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.Key words: cluster headache, pituitary adenoma, macroprolactinoma Abbreviation: CH cluster headache ( Headache 2001;41:723-725) 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). [2][3][4][5][6][7][8][9][10][11][12][13][14][15][16][17] 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 HISTORYA 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). His prolactin level was 4759 ng/mL,

Mitochondrial encephalomyopathies encompass a group of disorders that have impaired oxidative metabolism in skeletal muscles and central nervous system. Many compounds have been used in clinical trials on mitochondrial diseases, but the outcomes have been variable. It remains controversial whether treatment of mitochondrial diseases with coenzyme Q 10 is effective. This paper describes a case of mitochondrial myopathy, encephalopathy, lactic acidosis, strokelike episodes, and exercise intolerance successfully treated with coenzyme Q 10. Efficacy of this therapy in this patient is correlated to control of lactic acidosis and serum creatine kinase levels. Disappointingly, larger studies with coenzyme Q 10 failed to demonstrate a clear beneficial effect on the entire study population with regard to clinical improvement or several parameters of the oxidative metabolism. They suggest that the use of coenzyme Q in treatment of mitochondrial diseases should be confined to protocols. There is a confounding variation in phenotype and genotype, and the natural history of the disorders in individual patients is not accurately predictable. The unpredictable a priori efficacy of therapy suggests that a long-term trial of oral coenzyme Q may be warranted.

To our knowledge, this is the first case reported in the literature of MRI-reversible lesions in a patient with general paresis. We suggest that MRI is of prognostic value in patients with general paresis. Severe atrophy, especially in the temporal lobe, could be a marker of bad clinical outcome.

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This case reveals the importance of differential diagnosis in atypical migraine in which the symptomatology could be secondary to intracranial lesions. We propose venous stasis as a cause of symptoms.