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The relationship between pituitary tumors and headaches is explored, while citing various studies and treatments that help patients cope with severe headaches.
Headaches are a common complaint in patients with pituitary tumors. Although many patients presumably have headaches which are unrelated to their pituitary tumor, there are several important direct and indirect mechanisms by which pituitary tumors may elicit or exacerbate headaches. Pituitary tumors may directly provoke headaches by eroding laterally into the cavernous sinus, which contains the first and second divisions of the trigeminal nerve, by involvement of the dural lining of the sella or diaphragma sella (which are innervated by the trigeminal nerve), or via sinusitis, particularly after transsphenoidal surgery. Headache pain in these situations is typically characterized by steady, bifrontal or unilateral frontal aching (ipsilateral to tumor). In some instances, pain is localized in the midface (either because of involvement of the second division of the trigeminal or secondary to sinusitis).
In contrast to the insidious, subacute development of headaches in most patients with pituitary tumors, patients with pituitary apoplexy may experience acute, severe headaches, perhaps associated with signs and symptoms of meningeal irritation (stiff neck, photophobia), CSF pleocytosis or occulomotor paresis. Routine CT scans of the head occasionally skip the sella, hence the presence of blood or a mass within the sella may not be detected and patients can be misdiagnosed with meningitis or aneurysm. Because pituitary apoplexy represents a neurosurgical emergency, MRI should be used in patients with symptoms suggestive of this disorder. A subacute form of pituitary apoplexy has also been reported. Patients with subacute pituitary apoplexy experience severe and/or frequent headaches over weeks to months and have heme products within the sella on MRI scans.
In most instances, headaches are not attributable to direct effects of the pituitary tumor and indirect causes must be considered. Generally, indirect effects of pituitary tumors are caused by reduced secretion of pituitary hormones and are manifested by promotion of "vascular" headaches (e.g., migraine). The major exception to this rule relates to the potential for acromegalic patients to develop headaches secondary to cervical osteoarthritis. Vascular headaches may be exacerbated in association with disruption of normal menstrual cyclicity and impaired gonadal steroid secretion (e.g., from hyperprolactinemia or gonadotropin deficiency). Hyperprolactinemia, hypothyroidism and hyperthyroidism may also have direct effects, independent of gonadal hormones. Headaches are common in acromegaly, and in the majority of cases the etiology is not well understood.
Finally, drug management of pituitary tumors may inadvertently impact headaches. Octreotide results in extremely rapid headache improvement with patients with acromegaly. The rapid time course suggests it is not due to lowering of GH levels. Octreotide also has a dramatic beneficial effect on migraine and may be producing relief of headache by vascular mechanisms. Occasionally severe headaches surface in acromegalic patients after reduction or discontinuation of octreotide, as a "withdrawal" phenomenon.
Bromocriptine or other dopamine agonists occasionally trigger severe headaches. When this occurs, it is important to recognize that bromocriptine has been reported as a cause of pituitary apoplexy, and it may be necessary to perform an MRI or CT to rule out infarction or hemorrhage within the pituitary. Once it is established that the patient is not infarcting the pituitary, it is generally safe to treat the headaches symptomatically (not with an ASA containing drug) and consider alternative therapies for the prolactinoma if the problem remains severe.
Pituitary tumor patients with vascular headaches are generally quite responsive to standard prophylactic migraine drugs (e.g., tricyclic antidepressants, verapamil and beta-blockers). It is best to begin therapy with very low-dose medication (e.g., 10 mg of amitriptyline at bedtime) and resist the impulse to escalate the dose rapidly to higher levels. Often patients have an excellent response to 10-30 mg of a tricyclic antidepressant, although it may take up to six or more weeks to reach the ultimate benefit. The choice of tricyclic antidepressant should be based upon the desired side effects (e.g., either more sedation or less sedation) The newer, serotonin-selective antidepressants are generally less effective for headaches than tricyclics, although some patients do respond nicely to these agents. In some cases it may be necessary to use combination therapy (e.g., verapamil plus a tricyclic).
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