently results from focal lesions of the afferent fibers projecting to the inferior olive within the TGM. [1][2][3][4] Some reports recently showed HOD after many infra-and supratentorial lesions. We present a case of HOD following surgical excision of a tectal plate cavernoma and review the literature with an emphasis on the current knowledge of this disorder.…”

The Far Lateral Transpontomedullary Sulcus Approach to Pontine Cavernous Malformations

“…25 Interruption of physiological circuits, either by hemorrhage or surgical manipulation, of the structures composing the Guillain-Mollaret triangle (red nucleus, dentate nucleus, and olivary nucleus) have been, in some cases, associated with hypertrophic olivary degeneration, with symptoms including palatal myoclonus and "bobbing" ocular nystagmus, or oscillopsia. 8,[26][27][28][29][30][31][32] The superior olivary nucleus is considered part of the pons and is involved in the auditory system, such as sound localization and the measurement of time differences of sound arrival and intensity differences in the ears. 33 This nucleus is not at risk with the TPMS approach.…”

Hypertrophic Olivary Degeneration and Holmes' Tremor Secondary to Bleeding of Cavernous Malformation in the Midbrain

“… 1 The first description of HOD was published by Oppenheim in 1887, and the development of HOD was further described by Guillain and Mollaret in 1931. 2 , 3 …”