Chronic Headache Pain
Andrea Kohn Maikovich-Fong in Handbook of Psychosocial Interventions for Chronic Pain, 2019
Chronic cluster headache is a subtype of hemicrania continua. Cluster headache is characterized by unilateral head pain that occurs with autonomic features such as ptosis, miosis, eye lacrimation, eye conjunctival injection or redness, or rhinorrhea. These autonomic symptoms and the typically shorter duration of cluster headaches help to differentiate them from migraine headaches. Pain distribution is located in the unilateral trigeminal region. Episodic cluster headaches occur daily, usually one to eight times per day, for a period of a week. If no remission or painless period occurs, headaches are then classified as chronic cluster headaches. There is a positive correlation between chronic cluster headaches and a history of head injuries, and cluster headaches occur in males more than females at a ratio of roughly 5:1 (Pina-Garza, 2013).
Trigeminal autonomic cephalgias I – cluster headache: diagnosis and treatment
Stephen D. Silberstein, Richard B. Upton, Peter J. Goadsby in Headache in Clinical Practice, 2018
The key pathophysiological processes of cluster headache take place within the central nervous system. The most curious feature of the disorder is its episodic nature, from which the very apt name, cluster headache, is derived. During the cluster periods, patients note that their headaches turn on and off like clockwork, respecting some daily (circadian) rhythm that has the stamp of the biological clock; patients will often awaken with headache at the same time every night. Moreover, the occurrence of cluster periods often follow half-yearly, yearly, or even biennial cycles of recurrent bouts, one of the most fascinating cycling processes of human biology. These processes implicate involvement of the suprachiasmatic region, and unraveling the neurobiology will tell us much about human biological clocks.
Cluster Headache
Gary W. Jay in Clinician’s Guide to Chronic Headache and Facial Pain, 2016
The pathogenesis of cluster headache appears to be a central disorder involving an alteration of the hypothalamus characterized by its increased activity and subsequent increase in parasympathetic activity and changes in hypothalamically mediated hormonal activity and opioid-related analgesia. The linkage to the pineal gland neurologically and end ocrinolgically modulates the circadian components of the disorder. However, a central basis for the disorder is important, and the excessive parasympathetic activity that may be needed to produce the disorder of the sympathetic system in the periphery is also involved through an inhibitory process. Modulation of the pain, itself, occurs via the trigeminal vascular system, which may account for peripheral cervical spinal nerves in the clinical presentation.
Evaluating and managing severe headache in the emergency department
Published in Expert Review of Neurotherapeutics, 2021
Michelangelo Luciani, Andrea Negro, Valerio Spuntarelli, Enrico Bentivegna, Paolo Martelletti
There are other primary headache disorders that may present to the ED. Cluster headache is an easy diagnosis considering the clinical presentation with periodical attacks of severe, strictly unilateral pain, which is orbital, supraorbital or temporal, and lasting 15–180 minutes. The pain is typically associated with ipsilateral autonomic signs (nasal congestion and discharge, flushing, conjunctival injection, tearing, miosis, ptosis, restlessness, or agitation). Despite the headache attacks are short-lasting and self-limited, patients with cluster headache often visit the ED [50] and the main reason is because they are unaware of their condition and seek for a diagnosis. Patients with a known diagnosis may also visit the ED because of the inefficacy of the treatment prescribed as an outpatient; the urgent need of a drug prescription; an increase in the number of daily attacks since a few days; or a fear of adverse reactions because of the medication overuse due to a high daily frequency of the attacks.
A rational approach to migraine diagnosis and management in primary care
Published in Annals of Medicine, 2021
Vincent T. Martin, Alexander Feoktistov, Glen D. Solomon
The main differential diagnoses for migraine are tension-type headache and cluster headache [28]. Distinguishing features between these headache types include the typical location, quality, severity, and duration of pain, associated symptoms, and typical behaviour during attack, as shown in Figure 2 [32]. Briefly, tension headaches generally have mild-to-moderate, bilateral pain and lack migraine-associated symptoms (e.g. nausea and photophobia). Cluster headaches are associated with severe unilateral pain, ipsilateral autonomic symptoms (rhinorrhea, lacrimation, etc.), and duration <3 h. Medication overuse (≥15 days/month for simple analgesics; ≥10 days/month for triptans, ergots, combination analgesics or opioids) can increase the baseline frequency of any headache disorder and should be assessed once the primary headache is diagnosed.
CGRP pathway monoclonal antibodies for cluster headache
Published in Expert Opinion on Biological Therapy, 2020
The fremanezumab episodic cluster headache study used an endpoint of 4 weeks, and with this endpoint was terminated due to futility. It is plausible that the discordant results between the galcanezumab and fremanezumab trials are a result of the different study designs where the natural history of episodic cluster headache has not been sufficiently considered in setting the endpoint in the fremanezumab study. A cluster headache bout averages 8–9 weeks in duration [35]. Therefore, the study design will need to take this fact into account as a patient’s bout can spontaneously terminate and this can potentially be interpreted as an effect of the intervention [48]. The design of the galcanezumab episodic cluster headache trial, which included up to 15 days of screening and the preselected time point for the analysis of the primary endpoint of 3 weeks of double-blinded treatment, appears to be necessary to mitigate the placebo effect of spontaneous bout termination [19]. Examination of the response curve of the galcanezumab in the prevention of episodic cluster headache study showed the reduction in number of weekly attacks converged at 4 weeks and remained similar until the end of the double-blind phase [19]. The convergence of the treatment arm and placebo arm most likely represents spontaneous remission within both study arms [48]. Further examination of the response curve in the fremanezumab in the prevention of episodic cluster headache study suggests that by completing the study using the three-week endpoint, this study could also have been positive.
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