Trigeminal neuralgia (TN) is an extremely debilitating condition characterized by a unilateral sudden stabbing, shock-like, and electrocution type paroxysmal pain in one or more divisions of the trigeminal nerve triggered by innocuous stimuli. Under the International Classification of Headache Disorders (ICHD-3) diagnostic criteria, TN is divided into classical, secondary and idiopathic trigeminal neuralgia . New diagnostic criteria are developed based on several clinical pieces of research. [1-4] Classical trigeminal neuralgia, which is caused by neurovascular compression, is the most common form of TN. [3,5] Secondary TN, which accounts for approximately 15% of cases, results from an external cause like tumor or multiple sclerosis. [1,3,6] TN of unidentified etiology is labeled idiopathic. 
Anatomy of Trigeminal Nerve
The trigeminal nerve, the largest cranial nerve with three main branches, provides sensory innervations of the teeth, intracranial structures, neck, face and head. In addition, it has motor branches that innervate the masticatory muscles including the masseter, lateral pterygoid and temporalis muscles. The sensory root, which extends from the ganglion, enters into the pons and terminates three major nuclear complexes within the brainstem. 
Trigeminal sensory nuclei
The trigeminal nerve has three sensory nuclei, which extend from the superior part of the midbrain to the cervical region in continuity of each other.
The mesencephalic nucleus: Lies on the upper part of the principal nucleus, processing information from all three branches of the trigeminal nerve, sending fibers to the motor nucleus, thalamus reticular formation, and the cerebellum.
Principles nucleus: Also called the pontine trigeminal nucleus, is the largest nucleus of the trigeminal nerve. Though it processes many kinds of somatosensory information, its main function is to discriminate touch and pressure.
The spinal trigeminal nucleus: Also known as the spinal trigeminal tract nucleus, the main function of this third sensory nucleus is to process nociceptive information from the trigeminal system. It extends from the principal nucleus inferiorly and connects with the substantia gelatinosa of the cervical spinal cord. It was previously assumed that the spinal trigeminal nucleus ends at the C1-C2 spinal level. However, several researchers have demonstrated in cats that the spinal trigeminal tract conveys fibers that stretch through the substantia gelatinosa of the spinal cord as far caudally as the level of T9 or even throughout the spinal cord. [7-10] Other researchers have demonstrated that the spinal trigeminal tract continues in the spinal cord as far caudally as the eighth cervical vertebra, the ninth thoracic segment, and some through the entire length of the spinal cord. [11,12] The spinal trigeminal nucleus has three subdivisions, subnucleus oralis, subnucleus interpolaris, subnucleus caudalis.
The subnucleus oralis, is the most superior of the three subnuclei and is divided into three subdivisions. It extends from the caudal pole of the motor nucleus of the trigeminal nerve inferiorly to the rostral or superior pole of the nucleus of the facial nerve. It receives afferents transmitting the sensations of temperature and pain from the face. 
The subnucleus interpolaris, is localized between the subnucleus oralis and subnucleus caudalis, extending from the rostral pole of the hypoglossal nucleus caudally to the obex. It has been postulated that this subnucleus is responsible for processing dental pain. 
The subnucleus caudalis, is the most inferior or caudal portion of the spinal nucleus of the trigeminal nerve and is continuous inferiorly with the substantia gelatinosa in the dorsal horn of the cervical spinal cord. The nucleus is primarily responsible for transmitting pain from the face and mouth. [8, 11-13]
Clinical Rationale for the Study
It is well-known that vascular contact has not been observed in a wide range (4%–89%) of TN patients. [5,6,14-16] Similarly, a considerable number of patients in our clinic were diagnosed with idiopathic TN due to no etiological factors being present.
A recent new hypothesis suggests that pathological changes in the upper cervical region create a change in the trigeminal spinal tract that results in TN. It has been argued that TN can be a result of pathology in the subnucleus oralis because the distribution of the trigger zone in the facial area is in line with the subnucleus oralis.  Additionally, a number of case reports have identified that the lesion in the upper cervical region can cause TN. [17,18]
As far as we know, there are no studies that have illustrated upper cervical discopathy resulting in TN. The aim of this study is to investigate whether there is a relationship between TN and cervical discopathy.