Trigeminal Neuralgia is the most severe, highly disabling and difficult to treat neuropathic pain syndrome among multiple sclerosis patients with considerable burden for the individual suffering from. Trigeminal neuralgia characterized by recurrent paroxysms of unilateral, brief, stabbing, electric shock-like pain in one or more distribution of trigeminal nerve with sudden onset and termination bring triggered by innocuous stimuli. Trigeminal neuralgia prevalence is 20 times higher among multiple sclerosis patients than in general population. The most common cause of trigeminal neuralgia in multiple sclerosis is pontine demyelinating plaque. However, MRI findings and surgical approaches have suggested that neurovascular compression might also occur in association with multiple sclerosis as the concurring mechanism of demyelination along with pontine plaque. There is no specific well-defined strategy for the treatment of trigeminal neuralgia secondary to multiple sclerosis based on clinical evidence but is generally agreed on sodium channel blockers, i.e. Carbamazepine and Oxcarbazepine as the first line therapy. A new selective sodium channel 1.7 blocker with less central nervous system side effects is under development. Lamotrigine, baclofen, gabapentine, pregabalin, topiramate, phenytoin and onabotulinum toxin type A are possible treatment options for patients who do not respond to first-line prophylactic drugs. Surgical interventions including microvascular decompression, gamma knife radiosurgery and Gasserian ganglion procedures should be considered in multiple sclerosis patients with trigeminal neuralgia refractory to medical treatment options.