Review Article DOI: 10.18231/2395-6194.2017.0053 Journal of Oral Medicine, Oral Surgery, Oral Pathology and Oral Radiology, 2017; 3(4):222-224 222 Duloxetine- A novel therapeutic regimen for trigeminal neuralgia Akhilanand Chaurasia Assistant Professor, Dept. of Oral Medicine & Radiology, Faculty of Dental Sciences, King George’s Medical University, Lucknow Corresponding Author: Email:chaurasiaakhilanand49@gmail.com Abstract Duloxetine is a potent and selective inhibitor of serotonin and noradrenaline transporters and a weak inhibitor of dopamine transporters. Duloxetine is highly protein bound and is widely distributed throughout tissues. It is rapidly and extensively metabolized in the liver by cytochrome P450 (CYP) 1A2 and 2D6 and its numerous metabolites which are inactive are mainly excreted in the urine. It is more effective for recurrent/refractory type of TN. Duloxetine holds the promise in complete remission of TN in future. So in coming days it may be a drug of choice for medical management of TN. This article is an insight in chemical features, pharmacodynamics, pathophysiology and therapeutics of Duloxetine. Keywords: Antidepressants, Serotonin uptake inhibitors, Trigeminal Neuralgia, Major depressive disorders Introduction Trigeminal neuralgia (TN) is defined by the International Headache Society (IHS) as “unilateral disorder characterized by brief electric shock like pains, abrupt in onset and termination, and limited to the distribution of one or more divisions of the trigeminal nerve”. (1) Trigeminal neuralgia, a neuropathic pain syndrome is considered one of the most painful conditions experienced by people and is characterized by a severe, almost exclusively unilateral, neuropathic pain located within the distribution of the trigeminal nerve. Its relapsing-remitting and excruciating characteristics can severely and negatively affect the quality of life and increase the risk of depression in affected people. (2) The IHS has classified TN into classical type (CTN) and symptomatic type (STN). The classical TN is also known as essential/idiopathic TN. The pain in STN is indistinguishable from that of classical trigeminal neuralgia (CTN) but caused by a demonstrable structural lesion other than vascular compression. The diagnosis of CTN requires the absence of a clinically evident neurological deficit. CTN starts in the second or third divisions of trigeminal nerve affecting the cheek or the chin .(1) The ophthalmic division alone is involved in less than 5% of cases. (3) The single attack generally lasts from less than a second to a few seconds, but it may present in clusters of variable intensity with up to 2 minutes duration. In many cases it is followed by a brief refractory period during which a new stimulation is not able to evoke another attack. Between paroxysms the patient is usually pain free but a dull background pain may persist in some cases. (1) Growing neurosurgical data advocate the distinction of these two subtypes of TN into type 1 as defined as >50% episodic onset of TN pain and type 2 defined by >50% constant pain. (4,5) Trigeminal neuralgia (TN) is a facial pain syndrome characterized by paroxysmal, shock-like pain attacks located in the somato-sensory distribution of the trigeminal nerve. The prevalence of TN in the general population is 0.015%. (6) Facial pain has a considerable impact on quality of life. It has been recently shown that TN is the most frequent type of facial pain (7) and that, among facial pain syndromes, the overall incidence of TN has remained constant (8) ranging from 12.6/100,000/year (7) to 27/100,000/year. (8) TN is uncommon in population younger than 40 years (overall incidence of 0.2/100,000/year) and increases in incidence with advancing age, occurring in 25.9/100,000/year in individuals older than 80 years (9) TN appears to be slightly more common among women and has both classical and symptomatic (~15% of cases) subtypes with the former most often associated with a neurovascular conflict of the trigeminal nerve in the prepontine cistern. (10) The right side is more frequently involved. (11) When TN occurs in young age or presents with bilateral symptoms, lack of triggered pain, absence of a refractory period, or an abnormal neurologic examination, secondary causes such as multiple sclerosis (MS) should be suspected (10) Bilaterality may be seen in 5% of classical cases, but even in these cases, synchronous pain is not observed. Patients with bilateral TN often have a positive family history12. In patients affected by MS, prevalence is higher, ranging from 1% (13) to 6.3%. (14) Duloxetine is a potent and selective inhibitor of serotonin and noradrenaline transporters and a weak inhibitor of dopamine transporters. It has a low affinity for neuronal receptors like α adrenergic, dopamine D, Histamine H, Muscarinic, opioid and serotonin receptors as well as ion channel binding sites and other neurotransmitter transporters such as choline and GABA transporters. It does not inhibit monoamine oxidase types A or B. Duloxetine is highly protein bound and is widely distributed throughout tissues. It is rapidly and extensively metabolized in the live cytochrome P450 (CYP) 1A2 and 2D6 and itsnumerous