Cases reported "Cluster Headache"

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1/5. Persistence of attacks of cluster headache after trigeminal nerve root section.

    cluster headache is a strictly unilateral headache that occurs in association with cranial autonomic features. We report a patient with a trigeminal nerve section who continued to have attacks. A 59-year-old man described a 14-year history of left-sided episodes of excruciating pain centred on the retro-orbital and orbital regions. These episodes lasted 1-4 h, recurring 2-3 times daily. The attacks were associated with ipsilateral ptosis, conjunctival injection, lacrimation, rhinorrhoea and facial flushing. From 1986 to 1988, he had trials of medications without any benefit. In February 1988, he had complete surgical section of the left trigeminal sensory root that shortened the attacks in length for 1 month without change in their frequency or character. In April 1988, he had further surgical exploration and the root was found to be completely excised; post-operatively, there was no change in the symptoms. From 1988 to 1999, he had a number of medications, including verapamil and indomethacin, all of which were ineffective. prednisolone 30 mg orally daily rendered the patient completely pain free. sumatriptan 100 mg orally and 6 mg subcutaneously aborted the attack after approximately 45 and 15 min, respectively. He was completely anaesthetic over the entire left trigeminal distribution. Left corneal reflex was absent. Motor function of the left trigeminal nerve was preserved. Neurological and physical examination was otherwise normal. MRI scan showed a marked reduction in the calibre of the left trigeminal nerve from the nerve root exit zone in the pons to Meckel's cave. An ECG-gated three-dimensional multislab MRI inflow angiogram was performed. No dilatation was observed in the left internal carotid artery during the cluster attack. Blink reflexes were elicited with a standard electrode and stimulus. Stimulation of the left supraorbital nerve produced neither ipsilateral nor contralateral blink reflex response. Stimulation of the right supraorbital nerve produced an ipsilateral response with a mean R2 onset latency of 36 ms and a contralateral response with a mean R2 onset latency of 32 ms. Lack of ipsilateral vessel dilatation makes the role of vascular factors in the initiation of cluster attacks questionable. With complete section of the left trigeminal sensory root the brain would perceive neither vasodilatation nor a peripheral neural inflammatory process; however, the patient continued to have an excellent response to sumatriptan. The case illustrates that cluster headache may be generated primarily from within the brain, and that triptans may have anti-headache effects through an entirely central mechanism.
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2/5. Periods of cluster headache induced by nitrate therapy and spontaneous remission of angina pectoris during active clusters.

    Glyceryl trinitrate (GTN) is known to induce single extra attacks of cluster headache (CH) during active cluster periods, most probably via actions of nitric oxide (NO). Induction of whole periods of CH by organic nitrates has, however, attracted little attention in the literature. We report on eight patients with episodic CH and coexistent effort-induced angina pectoris. Cases 1-6 had been free of their headaches for many years but got recurrence of CH within a few weeks after the administration of long-acting organic nitrates (isosorbide-dinitrate, isosorbide-5-mononitrate or slow-release GTN) aimed at treating their chest pains. These nitrate-induced headache periods were more severe and had a longer duration than the previous spontaneous ones. Furthermore, one of the subjects and two additional cases experienced a marked reduction of their anginal attacks during successive CH periods. exercise time to effort-induced angina was increased in all three patients and one of them revealed a markedly elevated threshold for eliciting ischaemic cardiac symptoms by standardized physical exercise on a cycle ergometer. We hypothesize whether extra CH periods elicited by sustained nitrate therapy and remission of angina pectoris during active clusters are caused by central mechanisms involving inhibition of sympathetic tone and effects on both cranial vessels and cardiac functions.
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3/5. The cluster-tic syndrome and its surgical therapy.

    The term cluster-tic syndrome (CTS) is used to designate a clinical pain pattern in which symptoms of cluster headache (CH) and tic douloureux (TD) coexist. The TD elements of the attack occur in paroxysms of many seconds or minutes, always affect the maxillary or mandibular divisions of the trigeminal nerve, with spread into the ophthalmic division in some cases, and may be triggered by slight superficial stimuli. These features may occur independent of CH elements but more often the two blend together. Four patients with CTS unresponsive to medication underwent surgery. blood vessels were found to cross compress the trigeminal nerve in all four patients and the nerve was decompressed. A similar condition was found affecting the facial nerve in two of the three patients in whom that nerve was explored and the facial nerve was decompressed in these two. The TD component of the CTS disappeared after surgery in all four patients. The CH component of the syndrome returned after surgery but in a modified form. In three patients, the CH changed from what had been chronic cluster to infrequent episodic cluster periods; additionally in two patients, the duration of cluster was shorter and the pain was of lesser severity.
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4/5. cluster headache, hemicrania, and other head pains: morbidity of carotid endarterectomy.

    Carotid endarterectomy has become a widely used approach to the treatment of cerebrovascular disease. In spite of increasing experience, a significant and varied morbidity remains attached to the procedure. A poorly recognized complication is postoperative headache. In a series of 57 endarterectomies in 50 patients, 24 patients experienced postoperative headaches encompassing the entire spectrum of vascular headaches: nonspecific diffuse headaches, severe hemicranias, cluster headaches occurring early and delayed, chronic paroxysmal hemicranias, carotidynia, and Eagle's syndrome. Five patients had hemicranias, and all were homolateral to the endarterectomy. Therefore, we hypothesize that the spontaneously occurring hemicranias, the counterparts of postsurgical headache syndromes, also may be due to some overt or occult injury or disease of the carotid vessels or carotid sheaths in the regions from the carotid bifurcation to the base of the skull.
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5/5. Positron emission tomography studies in headache.

    Positron emission tomography (PET) allows the quantitative measurement of regional cerebral flow (rCBF) in humans in quantitative terms. Gross changes in rCBF are due to variation in vessel diameter. Changes of rCBF also reflect synaptic activity (inhibition and excitation). Therefore, PET was used to monitor changes in blood flow during the aura and headache phase of a migraine attack and to investigate focal areas of increased or decreased blood flow, e.g., in the brain stem and midbrain. Hemispheric rCBF was unchanged in spontaneous migraine attacks without aura. This was true for the headache side as well as for the nonheadache side. sumatriptan had no effects on cerebral blood flow. Regional cerebral blood flow was increased in midline brain stem structures during the headache phase, but also when the headache had been treated with sumatriptan. This persisting increased activity might reflect activity of a presumed migraine center in the brain stem. These changes are specific for migraine attacks and are not seen during attacks of cluster headache. Positron emission tomography measurements in the early phase of a migraine attack in a single subject showed flow reductions in the occipital cortex spreading forwards; an observation which would be compatible with the existence of spreading depression in humans. Our attempts to study the aura phase with PET have, to date, been unsuccessful.
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