The tensor veli palatini is innervated by the medial pterygoid nerve, a branch of mandibular nerve, the third branch of the trigeminal nerve (CN V) – the only muscle of the palate not innervated by the vagus nerve.
A focal, hyperintense, nonenhancing lesion and enlargement of the olivary nucleus with a coexisting pontine lesion suggest an injury of the dentato-rubro-olivary pathway, findings that are consistent with hypertrophic olivary degeneration). (3-5)
Hypertrophic olivary degeneration is a form of trans-synaptic degeneration caused by an insult to the neuronal connections of the dentato-rubro-olivary pathway (i.e., the triangle of Guillain and Mollaret) by a primary brainstem inury. (1,2) Disruption of this neuronal pathway affects the reflex arc that controls fine voluntary movements, resulting in signs and symptoms such as palatal myoclonus and dentatorubral tremor. (2,3) This type of astrocytic degeneration has been reported in both children and adults; there is no predilection to either sex. (4)
At any given time following a primary brainstem injury, there may be focal enlargement rather than atrophy of the inferior olivary nucleus. This finding is characteristically identified on MRI. However, failure to properly identify the enlargement may result in a misdiagnosis (e.g, a tumor or multiple sclerosis). (1,5,6)
The Guillain-Mollaret triangle is composed of the dentate nucleus, the red nucleus, and the inferior olivary nucleus. The red nucleus and the ipsilateral inferior olivary nucleus are connected via the central tegmental tract, and the dentate nucleus connects to the contralateral red nucleus through the superior cerebellar peduncle. There are no direct connections between the inferior olivary nucleus and the contralateral dentate nucleus. (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. (2,4)
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.
The central tegmental tract has several connections to the nucleus ambiguous, which gives rise to efferent motor fibers of the vagus nerve that innervates the muscles that control palatal movement. (2,5)
The clinical manifestations of hypertrophic olivary degeneration probably reflect a loss of inhibitory control as a result of disruption of the dentato-rubroolivary pathway. (1-3)
Below from this site:
The red nucleus receives most of its fibres from the dentate, but there are also contributions from the emboliform and globose nuclei. Efferents from the dentate nucleus ascend through the superior cerebellar peduncle or brachium conjunctivum and decussate in the caudal midbrain to finally reach the contralateral red nucleus. The rostral third of the red nucleus (parvicellular part) is the end point of the dentatorubral pathway where they have asymmetrical synapses. Fibers from the parvicellular part of the red nucleus descend ipsilaterally via the central tegmental tract to reach the dorsal lamella of the principal inferior olivary nucleus. The triangle is completed by decussating fibers originating from the inferior olivary nucleus, forming the largest component of the inferior cerebellar peduncle (corpus restiform) and terminating on the original dentate nucleus . M. Goyal, E. Versnick, P. Tuite et al., “Hypertrophic olivary degeneration: metaanalysis of the temporal evolution of MR findings,” American Journal of Neuroradiology, vol. 21, no. 6, pp. 1073–1077, 2000.
This is a bidirectional pathway, a coupled system likely to be of a feedback function, because there are also projections from the dentate nuclei to the contralateral caudal inferior olivary nucleus. The inferior olive has an intrinsic slow, rhythmic, and spontaneous activity . M. Goyal, E. Versnick, P. Tuite et al., “Hypertrophic olivary degeneration: metaanalysis of the temporal evolution of MR findings,” American Journal of Neuroradiology, vol. 21, no. 6, pp. 1073–1077, 2000.
it is olivary deafferentation that is thought to trigger the hypertrophic degenerative changes .
A midline lesion at the level of the brachium conjunctivum will result in bilateral HOD as the ducassating fibers of the right and left dentate olivary tracts are likely to be involved.
Many collaterals from the reticular formation and from the pyramids enter the inferior olivary nucleus.
Removal of one cerebellar hemisphere is followed by atrophy of the opposite olivary nucleus. Wikiapedia
The majority of red nucleus axons do not project to the spinal cord, but instead (via its parvocellular part) relay information from the motor cortex to the cerebellum through the inferior olivary complex, an important relay center in the medulla.
Inferior Olive Function
It is closely associated with the cerebellum, meaning that it is involved in control and coordination of movements, sensory processing and cognitive tasks likely by encoding the timing of sensory input independently of attention or awareness .  Lesions to the inferior olive have been associated with a decreased ability to perfect highly specialized motor tasks, such as improving one’s accuracy in hitting a target with a ball.
Alternatively, the downward smooth pursuit pathway could pass through the dentate nuclei.
Strategies which activate reflexogenic pathways such as optokinetic stimulations along with voluntary planned movements such as “no no” and “yes yes” head movement ( I usually do this with a head tilt ipsilateral to the weaker cerebellum and opposite to the weaker prefrontal cortex) which may effect activation / afferentation to the inferior olivary nucleus through projections from the reticular formation (possibly some through the cortiobulbar pathways). There are several other tricks I’ve used that have worked with these cases as well. There may be some aspect of dentate activation with smooth pursuits downward which the reflexogenic aspect of a downward optokinetic would create. Generally the OPK that augments the myoclonus has been in a oblique direction. Something that can be done using an app on an iPhone or iPad (OPTOK).
The most interesting aspect of my success has involved the use of endo-nasal balloon manipulations. These are done specifically based on testing done with the patient standing. There are various anatomical area’s challenged by pushing lightly and looking for an unstable reaction. These findings correlate to body positions and specific balloon placements within the nasal passages. The patient is then placed in that position usually using pelvic blocks, head flexed or extended and the head turned to one side. An assistant will hold one of the legs in a slightly flexed position with the foot with inversion and dorsiflexion. The balloon is inflated so that it travels through the nasal passage until just before it begins to enter the throat when it is then deflated and removed. Generally either one side or both will be inflated per day. There are 6 positions that can be used (lower, middle and upper) and I generally will only inflate one area per side. I will do this along with the specific brain activation that seems to decrease the PM symptoms for 4 days straight. Every patient has been a bit different and there has been such a diverse presentation and reaction to treatment. Some seem to be improved more with the balloons and others with the activation / exercise strategies described above. I’m still working on improving my care with these cases as they continue to fly in from around the world to seek care at my office.
Incidentally I have been working with using endo-nasal ballon manipulations for almost 20 years on a variety of conditions including many neurological with much success. I teach these methods as a technique called Functional Cranial Release. You can see more on my web site www.FuncationalCranialRelease.com