This is a recent article in Neurology Advisor discussing the role of the Hypothalamus in Chronic Migraine.
TMJ disorders are a primary cause of noxious input to the hypothalamus while Sphenopalatine Ganglion Blocks seem to act as a reset mechanism to the autonomic nervous system.
Activation of the Hypothalamus by Trigeminal Stimulation is greater in patients with Chronic Migraine than it is in Episodic Migraine. More than 50% of all input to the brain is through the trigeminal nervous system after amplification in the Reticular Activating System.
Reduction is activation of Trigeminal nerves by utilizing neuromuscular dentistry may be helpful in preventing progression of episodic migraine to chronic migraine. Neuromuscular dentistry works on both the Somatosensory nervous system and the Autonomic nervous system including both sympathetic and parasympathetic fibers.
While there are many conclusions to this study one definite concept that can be taken away is that reducing Nociception into the Trigeminal Nervous System can reduce both Episodic Migraines and to a greater degree Chronic Migraine. Again, Neuromuscular Orthotics are extremely effective at decreasing nociception and excessive trigeminal activity thru the trigeminal nervous system.
Chronic Migraine appears to affect the anterior hypothalamus more while the posterior hypothalamus was more affected by episodic migraine.
The Hypothalamus is part of the Limbic system and pain is actually felt in the limbic system as an emotional response to noxious system. The trigeminal nerves carry both sympathetic and parasympathetic nerves along its branches. The Sphenopalatine Ganglion is located on the maxillary division of the trigeminal nerve. It is the largest parasympathetic ganglion of the head but also has superior sympathetic chain neurons running thru it and along all branches of the hypothalamus.
Neuromuscular Dentistry utilizes the Myomonitor a ULF-TENS (ultra low frequency tens) that also will stimulates the sphenopalatine ganglion. The Myomonitor has a 50 year safety record.
Sphenopalatine Ganglion Blocks are extremely effective in treating Chronic headaches and migraines as well as Stress and Anxiety.
TMJ disorders causes have been classified as Axis 1 bring Physical, Musculoskeletal and Somatosensory causes and AXIS 2 represented by the H_P_A or Hypoothalamus-Pituitary- Adrenal Complex primarily the autonomic input.
Combination of Sphenopalatine Ganglion Blocks, SPG Stimulation and neuromuscular orthotics is an ideal approach to both chronic and episodic migraines.
Hypothalamus May Play a Central Role in Chronic Migraine
May 17, 2017
Examination of hypothalamic activity shows distinctly different patterns between episodic and chronic forms of migraine. Results of a recent study reported in Neurology demonstrate that activation of the hypothalamus increases in response to painful trigeminal stimulation in people with chronic migraine (CM) to a degree greater than for episodic migraine (EM) at the time of a headache, but not in healthy controls (HCs).
The investigators recruited 63 participants from the headache outpatient department of the University Medical Center in Eppendorf, Hamburg, Germany, and via an online ad. Following exclusions for errors in data acquisition, 17 patients with CM, 18 with EM, and 19 HCs remained. Migraine attacks were stimulated in the CM and EM participants through repeated exposure to 4 types of sensory experiences: pain (ammonia), olfactory activation (rose), a control condition (air), and visual excitation (checkerboard).
The hypothalamic activity was well differentiated in the two different types of migraine. Using functional magnetic resonance imaging (fMRI), the investigators recorded greater activity in the right anterior hypothalamic region in people with CM not only compared with HCs but also with EMs who were scanned at the time of a headache. Conversely, the posterior part of the hypothalamus was more activated during the painful headache phase in both CM and EM compared with the headache-free phase.
The repeated initiation (chronicity) of migraine attacks was associated with anterior activation, while acute attacks, and specifically the pain component, were linked to posterior activation. The investigators hypothesized that the hypothalamus mediates the anterior activity that precipitates and initiates migraines and that posterior excitation of the descending pain pathway is involved in acute attacks.
These two patterns suggest possible separate roles for the different regions of the hypothalamus in migraine that may each be part of a progressive continuum from EM to CM. The investigators theorized that participants with CM were more likely than participants with EM to have a migraine at the time of fMRI scanning. This was confirmed when they compared all patients with headache to patients without headache and found greater posterior activation linked to the acute pain of the attack.
This study provides important clues to the mechanisms of migraine and the increasing trend in overall hypothalamic activity from HCs to EMs to CMs pointed strongly to a progression in migraine chronicity over time. The investigators observed that the frequency of attacks in CM and lack of headache-free days made it difficult to distinguish the interdictal phase, suggesting that precursive anterior activation in EM may increasingly escalate toward CM, causing the threshold for future headaches to move lower by requiring less anterior stimulation for the re-initiation of chronic migraine attacks. Anterior hypothalamic activity, therefore, may provide a biomarker for future conversion to CM.
Schulte LH, Allers A, May A. Hypothalamus as a mediator of chronic migraine: evidence from high-resolution fMRI. Neurology. 2017;88:1-6.