Abstract:
Introduction. Posttraumatic headache (PTH) is defined as a headache attributed to trauma, or injury
to the head and/or neck. Acute PTH develops within 7 days after a traumatic brain injury (TBI),
whereas persistent PTH lasts longer than 3 months. Clinically, PTH may resemble migraine or tensiontype headache, while other forms include occipital neuralgia, cluster headache, low cerebrospinal fluid
pressure headache, supraorbital/infraorbital headache, cervicogenic headache and headache associated
with whiplash injuries. Posttraumatic hematomas may also cause headache. The aim of this study was
to highlight the pathophysiological mechanisms underlying posttraumatic headache.
Material and methods. A literature review was performed using PubMed, ResearchGate, Google
Scholar, medRxiv, EMBASE, and Cochrane library databases. The search term ‘posttraumatic
headache’ was used, and 21 eligible studies were included in the analysis.
Results. PTH is associated with complex neurochemical and structural changes, including the release
of excitatory neurotransmitters such as aspartate, glutamate, and acetylcholine. Elevated levels of
brain-derived neurotrophic factor (BDNF) have been reported during PTH episodes. Neuroimaging
studies suggest diminished choline concentrations in white matter, and decreased cortical thickness in
bilateral frontal regions. Traumatic injury could impair descending inhibitory pain pathways. Preexisting headache may be magnified following trauma. Discontinuation of the medication, regaining
the consciousness after a TBI, and the head injury itself are the triggers for PTH. The locus coeruleus
and periaqueductal gray matter play key roles in afferent pain modulation, and their involvement may
explain the frequent association between PTH and post-traumatic stress disorder (PTSD). Gender
differences in the incidence of PTH are controversive, although there is a higher incidence of migrainelike PTH in male veterans, and for tension-type PTH in elderly women. Genetic predisposition has
been suggested, with FMH1 and ATP1A2 gene variants associated with increased PTH severity. Loss
of consciousness is indicative of a more severe PTH. The treatment strategies for each PTH are similar
to the preceding, although there is debate that PTH could be completely distinct and require alternative
clinical approaches.
Conclusions. Posttraumatic headache is an important entity that needs to be expected, clinically
classified, and that requires pathophysiology-based management.
