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Table of Contents    
Year : 2019  |  Volume : 67  |  Issue : 5  |  Page : 1365-1366

Cluster Headache in a Case of Ophthalmic Cysticercosis

Department of Neurology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, Uttar Pradesh, India

Date of Web Publication19-Nov-2019

Correspondence Address:
Prof. Sunil Pradhan
Department of Neurology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow - 226 014, Uttar Pradesh
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0028-3886.271258

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How to cite this article:
Pradhan S, Das A, Bansal R. Cluster Headache in a Case of Ophthalmic Cysticercosis. Neurol India 2019;67:1365-6

How to cite this URL:
Pradhan S, Das A, Bansal R. Cluster Headache in a Case of Ophthalmic Cysticercosis. Neurol India [serial online] 2019 [cited 2020 Jul 10];67:1365-6. Available from:

Cluster headaches is considered to be a primary headache. They are characterized by recurrent episodes of unilateral pain involving the first division of the nerve along with autonomic symptoms. Although classified as primary headaches, some cluster headaches are associated with craniofacial organic etiologies, which activate the trigeminovascular reflex[1] resulting in trigeminal autonomic cephalgias. Much literature has been published for the apparent cluster headache-like conditions arising out of organic pathologies such as tumors, dissection, and infection in the craniofacial area, although the causal relationship still needs to be proved convincingly. In certain cases, treatment of the primary pathology such as sinusitis or otitis media leads to alleviation of the symptoms of headache. Neuroimaging has been recommended in atypical cases of cluster headache with atypical symptoms and signs or for those not responding to treatment. Neuroimaging in our case of cluster headache was suggestive of ophthalmic cysticercosis. To the best of our knowledge, cluster headache in ophthalmic cysticercosis has never been described.

A 28-year-old male presented with recurrent excruciating left-sided headaches for the last six years. The attacks were associated with congestion and lacrimation of the ipsilateral eye with nasal obstruction and severe restlessness. Each attack persisted for 30–40 minutes with a frequency of 5–6 per day, six days a week. The patient used to get these attacks initially at a frequency of 4–6 clusters per year, but in the last six months, he complained of about four clusters. These clusters were not seasonal. These attacks used to subside by oxygen inhalation at 10 L/min. Tenderness over the sinuses could not be elicited. Rest of the general and neurological examination was normal. He was diagnosed as a case of cluster headache as he fulfilled the revised International Classification of Headache Disorders criteria for a cluster headache.

ENT evaluation for acute sinusitis was performed which was normal. In view of increasing frequency of cluster attacks in the recent months, a possibility of secondary etiology of headache was kept and magnetic resonance imaging (MRI) of the brain was planned. MRI brain [Figure 1] with gadolinium contrast was done, which revealed a single ring enhancing lesion at orbital apex compressing left optic nerve. The lesion was T1 hypointense and T2 hyperintense with homogenous contrast enhancement. Magnetic resonance spectroscopy showed increased lactate and succinate peak favoring a diagnosis of cysticercosis of orbital apex.
Figure 1: MRI brain with orbital cuts showing T1 hypointense and T2 hyperintense lesion with homogenous contrast enhancement

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The acute attacks of the patient during the hospital visit were managed with oxygen inhalation and steroids, which was a treatment option for both cluster headache and ophthalmic cysticercosis. Neurosurgical consultation was taken and they advised for conservative treatment (for the symptom of cluster headache). The headache bouts also settled and he was discharged in stable condition on tapering steroid dose of eight weeks with the advice for regular follow-up. At 1-year follow-up, he had only one attack of cluster headache, which was managed symptomatically with oxygen therapy and indomethacin.

Secondary cluster headaches, although rare, should be suspected in cases of refractory ones, abnormal neurological signs and an age of onset of more than 50 years. Investigations in cases of primary headaches should also be done in cases of of recent changes in the character of the headache. A review of 31 secondary trigeminal autonomic cephalgia cases published by Favier et al. in 2007 suggested that since typical TAC cases fulfilling International Headache Society criteria can also be related to large cerebral mass lesions, neuroimaging should always be considered in patients with TAC[2],[3] In the previously described case series of unusual presentations of neurocysticercosis (NCC), a wide variety of CNS manifestations such as mesencephalic syndrome, tonsilar herniation, hemorrhagic stroke, TIAs, and cervical myelopathy has been described.[4] Migraine-like or tension-type headaches have been described with neurocysticercosis.[5] To the best of our knowledge, ophthalmic cysticercosis presenting as cluster headache has not been described.

The pathogenesis of secondary cluster headaches has not been convincingly proven, although they have been described in various case series. Primary cluster headaches have been related to the activation of trigemino-vascular reflex along with hypothalmic activation resulting in various autonomic symptoms of nasal congestion and conjunctival injection. The exact pathology in secondary cases like ours is not known. Pain in secondary causes has been attributed variously to autonomic disturbance caused by structural lesions or irritation of pain sensitive strictures and activation of trigeminal nerve endings.[4],[6] But whatever may be the cause of headache in our case, it was in some way related to ophthalmic cysticercosis as the headache frequency decreased after symptomatic treatment of the lesion by steroids. The lesion may have degenerated in the next 1 year resulting in near complete resolution of the cluster headache. Unfortunately, we could not repeat MRI brain with orbital cuts to prove the resolution of the cysticercosis due to financial constraints of the patient. However, following the clinical profile, we believe that this cysticercus was responsible for the attacks of cluster headache. The character of cluster headache in our case was not different from those of typical attacks of cluster headache, although it was probably a secondary phenomenon to ophthalmic cysticercus.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

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Conflicts of interest

There are no conflicts of interest.

  References Top

Nesbitt AD, Goadsby PJ. Cluster headache. BMJ. 2012;344:e2407.  Back to cited text no. 1
Favier I, van Vliet JA, Roon KI, Witteveen RJ, Verschuuren JJ, Ferrari MD, Haan J. Trigeminal autonomic cephalgias due to structural lesions: A review of 31 cases. Arch Neurol 2007;64:25-31.  Back to cited text no. 2
Carter DM. Cluster headache mimics. Curr Pain Headache Rep 2008;8:133-9.  Back to cited text no. 3
Wilbrink LA, Ferrari MD, Kruit MC, Haan J. Neuroimaging intrigeminal autonomic cephalgias: When, how, and of what? Curr Opin Neurol 2009;22:247-53.  Back to cited text no. 4
Cruz ME, Cruz I, Preux PM, Schantz P, Dumas M. Headache and cysticercosis in Ecuador, South America. Headache 1995;35:93-7.  Back to cited text no. 5
Leone M, Bussone G. Pathophysiology of trigeminal autonomic cephalalgias. Lancet Neurol 2009;8:755-64.  Back to cited text no. 6


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