A recently published report describes the case of a 24-year-old male patient who experienced a 6-year-long continuous headache that was resistant to over 20 different medical treatments but was successfully treated with venlafaxine.
The patient, who had no significant past medical history, described the headache pain as pulsatile in nature and rated it as “mostly constant at 8-9”, occasionally reaching 10, according to a self-reported numerical pain scale. He stated that it was associated with fatigue, nausea, position sensitivity, and photophobia and often led to schoolwork and social difficulty.
The patient consulted a neurologist after self-administration of Excedrin, ibuprofen, and acetaminophen led to no change in his symptoms. After a course of topiramate was found to be ineffective, a magnetic resonance imaging study with contrast, as well as a sleep study were conducted. Neither study yielded any information to note.
The patient then consulted a headache specialist, who found elevated cerebral spinal fluid (CSF) pressure in 1 of 2 lumbar punctures. Additional analyses and medication trials were conducted to rule out various conditions: CSF analysis ruled out meningitis, encephalitis, and other abnormalities; fundoscopic examination ruled out pseudotumor cerebri; indomethacin trial ruled out hemicrania continua.
A neuropsychiatric evaluation was eventually conducted and the patient was found to meet criteria for new daily persistent headache (NDPH). He was trialed on over 20 medications/treatments, all of which yielded no long-term benefit. It was found, however, that daily administration of venlafaxine greatly reduced the patient’s headache pain and resulted in improvement of his other symptoms (nausea, fatigue, neuropsychiatric deficiencies).
The patient was initiated on venlafaxine 37.5mg, which was further increased by 37.5mg every week. A dosage of 300mg was found to attenuate the patient’s headache pain and complete resolution of his symptoms occurred after 6 additional months of treatment.
At this time, the etiology of NDPH remains unclear. In this case, the authors hypothesized that the NDPH was caused by chronic inflammation via the cytokine tumor necrosis factor alpha (TNF-α) and that venlafaxine reduces NDPH symptoms by binding to the 5-HT2A receptor which causes inhibition of TNF-α signaling.
“Herein, we report on a patient who suffered with headache for 6 years failing to respond to over 20 different medical treatments, but found drastic improvement and eventual resolution with venlafaxine,” the study authors stated. They concluded, “Overall, venlafaxine should be considered specifically as a potential treatment for patients with NDPH.”
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