Avoiding Diagnostic Pitfalls in Facial Pain: A Case Report of Paroxysmal Hemicrania Initially Treated as Trigeminal Neuralgia
- 1Neurology Department, Consilium Medulla Multiprofile Clinic, Tbilisi, GEO
- 2School of Health Sciences, University of Georgia, Tbilisi, GEO
Abstract
A 21-year-old man presented with a two-year history of recurrent, strictly unilateral left-sided pain in the upper maxillary and orbital regions, radiating to the temporal and occipital areas. Individual attacks lasted 20 to 30 minutes and occurred 10 to 20 times daily, on most days throughout the two-year period. He had been diagnosed elsewhere with trigeminal neuralgia and treated with carbamazepine 200 mg twice daily without benefit. He denied photophobia, phonophobia, and ipsilateral cranial autonomic features, but described prominent restlessness during attacks. No cutaneous or mucosal trigger could be identified, and neurological examination was normal. The attack duration, the reported high attack frequency, the absence of tactile triggers, and the restlessness were inconsistent with classical trigeminal neuralgia and raised suspicion of a trigeminal autonomic cephalalgia, including probable paroxysmal hemicrania. Carbamazepine was withdrawn, and an escalating oral indomethacin trial was initiated, reaching 225 mg daily and maintained at that dose for 14 consecutive days. A headache diary begun on the first day of the trial recorded headache on all 20 days, and the patient reported no improvement at any point. Because the phenotype fulfilled all but the indomethacin-response criterion, the diagnosis was recorded as probable paroxysmal hemicrania, while cluster headache and other trigeminal autonomic cephalalgias remained in the differential diagnosis. Verapamil 240 mg daily was substituted on day 21. Headache days fell to 23 of 31 in the first month and 13 of 31 in the second, with the last 18 days of the second month free of headache. At telephone follow-up, the patient reported sustained resolution, with only mild headaches related to sleep deprivation that he considered distinct from his previous syndrome. He remains on verapamil. Whether verapamil produced the improvement cannot be established from a single uncontrolled case, as the drug was never withdrawn, and spontaneous remission remains possible. This case illustrates the clinical overlap between trigeminal neuralgia and the trigeminal autonomic cephalalgias and highlights the value of structured longitudinal symptom recording, ideally including individual attack count, duration, autonomic features, and triggers.
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BibTeX
@article{chehimi2026avoiding,
title = {{Avoiding Diagnostic Pitfalls in Facial Pain: A Case Report of Paroxysmal Hemicrania Initially Treated as Trigeminal Neuralgia}},
author = {Abdul Amir Chehimi and Marwan D Jaber and Ali Ba Nafea and Teimuraz Kakubava},
journal = {Cureus},
year = {2026},
month = oct,
doi = {10.7759/cureus.117284},
url = {https://europepmc.org/article/PMC/PMC13723051},
note = {CC BY},
}
RIS
TY - JOUR
TI - Avoiding Diagnostic Pitfalls in Facial Pain: A Case Report of Paroxysmal Hemicrania Initially Treated as Trigeminal Neuralgia
AU - Abdul Amir Chehimi
AU - Marwan D Jaber
AU - Ali Ba Nafea
AU - Teimuraz Kakubava
PY - 2026
DA - 2026/10/01
JO - Cureus
DO - 10.7759/cureus.117284
UR - https://europepmc.org/article/PMC/PMC13723051
AB - A 21-year-old man presented with a two-year history of recurrent, strictly unilateral left-sided pain in the upper maxillary and orbital regions, radiating to the temporal and occipital areas. Individual attacks lasted 20 to 30 minutes and occurred 10 to 20 times daily, on most days throughout the two-year period. He had been diagnosed elsewhere with trigeminal neuralgia and treated with carbamazepine 200 mg twice daily without benefit. He denied photophobia, phonophobia, and ipsilateral cranial autonomic features, but described prominent restlessness during attacks. No cutaneous or mucosal trigger could be identified, and neurological examination was normal. The attack duration, the reported high attack frequency, the absence of tactile triggers, and the restlessness were inconsistent with classical trigeminal neuralgia and raised suspicion of a trigeminal autonomic cephalalgia, including probable paroxysmal hemicrania. Carbamazepine was withdrawn, and an escalating oral indomethacin trial was initiated, reaching 225 mg daily and maintained at that dose for 14 consecutive days. A headache diary begun on the first day of the trial recorded headache on all 20 days, and the patient reported no improvement at any point. Because the phenotype fulfilled all but the indomethacin-response criterion, the diagnosis was recorded as probable paroxysmal hemicrania, while cluster headache and other trigeminal autonomic cephalalgias remained in the differential diagnosis. Verapamil 240 mg daily was substituted on day 21. Headache days fell to 23 of 31 in the first month and 13 of 31 in the second, with the last 18 days of the second month free of headache. At telephone follow-up, the patient reported sustained resolution, with only mild headaches related to sleep deprivation that he considered distinct from his previous syndrome. He remains on verapamil. Whether verapamil produced the improvement cannot be established from a single uncontrolled case, as the drug was never withdrawn, and spontaneous remission remains possible. This case illustrates the clinical overlap between trigeminal neuralgia and the trigeminal autonomic cephalalgias and highlights the value of structured longitudinal symptom recording, ideally including individual attack count, duration, autonomic features, and triggers.
SN - 2168-8184
ER -