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

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