Tumors and Headaches
by Peter N Riskind, M.D.,Ph.D.
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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, MRl 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, 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).
therapies for headache such as cafergot or imitrex are probably
effective in patients with pituitary tumors, I believe that
it is prudent to avoid these drugs in patients with macroadenomas
because of the potential for precipitating pituitary apoplexy.
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