One of the best articles I’ve found on the neurology of Palatal Myoclonus.

This article might explain why FCR works for PM. I’ll explain at the end.

Palatal myoclonus secondary to hypertrophic olivary degeneration

by Enrique Palacios, Ewa Wasilewska, Jorge E. Alvernia, Ramon E. Figuero.

A 64-year-old woman with a history of hypertension and stroke presented with palatal tremor and myoclonus 11 months after experiencing a vascular insult in the brainstem. The myoclonus was characterized by rhythmic involuntary movement of the soft palate, uvula, pharynx, and larynx. Magnetic resonance imaging (MRI) detected the presence of an old pontine vascular insult associated with a prominence and abnormal hyperintensity in the area of the right inferior olivary nucleus (figures 1-3). These findings were consistent with hypertrophic olivary degeneration. (1,2)

MRI is the most sensitive modality for the diagnosis of hypertrophic olivary degeneration because of its high diagnostic sensitivity in the area of the brainstem. On imaging, hypertrophic olivary degeneration occurs in three characteristic stages (3-5):

* In the first 4 to 6 months, no significant morphologic change in the olive or signal intensity is seen. This period corresponds with the initial phase of gliosis, demyelination, and vacuolization.

* From 6 months through 4 years, hypertrophy and an abnormal signal intensity of the olive are seen. These findings are related to neuronal and astrocytic hypertrophy (figures 1 and 2).

* After 4 years, the hypertrophy resolves, and abnormal signal intensity can be observed.

No evidence of contrast enhancement is seen during any of these stages.

The differential diagnosis of an abnormal localized signal intensity in the olive and pontomedullary area includes ischemic infarction, demyelination, tumor, an inflammatory process (including sarcoidosis), and focal rhomboencephalitis. 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)

There are three patterns of hypertrophic olivary degeneration as they relate to the location of the primary lesion. When the lesion is in the dentate nucleus or superior cerebellar peduncle, the olivary degeneration is contralateral. When the primary lesion is in the central tegmental tract, olivary degeneration is ipsilateral, as occurred in our patient. When the lesion involves both pathways, the olivary degeneration is bilatera. (1,6)

Hypertrophy of the olivary nucleus following a primary brainstem injury is believed to represent a combination of cell body enlargement, vacuolation of the cytoplasm, astrocytic proliferation, demyelination, and fibrillary gliosis. (2,6) The degree of the hypertrophic olivary nucleus is variable, depending on the time interval from the insult to the Guillain-Mollaret triangle. As seen on imaging, olivary hypertrophy develops 4 to 6 months after the primary insult, and it may resolve 10 to 16 months later. However, abnormal hyperintensity of the inferior olivary nucleus on T2-weighted MRI may continue for years despite the persistence of the signs and symptoms of palatal myoclonus and dentatorubral tremor. (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) The most common symptom is palatal myoclonus, which is characterized by rhythmic involuntary movement of the soft palate, uvula, pharynx, and larynx. (2,6) Other clinical signs and symptoms include dentatorubral tremor, severe myoclonus of the cervical muscles and diaphragm, and symptoms of cerebellar or brainstem dysfunction. (2) 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) Our patient exhibited the classic signs and symptoms of palatal myoclonus, which correlated with imaging findings involving the central tegmental tract.

Not all patients with hypertrophic olivary degeneration develop the classic symptoms, but virtually all patients who develop palatal myoclonus after a brainstem insult will develop hypertrophic olivary degeneration. (1,2) Hypertrophic olivary degeneration is a sequela of a brainstem injury of various etiologies, and its clinical presentation is variable. Identification of the characteristic MRI findings of the olivary nucleus indicating an associated lesion involving the dentatorubro-olivary pathway allows for correct diagnosis. Therefore, it is important to understand the potential clinical pattern that may lead to recognition of the MRI findings of hypertrophic olivary degeneration.


(1.) Salamon-Murayama N, Russell EJ, Rabin BM. Diagnosis please. Case 17: Hypertrophic olivary degeneration secondary to pontine hemorrhage. Radiology 1999;213(3):814-17.

(2.) Krings T, Foltys H, Meister IG, Reul J. Hypertrophic olivary degeneration following pontine haemorrhage: Hypertensive crisis or cavernous haemangioma bleeding? J Neurol Neurosurg Psychiatry 2003;74(6):797-9.

(3.) Hirono N, Kameyama M, Kohayashi Y, et al. MR demonstration of a unilateral olivary hypertrophy caused by pontine tegmental hematoma. Neuroradiology 1990;32(4):340-2.

(4.) Uchino A, Hasuo K, Uchida K, et al. Olivary degeneration after cerebellar or brain stem haemorrhage: MRI. Neuroradiology 1993;35(5):335-8.

(5.) Osborn AG, Blaser SI, Salzman KL. Toxic/metabolic/degenerative disorders, acquired. In: Osborn AG, Blaser SI, Salzman KL. Diagnostic Imaging: Brain. Salt Lake City: Amirsys; 2004.

(6.) Kitajima M, Korogi Y, Shimomura O, et al. Hypertrophic olivary degeneration: MR imaging and pathologic findings. Radiology 1994;192(2):539-43.

Enrique Palacios, MD, FACR; Ewa Wasilewska, MD; Jorge E. Alvernia, MD; Ramon E. Figueroa, MD, FACR

From the Department of Radiology (Dr. Palacios and Dr. Wasilewska) and the Department of Neurosurgery (Dr. Alvernia), Tulane University Hospital and Clinic, New Orleans; and the Department of Radiology, Medical College of Georgia, Augusta (Dr. Figueroa).

COPYRIGHT 2009 Vendome Group LLC
COPYRIGHT 2010 Gale, Cengage Learning
In this article they mention 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.

Read the following definition of the Nucleous Ambiguus.

The nucleus ambiguus (literally “ambiguous nucleus”) is a region of histologically disparate cells located just dorsal (posterior) to the inferior olivary nucleus in the lateral portion of the upper (rostralmedulla. It receives upper motor neuron innervation directly via the corticobulbar tract.

This nucleus gives rise to the branchial efferent motor fibers of the vagus nerve (CN X) terminating in the laryngealpharyngeal muscles, and musculus uvulae[citation needed]; as well as to the efferent motor fibers of theglossopharyngeal nerve (CN IX) terminating in the stylopharyngeus.

Now read this Definition of the corticobulbar tract.
The corticobulbar (or corticonucleartract is a white matter pathway connecting the cerebral cortex to the brainstem. The ‘bulb’ is an archaic term for the medulla oblongata; in modern clinical usage, it sometimes includes the pons as well. The word ‘bulbar’ therefore refers to the nerves and tracts connected to the medulla, and also by association to the muscles thus innervated, those of the tongue, pharynx and larynx.
Something to keep in mind is the innervation of the face and nasal passages is from the trigeminal nucleus. When I perform FCR I’m creating a stimulation through these very pathways! Your nerve cells need 3 things to be healthy. Oxygen, Glucose and activation. Activation is stimulation and if your brain isn’t stimulated it is programed to start dyeing off. To stabilize the area’s of your brain that cause PM you need to look at healthy area’s that can be activated that will support the unhealthy area’s. This is called augmenting neurology. Stabilizing these area’s of the brain as well as improving activation will be the answer to overcoming PM.
Your’s in Health,
John Lieurance, DC, ND

Therapies for Palatal Myoclonus, treatment for palatal myoclonus




Etymology: Gk, optikos, sight, kinesis, motion
pertaining to movement of the eyeballs in response to the movement of objects across the visual field, such as in optokinetic nystagmus. Also called opticokinetic.
Mosby’s Medical Dictionary, 8th edition. © 2009, Elsevier.

nystagmus [nis-tag´mus]

involuntary, rapid, rhythmic movement (horizontal, vertical, rotatory, or mixed, i.e., of two types) of the eyeball. adj., adj nystag´mic.
amaurotic nystagmus nystagmus in the blind or in those with defects of central vision.
amblyopic nystagmus nystagmus due to any lesion interfering with central vision.
aural nystagmus labyrinthine nystagmus.
caloric nystagmus rotatory nystagmus in response to caloric stimuli in the ear, seen during the caloric test.
Cheyne’s nystagmus a peculiar rhythmical eye movement resembling Cheyne-Stokes respiration in rhythm.
congenital nystagmus (congenital hereditary nystagmus) nystagmus usually present at birth, usually horizontal and pendular, but occasionally jerky and pendular; the nystagmus may be caused by or associated with optic atrophy, coloboma, albinism, bilateral macular lesions, congenital cataract, severe astigmatism, and glaucoma.
dissociated nystagmus that in which the movements in the two eyes are dissimilar.
end-position nystagmus that occurring only at extremes of gaze.
fixation nystagmus that occurring only on gazing fixedly at an object.
gaze nystagmus nystagmus made apparent by looking to the right or to the left.
labyrinthine nystagmus vestibular nystagmus due to labyrinthine disturbance.
latent nystagmus that occurring only when one eye is covered.
lateral nystagmus involuntary horizontal movement of the eyes.
optokinetic nystagmus nystagmus induced by looking at objects moving across the visual field.
pendular nystagmus nystagmus in which the oscillations of the eyes have an equal rate, amplitude, direction, and type of movement.
positional nystagmus that which occurs, or is altered in form or intensity, on assumption of certain positions of the head.
retraction nystagmus (nystagmus retracto´rius) a spasmodic backward movement of the eyeball occurring on attempts to move the eye; a sign of midbrain disease.
rotatory nystagmus involuntary rotation of the eyes about the visual axis.
secondary nystagmus nystagmus occurring after the abrupt cessation of rotation of the head, caused by the labyrinthine fluid continuing to move.
spontaneous nystagmus that occurring without specific stimulation of the vestibular system.
vertical nystagmus involuntary up-and-down movement of the eyes.
vestibular nystagmus nystagmus due to disturbance of the labyrinth or of the vestibular nuclei; the movements are usually jerky.
Take a look at an eye phone application called OPTIK. Try and see if your myoclonus changes with the direction, speed and even whether the phone is in your periphery in various feilds.
I find many PM patients have an effect. Usually it will speed up the myoclonus.
John Lieurance, DC