Trigeminal Nerve Block 

Updated: Dec 09, 2020
Author: Anusha Cherian, MD, MBBS, DNB; Chief Editor: Meda Raghavendra (Raghu), MD 

Overview

Background

Trigeminal nerve block provides hemifacial anesthesia and is used predominantly in the diagnosis and treatment of neuralgia. It is a relatively underused procedure, mainly owing to the difficulty of achieving a reliable block. Before proceeding with the block, one should have a precise knowledge of the anatomy, should be thoroughly familiar with the details of the procedure, and should be fully aware of the potential complications.

Indications

Trigeminal nerve block is indicated for the following[1, 2] :

  • Treatment of trigeminal neuralgia

  • Diagnostic testing

  • Recalcitrant herpes zoster ophthalmicus

  • Postherpetic neuralgia

Trigeminal neuralgia is characterized by spontaneous, paroxysmal lancinating pain in the trigeminal nerve distribution. Often, the cause is not known. Occasionally, tumor infiltration, vascular compression of the nerve, or diseases such as multiple sclerosis may be the causative factors. Therefore, these patients should undergo complete neurologic evaluation.

Oral carbamazepine is the drug of choice and is effective in the majority of cases; trigeminal nerve block is reserved for patients who do not respond to medical treatment or patients in whom neurologic decompression of the canal is not feasible or has failed.[3, 4]

Before neurolysis is carried out, the patient’s response to a diagnostic block with local anesthetic must be assessed.

Contraindications

Trigeminal nerve block is contraindicated for the following:

  • Patients who refuse the procedure

  • Patients who have coagulation abnormalities or are taking anticoagulant drugs

  • Patients on antiplatelet medications

  • Pregnant women

Technical Considerations

The trigeminal nerve is the fifth cranial nerve and supplies sensory innervations to the face via its branches (see the image below). The trigeminal nerve ganglion (also referred to as the gasserian ganglion) lies in the trigeminal cave (also known as the Meckel cave), which is a dural invagination in the petrous part of the temporal bone. This ganglion is formed by 2 roots that exit the ventral surface of the brainstem at the midpontine level and travel forwards and laterally to enter the trigeminal cave.

Sensory distribution of the trigeminal nerve Sensory distribution of the trigeminal nerve

The trigeminal ganglion is bounded medially by the cavernous sinus, superiorly by the inferior surface of the temporal lobe, posteriorly by the brainstem, and anteriorly by its exiting 3 branches (ophthalmic, maxillary, and mandibular; see the image below). The dural pouch (trigeminal cistern) contains cerebrospinal fluid (CSF) and lies behind the ganglion. The postganglionic fibers are the sensory nerves to the face and exit via various foramina at the base of the skull.

Trigeminal ganglion and its major branches Trigeminal ganglion and its major branches

The structures supplied by the branches of the trigeminal ganglion are as follows (see the image above):

  • Ophthalmic branch (V1) – This provides the sensory supply to the eyes and forehead; it exits at the superior orbital fissure, and its branches are the nasociliary, lacrimal, and frontal nerves

  • Maxillary branch (V2) – This supplies the midface and upper jaw; it exits via the foramen rotundum, and its branches include the zygomatic, infraorbital, superior alveolar, and sphenopalatine nerves

  • Mandibular branch (V3) – This supplies the lower jaw; it exits via the foramen ovale, and its branches are the lingual, auriculotemporal, inferior alveolar, buccal, and mental nerves

The ophthalmic and maxillary nerves are purely sensory. The mandibular nerve has sensory and motor functions. For more information about the relevant anatomy, see Trigeminal Nerve Anatomy.

Outcomes

The success of a trigeminal nerve block depends on proper identification of the anatomic landmarks and the nerve itself. The duration of the block depends on the agent used. Local anesthetics typically provide analgesia lasting up to 12 hours, whereas neurolytic agents such as glycerol or alcohol have effects lasting for up to 6 months. Radiofrequency ablation has a 98% success rate and yields a longer pain-free period. Treatment with glycerol has a success rate of 70-90% and a recurrence rate of 54% at 4-year follow-up.

In a study of 79 patients who underwent either percutaneous anhydrous glycerol rhizolysis (PRGR) or radiofrequency (RF) thermocoagulation, 23 (58.9%) of the 40 PRGR patients and 33 (84.6%) of the 39 RF patients experienced excellent pain relief. The mean duration of excellent pain relief in the 2 groups was comparable.[5] By the end of the study period, 39.1% of the PRGR patients and 51.5% of the RF patients had experienced recurrence of pain.

 

Periprocedural Care

Patient Education and Consent

Patients are asked not to eat or drink anything for 6 hours before the procedure. Except for anticoagulants and antiplatelet agents, routine drugs are allowed. Patients should be accompanied by a responsible adult.

The physician must explain the procedure, complications, and expected outcomes. Patients should be informed that a local anesthetic will be used to block the nerves causing the pain. They should be warned of possible facial numbness and weakness of facial muscles, especially decreased ability to chew (usually transient, resolving within 24 hours). They should understand that pain may recur after the drug wears off. They should notify the treating physician of the intensity of pain experienced and the amount of relief achieved during the block.

Patients should be made aware of potential side effects, the most common of which is swelling and bruising of the face. Rarely, some residual weakness of muscles or difficulty in breathing or swallowing can occur as a consequence of the involvement of other nerves. If these side effects arise, this must be communicated to the physician, and appropriate treatment must be administered. Patients may have to be kept under observation for at least 2 hours after the procedure.

Equipment

Trigeminal nerve block should be performed only in a predesignated room that has the essential facilities for conducting the block safely and for resuscitating the patient in case of any major adverse events.

Necessary equipment includes the following:

  • 22-gauge long spinal needle (10 cm)

  • 5-mL syringe (for the block)

  • 1-mL syringe (for infiltration of skin)

  • Sterile drapes

  • Skin disinfectant – Alcohol, povidone-iodine, or chlorhexidine

  • Local anesthetic – Lidocaine or bupivacaine

  • Neurolytic agent – Alcohol, glycerol, or phenol

  • Sterile gloves

  • C-arm with fluoroscopy unit

This procedure must be done with appropriate monitoring in place. This may involve pulse oximetry, noninvasive blood pressure (NIBP) monitoring, electrocardiography (ECG), end-tidal carbon dioxide or respiratory rate monitoring, or a combination of 1 or more of these methods. Resuscitation drugs and equipment should be readily available.

Patient Preparation

For trigeminal nerve block, the patient undergoes mild sedation with midazolam 0.5-1 mg or fentanyl 50-100 µg. Local anesthetics (eg, lidocaine 2% or bupivacaine 0.5%) may be used to provide temporary pain relief until the drug is metabolized.

The patient is placed in a supine position on an imaging table with an intravenous line in place and all monitors attached. The positioning of the head depends on the specific approach to the procedure (see Technique).

 

Technique

Approach Considerations

Neurolytic agents provide a longer duration of pain relief, typically lasting for a few months. They achieve this by causing destruction of nerve fibers and wallerian degeneration of axonal fibers and Schwann cells. The neurons regenerate in 3-5 months. Often, it might take 1-2 weeks before complete pain relief is experienced.

The neurolytic agents used in trigeminal nerve block include the following:

  • Glycerol (100%) – This agent is typically used for treating trigeminal neuralgia; it is a mild neurolytic agent, but it can also cause perineural damage

  • Alcohol (50-70%) – Currently, this agent is rarely used because of its high rate of complications; it can seep into surrounding tissues and cause necrosis and cellular injury, and it can also cause vasospasm

  • Phenol (4-10%) – This agent is also commonly used; it can cause warmth and numbness on injection, and it can cause convulsions and cardiovascular collapse if inadvertently injected intravascularly

Techniques for Trigeminal Nerve Block

Trigeminal nerve block can be accomplished either via the classic approach (guided by the anatomic landmarks) or with the help of imaging (guided by fluoroscopy or computed tomography [CT]).

Classic approach

The patient is placed in a supine position with the head in a neutral position and the eyes staring straight ahead. The key anatomic landmark—a point 2-3 cm lateral to the angle of the mouth on the side to be blocked—is marked.

The skin over the cheek on the involved site is prepared with iodophor or povidone-iodine and draped. A skin wheal is raised with a local anesthetic. A 22-gauge 10-cm long spinal needle is inserted here and advanced upward toward the mandibular condyle (see the images below). This plane should be in line with the pupil as the patient’s eyes stare ahead, and the trajectory should be cephalad toward the external auditory meatus.

Direction of needle entry for gasserian ganglion b Direction of needle entry for gasserian ganglion block
Trigeminal nerve block Trigeminal nerve block

At a depth of 4-6 cm, the greater wing of the sphenoid at the base of the skull is contacted. The needle is withdrawn and redirected more posteriorly so as to enter the foramen ovale. It is then advanced 1-1.5 cm. Paresthesia at the mandible is elicited, followed by paresthesia in the maxilla and orbit.

Image-guided approach

The foramen ovale is identified by using the C-arm image intensifier. The patient’s head is placed in the reverse occipitomental position (chin up and neck extended), turned 30° to the opposite side. The x-ray beam is directed with a 30° caudal angulation. A small focal point and a small field size are recommended. The foramen ovale can be imaged here; in some cases, this proves quite difficult.

The 22-gauge spinal needle is advanced to reach the foramen ovale in much the same fashion as in the classical approach (see above). Lateral screening is done to check the depth of insertion. As the needle enters the trigeminal cistern, cerebrospinal fluid (CSF) is aspirated. The needle is then gradually withdrawn until CSF is no longer aspirated.

Contrast is injected to visualize the filling of the cistern and to confirm that the needle has not entered a vessel. Next, 0.3 mL of bupivacaine 0.25% is injected, and the patient’s response to this is assessed. Longer-lasting blockade with alcohol or glycerol can be planned later, after the response to the local anesthetic has been evaluated.

When a hyperbaric solution is used, the patient must be seated in an upright position to help the drug settle in the inferolateral position of the cistern through the action of gravity. The patient is left in this position for at least 1 hour.

Trigeminal nerve block may also be performed under ultrasound guidance. The advantage of using ultrasonography is that vascular structures, particularly the maxillary artery, can be visualized throughout its course in the infratemporal and the pterygopalatine fossa and inadvertent intravascular injection of the agent used to block the nerve may be prevented. It also prevents exposure to radiation as occurs during x-ray imaging. A recent article published a case series on 15 consecutive adult patients with uncontrolled facial pain due to various causes. Trigeminal nerve block was performed under ultrasound guidance in these patients. The authors confirmed this technique to be feasible, safe, and effective.[6]  Five ml of local anesthetic placed below the lateral pterygoid muscle in the pterygopalatine fossa results in immediate sensory block in the distribution of trigeminal nerve in most patients.

Complications

Hematoma of the face and subsclera is a common complication of this technique; the pterygopalatine space is highly vascular and is close to the middle meningeal artery. Direct intravascular injection of the drug into the carotid artery may occur. Total spinal anesthesia may develop. CSF is frequently encountered on withdrawal of the syringe in the trigeminal cistern. Injection of local anesthetic in this area can cause cardiac and respiratory arrest as the drug spreads on the ventral surface of the brainstem.

For these reasons, trigeminal nerve block must be performed only by experienced personnel. Maximal caution must be exercised, and resuscitative equipment must be kept ready. Performing the block under imaging guidance can prevent these complications to a large extent.

With an intravascular injection, drug toxicity can manifest as cardiovascular or central nervous system effects. Pain, masticatory weakness, neurolysis, or persistent paresthesia may occur. Facial numbness may be profound. Abolition of corneal reflexes can produce exposure keratitis and dryness of eyes.

 

Medication

Medication Summary

The goals of pharmacotherapy are to reduce morbidity and to prevent complications.

Local Anesthetics, Amides

Class Summary

Local anesthetics block the initiation and conduction of nerve impulses.They are used to increase patient comfort during the procedure.

Bupivacaine and epinephrine (Marcaine with epinephrine, Vivacaine, Sensorcaine with epinephrine)

This decreases permeability to sodium ions in neuronal membranes, resulting in the inhibition of depolarization, thereby blocking the transmission of nerve impulses. Epinephrine prolongs the duration of the anesthetic effects from bupivacaine by causing vasoconstriction of the blood vessels surrounding the nerve axons.

An 18-gauge needle is introduced medial to the tibialis anterior tendon, and 15-20 mL of saline or 0.25% bupivacaine solution with epinephrine is injected to distend the ankle joint.

Bupivacaine (Marcaine)

Bupivacaine decreases permeability to sodium ions in neuronal membranes, resulting in the inhibition of depolarization, thereby blocking the transmission of nerve impulses.

Lidocaine (Xylocaine)

Lidocaine is an amide local anesthetic used in a 1-2% concentration. The 1% preparation contains 10 mg of lidocaine for each 1 mL of solution; the 2% preparation contains 20 mg of lidocaine for each 1 mL of solution. Lidocaine inhibits depolarization of type C sensory neurons by blocking sodium channels.

To improve local anesthetic injection, cool the skin with ethyl chloride before injection. Use smaller-gauge needles (eg, 27 gauge or 30 gauge). Make sure the solution is at body temperature. Infiltrate very slowly to minimize the pain. The time from administration to onset of action is 2-5 minutes, and the effect lasts for 1.5-2 hours.

Lidocaine and epinephrine (Xylocaine with epinephrine, Lignospan)

Lidocaine inhibits depolarization of type C sensory neurons by blocking sodium channels. Epinephrine prolongs the duration of the anesthetic effects from bupivacaine by causing vasoconstriction of the blood vessels surrounding the nerve axons.

Neurologics, Other

Class Summary

Neurolytic agents provide a longer duration of pain relief, typically lasting for a few months. They achieve this by causing destruction of nerve fibers and wallerian degeneration of axonal fibers and Schwann cells. The neurons regenerate in 3-5 months. Often, it might take 1-2 weeks before complete pain relief is experienced.

Glycerol

Glycerol is a mild neurolytic agent used for treating trigeminal neuralgia but may cause perineural damage. Glycerol may down-regulate central neuronal hyperexcitability.

Alcohol

Alcohol is used in therapeutic neurolysis; however, because of its high complication rate, it has fallen out of favor. Concentrations of 95% will reliably lyze sympathetic, sensory, and motor components of a nerve.

Phenol

Phenol causes nerve destruction by inducing protein precipitation. It causes a separation of the myelin sheath from the axon and axonal edema. The use of higher concentrations of phenol may predispose to a higher incidence of vascular injury.

CNS Depressants

Class Summary

For trigeminal nerve block, the patient undergoes mild sedation.

Midazolam

Midazolam increases the presynaptic GABA inhibition and reduces the monosynaptic and polysynaptic reflexes. It suppresses muscle contractions by facilitating inhibitory GABA neurotransmission and other inhibitory transmitters. The patient undergoes mild sedation with midazolam 0.5-1 mg.

Fentanyl (Duragesic, Actiq, Abstral)

Fentanyl citrate is a synthetic opioid that has 75-200 times more potency and a much shorter half-life than morphine sulfate. It has fewer hypotensive effects than morphine and is safer in patients with hyperactive airway disease because of minimal or no associated histamine release. By itself, fentanyl citrate causes little cardiovascular compromise, although the addition of benzodiazepines or other sedatives may result in decreased cardiac output and blood pressure.