Trigeminal neuralgia

Abstract

Trigeminal neuralgia (TN) is a sudden, severe, brief, stabbing, and recurrent pain within one or more branches of the trigeminal nerve. Type 1 as intermittent and Type 2 as constant pain represent distinct clinical, pathological, and prognostic entities. Although multiple mechanism involving peripheral pathologies at root (compression or traction), and dysfunctions of brain stem, basal ganglion, and cortical pain modulatory mechanisms could have role, neurovascular conflict is the most accepted theory. Diagnosis is essentially clinically; magnetic resonance imaging is useful to rule out secondary causes, detect pathological changes in affected root and neurovascular compression (NVC). Carbamazepine is the drug of choice; oxcarbazepine, baclofen, lamotrigine, phenytoin, and topiramate are also useful. Multidrug regimens and multidisciplinary approaches are useful in selected patients. Microvascular decompression is surgical treatment of choice in TN resistant to medical management. Patients with significant medical comorbidities, without NVC and multiple sclerosis are generally recommended to undergo gamma knife radiosurgery, percutaneous balloon compression, glycerol rhizotomy, and radiofrequency thermocoagulation procedures. Partial sensory root sectioning is indicated in negative vessel explorations during surgery and large intraneural vein. Endoscopic technique can be used alone for vascular decompression or as an adjuvant to microscope. It allows better visualization of vascular conflict and entire root from pons to ganglion including ventral aspect. The effectiveness and completeness of decompression can be assessed and new vascular conflicts that may be missed by microscope can be identified. It requires less brain retraction.

A charcot‐marie‐tooth type 1B kindred associated with hemifacial spasm and trigeminal neuralgia

“…The mechanism for this extreme predilection to develop HFS/TN is unclear. As in our kindred, sporadic cases of HFS and TN demonstrate advancing incidence with age and the onset age for sporadic HFS and TN is similar to that in our kindred . Sporadic HFS/TN is believed to be caused by compression of the cranial nerves by adjacent vasculature and this risk could be increased by nerve hypertrophy.…”

“…As in our kindred, sporadic cases of HFS and TN demonstrate advancing incidence with age and the onset age for sporadic HFS and TN is similar to that in our kindred. 32,33 Sporadic HFS/TN is believed to be caused by compression of the cranial nerves by adjacent vasculature 34,35 and this risk could be increased by nerve hypertrophy. Using neuromuscular ultrasound, we have previously shown that this family has hypertrophic nerves including the vagus nerve 36 and other MPZ mutations have been associated with cranial nerve thickening.…”

Trigeminal neuralgia: case report and literature review

“…The attacks of pain occur more frequently and more severely with time [6,7] and may manifest with one or several symptoms such as intense, shooting, stabbing pain that is similar to electric shocks, intermittent twinges of mild pain,spasms of pain, episodes of cluster attacks. TN pain can be focused in a specific area or spread over a widespread area [7,8,9] . TN pain episodes can last from a few seconds to several minutes, usually unilaterally, or less frequently on both sides of the face.…”

“…The attacks of pain may go into remission and patients maybe symptomless for months or years [5,7] . Women are twice as likely to be affected with this condition as men and in both genders, it is more prevalent after the age of 40 years [1,3] , with a prevalence of 4.3 per 100,000 [8,10] .…”

“…TN is classified as classical or symptomatic TN [5,8] and symptomatic TN is caused by disease that leads to neural damage such as multiple sclerosis, herpes zoster, trauma, space-occupying lesion or tumours of the cerebellopalatine angle [2,4] . Classical TN is caused by neurovascular conflict and is divided into type 1 and 2 [1,5] .…”