Cluster Headache Pharmacotherapy

Abstract

Cluster headache is a well-known primary headache syndrome with a prevalence of about 5/10,000 of the adult population, making it much less common than migraine. Diagnostic terms such as histaminic cephalalgia, Horton's headache and ciliary neuralgia have been used for what is now known as cluster headache. This disorder can be differentiated from migraine by clinical and pathophysiologic features. Cluster headache also exhibits a differing therapeutic response to medications when compared with migraine. The pharmacologic treatment of cluster is reviewed in this article. In contrast to migraine, men are 3-4 times more likely to be diagnosed with cluster headache than women, and the cluster headache population is older. Cluster attacks are known for their brief intense unilateral excruciating pain during susceptible periods known as cluster periods, which typically last weeks. Attack-free months generally follow. Pain is experienced in the distribution of the trigeminal nerve, with unilateral autonomic features. Most patients are successfully managed with medical therapy. Medication management can be divided into abortive treatments for an ongoing attack and prophylactic treatment. Prophylaxis aims to induce and maintain a remission. There are a variety of different medications for abortive and prophylactic therapy, accompanied by a variable amount of evidence-based medicine. For patients refractory to medical management, interventional procedures are available as a last resort. Most procedures are directed against the sensory trigeminal nerve and associated ganglia, eg, anesthetizing the sphenopalatine ganglion.

Unsuccessful Pulsed Radiofrequency of the Sphenopalatine Ganglion in Patients with Chronic Cluster Headache and Subsequent Successful Thermocoagulation

“…Even though the physiopathology of CH is still unknown, the hypothalamus is thought to be the generator of this disease because of its circadian and circannual periodicity and the activation of the posterior hypothalamus found in neuroimaging studies that were undertaken during the attacks. Furthermore, activation of the parasympathetic outflow from the superior salivary nucleus via the SPG is supposed, explaining the autonomic manifestations of CH and the likely role of the SPG at least in this aspect of the disease . Indeed, it was shown that low frequency (5 Hz) SPG stimulation could induce cluster‐like attacks with autonomic features.…”

“…The increased parasympathetic outflow may be originated centrally because of a hypothalamic disturbance, with likely involvement of a trigemino‐hypothalamic pathway. Also, descending fibers from the hypothalamus to the trigeminal nucleus caudalis could trigger the pain …”

“…In these cases, as well as those in which the side effects of the medications are intolerable a sphenopalatine ganglion (SPG) block may be indicated. Although several methods for blockade are proposed in the literature, we previously used continuous radiofrequency (CRF) of the SPG in patients with medically refractory CCH . However, there may be some complications following this procedure, such as hyperpathia or deafferentation pain in the territory of the maxillary branch of the trigeminal nerve; permanent or transient hypesthesia; hypersensitivity or dysesthesia in the palate; maxilla;, gums; cheek or posterior pharynx; in addition to dryness of the eye and reflex bradycardia during radiofrequency lesioning .…”

“…Cluster headache (CH) is a trigeminal autonomic cephalalgia, a condition that is characterized by severe unilateral headache and cranial parasympathetic manifestations. [1][2][3][4][5][6][7][8][9] Approximately 10% to 15% of patients develop chronic cluster headache (CCH). 6,7,10,11 Although its treatment is essentially pharmacological, involving both prophylactic and acute measures, up to 15% to 20% of patients do not respond adequately to conservative management.…”

Cluster headache: Acase-based review of diagnostic and treatment approaches

“…Because hypothyroidism and nephrogenic diabetes insipidus can occur with long-term use, renal and thyroid function are assessed prior to and during treatment. Concomitant use of diuretics and nonsteroidal anti-inflammatory drugs should be avoided because they can increase lithium levels by decreasing renal excretion [1•, 22,35].…”