My impression is that most of our UK folks have the same story to tell abou their docs, i.e., there is a marked absence of training in headache among your docs. Which is to say: you must do, as many of us in the US have done--learn enough about CH so that you can inform the docs on how to care for you. The approach is to get MEDICAL materials here to give to our doc in hopes that he will recognize and respect the source (medical journals, etc.)
Print out these items--both to help you to understand what good treatment involves and to give the doc.
PDF file below and the print out the full article of the abstract which follows.
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Cluster headache.
From: Multimedia File Viewing and Clickable Links are available for Registered Members only!! You need to
or
(Orphanet Journal of Rare Diseases)
[Easy to read; one of the better overview articles I've seen. Suggest printing the full length article--link, line above--if you are serious about keeping a good medical library on the subject.]
Leroux E, Ducros A.
ABSTRACT: Cluster headache (CH) is a primary headache disease characterized by recurrent short-lasting attacks (15 to 180 minutes) of excruciating unilateral periorbital pain accompanied by ipsilateral autonomic signs (lacrimation, nasal congestion, ptosis, miosis, lid edema, redness of the eye). It affects young adults, predominantly males. Prevalence is estimated at 0.5-1.0/1,000. CH has a circannual and circadian periodicity, attacks being clustered (hence the name) in bouts that can occur during specific months of the year. ALCOHOL IS THE ONLY DIETARY TRIGGER OF CH, STRONG ODORS (MAINLY SOLVENTS AND CIGARETTE SMOKE) AND NAPPING MAY ALSO TRIGGER CH ATTACKS. During bouts, attacks may happen at precise hours, especially during the night. During the attacks, patients tend to be restless. CH may be episodic or chronic, depending on the presence of remission periods. CH IS ASSOCIATED WITH TRIGEMINOVASCULAR ACTIVATION AND NEUROENDOCRINE AND VEGETATIVE DISTURBANCES, HOWEVER, THE PRECISE CAUSATIVE MECHANISMS REMAIN UNKNOWN. Involvement of the hypothalamus (a structure regulating endocrine function and sleep-wake rhythms) has been confirmed, explaining, at least in part, the cyclic aspects of CH. The disease is familial in about 10% of cases. Genetic factors play a role in CH susceptibility, and a causative role has been suggested for the hypocretin receptor gene. Diagnosis is clinical. Differential diagnoses include other primary headache diseases such as migraine, paroxysmal hemicrania and SUNCT syndrome. At present, there is no curative treatment. There are efficient treatments to shorten the painful attacks (acute treatments) and to reduce the number of daily attacks (prophylactic treatments). Acute treatment is based on subcutaneous administration of sumatriptan and high-flow oxygen. Verapamil, lithium, methysergide, prednisone, greater occipital nerve blocks and topiramate may be used for prophylaxis. In refractory cases, deep-brain stimulation of the hypothalamus and greater occipital nerve stimulators have been tried in experimental settings.THE DISEASE COURSE OVER A LIFETIME IS UNPREDICTABLE. Some patients have only one period of attacks, while in others the disease evolves from episodic to chronic form.
PMID: 18651939 [PubMed]
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Explore, for your personal use, the buttons, left side, starting with the OUCH.
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Also print for your doc:
Curr Opin Neurol. 2009 Jun;22(3):247-53.
Neuroimaging in trigeminal autonomic cephalgias: when, how, and of what?
Wilbrink LA, Ferrari MD, Kruit MC, Haan J.
Department of Neurology, Leiden University Medical Centre, Leiden, The Netherlands.
PURPOSE OF REVIEW: Trigeminal autonomic cephalgias (TACs) are characterized by frequent, short-lasting headache attacks with ipsilateral facial autonomic features. They include CLUSTER HEADACHE, paroxysmal hemicrania, and short-lasting unilateral neuralgiform headache attacks with conjunctival injection and tearing. The pathogenesis of TACs is largely unknown, but many case reports in the literature suggest that TACs are secondary to structural lesions. Thus, the question arises whether TAC patients should undergo neuroimaging. Here, we review the recent literature on secondary TACs and attempt to formulate guidelines for neuroimaging. RECENT FINDINGS: Recently, we published two reviews of, in total, 33 case reports of patients with a secondary TAC or TAC-like syndrome. Since then, 23 additional cases have been published. Here, we provide a summary of these 56 case reports. TACs were found to be associated with a wide range of both intracranial and extracranial neurovascular and structural lesions. We could not identify a 'typical' clinical warning profile for secondary TACs as these patients could present with clinical features that are entirely characteristic of a TAC, including alternating attack and attack-free periods, and excellent response to TAC-specific treatments.
SUMMARY: EVEN CLINICALLY TYPICAL TACS CAN BE CAUSED BY STRUCTURAL LESIONS. THERE ARE NO 'TYPICAL' WARNING SIGNS OR SYMPTOMS. NEUROIMAGING SHOULD BE CONSIDERED IN ALL PATIENTS WITH TAC OR TAC-LIKE SYNDROMES, NOTABLY IN THOSE WITH ATYPICAL PRESENTATION. DEPENDING ON THE DEGREE OF SUSPICION, ADDITIONAL IMAGING SHOULD BE CONSIDERED ASSESSING INTRACRANIAL AND CERVICAL VASCULATURE, AND THE SELLAR AND PARANASAL REGION.
Publication Types:
Research Support, Non-U.S. Gov't
PMID: 19434790 [PubMed]
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