Low-level Laser Therapy for Trigeminal Neuralgia

Case reports on two patients whose unrelenting facial pain and hypersensitivity from their diagnosed trigeminal neuralgia resolved with low-level laser therapy.
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In this issue, Drs. Leonard Vernon and Rafael Hasbun present two case reports of trigeminal neuralgia pain successfully treated with low-level laser therapy (LLLT). Trigeminal neuralgia can be a challenging painful condition to treat and/or manage. This article also includes a review of the etiology, involved anatomy, and typical outcomes of conventional modalities in comparison to LLLT.

William J. Kneebone, CRNA, DC, CNC, DIHom

Low-level laser therapy (LLLT) has been used extensively as modality in the treatment of a wide variety of clinical conditions. Until recently, most of this clinical use has been outside of the United States. Although this therapy method remains controversial, many authors have reported significant pain reduction in a number of conditions such as rheumatoid arthritis, osteo-arthritis, fibromyalgia, post-operative pain, and low back pain.

LLLT has been shown to effect many sub-cellular and cellular processes and, although the exact mechanism have not been well defined, it is believed that light is absorbed by mitochondrial chromophores leading to an increase in adenosine triphosphate (ATP), reactive oxygen species and/or cyclic AMP production, and consequent gene transcription via activation of transcription factors. Despite the many case reports, the use of LLLT remains controversial.

In this article, we report on two patients who were diagnosed with trigeminal neuralgia (CN V). Both patients had unrelenting facial pain, with one of the two patients experiencing a motor nerve component (CN VII), as well as a hyper-sensitivity. Both patients had tried various medications including analgesics, NSAIDs, and steroids—all of which offered no relief. Both patients were treated with a Ga-Al-As diode system that produces low-energy infrared light (808nm diodes/200mW). The laser was applied to the multiple locations within a defined region of the facial area. Both patients were treated once per day for five consecutive days, followed by a two-day interval. This regimen continued until the total number of applications reached 20.

Etiology

Trigeminal neuralgia (TN) has been referred to in the medical literature for centuries. References to unilateral facial pain causing facial spasms can be seen in the writings of Aretaeus of Cappadocia in the 2nd century A.D.1 and those of the Arab physician Jujani in the 11th century A.D.2 John Fothergill,3 in a paper published in 1773, described the typical features of TN, including its paroxysmal nature and association with triggering factors such as eating, speaking, or touching the face. In 1756, the French surgeon Nicholas André coined the term “tic douloureux” to describe at least three patients with TN.4

Trigeminal neuralgia (TN), or tic douloureux (also known as prosopalgia), is a neuropathic disorder of the trigeminal nerve that causes episodes of intense pain in the eyes, lips, nose, scalp, forehead, and jaw, with the majority of cases being unilateral.(>95%).5 This lancinating pain is typically in the distribution of the second and third divisions of the trigeminal nerve and can be triggered by facial movement, cold temperature, talking, and other common activities.6 Trigeminal neuralgia is considered by many to be among the most painful of conditions and is often labeled the “suicide disease” because of the significant numbers of people taking their own lives when they cannot find effective treatments. An estimated 1 in 15,000 people suffers from trigeminal neuralgia, although numbers may be significantly higher due to frequent misdiagnosis. It usually develops after the age of 40, although there have been cases with patients being as young as 13 months of age.7

On physical examination, the neurological examination of other cranial nerves is usually within normal limits, as neurological signs rarely accompany TN. If a neurological abnormality is revealed, such as absent or diminished corneal reflex, it is important to consider an alternative diagnosis such as a central lesion (posterior fossa tumor) or MS.8 When attempting to examine the affected side, the patient will shrug away or prevent the examiner’s hand from touching the face for fear of inducing pain. If the examiner can examine the area, there may be a mild light touch or pin perception loss in the central area of the face.9

The mechanism of pain production remains controversial. One theory suggests that peripheral injury or disease of the trigeminal nerve increases afferent firing in the nerve. Failure of central inhibitory mechanisms may be involved as well. Some authors have hypothesized that trigeminal neuralgia has a peripheral cause as well as a central pathogenesis. They speculate that chronic irritation of the trigeminal nerve apparently leads to both a failure of segmental inhibition in the trigeminal nucleus, and ectopic action potentials in the trigeminal nerve. In 90-95% of cases, no lesion is identified, and the etiology is labeled idiopathic by default.10 Some authors have speculated that, like Bell’s palsy, a neurotropic virus may be the causative agent and the proximity of the two nerves may give cause to further support this theory.7 Ch’ien and Halsey reported two cases of concomitant trigeminal sensory neuropathy and Bell’s palsy.11Although the exact pathogenesis is unknown, it is, however, generally accepted that focal demyelination in the root of the trigeminal nerve is involved.12,13 Of course, any injury to the trigeminal nerve may also cause the condition. Trigeminal Neuropathy or Post-Traumatic TN may develop following cranio-facial trauma (such as from a car accident), dental trauma, or sinus trauma.

The syndrome presents as classic episodes of shooting pain in areas of the face. The disorder is frequently associated with gradual worsening of the pain pattern and shortening of pain-free intervals. If left untreated, it may develop new features, including sensory disturbances and constant pain, which are uncharacteristic of trigeminal neuralgia and evolve toward another pain syndrome, generally known as atypical trigeminal neuralgia.14

Anatomy

The trigeminal nerve is the largest of all the cranial nerves. It exits laterally at the mid-pons level and has two divisions-a smaller motor root (portion minor) and a larger sensory root (portion major). The motor root supplies the temporalis, pterygoid, tensor tympani, tensor palati, mylohyoid, and anterior belly of the digastric. The motor root also contains sensory nerve fibers that particularly mediate pain sensation.

The gasserian ganglion is located in the trigeminal fossa (Meckel cave) of the petrous bone in the middle cranial fossa. It contains the first-order general somatic sensory fibers that carry pain, temperature, and touch. The peripheral processes of neurons in the ganglion form the three divisions of the trigeminal nerve.

Figure 1. Here the patient is treated with the laser at the point where an incision would be made if decompression surgery was being performed on trigeminal nerve (about two-inches deep). The ophthalmic nerve (V1), which exits the cranium via the superior orbital fissure, is a sensory nerve that controls feeling in the skin on the top of the head, the mucous membrane of the nose and sinuses, the cornea, and the conjunctiva. In trigeminal neuralgia, damage to, or pressure on, the ophthalmic nerve can cause pain along the jaw line, to the eye, and back across the forehead.

The maxillary nerve (V2) ,which exits via the foramen rotundum, controls sensation in the dura mater of the brain and spinal cord, the gums and teeth in the upper jaw, the upper lip, and the orbit. If this nerve is affected, pain often radiates from the jaw to the upper lip, nose, and underneath the eye.

First published on: July 1, 2008