Regístrese
Buscar en
Neurología (English Edition)
Toda la web
Inicio Neurología (English Edition) Influenza A virus: A possible trigger factor for hypnic headache?
Journal Information
Vol. 32. Issue 1.
Pages 67-68 (January - February 2017)
Vol. 32. Issue 1.
Pages 67-68 (January - February 2017)
Letter to the Editor
DOI: 10.1016/j.nrleng.2015.03.016
Open Access
Influenza A virus: A possible trigger factor for hypnic headache?
¿Virus de la gripe A como factor desencadenante de una cefalea hípnica?
Visits
...
A. Pérez Hernándeza,
Corresponding author
Azuquahe@gmail.com

Corresponding author.
, E. Gómez Ontañónb
a Servicio de Neurología, Hospital General de La Palma, Breña Alta, Santa Cruz de Tenerife, Islas Canarias, Spain
b Servicio de Neurología, Hospital Universitario Nuestra Señora de Candelaria, Santa Cruz de Tenerife, Islas Canarias, Spain
Article information
Full Text
Bibliography
Download PDF
Statistics
Tables (2)
Table 1. ICHD-3 beta diagnostic criteria for hypnic headache.
Table 2. ICHD-3 beta diagnostic criteria for probable hypnic headache.
Show moreShow less
Full Text
Dear Editor:

Hypnic headache (HH), a primary headache first described by Raskin1 in 1988, is listed in group 4 of the third edition of the International Classification of Headache Disorders, beta version (ICHD-3 beta), which was published in 2013.2 HH usually begins after the age of 50 and presents as recurrent oppressive headache in most cases. This type of headache presents only during sleep, waking the patient (‘alarm clock’ headache) and lasting for up to 4 hours, without any characteristic associated symptoms. To diagnose HH, other possible causes of nocturnal headache must first be ruled out, with special attention to sleep apnoea/hypopnoea syndrome (SAHS), nocturnal hypertension, hypoglycaemia, and medication overuse. However, presence of SAHS does not rule out a diagnosis of HH.

The ICHD-3 beta differentiates between hypnic headache (Table 1) and probable hypnic headache (Table 2).

Table 1.

ICHD-3 beta diagnostic criteria for hypnic headache.

Recurrent headache attacks fulfilling criteria B-E 
Developing only during sleep and causing wakening 
Occurring on ≥10 days per month for >3 months 
Lasting ≥15 minutes and for up to 4 hours after waking 
No cranial autonomic symptoms or restlessness 
Not better explained by another ICHD-3 diagnosis 
Table 2.

ICHD-3 beta diagnostic criteria for probable hypnic headache.

Recurrent headache attacks fulfilling criterion B and 2 of criteria C-E 
Developing only during sleep and causing wakening 
Occurring on ≥10 days per month for >3 months 
Lasting ≥15 minutes and for up to 4 hours after waking 
No cranial autonomic symptoms or restlessness 
Not fulfilling ICHD-3 criteria for any other headache disorder 
Not better explained by another ICHD-3 diagnosis 

We present the case of a 41-year-old woman with a history of essential hypertension, type 2 diabetes mellitus, class II obesity, migraine without aura, and obesity-hypoventilation syndrome (OHS). She had been hospitalised due to a viral respiratory infection with influenza A; during her hospital stay she only required nasal cannula oxygen therapy in the first few days and experienced a mild headache that resolved as symptoms improved. In the month following discharge, our patient was referred to the headache unit due to episodes of headache appearing only at night (usually around 2.00-3.00 a.m.), with a frequency of 2-4 episodes. Headache was either hemicranial (affecting both sides) or holocranial, pulsating and stabbing, and of moderate intensity. Episodes lasted a mean of 15 minutes and made her get out of bed to engage in motor tasks until symptoms subsided completely. She displayed no other neurological signs or symptoms, whether general or local, except for occasional nausea.

Headache met the ICHD-3 beta diagnostic criteria for HH. A physical examination, analyses, and a neuroimaging study revealed no abnormalities, which ruled out symptomatic headache secondary to an intracranial structural process.

As HH was suspected, we started preventive treatment with lithium carbonate given that this is the most studied treatment for HH and our patient had no contraindications for this drug. Treatment achieved excellent response, with complete remission of the episodes. The treatment was discontinued once the patient had been asymptomatic for approximately 6 months, and headache episodes did not reappear.

Respiratory infection and essential hypertension (which exacerbates at night) may have played an important role in the pathogenesis of HH. However, other factors should also be considered, namely adequate management of hypertension during hospitalisation and the exceptional response to lithium carbonate before starting non-invasive mechanical ventilation, on the one hand, and the temporal connection between headache episodes and respiratory infection due to influenza A virus, on the other.

Although the literature describes a number of neurological complications associated with influenza A (H1N1) virus infection (posterior reversible encephalopathy syndrome, myelitis, acute necrotising encephalitis, etc.3–6), these conditions occur during the acute phase of infection, which suggests a parainfectious immune-mediated aetiology.7,8 In theory, a direct association between influenza A virus infection and HH cannot be established since there is little understanding of the pathophysiology of either entity. However, given that other viruses have been suggested to be linked to other forms of primary headache,9–11 influenza A virus infection may be considered a potential trigger factor for HH in at-risk patients.

Although our patient was diagnosed with primary HH and received pharmacological treatment, we hypothesise that HH in this case may have been a subacute/chronic complication of influenza A virus infection. However, this hypothesis is not likely to be confirmed in the near future given the low frequency of influenza A virus infection (patients with HH rarely have a history of influenza according to the series described in the literature). In any case, HH should be considered within the spectrum of neurological alterations secondary to influenza A virus infection.

References
[1]
N.H. Raskin.
The hypnic headache syndrome.
Headache, 28 (1988), pp. 534-536
[2]
The International Classification of Headache Disorders, 3rd edition (beta version).
Headache Classification Committee of the International Headache Society (IHS).
Cephalalgia, 33 (2013), pp. 629-808
[3]
S. Toovey.
Influenza-associated central nervous system dysfunction: a literature review.
Travel Med Infect Dis, 6 (2008), pp. 114-124
[4]
S.M. Maricich, J.L. Neul, T.E. Lotze, A.C. Cazacu, T.M. Uyeki, G.J. Demmler, et al.
Neurologic complications associated with influenza A in children during the 2003–2004 influenza season in Houston, Texas.
Pediatrics, 114 (2004), pp. e626-e633
[5]
W.S. Bartynski, A.R. Upadhyaya, J.F. Boardman.
Posterior reversible encephalopathy syndrome and cerebral vasculopathy associated with influenza A infection: report of a case and review of the literature.
J Comput Assist Tomogr, 33 (2009), pp. 917-922
[6]
C.A. Glaser, K. Winter, K. DuBray, K. Harriman, T.M. Uyeki, J. Sejvar, et al.
A population-based study of neurologic manifestations of severe influenza A(H1N1)pdm09 in California.
Clin Infect Dis, 55 (2012), pp. 514-520
[7]
H. Aiba, M. Mochizuki, M. Kimura, H. Hojo.
Predictive value of serum interleukin-6 level in influenza virus-associated encephalopathy.
Neurology, 57 (2001), pp. 295-299
[8]
T. Ichiyama, H. Isumi, H. Ozawa, T. Matsubara, T. Morishima, S. Furukawa.
Cerebrospinal fluid and serum levels of cytokines and soluble tumor necrosis factor receptor in influenza virus-associated encephalopathy.
Scand J Infect Dis, 35 (2003), pp. 59-61
[9]
F. Díaz-Mitoma, W.J. Vanast, D.L. Tyrrell.
Increased frequency of Epstein-Barr virus excretion in patients with new daily persistent headaches.
Lancet, 1 (1987), pp. 411-415
[10]
D. Li, T.D. Rozen.
The clinical characteristics of new daily persistent headache.
[11]
P. Meineri, E. Torre, E. Rota, E. Grasso.
New daily persistent headache: clinical and serological characteristics in a retrospective study.
Neurol Sci, 25 (2004), pp. S281-S282

Please cite this article as: Pérez Hernández A, Gómez Ontañón E. ¿Virus de la gripe A como factor desencadenante de una cefalea hípnica? Neurología. 2017;32:67–68.

This study has not been presented at the SEN's Annual Meeting or at any other meetings or congresses, nor has it received funding from any public or private institutions.

Copyright © 2014. Sociedad Española de Neurología
Article options
Tools
es en pt

¿Es usted profesional sanitario apto para prescribir o dispensar medicamentos?

Are you a health professional able to prescribe or dispense drugs?

Você é um profissional de saúde habilitado a prescrever ou dispensar medicamentos

es en pt
Política de cookies Cookies policy Política de cookies
Utilizamos cookies propias y de terceros para mejorar nuestros servicios y mostrarle publicidad relacionada con sus preferencias mediante el análisis de sus hábitos de navegación. Si continua navegando, consideramos que acepta su uso. Puede cambiar la configuración u obtener más información aquí. To improve our services and products, we use "cookies" (own or third parties authorized) to show advertising related to client preferences through the analyses of navigation customer behavior. Continuing navigation will be considered as acceptance of this use. You can change the settings or obtain more information by clicking here. Utilizamos cookies próprios e de terceiros para melhorar nossos serviços e mostrar publicidade relacionada às suas preferências, analisando seus hábitos de navegação. Se continuar a navegar, consideramos que aceita o seu uso. Você pode alterar a configuração ou obter mais informações aqui.