BACKGROUND: Adenosine is a purinergic signaling molecule with a wide range of physiological functions including anti- and pronociceptive properties. Adenosine receptors are expressed in the trigeminovascular system, and adenosine receptor antagonist, caffeine, relieves migraine headache. We performed a systematic review of the literature of preclinical data addressing the role of adenosine in migraine pathophysiology.
METHODS: PubMed and EMBASE were searched for pre-clinical studies on the role of adenosine in migraine pathophysiology on September 5th, 2021.
RESULTS: A total of 2510 studies were screened by title and abstract. Of these, thirteen pre-clinical studies evaluating adenosine, adenosine A1, A2A and A3 receptors were included. These studies showed that adenosine signaling pathway is involved in controlling vascular tone. Furthermore, electrical stimulation of the trigeminal ganglion modulates the expression of adenosine A1 and A2A receptors in the trigeminal ganglion and trigeminal nucleus caudalis implicating adenosine signaling pathway in pain transmission.
CONCLUSIONS: Preclinical studies showed that adenosine has a dual effect on vasodilation and trigeminal pain pathway due to different receptor activation, suggesting a possible role of adenosine in migraine pathophysiology. Studies investigating pharmacological characteristics of subtypes of adenosine receptors are needed to further elucidate their role as a potential target for migraine treatment.

BACKGROUND: The anterior surgical approach to the cervical spine is known to be safe, and damage to the hypoglossal nerve and trigeminal pathway after the surgery is uncommon. However, once damage to those nerves occurs, the patient\'s quality of life can be severely impaired by discomfort and disability.
METHODS: We report the case of a 59-year-old male with concomitant and irreversible hypoglossal nerve and trigeminal system dysfunction after cervical spine surgery by the anterior approach confirmed by an electrodiagnostic study. He had undergone anterior cervical disc fusion through right-sided approach for a herniated intervertebral disc on the C3-4 level and direct cord compression. He had difficulty with tongue movement, dysarthria, and hypesthesia along the lower margin of the right mandible immediately after the surgery. An electrodiagnostic study revealed hypoglossal neuropathy and trigeminal somatosensory pathway dysfunction. Even though the patient received rehabilitation therapy for impaired tongue movement for more than 2 years, this function did not recover.
CONCLUSIONS: It is important to be aware of the complexity of the anatomy of vulnerable structures, including hypoglossal nerves and the trigeminal nerve system at the cervical spine level, to prevent damage to important neural structures during surgical procedures.

In this paper, we present evidence that neurons in the dorsal part of the trigeminal main sensory nucleus participate in the patterning of mastication. These neurons have special membrane properties that allow them to generate rhythmical bursts of action potentials in the frequency range of natural mastication even when cut off from synaptic inputs. These properties mature during the third postnatal week in rats at the same time as mastication begins. Finally, we present evidence that a reduction on extracellular calcium concentration is an important step in the initiation of mastication.

The article presents an overview on the peripheral and central neural mechanisms underlying pain in the orofacial area. First a definition of pain and a description of general aspects of orofacial pain are presented. Characteristics of acute and chronic pain are also described. The study highlights the sense organs, the molecular mechanisms and categories of primary afferents involved in peripheral events of orofacial pain. After describing the brain-stem nuclei participating in trigeminal pain and their functional role, primary afferents involved in nociceptive sensation from the tooth pulp, explanations of dentinal sensitivity and differences between the brain-stem endings of primary afferents among different species are discussed in details. The role of higher brain centres, with a special emphasis on the thalamus and somatosensory cortex in the development of orofacial pain sensation is considered. The last section provides a review about how the activities of nociceptive neurons are controlled by higher brain centres and neurochemicals involved in pain transmission.

OBJECTIVE: To study the concept of facial muscle reinnervation from the trigeminal pathway following facial nerve paralysis.
METHODS: We studied this phenomenon in an animal model using the neuronal marker, horseradish peroxidase (HRP). The temporalis transposition procedure was performed at varying intervals post facial nerve transection. To evaluate the trigeminal-facial reinnervation process and its timing, the zygomaticus major muscle was injected with HRP at varied periods after temporalis transposition, and histologic sections of the brainstem nuclei were examined for the final location of the HRP.
RESULTS: The presence of HRP in the trigeminal nucleus provided evidence of trigeminal-facial neurotization in those animals that underwent temporalis transposition up to 2 months following facial denervation and in which the HRP injection was performed 4 months after temporalis transposition.
CONCLUSIONS: The findings of our pilot study are strongly supportive of the trigeminal-facial neurotization hypothesis in those animals that underwent temporalis transposition up to 2 months post facial denervation and in which 4 months were allowed thereafter for adequate neurite ingrowth and neurotization to occur. This suggests that the neurotrophic signals are greatest up to 2 months post denervation and denotes the optimal time for performance of reconstructive procedures. Future studies with a larger number of animals in each group will be necessary to ensure more potent statistical significance and to augment our experimental evidence that trigeminal-facial crossover does occur and can be used as an adjunctive concept to maximize early rehabilitation of the paralyzed face.

The anatomical basis for facial itch after epidural morphone is outlined. CNS nuclear events which reactivate latent herpes simplex and immune inhibition resulting in maternal mouth vesicles or neonatal infections are described. Morphine is hypothesized to affect these processes and facial itch is only a marker, not a trigger of this trigeminal opioid activity.

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