Classic trigeminal neuralgia: a surgical perspective.
Trigeminal neuralgia (TN), also known as tic douloureux, is a disease that affects the fifth cranial nerve. It is characterized by intense shooting spasms of pain, usually isolated to one side of the face. Although it can involve one or more branches of the trigeminal nerve, the maxillary (V2) and mandibular (V3) divisions are the most commonly affected regions (Hickey, 2002). The pain may occur spontaneously or can be triggered by light touch, chewing, talking, or even temperature changes. Although the exact etiology is unknown, one possible explanation is compression of the nerve root by an adjacent vessel (Hickey).
Although TN is relatively rare, affecting four people per 100,000 population, those afflicted describe it as both debilitating and unbearable (Wilkins, 2002). Drug therapy is often used as the initial approach to treatment. Surgery may be incorporated when drug therapy fails or when the patient is unable to tolerate the drugs.
Neurosurgical nurses are an important part of the multidisciplinary team working together to improve the quality of life for these patients. Additional clinical knowledge and skills are required to provide safe and competent perioperative and postoperative care to the TN patient and his or her family. This article provides an overview of the anatomy, pathophysiology, etiology, and surgical management options available to TN patients.
The trigeminal nerve is classified as a mixed cranial nerve consisting of both sensory and motor fibers. The larger sensory component arises from the ventrolateral aspect of the pons; the much smaller motor root emerges medially (Netter, 1995). The motor and sensory roots follow a path from the pons across the petrous ridge of the temporal bone. The sensory root expands to become the semilunar shaped Gasserian ganglion, which divides into the three peripheral sensory branches: ophthalmic, maxillary, and mandibular (Table 1). The motor root passes under the ganglion to join the mandibular branch. The Gasserian ganglion rests in a groove, the trigeminal impression, on the petrous portion of the temporal bone (Kruger & Young, 1981).
The Gasserian ganglion and the proximal sensory and motor roots are enclosed in a dural envelope, which forms Meckel's cave (Kruger & Young, 1981). Ventromedial to the ganglion, a thick plate of bone, which forms the floor to Meckel's cave, separates the ganglion and root fibers from the underlying internal carotid artery and the posterior part of the cavernous sinus (Kruger & Young). The sensory impulses for touch, pain, temperature, and sensation are conveyed from most of the face, while the muscles of mastication are supplied by the motor component (Hickey, 2002).
The trigeminal nerve also carries proprioceptive impulses from the orbital and masticatory muscles. Numerous parasympathetic and sympathetic fibers join branches of the trigeminal nerve through interconnections with the oculomotor (III), trochlear (IV), facial (VII), and glossopharyngeal (IX) nerves (Netter, 1995). It is through these interconnections that the trigeminal nerve is able to act as a vehicle in the distribution of sympathetic and parasympathetic fibers (Netter).
Classic TN is a disease characterized by intense shooting spasms of pain, usually lasting a few seconds to a few minutes in duration. The pain is usually unilateral, and the right side of the face is affected more often than the left (Tekkok & Brown, 1996). The pain may occur spontaneously or can be triggered by light touch, chewing, talking, or even temperature changes (Netter, 1995). The cutaneous or mucosal trigger point or zone can usually be identified and may change location over time (Tekkok & Brown, 1996; Jannetta, 1981b).
Bouts of pain may occur over several weeks or months followed by a spontaneous, unpredictable remission. Motor and sensory deficits usually are not observed. However, the ipsilateral corneal reflex may be decreased or absent when the ophthalmic division of the nerve is involved (Hickey, 2002; Jannetta, 1981b). TN most commonly occurs in the fifth or sixth decades of life and occurs more often in women than in men.
The exact etiology of classic TN is unknown. One possible explanation is that of vascular compression. With age, the brain will shrink and sag caudally, and this may allow the root entry zone to be compressed by an elongated arteriosclerotic artery (Janetta, 1981a). A loop of the superior cerebellar artery (SCA) and occasionally the anterior inferior cerebellar artery (AICA) or the petrosal vein is identified as the vessel causing the compression. There also may be demyelination of the trigeminal roots from contact with the adjacent vessel. This is believed to occur at the transition area between the peripheral myelin, which is formed by Schwann cells, and the central myelin, formed by oligodendrocytes. It is possible that with demyelination these nerve fibers at the myelin transition area may generate ectopic impulses and fail to inhibit continuous sensory input from the smaller fibers of the trigeminal nerve (Tekkok & Brown, 1996). However, it is important to remember that, in some cases, a cause for the pain cannot be found.
An accurate history and a detailed neurological examination are important in the diagnosis of classic TN. Magnetic resonance imaging (MRI) is performed to rule out the presence of a structural lesion, such as a tumor, an arteriovenous malformation, or multiple sclerosis involving the trigeminal system, because these may also cause the symptoms of TN. It is important to rule out atypical facial pain, vasomotor or postherpetic neuralgia, and dental pain. These patients will not benefit from microvascular decompression, and the pain may worsen with certain percutaneous procedures (Adler, 1989). In some cases MRI studies can clearly demonstrate the presence of a vascular structure at the root entry zone. However, the exact vascular relationships are not usually appreciated until the root entry zone is exposed at the time of surgery (Tekkok & Brown, 1996).
Trigeminal neuralgia was described as early as the first century AD in the writings of Aretaeus when treatments ranged from bloodletting to the application of poison-laden bandages (Facial Neuralgia Resources, 2002). Current medical treatment utilizes a variety of drug therapies. Surgery is reserved for those who cannot tolerate the medical therapy, fail to achieve long-term control, or do not respond to medication (Siegfried, 1981).
Microvascular decompression is the only surgical option aimed at the etiology of the disease, whereas percutaneous balloon microcompression, radiofrequency thermocoagulation, and glycerol injection are used to treat the symptoms (Tekkok & Brown, 1996). The operative procedure selected is one that will give the individual patient the greatest chance of long-term pain relief with the fewest complications (Siegfried, 1981). The elderly, medically unfit, those patients who have undergone destructive procedures, or those unwilling to assume the risks of surgery may choose a percutaneous procedure. The younger patient who wishes to avoid any facial dysesthesias may initially opt for a microvascular decompression (Tekkok & Brown, 1996).
Microvascular decompression is an operative procedure used to relieve the compression and/or contact between a vessel and the root entry zone of the trigeminal nerve. The patient is anesthetized, intubated, and then positioned in a lateral or park bench position using three-pin skull fixation. Through a retromastoid incision the muscle, fascia, and pericranium are dissected away from the calvaria. A craniectomy or craniotomy is performed, using a high-speed drill, to expose the underlying junction of the transverse and sigmoid sinuses. The dura is incised and sutured to the galea to tent the sinus up and away.
The operating microscope, in a diploscope arrangement, is then introduced. Aspiration of cerebrospinal fluid from the basal cisterns allows the cerebellum to be gently retracted. The arachnoid is then opened and the root entry zone of the trigeminal nerve is exposed. The arachnoid is bluntly dissected away from the nerve to allow for the identification and repositioning of the compressing vessel (Fig 1). One or more pieces of Teflon felt are positioned between the nerve and the artery while compressing veins may be coagulated and divided. Meticulous hemostasis is maintained throughout the entire operative procedure with the use of electrocoagulation, absorbable gelatin sponge, oxidized regenerated cellulose, and bone wax.
[FIGURE 1 OMITTED]
The cerebellar retractor is then removed and the dura closed. Fibrin sealant also may be used to provide a water-tight dural seal. The bone flap is replaced, in a craniotomy, and securely held with titanium plates and screws. The galea is then closed. Microvascular decompression is an effective surgical means of relieving the patient's intense pain while retaining the facial sensation. It is not completely understood whether this is accomplished by relieving the compressing adjacent vessel or through the manipulation and trauma to the nerve during surgery (Tekkok & Brown, 1996).
Aseptic meningitis, cerebrospinal fluid leak, ataxia, profound ipsilateral hearing loss, and seventh and eighth nerve deficits are the most common postoperative complications. Once a microvascular decompression has been performed, the average time for the pain to reoccur is 1.9 years, with 47% of recurrences in the first year (Tekkok & Brown, 1996).
Percutaneous Balloon Microcompression
Percutaneous balloon microcompression is a procedure that selectively injures the large myelinated fibers that mediate light touch and trigger the pain in all three sensory branches of the trigeminal nerve (Tekkok & Brown, 1996). The smaller fibers, which mediate the corneal reflex and pain, are usually spared from injury (Tekkok & Brown).
Fluoroscopy is used to guide a 14-gauge access needle through the skin of the cheek into the entrance of the foramen ovale. Because entry into this area can cause excruciating pain, it is performed under a general anesthetic. A 4.0 french (1.35 mm) balloon catheter is inserted through the cannula of the needle and advanced to the entrance of Meckel's cave (Fig 2). The balloon, filled with approximately 0.75-1 ml of a contrast material, is inflated to compress the Gasserian ganglion and nerve root against the dura and the petrous ridge for 1 minute (Fig 3). The contrast material allows the position of the balloon to be verified under fluoroscopy (Tekkok & Brown, 1996). After deflation, the balloon and cannula are removed concurrently (Tekkok & Brown).
[FIGURES 2-3 OMITTED]
Percutaneous balloon microcompression is usually effective immediately in treating the pain from all branches of the trigeminal nerve. With stimulation of the autonomic nervous system during needle placement and the balloon compression, bradycardia and hypotension may occur (Tekkok & Brown, 1996).
Masseter weakness, hypesthesia, and dysesthesia also may be experienced in the face after surgery. Percutaneous balloon microcompression relieves first division neuralgia while sparing corneal sensation (Tekkok & Brown, 1996). The recurrence rate is approximately 25% at 3 years (Tekkok & Brown).
Radiofrequency Thermal Coagulation
Radiofrequency thermal coagulation, a percutaneous procedure, creates a precise thermal lesion on the root fibers of the trigeminal nerve. The small sensory fibers that carry pain impulses are more sensitive to thermal lesions and can be sufficiently destroyed without compromising touch or motor function (Hickey, 2002).
The patient receives sedation and local anesthesia to the puncture site prior to the beginning of the procedure. Fluoroscopy is used to guide an insulated cannula through the cheek into the foramen ovale, while maintaining the integrity of the oral mucosa. The patient usually experiences substantial pain as the cannula advances into the entrance of the foramen. As the stylet of the cannula is removed, cerebrospinal fluid is encountered.
A curved tip thermistor electrode is then inserted through the cannula. Sensory and motor testing is performed to ensure the proper target location has been reached. Once the testing has been completed, a small graded lesion can be created with the use of a radio frequency generator. The electrode is then allowed to cool before it is removed from the cannula.
Immediate pain relief is usually experienced; however, anesthesia dolorosa and dysesthesia to the face, as well corneal anesthesia, may occur (Tekkok & Brown, 1996). The average recurrence rate is 25%-37% at 5 years after radiofrequency rhizotomy (Tekkok & Brown).
Glycerol is a hyperbaric solution that is injected into the Meckel's cave to cause destruction to the myelinated fibers of the nerve. While sedated, the patient is given local anesthesia at the puncture site in the cheek. An 18-gauge needle is then guided into the foramen ovale with the use of fluoroscopy. The patient experiences substantial pain with the advancement of the needle. Once the proper placement of the needle is verified with the use of contrast material, glycerol is injected into the cistern surrounding the nerve. The head is kept in a flexed position for approximately 1 hour to prevent its escape into the posterior fossa (Tekkok & Brown, 1996).
Relief from the glycerol injection is not instantaneous. It may take up to 21 days for the patient to experience a reprieve from the pain. In spite of the delay, this technique is beneficial because it causes little or no sensory loss and may avoid facial numbness (Tekkok & Brown, 1996). Hypalgesia and aseptic meningitis are the most common complications associated with glycerol injection (Tekkok & Brown, 1996). The recurrence rate is 24% at 1.9 years (Tekkok & Brown).
It is important for neurosurgical nurses to remember that patients with TN will experience anxiety and stress related to undergoing microvascular decompression or any of the percutaneous procedures. Demonstrating a caring attitude, providing support, as well as providing explanations to the patient and family can help to alleviate this fear of the unknown.
Despite the ongoing research into TN, much about the disease remains unknown. Percutaneous balloon micro-compression, radiofrequency thermal coagulation, and glycerol injection are usually the first surgical options considered for the elderly, medically unfit, and those unwilling to assume the risks involved with a microvascular decompression. Although the pain is likely to return with these percutaneous procedures, they can be repeated. In classic TN no single treatment is effective for all patients. The main function of any of these procedures, however, is to improve a patient's quality of life, by establishing effective pain relief while limiting side effects.
Table 1. Three Peripheral Sensory Branches of Trigeminal Neuralgia (Netter, 1995) V1 Ophthalmic This branch passes through the superior Sensory orbital fissure. Conveys sensation from the upper face (eyes, forehead, nose), cornea, meninges of the anterior cranial fossa, paranasal sinuses, and part of the nasal mucosa. V2 Maxillary This branch exits the skull through the Sensory foramen rotundum. Conveys sensation from the midface (upper teeth, gums, upper lip and cheeks, lower eyelid and the side of the nose), hard palate, maxillary sinus, part of the nasal mucosa, meninges of the middle cranial fossa. V3 Mandibular The largest branch is joined by the Sensory motor root and exits the skull through Motor the foramen ovale. Conveys sensation from the lower face (lower teeth, gums and lower lip), buccal mucosa, tongue, part of the external ear, auditory meatus, meninges of the middle cranial fossa. Motor nerves supply the muscles of mastication (temporal and masseter), and the tensors of the soft palate and tympanic membrane.
I thank Matt Wheatley, MD, J. Max Findlay, MD, the neurosurgical associates, and Cathie Christensen for their input and guidance in the preparation of this paper.
Adler, R.J. (1989). Trigeminal glycerol chemoneurolysis: Nursing implications. Journal of Neuroscience Nursing, 21, 337-341.
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Kruger, L., & Young, R.F. (1981). Specialized features of the trigeminal nerve and its central connections. In M. Samii & P.J. Jannetta (Eds.), The cranial nerves (pp. 273:-296). Berlin: Springer-Verlag.
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Siegfried, J. (1981). Percutaneous controlled thermocoagulation of gasserian ganglion in trigeminal neuralgia. Experiences with 1000 cases. In M. Samii & P.J. Jannetta (Eds.), The cranial nerves (pp. 322-330). Berlin: Springer-Verlag.
Tekkok, I., & Brown, J.A. (1996). The neurosurgical management of trigeminal neuralgia. Neurosurgery Quarterly, 6(2), 89-107.
Wilkins, R.H. (2002). Trigeminal neuralgia: Historical overview, with emphasis on surgical treatment. In K.J. Burchiel (Ed.), Surgical management of pain (pp. 288-302). New York: Thieme Medical Publishers, Inc.
Questions or comments about this article may be directed to: Debbie Filipchuk, RN CPN (C), by phone at 780/407-6955 or by e-mail at firstname.lastname@example.org. She is a staff nurse and a registered nurse first assist in the neurosurgery theaters in the surgical suite at the University of Alberta Hospital, Edmonton, Alberta, Canada.
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|Title Annotation:||neuroscience nursing research; includes table|
|Publication:||Journal of Neuroscience Nursing|
|Date:||Apr 1, 2003|
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