Treatment-resistant cases of trigeminal neuralgia may be treated with duloxetine, according to a new case study.
Duloxetine may be effective in treating trigeminal neuralgia with comorbid major depressive disorder, especially in treatment-resistant cases, according to a case study published in The Annals of Pharmacotherapy.
Researchers in Taipei, Tawain, describe the case of a 37-year-old woman treated with duloxetine for trigimenal neuralgia, a neuropathic pain condition that affects one or more branches of the trigeminal nerve. Typically, attacks are brief but painful, like shocks, and are distributed among the trigeminal nerve branches, according to the authors. The sudden shocks of pain often come without warning or symptoms to alert patients about potential problems.
Initially, the patient was treated with daily 800mg of carbamazepine, which did not show signs of providing pain relief. Over a period of 3 years, the patient was generally unresponsive to a myriad of combination therapies and medications, including: carbamazepine, valproate, baclofen, dicofenac, and acetaminophen. The patient underwent multiple gamma knife radiosurgery procedures, which also did not relieve her symptoms.
After developing what the researchers called “clinically significant” depressive symptoms, the patient was diagnosed with major depressive disorder. To manage her depression, she was prescribed a daily dose of 30 mg of duloxetine. The dosage was gradually increased to 60 mg daily.
The researchers reportedly were surprised to find that at 60 mg daily, the patient described improvement in trigeminal neuralgia pain within the first 7 days. The patient’s mood also gradually improved over the following 3 weeks.
At the time of a 4-year follow-up, the patient had been tapered off the various medications. The woman’s major depressive disorder and trigeminal neuralgia were managed on a daily combination of 60 mg duloxetine and 600 mg carbamazepine.
“The mechanisms may be related to duloxetine’s ability to modulate norepinephrine and serotonin and antagonize N-methyl-d-aspartate (NMDA) receptors,” the authors concluded. “The ignition hypothesis is a proposed etiology of trigeminal neuralgia, in that any individual hyperexcitable neuron can spread its discharge quickly to activate the entire population of neurons. We suggest that duloxetine exerts desynchronizing effects through its NMDA antagonism, modulating the hyperexcitable state of the trigeminal afferents.”