A traumatic brain injury (TBI) can cause migraines. A TBI is defined as an alteration in brain function or other evidence of brain pathology caused by an external force, such as a blow to the head or a rapid acceleration/deceleration movement. Headaches are the most common symptom following a TBI, and these post-traumatic headaches (PTH) frequently manifest with features that meet the diagnostic criteria for migraine.
Understanding Traumatic Brain Injury Classifications
The severity of a traumatic brain injury is categorized to guide immediate treatment and predict long-term prognosis. Classification relies on the Glasgow Coma Scale (GCS) score, the duration of lost consciousness, and the length of post-traumatic amnesia. The GCS is an objective scoring measure that assesses a person’s eye-opening, verbal, and motor responses, with scores ranging from 3 to 15.
A mild TBI (mTBI), often called a concussion, is the most prevalent type, accounting for approximately 80% of all cases. This classification involves a GCS score of 13 to 15, a loss of consciousness lasting less than 30 minutes, and post-traumatic amnesia of less than 24 hours. Moderate TBI is characterized by a GCS score between 9 and 12, while a severe TBI involves a GCS score of 8 or less, often signaling a comatose state. The majority of TBI-related headaches and subsequent migraines occur following a mild TBI, demonstrating that injuries without severe initial symptoms can lead to chronic pain.
The Direct Link Between TBI and Migraine Onset
The headache that follows a TBI is known as a Post-Traumatic Headache (PTH), which starts within seven days of the injury. These headaches are a common consequence of head trauma, with acute PTH reported by 60% of patients with mild TBI two weeks post-injury. The clinical features of PTH frequently overlap with those of primary headache disorders, most often resembling migraine or tension-type headache.
PTH is classified as either acute, meaning it resolves within three months, or persistent (chronic) if it lasts beyond that three-month window. A significant proportion of initial sufferers continue to experience chronic headaches, with approximately 29% of those with acute PTH still reporting symptoms one year later. When this persistent headache meets the criteria for migraine—including features like throbbing pain, sensitivity to light and sound, and nausea—it is specifically diagnosed as post-traumatic migraine. The severity of the initial injury does not correlate with the persistence of the headache, as patients with mTBI can suffer for months or years.
Physiological Changes Driving Post-Traumatic Migraines
The development of a chronic, migraine-like headache after a TBI is driven by several complex changes within the central nervous system. The physical trauma initiates a state of neuroinflammation, where the injury triggers a persistent inflammatory response in the brain. This response involves the release of pro-inflammatory mediators and cytokines, which can alter the function and sensitivity of structures involved in head pain, such as the trigeminovascular system.
This initial neuroinflammatory cascade leads to the sensitization of pain pathways, particularly within the trigeminal nucleus caudalis (TNC) in the brainstem. This phenomenon, known as central sensitization, lowers the pain threshold, causing normally non-painful stimuli to be perceived as painful (allodynia). The prolonged activation of these sensory neurons creates a state of hyperexcitability, which is a hallmark of chronic pain conditions like migraine.
Chemical imbalances further contribute to the chronic pain state, involving Calcitonin Gene-Related Peptide (CGRP). CGRP is a potent vasodilator and pain transmitter released by trigeminal nerve endings, and its release is strongly implicated in migraine pathophysiology. Following TBI, inflammatory processes can upregulate CGRP synthesis and release, creating a positive feedback loop that promotes neurogenic inflammation and sustains the sensitization of the trigeminal system.
Managing and Treating Post-Injury Headaches
Managing post-traumatic headaches typically involves a multi-modal approach that addresses both the acute attacks and the long-term prevention of chronic pain. Acute treatment focuses on stopping a headache once it has started, often utilizing migraine-specific medications such as triptans, which target serotonin receptors to constrict blood vessels and block pain pathways. Non-steroidal anti-inflammatory drugs (NSAIDs) and combination analgesics are also commonly used, but caution is necessary to prevent medication overuse headache (MOH), a risk in chronic sufferers who take acute medications too frequently.
For persistent post-traumatic migraine, prophylactic (preventative) treatment is initiated to reduce the frequency and severity of attacks. Traditional preventative agents include certain anti-seizure medications like topiramate and valproate, as well as beta-blockers and some antidepressants. Newer, highly effective options target the CGRP pathway, such as CGRP monoclonal antibodies, which are recommended due to their proven efficacy in reducing monthly migraine days.
Non-pharmacological strategies are also integrated into the treatment plan to provide comprehensive care. These include physical therapy to address any associated neck pain or musculoskeletal issues, biofeedback training for pain management, and cognitive behavioral therapy (CBT) to address common comorbidities like anxiety and depression. A specialized headache provider is often necessary to tailor these treatments, as the optimal strategy depends on the headache’s specific characteristics and any co-occurring symptoms.