The pain attacks last for seconds or minutes and are typically triggered by stimuli such as touch, chewing, speaking, swallowing or brushing the teeth. The pain is so excruciating that in severe cases it is no longer possible to eat. On a pain scale of 1-10, the intensity is at the highest level. Pain attacks are often followed by vegetative symptoms such as redness and secretion from the tear, nasal and/or saliva glands. The attacks can occur several times a day for weeks and months. There may be pain-free intervals lasting weeks or months, but the individual trigger mechanism can cause new symptoms at any time. As a rule, the intensity increases and destroys the quality of life. 

The diagnosis of TN is based on the typical symptoms. At each initial diagnosis, an MRI examination is indicated. Contrast-enhanced imaging can detect, or, in most cases rule out, symptomatic TN. Using modern T2 thin-film technology (CISS sequences), the pathological neurovascular contact can be detected in the classical form. 

Therapy has evolved significantly in recent years. On the one hand, modern imaging has made it easier to secure the diagnosis. On the other hand, long experience with conservative and surgical methods have made it possible to define an optimal treatment pathway based on the cause of the suffering and the condition of the patient. An individual treatment concept with interdisciplinary patient care is the key to long-term therapeutic success. With symptomatic TN, the primary disease is treated. With classic TN, conservative drug therapy comes to the fore, and, due to the short duration of the attacks, this is usually a prophylaxis. The drugs must be selected and dosed individually. The dosage will be increased until satisfactory freedom from pain is achieved or intolerable side effects occur. 

A surgical procedure should always be considered if long-term drug therapy leads to side effects or only achieves insufficient results. In general, destructive-ablative and function-preserving methods are available. 

The ablative method causes thermal, chemical or mechanical damage to the trigeminal nerve. However, the special feature of treatment at our centre is not a destructive, but a function-preserving procedure: endoscopic microvascular decompression. The neurovascular conflict is remedied microsurgically and a curative solution is sought. The trigeminal nerve is exposed using a purely endoscopic technique, through a tiny keyhole-like opening behind the ear. At the nerve entry zone, the neurovascular conflict is identified with the aid of neuronavigation and the compressing vessel is detached from the nerve. By inserting a teflon piece, the nerve is then padded against the vessel, and the functions of the brain stem and the basal cranial nerves are tested with continuous electrophysiological monitoring. 

A particularly high success rate has been reported in recent years through the use of navigation-assisted, minimally invasive endoscopic methods. The essential advantage of endoscopy is that the site of the conflict can be represented particularly well and the decompression can be reliably assessed. Recurrences are rare with this disease, and definitive healing can be assumed in more than 90-95% of cases.