Glial activation subsequent to trigeminal disturbance

Types of glial cells in brain

Glial activation is a condition of the brain where the white matter (glial cells) become inflamed.  This causes the glial cells to not perform their function properly.  Glial activation is believed to cause a major part of the pathology in a wide assortment of diseases (MS, Parkinson’s, ALS, Alzheimers,  fibromyalgia, autism, diabetes, etc.).

Glial activation subsequent to a trigeminal disturbance is well documented in the literature.  As glial activation is a major part of Parkinson’s pathology, this lends a great deal of support to the theory that bite disturbances are a major contributor to Parkinson’s disease.

Articles on glial activation subsequent to trigeminal disturbance:

Central sensitization and MAPKs are involved in occlusal interference-induced facial pain in rats.    Cao Y, Li K, Fu KY, Xie QF, Chiang CY, Sessle BJ.
J Pain. 2013 Aug;14(8):793-807. doi: 10.1016/j.jpain.2013.02.005. Epub 2013 May 1.
PMID: 23642433 Free PMC Article

Temporomandibular joint inflammation activates glial and immune cells in both the trigeminal ganglia and in the spinal trigeminal nucleus.
Villa G, Ceruti S, Zanardelli M, Magni G, Jasmin L, Ohara PT, Abbracchio MP.
Mol Pain. 2010 Dec 10;6:89. doi: 10.1186/1744-8069-6-89.
PMID: 21143950 Free PMC Article

Substance P and Parkinson’s

Substance P and Parkinson’s

Substance P is considered a possible cause of Parkinson’s.  One of the likely ways that  jaw alignment therapy impacts Parkinson’s is by lowering substance P levels.  The effect of substance P on Parkinson’s is well researched and documented (for example see article).  Substance P levels are highest in the brain within the sustantia nigra, the area of the brain where dopamine cells die off in Parkinson’s.

Substance P levels become elevated by many types of sensory stimulation to the body (“C” fibers are polymodal), but due to the high density of C fibers within the trigeminal nerve (100 times more dense than any other nerve), trigeminal disturbances have disproportionate impact on substance P levels.  The trigeminal system includes upper cervical and visceral sensory (vegus nerve).

Hence, with a chronic misaligned jaw/ trigeminal disturbance, substance P levels become elevated, and consequently cause glial activation and central sensitization.  This further elevates substance P levels as well as impacts brain blood flow.  Prolonged elevated substance P levels down regulates the precursor to substance P, nerve growth factor.  With lowered nerve growth factor brain cells can not be sustained or repaired.

Substance P levels are measured by Quest Diagnostics as a blood test, though their reported norm levels are way off by their own admission.  Research suggests that it should be below 100 pg/ml.

Parkinsons Treatment in San Francisco Bay Area

Parkinsons Treatment in San Francisco Bay Area

Northern California Cranio-facial Diagnostic Center is the premiere center for Parkinsons treatment in San Francisco Bay Area for TMJ type services.  Dr. Jennings at Northern California Cranio-facial Center was the first to publish on the link between jaw misalignment and Parkinsons (see Parkinsons TMJ treatment ).  We have extensive experience with Parkinsons patients and their wide assortment of symptoms.

In most Parkinsons cases, there is an excess amount of space between the upper jaw and lower jaw at rest (patient is agape).  This is also evident with speech: there being an excess of space between upper and lower jaw during speech.  This gives the voice a hollow/ nasal sound and in some cases a lispy quality.  The excess space causes the jaw posturing muscles to have to over contract to put the teeth together, causing the trigeminal nerve to become hyper tonic.  It is theorized that this leads to elevated substance P and subsequently glial activation, a primary pathology of Parkinsons.  It is also known that jaw alignment sensors are a major influence on the part of the brain that causes tremors.

Parkinsons treatment in San Francisco Bay Area

Treatment that is most often needed for the excess space between the teeth is a tall splint.  This is worn full time for diagnostic purposes to see if it resolves tremors, balance, cognitive function, and other symptoms.  In a large number of cases, placing tongue blades between the teeth will substantially reduce tremors immediately.

Parkinsons voice initiative

Parkinson’s voice initiative:

Recently there has been news stories on at least Fox and NPR about the Parkinson’s Voice Initiative ( They are asking for 10,000 people to call in for 3 minutes to analyze their voice to develop a data base that will diagnose whether or not one has Parkinson’s disease.  They have found that defects in the voice are very accurate at determining whether or not you have Parkinson’s disease.  The phone number if you would be interested in making the call is 857-284-8035 for the U.S.  Please see their website for other countries.

I think that this finding in the Parkinson’s voice initative is further evidence that there is a jaw misalignment component to Parkinson’s disease.  The consensus of clinical experience indicates that bite dysfunction is at the foundation of many forms of movement disorders, and speech abnormalities would be expected.

Case history: I recently saw a 20 year old male with speech apraxia (wiki:, tremors, and poor balance. Not only was his speech compromised, but also was  his gross motor movements (both noticeably jerky).  His symptoms had increased at age 14 when he had head trauma at the same time he was under going orthodontic treatment with extractions.  His orthodontic treatment has left him with a major jaw misalignment. I expect that jaw reposition therapy will resolve many of his issues, particularly his fine motor control and speech apraxia.

The following abstract points out that apraxia is due to defects in  sensory integration, known to be from the reticular formation, not the cerebrum as is thought in apraxia. It is the reticular formation where tremors are generated and where bite dysfunction manifests its pathology . And it will be defects in the reticular formation that accounts for the defects found in the voice analysis of the  Parkinson’s voice initiative.

Novartis Found Symp. 1998;218:308-25; discussion 326-31.

The apraxias are higher-order defects of sensorimotor integration.


University Department of Clinical Neurology, Institute of Neurology, National Hospital for Neurology and Neurosurgery, London, UK.


The classical features of motor disorders due to neurological disease affecting the pyramidal pathways, cerebellum and basal ganglia in humans are well known. What is less understood is the clinical world of apraxia–‘inability to perform purposeful skilled movements in the absence of any elementary motor (weakness, akinesia, abnormal posture or tone) or sensory deficits, or impaired comprehension or memory’. Much of what clinicians call apraxia is a failure of gesture production to command, due to problems of transcoding language into motor action, without motor deficit in ordinary life. However, damage to premotor regions and superior parietal lobules provokes devastating spontaneous higher-order motor deficits, including limb-kinetic apraxia, diagnostic apraxia, visuomotor apraxia and ideational apraxia.









Parkinson’s TMJ patients trends

Trends in Parkinsons TMJ patients:

From the moderate sample of Parkinsons TMJ patients that I have seen, there are emerging trends that I think need to be pointed out.  Four of the last six patients have been orthodontically treated four bicuspid extraction cases.  The Parkinsons TMJ patients all had severe jaw alignment defects; some severely retruded, some with excess vertical space between the teeth when the jaw is relaxed (i.e. excess freeway space).  The over riding symptoms have been rigidity and various types of movement disorders, but not necessarily tremors.

Extraction of teeth is almost never good with orthodontic treatment.  It is typically done when an orthodontist erroneously takes no functional records (i.e. only skeletal records=traditional records = ceph, study models, pictures). Orthodontists are not taught much about jaw alignment (jaw orthopedics), hence they treat only to a cosmetic ideal, typically disregarding functional requirements, and causing stressful bites.  This leads to elevated neurological activity, elevated neuropeptides, and ultimate neurological degeneration. It is frightful to think that a significant percentage of extraction cases would turn into Parkinsons TMJ patients since so many people have been treated orthodontically with extractions.

Trends in Parkinsons TMJ patients:

The last new Parkinsons TMJ case I saw this week, was a non-orthodontically treated female with intermittent tremor, right side rigidity, lots of TMJ symptoms, and an occlusion in which her lower jaw was 3 mm left of the upper jaw (congenital defect).  Palpation of her inner ear showed the left TMJ to be severely displaced backwards into her ear space as a result of her bite being shifted 3mm to the left.  The rigidity would be expected on the right side as a result of the jaw shifted to the left (animal studies show that lowering bite on left causes hypertonicity on the right). Treatment will entail jaw repositioning with twin block crozat appliances (phase I) similar to the attached picture.orthopedic appliances for parkinson's patient

With the diagnostic repositioning it is expected that her tremor and rigidity will resolve.  If successfully resolved, she will need to be stabilized in the therapeutic position with a combination of orthodontics and overlay crowns ( to make back teeth taller).

Implication of blink reflex defect and Parkinson’s

Blink reflex has been found to be abnormal in 70% of Parkinson’s patients. This associated pathology  very strongly supports the jaw misalignment hypothesis of Parkinsonism since trigeminal stimulation impacts blink response.

Blink reflex (see corneal reflex/ Wikipedia)is the closing of the eyelid when the eye is endangered.  Blink reflex defects usually involves excess frequency of blinking or decreased frequency of blinking.  Greater activation of dopaminergic pathways dopamine production in the striatum is associated with a higher rate of spontaneous eye blinking.  Conditions in which there is reduced dopamine availability such as Parkinson’s disease have reduced eye blink rate, while conditions in which it is raised such as schizophrenia  have an increased rate.  Generally, between each blink is an interval of 2–10 seconds; actual rates vary by individual averaging around 10 blinks per minute.  Eye blinking can be a criterion for diagnosing medical conditions. For example, excessive blinking may help to indicate the onset of Tourette syndrome, strokes or disorders of the nervous system. A reduced rate of blinking is associated with Parkinson’s disease. Parkinson’s patients have a distinct serpentine stare that is very recognizable (Wikipedia: blink).

Blink reflex involves trigeminal sensory input, and seventh cranial nerve output. Bite dysfunction can cause altered trigeminal sensory input and thus cause abnormal blink reflex (supported by published literature and case histories in my practice).  This close connection with the trigeminal has been overlooked in all the articles I have found on Parkinson’s and blink reflex; most articles assume that the blink reflex defect is caused by dysfunction within the brain stem.

Blink reflex defect is also associated with ALS and scleraderma.  I am currently writing an article hypothesizing that bite therapy will likely be effective at reversing ALS.

Dr. Jennings

Parkinson’s and comorbidities

Today a patient told me of a relative who was recently diagnosed with Parkinson’s, but also has lymphoma.  These two conditions together increase the likelihood that the cause of both is a bite problem.  When the bite is off it affects the reticular formation (hence tremor) and it causes elevated “substance P” with consequently altered blood formation.

Dystonia and other forms of movement dysfunction

Many case histories have shown that jaw malalignment can cause a wide spectrum of movement disorders: trigger finger, blink reflex, torticollis, scoliosis, poor gait, weak limbs, etc.  Some of these case histories have also shown that dystonia is but another form of movement dysfunction often caused by jaw malalignment.  That came to light this week when I examined a new patient with a Parkinson’s diagnosis.  Her primary symptom was not tremor, but moderately severe dystonia.  She could not sit in the exam chair without considerable twisting, turning, and head movement.  When I propped her jaw open with bite material her dystonia immediately ceased by over 90%.  Hence, once again the traditional Parkinson’s model based on neurotransmitter imbalances has failed to explain another aspect of the disease.

Use of Jaw Orthopedic Therapy in an Anti-aging Regimen

TMJ manifests as a lot of different conditions, from mild to life threatening.  One area that is often overlooked is the effect of a poor aligned jaw on elder persons.  This can be critical to quality of life.  In some instances where the TMJ condition is affecting blood flow to the brain, it can be life threatening.  The following article discusses many of the ways jaw malalgnment affects the elderly (Use_of_Jaw_Orthopedic_Therapy_in_an_Anti-aging regimen).

Trigeminal disturbance hypothesis of Parkinson’s

Dr. Jennings

Dr. Jennings’s Parkinson’s Etiology Hypothesis:

Long term disturbances in the trigeminal system are the cause of most forms of Parkinson’s.  In most cases this is going to be due to jaw malalignment, though it could be other disturbances within the trigeminal system.

There is massive evidence within the medical literature that this is a valid hypothesis.  I shall be presenting the evidence in support of this hypothesis over the next few months in this website.

November 20, 2011

Dwight Jennings, DDS