Cocaine-induced cluster-like headache

Abstract

Cluster headache (CH) is the paradigm of trigeminal autonomic cephalalgias (TACs). According to the guidelines of the International Classification of Headache Disorders [1], CH is characterized by attacks of severe, strictly unilateral pain which may be orbital, supraorbital, temporal or any combination of these sites, lasting 15–180 min and occurring from once every other day to eight times per day. The pain is associated with ipsilateral conjunctival injection, lacrimation, nasal congestion, rhinorrhea, forehead and facial sweating, myosis, ptosis and/or eyelid oedema and/or with restlessness/agitation [1]. However, there have been some cases where, although the headache had clinical features that mimicked primary CH, even in the typical time pattern and response to treatment, they were of secondary origin [2] and thus named cluster-like headache (CLH). A recent review reported that the most frequent pathologies associated with CLH were of vascular origin (38.5 %), followed by tumours (25.7 %) and inflammatory/infectious diseases (13.5 %), where iatrogenic or drug-related conditions represented 4.7 % of the CLH [3]. Cocaine is involved in several neurological complications: ischaemic stroke, transient focal deficits, dizziness, seizures and even headache [4]. Headache usually has migrainous features in cocaine abusers, even if cocainerelated cases of cluster-like headache and orofacial pain have occasionally been reported [5]. Herein, we report a case where cocaine abuse gave rise to head and facial pain, accompanied by autonomic features, mimicking CH. In November 2010, a 24-year-old woman, smoker, had a neurological evaluation for right zygomatic and periorbital pain which was so severe and recurrent as to make her return to the Emergency Department of Campo di Marte Hospital in Lucca five times in 1 week. The patient complained of 1 or 2 daily pain attacks, mostly in the evening (about 8:00–9:00 p.m.), associated with rhinorrhea, lacrimation, conjunctival injection and reduced palpebral opening (ptosis) on the right of her face and reported having had two similar, less painful, episodes on the left side. Each pain crisis lasted 45–180 min, with severe, throbbing and burning pain. She was restless and extremely nervous during the attacks and reported having had a nosebleed three times before the onset of facial pain in the last week. Both neurological examination and CT scan were unremarkable, as was brain MRI. Treatment with i.v. ketorolac, ibuprofen, tramadol and diclofenac had no effect. Only i.v. paracetamol (1,000 mg/day) and i.m. dexamethasone (8 mg/day), administered in the Emergency Department, seemed to provide partial relief, even though a spontaneous cessation of the attack could not be ruled out. Although some of the facial pain features were consistent with CH, according to the HIS diagnostic criteria, they had some atypical characteristics, i.e. nose G. Cafforio (&) M. Mazzoni Neurological Department, Campo di Marte Hospital, Via dell’Ospedale, Lucca, Italy e-mail: gcafforio@libero.it