Prolactinomas, dopamine agonists and headache: two case reports

Abstract

Headache is a common problem in patients with pituitary tumours. Small pituitary lesions can cause debilitating headache, suggesting that the size of the pituitary tumour may not be the only causal factor in pituitary-related headache. We present two cases of prolactinoma-associated headache. The first case has a clinical diagnosis of short-lasting unilateral headache attacks with conjunctival injection and tearing (SUNCT). The second case has a clinical diagnosis of hemicrania continua and idiopathic stabbing headache. In each case, the administration of dopamine agonists has led to an exacerbation of symptoms. We review the relevant literature to understand the pathophysiological implications of these cases.

The Role of Dopamine in a Model of Trigeminovascular Nociception

“…Despite the evidence that dopamine receptors may be present in the trigeminovascular system (Peterfreund et al, 1995) and that dopamine agonists have been found to exacerbate certain types of headache (Levy et al, 2003), only the D 1 receptor is able to attenuate or inhibit the activation of dural blood vessels or trigeminal neurons, and this response was only a partial effect, suggesting perhaps a small role in the acute phase of migraine. There were other effects, perhaps due to vasoconstriction caused by activation of the ␣ 2 -adrenoceptor.…”

SUNCT and high nocturnal prolactin levels: some new unusual characteristics

“…A few studies reported how patients with micro-adenoma may suffer from severe headache, while patients with macro-adenoma may not have headache. This suggests that mass effect of the tumour is not correlated to the presence or intensity of the headache [11], but rather the headache syndromes may result from alterations in the neuro-endocrine system. Recently, in the case reported by Rozen, the complete cessation of headaches after the removal of an acromegalic micro-adenoma was documented, suggesting a potential role also for GH in SUNCT pathogenesis [15].…”

“…Therefore, dopaminergic hypofunction could be the consequence of serotoninergic hyperfunction, because of the inhibitory effect of serotonin on dopamine neurons. In fact, in patients with SUNCT the treatment with dopamine-agonists can determine various responses, with worsening in some cases [7] and improvement in others [11,12]. Most cases of SUNCT syndrome are primary but several cases of SUNCT are secondary and occur in patients with pituitary tumours, further supporting involvement of the hypothalamic-hypophysial axis.…”

“…Most cases of SUNCT syndrome are primary but several cases of SUNCT are secondary and occur in patients with pituitary tumours, further supporting involvement of the hypothalamic-hypophysial axis. There are seven cases reported of SUNCT syndrome secondary to pituitary adenomas in the medical literature, of which four cases had prolactinomas [10][11][12], two non-secreting macro-adenoma [13,14] and one case had micro-adenoma linked to acromegaly [15]. In all the case reports with prolactinoma, the tumour was ipsilateral to the side of the attacks, producing a possible mass effect or mechanical mode of action, which may have played a role in SUNCT onset.…”

Pituitary Adenoma Presenting As Trigeminal Neuralgia

“…8,9 Many patients report headaches after starting pharmacotherapy for adenoma; one explanation given for why headaches get worse after taking dopamine agonist is that the growth of the tumor is transitory or that a neurohormonal mechanism is possible. 10,11 The degree of extension into the cavernous sinus is not associated with the presence or extent of headache.…”