Neuralgias

Trigeminal neuralgia

The diagnosis is established exclusively on the basis of clinical and anamestic data. Confirmation requires the presence of three or more attacks of unilateral pain strictly limited to the branches of the nervus trigeminus.

Key characteristics of the pain syndrome:

• Paroxysmal nature: attacks last from a couple of seconds to two minutes.
• Character: acute pain resembling a dagger stab or an electric shock.
• Triggering: attacks are provoked by touching specific trigger zones on the affected side of the face.
• Absence of focal neurological deficit and other causes for pain.

Two clinical types are distinguished. In classic neuralgia (type I), there is no facial pain whatsoever between attacks. If the disease progresses, it can transition to type II, where background burning, boring, or throbbing pain persists between shooting pains. This transition is caused by central sensitization—a pathological increase in the excitability of the sensory nucleus of the nerve and brain structures.

The basis of treatment is anticonvulsants, which block ectopic impulse generation. They help approximately 80% of patients. MRI and MR angiography are used to rule out tumors, multiple sclerosis, or to look for vascular compression prior to surgical intervention.

Postherpetic trigeminal neuralgia

Occurs as a consequence of herpetic involvement of the ganglion. In the acute phase (first 3 months), vesicular rashes appear on the skin and mucous membranes, along with pain, most often in the ophthalmic branch zone. If the pain syndrome persists for more than 3 months, postherpetic neuralgia is diagnosed. About 10% of patients are susceptible to this complication, mostly elderly individuals.

Due to damage to thick and thin myelin fibers, spontaneous neuronal activity increases. Clinically, this manifests as sensory disturbances, constant burning pain with shooting pains, and allodynia—a condition where even a light, non-painful touch causes severe pain. The pathology is treated similarly to the classic form.

Glossopharyngeal neuralgia

Glossopharyngeal nerve involvement is 10 times less common than trigeminal involvement (about 0.8 cases per 100,000 population). It typically debuts in middle and older age (around 50 years), with women being affected twice as often as men.

In most situations, the idiopathic form occurs, caused by compression of the nerve root at the brainstem (most often by the posterior inferior cerebellar artery). Rare symptomatic forms are provoked by pharyngeal or cerebellopontine angle tumors, metastases, tonsillar infections, vascular malformations, an elongated styloid process, or multiple sclerosis.

Atypical and muscular facial pain

Not all facial pain is neuralgia. Atypical facial pain is characterized by a constant, dull, and aching course (most commonly in the maxillary or frontal region) without objective somatic causes. The pain lasts for at least 6 months, causes severe distress, and often masks underlying depression, schizophrenia, or hypochondriacal disorder. Unlike neuralgia, there are no trigger zones, and symptoms are aggravated by stress, cold, or physical exertion. It is often accompanied by insomnia, decreased libido, and irritability.

Muscular facial pain is treated non-medically (post-isometric relaxation, acupuncture) and with trigger point blocks using 0.5% procaine solution. Dental correction for jaw occlusion disorders is mandatory, as is the elimination of functional factors using psychotherapy, tranquilizers, and antidepressants.

Class and exam questions

What else to study on this topic

• Mechanisms of central sensitization in pain chronification
• Neurovascular conflict: anatomy of the cerebellopontine angle
• Differential diagnosis of somatoform pain disorders
• Technique of therapeutic blocks in muscular facial pain
• The role of dental pathology in the development of facial pain

Other topics in "Chapter 29. Facial Pain"

Prepared by WhiteCoat Pro faculty in accordance with the medical school curriculum. For educational purposes only.