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.

No abstract

BACKGROUND: Neurogenic claudication secondary to degenerative lumbar stenosis is typically managed with nonsurgical options, such as epidural corticosteroid injections. As a standard and effective treatment for lumbar stenosis, clinicians must be aware of the corticosteroids choice when injecting in the epidural space. CASE REPORT: A 62-year-old man presenting with sciatic pain is treated with multiple neuroforaminal, facet, and caudal corticoid injections over the course of several months without any symptomatic resolution. A magnetic resonance imaging of his lumbar spine revealed focal bilateral central stenosis at the L4-L5 level. A computed tomography revealed hyperdense lesions at that level. The patient was referred for a surgical option. He underwent complete minimally invasive resection of the bilateral lesion with instrumented and interbody fusion. The final pathology report identified the mass as a calcified granuloma. CONCLUSIONS: Following repetitive methylprednisolone acetate injections, one must be aware of all the potential complications arising from particulate corticosteroids. KEY WORDS: Spinal stenosis, epidural injections, granulomas, corticosteroids

No abstract