MRI evaluation of trigeminal neuralgia patients in a rural hospital of central India

Introduction

Trigeminal neuralgia is a disease characterized by severe paroxysmal, electric shock-like pain involving the distributions of the trigeminal nerve. The pain may occur in one or more divisions of the trigeminal nerve. Patients often describe the pain as unilateral, abrupt in onset and brief but tend to occur repeatedly many times a day.¹

The trigeminal nerve is a mixed cranial nerve, i.e., it has sensory and motor components. It has one motor nucleus and three sensory nuclei in the brainstem. The motor nucleus is involved in the control of muscles of mastication and is located in pons. Among sensory nuclei, there are three divisions. The mesencephalic nucleus mediates proprioception of muscles of mastication, face, tongue, and orbit. The primary sensory nucleus is involved in facial tactile sensation and supplies touch fibres to all the divisions of the trigeminal nerve. The spinal nucleus extends from the posterior region of the pons to the upper part of the cervical cord and controls facial pain and temperature.^1,2

The cisternal segment of the trigeminal nerve comprises a sensory portion which forms a large part of the nerve and a few smaller motor roots; the segment arises from the anterolateral aspect of the pons and is most involved in the neurovascular conflict. The root entry zone [REZ] in this segment, wherein conversion from central to peripheral myelin occurs, is most implicated in neurovascular compression.¹

The nerve traverses through the cisternal space and reaches the Meckel’s cave via porus trigeminus. The Meckel’s cave is a CSF (Cerebrospinal fluid-filled space in the petrous apex; the trigeminal nerve forms gasserian or trigeminal ganglion. The three divisions of trigeminal nerve i.e., ophthalmic (V1), maxillary (V2) and mandibular (V3) arise from gasserian ganglion. V1, V2, and V3 separately provide sensory innervation to the face’s top, middle, and bottom thirds.²

Trigeminal neuralgia is more prevalent in women than men, with the right side of the face involved more commonly than the left side; the peak age of onset ranges from the fifth to the eighth decade of life and is more commonly found in rural populations.³

As per available literature, the most common cause for trigeminal neuralgia is neurovascular contact in the prepontine cistern, and the most implicated artery is the superior cerebellar artery and its branches.¹ Other causes of trigeminal neuralgia vary upon the site of involvement; in the prepontine cistern, common causes include neurovascular compression, cerebellopontine angle tumours and aneurysms, while at the level of brainstem lesions like brainstem glioma, infarction, multiple sclerosis and cavernoma have been identified as potential causes.¹

MRI is the primary imaging modality for evaluating trigeminal neuralgia, with sequences like 3D- FIESTA (Fast Imaging employing steady-state acquisition) being the mainstay. These are heavily T2-weighted sequences.¹

The artefact produced by natural fluid flow is one of the challenges in imaging CSF spaces with MRI. As a result, approaches that shorten scanning time should provide higher-quality images. Here, there is the role of S.S.F.P. sequences like FIESTA. FIESTA MRI employs ultrashort repetition and echo periods to achieve highly rapid acquisition times. With solid signals from fluid and reduction of background tissue, the signal-to-noise ratio is high, resulting in superb contrast and, more crucially, anatomical features of minute structures. Therefore, allowing for better visualization of the cranial nerves.⁴

Microvascular decompression (MVD) has become the mainstay therapy for treating patients with trigeminal neuralgia, as neuro-vascular compression is the most common cause. Though a patient’s history is essential in prognosis post-MVD, Imaging plays a vital role in surgical planning. Surgeons rely on specific imaging findings in planning MVD. These are whether the compressing vessel is an artery or a vein, the name of the compressing vessel and whether it is compressing the proximal or distal half of the cisternal segment.⁵

Methods

Discussion

Rangaswamy, Vijaykumar Kenchanahalli et al. (2016) studied the use of MRI in evaluating cases of trigeminal neuralgia. They studied 75 patients in the age group of 18-60 years retrospectively over one year to find out about common causes of trigeminal neuralgia. They found neurovascular compression at REZ as the most common cause. Other causes identified include Cerebellopontine angle tumour, multiple sclerosis and brain stem infarction.¹

Hughes, Marion A. et al. (2016) studied trigeminal nerve anatomy and tried to find relevant strategies for radiologists to delineate significant imaging findings in patients with trigeminal neuralgia on MRI. They concluded that Imaging and clinical history play a vital role in identifying patients who are suitable candidates for microvascular decompression.⁵

Geneidi, Eman A. Sh, et al. (2016) studied 45 patients with trigeminal pain to evaluate underlying pathology and compared the imaging findings with relevant clinical info. MRI revealed the underlying aetiology in 25 out of 45 patients. The most common cause in their study is neurovascular compression in the prepontine segment of the nerve, followed by brainstem lesions.⁷

Anwar, Hameed Arafath, et al. (2022) studied 67 patients with trigeminal neuralgia for neurovascular conflict using 1.5 Tesla MRI Their study focused on various parameters of neurovascular conflict, such as side, site of neurovascular conflict, and whether there was any deviation or atrophy at the site of neurovascular conflict. They looked out for features of the vascular loop causing the neurovascular conflict. They concluded that neurovascular compression involving the root entry zone strongly correlates with trigeminal neuralgia symptoms on the ipsilateral side. Also, trigeminal nerve thinning correlates with trigeminal neuralgia on the same side.⁶