It should be kept in mind that since the spinal trigeminal tract extends inferiorly up to the level of C3, this tract can be involved clinically in a patient having a craniovertebral junction tumor.

Lateral Medullary Syndrome

Lateral medullary syndrome, also known as medullary or posterior inferior cerebellar artery syndrome, occurs due to the occlusion of the posterior inferior cerebellar artery or the vertebral artery. An occlusion to either of these arteries can result in a lack of blood flow to the lateral medulla, the location of the spinal trigeminal nucleus. The primary ischemic events that trigger lateral medullary syndrome can be a result of stenotic blood vessels as is seen in adults, often with other comorbid conditions. In children, however, ischemia can be due to injury to the vertebral artery following a hyperextension neck injury.[3] The lateral medullary syndrome presents with many symptoms including contralateral loss of pain and temperature sensation in the body with ipsilateral Horner syndrome, dysphagia, and loss of sensation in the face. This ipsilateral loss of facial sensation is due to lack of blood supply via the posterior inferior cerebellar artery to the spinal trigeminal nucleus. SpV is responsible for relaying sensory information from the trigeminal nerve to the primary sensory cortex, making it a key player in the presentation of the lateral medullary syndrome.[4]

Trigeminal Neuralgia

Trigeminal neuralgia is a condition that most often presents with unilateral, stabbing, and paroxysmal painful sensation from the face along the distribution of the trigeminal nerve.[5] There are myriad theories in regard to the underlying mechanism of this condition. The etiologies have been broken down into idiopathic, primary, and secondary trigeminal neuralgia. Suggested peripheral mechanisms involve defects along the pathway of the trigeminal nerve before entering the brainstem. A recent hypothesis attributes the pain of trigeminal neuralgia to a central mechanism involving the subnucleus oralis of the spinal trigeminal nucleus.[6] This theory has as its basis the characterization of trigeminal neuralgia as focal epileptic and neuronal hyperactivity. An increase in activity at the spinal trigeminal nucleus has been shown to precipitate the pain seen in trigeminal neuralgia in both cats and monkeys. Furthermore, the administration of anti-epileptic medications in cats and monkeys was able to decrease the intensity and duration of the attacks. The difficulty of treatment approaches makes the understanding of trigeminal neuralgia imperative.[7] Though there is not a consensus on the underlying mechanism of trigeminal neuralgia, recent evidence suggests that the spinal trigeminal nucleus, in particular, the subnucleus oralis, plays a vital role in this process.

Chronic Orofacial Pain

Understanding chronic orofacial pain is important as it has been determined as a source of significant psychological distress in patients. This distress is likely because often procedures and medications are unable to provide relief of symptoms.[8] A better understanding of the underlying mechanism may help in creating new solutions to this lack of treatment efficacy. In the processing of orofacial pain, the spinal trigeminal nucleus specifically, the subnucleus caudalis, projects to both the ventral posteromedial thalamic nucleus as well as the parabrachial nucleus.[9] A recent study was conducted in humans to demonstrate changes in synapses of patients with chronic orofacial neuropathic pain. Utilizing T1-weighted MRI imaging, the study showed that alterations in the anatomy of primary synapses of the trigeminal nerve, particularly in the subnucleus oralis, is critical for both the generation and maintenance of chronic pain in the distribution of the trigeminal nerve. These changes included significant regional gray matter volume reduction, a decrease in mean diffusivity, and fractional anisotropy increase.[10] Imaging of the peripheral pathways of the trigeminal nerve showed no significant change in the anatomy in the setting of chronic orofacial pain, thus decreasing the likelihood of its involvement in the pathophysiology of this condition. Anatomical changes to the subnucleus oralis of the spinal trigeminal nerve are responsible for the presentation of chronic orofacial pain.

There is evidence in rats suggesting the presence of oxytocin receptors in both the medulla oblongata and pons.[11] These oxytocin receptors are present in the spinal trigeminal nucleus; however, as is seen with oxytocin receptors in other regions of the medulla and pons, they disappear by postnatal day 10. At the time of birth, there is an increase in the maternal release of oxytocin, likely acting on these oxytocin receptors as well; this indicates an early and transient role of oxytocin in the neuronal development of the neonatal period. The full extent of the effect of oxytocin on neuronal development postnatally is yet to be determined.