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Keywords:

  • cluster headache;
  • pituitary adenoma;
  • macroprolactinoma

Abstract

  1. Top of page
  2. Abstract
  3. CASE HISTORY
  4. COMMENTS
  5. REFERENCES

We report a case of cluster headache in a patient with a macroprolactinoma. Symptomatic cluster headache was suspected because of an unsatisfactory response to medications that are usually effective in idiopathic cluster headache. The neurological examination was normal. However, magnetic resonance imaging demonstrated a large pituitary tumor. One year after starting treatment with cabergoline, the patient remains asymptomatic. Symptomatic cluster headache should be suspected when the clinical features of the headache are atypical. By inducing vascular mechanisms, the parasellar lesion may have played a role in initiating the cluster headache.

Abbreviation:
CH

cluster headache

Cluster headache (CH) is a disease with a typical periodic pain pattern. The diagnostic criteria are based on clinical features and the temporal pattern. In primary CH, neuroradiological investigations should not demonstrate any pathological or morphological lesion in the central or peripheral nervous system. Like other vascular headaches, CH is presumed to develop from pathophysiological events, which ultimately activate the trigeminovascular system.1 Several reports have described the association of clusterlike headache with structural neurological disturbances (Table 1).2-17

Table 1.—.  Underlying Intracranial Lesions Described in Symptomatic Cluster Headache
Parasellar and upper cervical meningiomas
Pituitary adenomas
Prolactinomas
Growth hormone-secreting pituitary adenoma
Trigeminal neurinomas
Nasopharyngeal carcinomas
Brain metastases
Lymphomatous meningitis
Calcified lesions in the region of the third ventricle
Anterior carotid artery aneurysms
Pseudoaneurysm of intracavernous carotid artery
Hemispheric arteriovenous malformations
Posterior communicating artery aneurysm
Vertebral artery aneurysm
Vertebral artery dissection
Giant cell arteritis
High cervical spinal cord infarction
Facial, head, or neck trauma
Orbitosphenoidal Aspergillosis
Maxillary sinusitis

We report the occurrence of clusterlike headache in a patient with a pituitary adenoma. The neurological examination was normal, but both neuroradiological and endocrine investigations revealed the presence of a pituitary prolactinoma.

CASE HISTORY

  1. Top of page
  2. Abstract
  3. CASE HISTORY
  4. COMMENTS
  5. REFERENCES

A 30-year-old man presented with complaints of recurrent headache of 2 years' duration. The pain was severe, sharp, and invariably in the left eye and periorbital region, and usually lasted less than 120 minutes. The attacks were associated with ipsilateral lacrimation, rhinorrhea, injection of conjunctiva, ptosis, and miosis. The pain was never associated with nausea or vomiting and did not increase with Valsalva maneuver. The pain never awakened the patient. Initially, the attacks occurred sporadically, once a day for a period of 20 days, and then he was asymptomatic for a couple of months. The frequency increased in the previous 6 months to three or more episodes per day without any temporal pattern. Because analgesic treatment was not effective and the clinical characteristics had changed, he decided to consult a specialist. The initial neurological examination was normal. There were no signs of cranial nerve involvement. The patient was started on verapamil and given zolmitriptan for pain crises. A cranial computed tomography scan showed a parasellar and suprasellar tumor with left extension into the cavernous sinus. Magnetic resonance imaging (MRI) again demonstrated a left-sided adenoma with cavernous sinus invasion (Figure 1). His prolactin level was 4759 ng/mL, and evaluation of other pituitary function was normal. Visual fields were normal. Because there was no visual impairment, the patient was given cabergoline, 1 mg, per week and became asymptomatic after 4 weeks. The visual fields have been checked repeatedly and remain normal. An MRI 4 months after starting treatment and again at 10 months after starting treatment both showed the prolactinoma to be smaller. A year later, the patient remains totally free from further attacks.

image

Figure 1.—. Magnetic resonance image showing a left-sided adenoma with cavernous sinus invasion.

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COMMENTS

  1. Top of page
  2. Abstract
  3. CASE HISTORY
  4. COMMENTS
  5. REFERENCES

Although the pathophysiology of CH remains undetermined, it has a neuronal component with possible involvement of the trigeminal nerve. The strictly unilateral nature of the pain, the periodicity, and the observation that pain precedes the onset of increased blood flow and other autonomic features associated with CH support the role of the trigeminovascular system as in migraine.18 The majority of reported symptomatic CHs are associated with parasellar pathology around the distal portions of the carotid artery in the cavernous sinus area. In this area, the nociceptive fibers of the trigeminal nerve and sympathetic and parasympathetic nerves come together.18

Symptomatic CH should be suspected when the clinical features of the headache are atypical: absence of the typical periodicity or duration seen in episodic CH, a persistent headache between attacks, unsatisfactory response to medications that are normally effective in idiopathic CH (such as ergotamine, triptans, oxygen inhalation, steroids, verapamil), and the presence of atypical neurological signs or symptoms.8,19

Our patient presented with a history of recurrent headache for 2 years, and 2 weeks after starting treatment with a dopamine agonist became asymptomatic; he remains asymptomatic 1 year later. This indicates a relationship between the sellar-suprasellar lesion and CH. Because there are several reports of nonendocrine lesions related to CH (Table 1), it is unlikely that CH could be induced by hormonal changes.

The only atypical feature was the lack of response to CH medications. This observation is consistent with the convenience of excluding symptomatic CH in patients with atypical evolution.

REFERENCES

  1. Top of page
  2. Abstract
  3. CASE HISTORY
  4. COMMENTS
  5. REFERENCES