Poster #: 15A
Session/Time: A
Author: Anjani Patibandla, BS
Mentor: Yifan Guo, MD
Research Type: Case Report

Abstract

Introduction

Headache is a frequent neurologic manifestation of Long COVID, defined as persistent or newly developed symptoms following acute SARS-CoV-2 infection. However, the mechanisms underlying persistent headache and effective treatments remain uncertain. Headaches may develop after infection in patients without a prior headache disorder and can resemble migraine, tension-type headache, or mixed phenotypes. Management is generally directed toward the presenting phenotype and may provide limited relief in refractory cases. Although peripheral nerve dysfunction has increasingly been recognized in Long COVID, the role of focal nerve compression in post-COVID headache remains unclear. We describe a young woman with new-onset, treatment-resistant chronic daily headache following COVID-19 who experienced sustained resolution after peripheral nerve decompression.

Case Info

A 19-year-old woman with postural orthostatic tachycardia syndrome and complex regional pain syndrome type I of the left lower extremity, but no history of migraine or other primary headache disorder, developed severe headaches approximately three weeks after SARS-CoV-2 infection. Symptoms included diffuse head pain, retro-orbital pressure, visual changes, photophobia, and phonophobia. Over two years, headaches became continuous and significantly impaired school attendance and daily functioning. Multiple medications, botulinum toxin injections, and repeated peripheral nerve blocks provided inadequate or temporary relief. Severe nausea and poor oral intake resulted in a 25-pound weight loss and temporary nasogastric feeding. Brain and spine magnetic resonance imaging and rheumatologic evaluation were unrevealing. Targeted blocks of the bilateral supraorbital, supratrochlear, and greater occipital nerves produced substantial temporary relief, prompting staged peripheral nerve decompression. Surgical exploration demonstrated vascular compression, fascial scarring, and muscular fibrosis surrounding the affected nerves. Following decompression, headache severity and frequency progressively declined, with complete resolution by one-year follow-up. The Pediatric Migraine Disability Assessment (PedMIDAS) score improved from >50 to 0, and the Headache Impact Test-6 (HIT-6) score was 42. She reported only mild headaches approximately once weekly and returned to school and subsequently college.

Disc Clinical

The pathophysiology of Long COVID headache is likely multifactorial, with proposed contributions from inflammation, altered pain signaling, autonomic dysfunction, and peripheral nerve abnormalities. Recent studies demonstrating small-fiber dysfunction in Long COVID provide increasing evidence of peripheral nervous system involvement in persistent post-COVID pain. Peripheral nerve compression has also been implicated in other refractory headache syndromes and may respond to surgical decompression. In this patient, improvement after targeted nerve blocks and direct evidence of nerve compression at surgery suggest that focal peripheral pathology contributed to her symptoms. This response raises the possibility that diagnostic nerve blocks could identify patients with Long COVID headache who have a surgically addressable peripheral pain source. Further investigation is warranted to evaluate this potential treatment pathway.

Conclusion

This case demonstrates a novel therapeutic approach to refractory Long COVID headache in a patient without a pre-existing headache disorder. Targeted nerve blocks identified potential sites of peripheral involvement, while staged decompression was followed by sustained resolution of chronic daily headache and substantial functional recovery. Peripheral nerve evaluation may warrant consideration in selected patients with treatment-resistant Long COVID headache.