Motor vehicle accidents are the most frequent cause of head injury (42%), and men 15 to 24 years old are at the highest risk. Other causes of head injury include falls (23%), assaults (14%), and sports accidents (6%) (58).
Many of these patients suffer from posttraumatic syndrome and have additional somatic and neuropsychologic symptoms.

MHI accounts for more than 75% of brain injuries (26) and its annual incidence varies from 131 to 511 per 100,000 inhabitants (15). PTHA follows head trauma and whiplash injury in 30 to 90% of patients (14,25). The reported incidence of chronic PTHA also varies from one study to another, in part because of disagreement on the duration of symptoms from the time of injury. The new IHS diagnostic criteria define chronic PTHA when symptoms persist beyond 3 months of the original insult (22). Up to 32% of patients with head injury report persistent headaches 3 months after trauma, and approximately one in four continues to report headache at 4 years (4,6, 13,25).

The IHS criteria require the onset of PTHA to be within 1 week of head trauma (22). However, some studies indicate that late-acquired headaches (starting more than 2 weeks after the trauma) may be as common (6,29) or more common (10) than those of early onset. Until well-designed case-control studies are performed, it is difficult to ascertain that these “late-onset headaches” are, indeed, posttraumatic in nature.

Posttraumatic syndrome is probably not a single pathologic entity but a group of traumatically induced disorders with overlapping symptoms. Headache is mainly a manifestation of brain dysfunction with occasional contributions from persistent musculoskeletal injuries. Axonal injury, soft tissue damage, cerebral metabolic derangements, and altered cerebral hemodynamics have been implicated in the genesis of symptoms, including headache, following head trauma.

Neck, jaw, and scalp tissue injuries may contribute to acute PTHA. Most of these injuries heal completely and cannot, by themselves, account for chronic PTHA. However, soft tissue or skeletal injuries may initiate or trigger a transformation process in headache-prone patients somewhat akin to the process of chronic migraine that evolves from an episodic disorder. Perhaps these injuries induce wind-up and sensitization, resulting in a permanently altered neuronal function (44).

Shear forces are applied to the brain during head injury, resulting in diffuse axonal insult, which varies in severity from functional abnormalities to widespread structural damage. Experimental and clinical data suggest that diffuse axonal injury occurs with MHI, but its extent and relevance remain elusive. A better understanding of the nature of neuroimaging abnormalities after MHI could shed light on the pathologic basis for the long-term neurologic disability that some patients with chronic PTHA develop. Indeed, newer magnetic resonance imaging (MRI) techniques (e.g., diffusion tensor imaging and magnetization transfer ratio) (1,23) may better delineate small parenchymal brain lesions, diffuse axonal injury secondary to disruption of axonal membranes, or delayed cerebral atrophy. Furthermore, magnetic resonance spectroscopy studies may detect metabolic brain changes (an early reduction in N-acetyl aspartate and an increase in choline compounds) that correlate with head injury severity (17,50). Lastly, positron emission tomography (PET), single-photon emission computed tomography (SPECT), and 133Xenon inhalation techniques provide additional insight into brain perfusion abnormalities after MHI and chronic posttraumatic symptoms (45,52).

The mechanisms of PTHA may mirror those of primary headaches. Neurochemical changes that are observed in typical migraine and in experimental traumatic brain injury include excessive release of excitatory amino acids (primarily glutamate); increase in extracellular potassium, intracellular sodium, or calcium; and accumulation of serotonin. Also, changes in levels of catecholamines and endogenous opioids, decline in magnesium levels, abnormalities in nitric oxide formation, and alterations in neuropeptides are observed (41,48). Furthermore, patients with PTHA may develop a central sensitization phenomenon as a result of traumatic focal lesions (27). Finally, both central and peripheral sensitization have been proposed to occur in PTHA (5,31,39).