An article published in Neurología by Dr Sanchez-Hernandez et al.1 presents 2 cases of possible hypertrophic olivary degeneration secondary to a lesion of the upper cerebellar peduncle and central tegmental tract. These cases are similar to others reported previously.2 I would like to comment on the anatomical background they provide in the article.
It is true that the dentate nucleus projects to the red nucleus and projections extend from that location to other structures of the brainstem, including the inferior olivary nucleus and thalamus. Nevertheless, the main dentato-olivary pathway does not pass through the red nucleus. It is a direct pathway that passes by the red nucleus without forming synapses there (Figure 17.24 and Figure 1).3,4 This explains hypertrophic degeneration of the olivary nucleus, one of the best examples of trans-synaptic degeneration in the human brain. If the main dentato-olivary pathway were to form a synapsis in the red nucleus, any trans-synaptic degeneration would take place at that location and not the olivary nucleus, which would mainly receive a second projection. Furthermore, this scenario would not respect the precise topographical relationship existing between the dentate nucleus and the olivary nucleus, which I will explain below.
The lower side of the famous triangle of Guillain-Mollaret, described by Sanchez-Hernandez et al. as a direct olivo-dentate pathway, does not exist, as I have already stated in another publication.5 The main projections from the olivary nucleus pass through the inferior cerebellar peduncle and ascend as climbing fibres (described by Cajal) to the Purkinje cell dendrites but not to the dentate nucleus. It is true that some textbooks (see Figure 20.12)6 include drawings of abundant direct olivo-dentate fibres. While this may accurately describe the brains of certain animal species, it does not correspond to the human brain in which these direct fibres do not exist. The olivo-dentate connection is established by means of collateral projections of climbing fibres and these collateral projections are scarce (“olivocerebellar fibres only branch very sparingly”).7
In any case, the hypothetical olivo-dentate connection is irrelevant to phenomena of interest in clinical medicine, such as palate tremor, since injury to olivary projections (in the inferior cerebellar peduncle) cannot cause hypertrophic olivary degeneration whether directly or indirectly.
Given that these authors not only analyse neuroimaging in hypertrophic olivary degeneration but also elaborate on the neuroanatomy and neuropathology of the dentato-olivary pathway, I would like to have read the name of my professor Jean Lapresle among the references. Lapresle has probably contributed more to this topic than any other author by describing the precise topographical connections between these two structures and the mesencephalic tract of the dentato-olivary pathway adjacent to the red nucleus.4,8–11
Please cite this article as: Zarranz Imirizaldu JJ. Sobre el famoso «triángulo» de Mollaret. Neurología. 2014;29:441–442.
