A 19-year-old female, university student with a long-standing history of migraine headaches presented to the emergency department (ED) with a 36-hour history of gradual onset of left-sided headache, preceded by visual aura. She stated that her headache was worse than usual and now associated with nausea, vomiting, and photophobia, despite use of oral ibuprofen. On examination, she was afebrile, her SaO2 = 98% on room air, her pulse was 110 beats/minute, and she was breathing 20 breaths/minute. She received a Canadian Triage and Acuity Scale score of 2 due to her pain score of 8/10 on a Visual Analogue Scale (VAS). Her neurological examination was normal and her neck was supple with full range of motion. She was a non-smoker, infrequent cannabis user, and her last menstrual period was normal.

The most common symptom of post-concussive syndrome (PCS) is post-traumatic headache (PTH) accompanied by photophobia. Post-traumatic headache is currently categorized as a secondary headache disorder with a clinical phenotype described by its main features and resembling one of the primary headache disorders: tension, migraine, migraine-like cluster. Although PTH is often treated with medication used for primary headache disorders, the underlying mechanism for PTH has yet to be elucidated. The goal of this narrative literature review is to determine the current level of knowledge of these PTHs and photophobia in mild traumatic brain injury (mTBI) in order to guide further research and attempt to discover the underlying mechanism to both symptoms. The ultimate purpose is to better understand the pathophysiology of these symptoms in order to provide better and more targeted care to afflicted patients. A review of the literature was conducted using the databases CINAHL, EMBASE, PubMed. All papers were screened for sections on pathophysiology of PTH or photophobia in mTBI patients. Our paper summarizes current hypotheses. Although the exact pathophysiology of PTH and photophobia in mTBI remains to be determined, we highlight several interesting findings and avenues for future research, including central and peripheral explanations for PTH, neuroinflammation, cortical spreading depolarization and the role of glutamate excitotoxicity. We discuss the possible neuroanatomical pathways for photophobia and hypothesize a possible common pathophysiological basis between PTH and photophobia.

A comparative study was carried out between a control group and different patient subgroups suffering from psychosonratic disorders: headache, insomnia and loss of consciousness due to neurocirculatory dystonia.

Different personality questionnaires (Minnesota Multiphasic Personality Inventory, Sensation Seeking Scale, Susceptibility to Punishment Scale), neurobioelectric parameters (Hjörth descriptors, alpha percentage, P100, N120 P200 of visual evoked responses) and platelet monoamine oxidase B (using phenylethylamine as substrate) were evaluated.

The results show a significant increase in anxiety indicators (at a psychometric and bioelectric level) in the headache and insomnia groups. MAO B activity was higher in patients, especially in the insomniac group; but no significant differences were found in any of the groups studied.