The stabbing, lancinating, recurrent facial pain associated with trigeminal neuralgia (TN) is considered one of the most painful sensations in human experience. It can impact mood, sleep, overall health, and employment and, in some cases, has led to suicide.
Treatment ranges from drug therapy to surgery. Therapeutic success is particularly dependent on differential diagnosis to distinguish classic TN from other types of facial pain, some of which share clinical features with TN.
TN1, or classic TN, generates repetitive volleys of piercing, paroxysmal pain that can last seconds or minutes and sometimes hours. It is almost always unilateral and typically occurs in the mandibular and maxillary divisions of the trigeminal nerve. TN1 can be triggered by everyday activities that stimulate the nerve, such as eating, speaking, or touching the face. Pain-free intervals range from several days to years, but typically the pain increases in frequency and severity over time.
TN1 is most often caused by vascular compression at the trigeminal nerve root. In rare cases, the nerve root may be compressed by a tumor, an aneurysm, or an arteriovenous malformation. Over time, demyelination of the nerve due to compression may generate random, spontaneous afferent discharges.
Sometimes misdiagnosed as dental pain, the pain in TN2 is distinguished by a throbbing, burning sensation that is constant rather than episodic. Some patients with TN2 report the shooting pain of TN1 as occurring within a background of chronic dull pain. TN2 can arise from various sources, including:
Although demyelinating disease and structural anomalies may be evident on high-resolution magnetic resonance imaging, neurovascular compression may not always be seen. For this reason, the clinical examination is critical in determining the best approach to treatment.
Management of TN and other types of neurologically based facial pain is best served by a team approach with close communication between neurologists and neurosurgeons.
In TN, the goal of pharmacologic intervention is to block or suppress painful trigeminal nerve discharges. TN1 does not respond well to analgesics but does to antiepileptic drugs such as carbamazepine, sometimes at lower doses than those used to treat epilepsy.
Although initial pain control usually can be achieved within days to weeks, the effect may wear off. Incremental dosing helps prevent dose-dependent adverse effects that might discourage patients from continuing a pharmacologic approach when it could be of great benefit.
Depending on the probable cause of TN, surgical options include microvascular decompression for classic TN1 and percutaneous denervating procedures or stereotactic radiosurgery to block the pain signal.
For cases of microvascular compression, surgery directed at the site of compression can stop the pain immediately and has excellent long-term durability. One advantage of this approach is that it minimizes the risk of facial numbness, a complication associated with ablation techniques.
Percutaneous ablation techniques, such as balloon compression or glycerol rhizotomy (the injection of an alcohol-like substance into the nerve), are less invasive but are also less durable because the nerve may recover over time. Stereotactic radiosurgery, another ablative technique, is the least invasive surgical approach, with excellent outcomes.
All ablative techniques intentionally damage the nerve and thus increase the patient's risk of facial numbness. Motor cortex stimulation is not used for TN1, but it has been found effective for selected cases of intractable trigeminal neuropathic pain arising from deafferentation or previous nerve injury in TN2.