**Letter to the Editor: New Observation**

# Traumatic Brain Injury Temporal Lesion Causing Hemicrania Continua

Caitlin R. Christensen ID, Collin C. Luk ID and Mohammed Wasif Hussain ID

Faculty of Medicine, Division of Neurology, University of Alberta, Edmonton, AB, Canada

**Keywords:** Trigeminal autonomic cephalgia; Hemicrania continua; Traumatic brain injury; Encephalomalacia

There have been scant reports of hemicrania continua (HC) fol-
lowing head trauma resulting in concussion or traumatic brain
injury (TBI). Even more rare are reports of HC resulting from
lesional pathology. A review from 2004 found five documented
cases of HC secondary to head trauma including a 38-year-old
female with onset following a motor vehicle accident (MVA), a
48-year-old female with onset after a syncopal episode causing
head injury, a 32-year-old female with onset after a fall resulting
in TBI, a 30-year-old male with onset after a head injury on a
bicycle, and a 34-year-old female (Trucco et al.).¹ All of these cases
had normal neuroimaging. Prakash et al. reported two more cases
in 2009, namely a 52-year-old male with a closed head injury ten
years prior secondary to a MVA and a 44-year-old female with
onset after MVA that caused a left-sided parietal hematoma requir-
ing surgical evacuation. Finally, Finkel et al. (2017) reported 12
military personnel who developed HC following mild TBI.²

We encountered a young adult, right-hand dominant, male
who presented for the assessment of headache. He was otherwise
healthy and taking no medications. Fifteen years prior, he sus-
tained a blunt force trauma to the head in South America. He
developed a headache the following day, and workup revealed
intracranial hemorrhage for which surgery was suggested but
the patient declined.

Since his injury, there was mild continuous headache and
weekly exacerbations. Exacerbations had moderate intensity (rated
as a 4/10), but became severe (10/10) when periorbital edema was
present. Headaches were strictly left-sided and had a pulsatile and
pressure-type quality in the periorbital area. Exacerbations were
associated with nausea and vomiting, diplopia, left-sided periorbi-
tal edema, conjunctival injection, and tearing. Red discoloration of
his vision also occurred during these episodes. There was no photo-
or phonosensitivity. Headaches were not exacerbated by activity.
There was no relief with oral naproxen. Physical examination
was unremarkable.

Magnetic resonance imaging of the brain revealed multiple
abnormalities (Figure 1) including left mesial temporal encephalo-
malacia and T2-weighted imaging hyperintensities scattered
throughout the supratentorial white matter. There was no abnor-
mal enhancement.

He was diagnosed with persistent headache attributed to mod-
erate or severe traumatic injury to the head with clinical features
consistent with HC, unremitting type, and indomethacin was
trialed at a dose of 75 mg PO TID. Within two weeks, he had
complete resolution of headaches. Consumption of alcohol no
longer triggered headaches. He gradually decreased the dose of

<figure><img src="image_1.png" /><figcaption>**Figure 1:** Neuroimaging findings. Axial T1-weighted image (A), axial T2-weighted image (B), and coronal T1-weighted image with gadolinium (C) demonstrate left mesial temporal encephalomalacia and atrophy.</figcaption></figure>

**Corresponding author:** Mohammed Wasif Hussain, Faculty of Medicine, Division of Neurology, 7-135 Clinical Sciences Building, University of Alberta, 8440 112 Street NW, Edmonton, AB T6G 2B7, Canada. Email: mhussain@ualberta.ca

**Cite this article:** Christensen CR, Luk CC, and Hussain MW. (2023) Traumatic Brain Injury Temporal Lesion Causing Hemicrania Continua. *The Canadian Journal of Neurological Sciences* **50**: 645–646, https://doi.org/10.1017/cjn.2022.84

© The Author(s), 2022. Published by Cambridge University Press on behalf of Canadian Neurological Sciences Federation. This is an Open Access article, distributed under the terms of the Creative Commons Attribution licence (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted re-use, distribution and reproduction, provided the original article is properly cited.
indomethacin, and it was discontinued after 6 months. The patient remained headache-free.

HC is a rare primary headache disorder. It presents as a strictly unilateral, 'side locked' headache with ipsilateral autonomic features. There is typically a mild-to-moderate continuous headache with episodic exacerbations; however, the robust response to indomethacin is required for diagnosis.

Headache attributed to traumatic injury to the head, previously called post-traumatic headache, is a common cause of secondary headache and can have numerous clinical phenotypes that may mimic primary headache disorders.

Classically, there is no identifiable underlying pathology of HC; however, increasing numbers of symptomatic cases have been reported. Head trauma is a rare cause of HC, and this represents the first case due to a temporal lobe lesion. Such cases have been referred to as 'secondary HC' in the literature³,⁴; however, a more accurate diagnosis in accordance with The International Classification of Headache Disorders, 3rd edition (ICHD-3) is persistent headache attributed to moderate or severe traumatic injury to the head with clinical features consistent with HC.⁵ While the relationship between TBI and onset of headache with features of HC may be spurious, the temporal relation in this case suggests causation. The authors hypothesize that the connections between the mesial temporal

lobe and the posterior hypothalamus were disrupted, resulting in clinical HC.

**Funding.** The authors have no relevant funding to this article.

**Conflicts of Interest.** No conflicts of interest was reported by the authors.

**Statement of Authorship.** CRC drafted the manuscript and wrote the figure legend. CCL performed the patient's clinical assessment, edited the manuscript, and created the figure. MWH assisted in the patient's clinical assessment and performed critical revisions of the manuscript for intellectual content.

## References

1. Trucco M, Mainardi F, Maggioni F, Badino R, Zanchin G. Chronic paroxysmal hemicrania, hemicrania continua and SUNCT syndrome in association with other pathologies: a review. Cephalalgia. 2004;24:173-84.

2. Finkel AG, Yerry JA, Klaric JS, Ivins BJ, Scher A, Choi YS. Headache in military service members with a history of mild traumatic brain injury: a cohort study of diagnosis and classification. Cephalalgia. 2017;37:548-59.

3. Prakash S, Shah ND, Soni RK. Secondary hemicrania continua: case reports and a literature review. J Neurol Sci. 2009;280:29-34.

4. Prakash S, Patel P. Hemicrania continua: clinical review, diagnosis and management. J Pain Res. 2017;10:1493-509.

5. Headache Classification Committee of the International Headache Society (IHS). The international classification of headache disorders, 3rd edition (beta version). Cephalalgia. 2013;33:629-808.