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Cluster Headache Associated With a Pituitary Adenoma

´╗┐Cluster Headache Associated With a Pituitary Adenoma

Discussion


This case study involved a patient with CH responding to treatment. An assessment revealed a clinically non-functioning pituitary adenoma. The patient became headache-free after treatment and remained so at follow-up.

Tumors have been documented in patients with CH. The symptoms may be in line with the criteria for CH. Pituitary lesions have been reported within the range of autonomic headache syndromes (trigeminal autonomic cephalalgias). This had led to interest in the link between pituitary tumors and headache. Headache is a common symptom of pituitary disease. Levy et al. observed in a study of pituitary tumors and headache that 4% of patients had CH. Functioning adenomas were above all linked to CH. Prolactinomas may be particularly associated with headache. Levy et al. described a case of macroprolactinoma associated with CH, which responded to dopamine agonists with complete resolution of the headache. In a reappraisal, Mainardi et al. found that pituitary adenomas accounted for 3% of secondary CH cases. The most frequent adenomas were prolactinomas.

The etiology and pathophysiology of CH are unknown. The current hypothesis proposes that primary CH is characterized by hypothalamic activation with secondary activation of the trigeminal-autonomic reflex, probably by a trigeminal-hypothalamic pathway. In this case, the tumor will be non-functioning. The underlying pathophysiology could be due to the structural effects of the tumor itself. Symptomatic CHs due to sellar pathology have also been reported. Olesen et al. point to the role of the cavernous sinus and/or hypophyseal region in the pathophysiology of symptomatic CH. The trigeminal nerve may be affected within the cavernous sinus and hypophyseal region by the sympathetic, parasympathetic and sensory fibers of the trigeminal nerve coming together as a plexus in this region. There are patients with pituitary tumor-associated headache who have headache and cranial autonomic symptoms on the same side as the lesion. A local mechanical effect or invasion may be important for the symptoms in those cases. This structural mechanism might have been involved in the pathophysiology of this case.

However, there are studies that contradict this explanation. These studies have failed to show an association between cavernous sinus invasion or tumor volume and headache. Thus, a pituitary tumor-linked headache may not just be a structural problem. It is likely that CH due to sellar pathology has a more multifaceted pathogenesis. The underlying mechanism in these cases remains to be illuminated.

Symptomatic CH should be suspected when the clinical features of the headache are atypical and in patients with pathological findings on neurological examination. Cittadini and Matharu suggest that all patients with CH should be evaluated for pituitary symptoms or disease. They also advocate that enhanced MRI should be carried out in all patients with CH who have an atypical symptomatology, abnormal examination, and a poor response to the appropriate treatments. Many authors propose that neuroimaging should be done in all patients with CH. The motive for this is that symptomatic CH may be indistinguishable from typical episodic CH.

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