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Trigeminal Neuralgia After Bromocriptine Therapy in a Stroke Patient - a Case Report

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Trigeminal Neuralgia After Bromocriptine Therapy in a Stroke Patient - a Case Report J Korean Acad Rehab Med 2010; 34: 777-780 Case Report Trigeminal Neuralgia after Bromocriptine Therapy in a Stroke Patient - A Case Report - Joo Hyun Park, M.D., Ph.D.2, Geun Young Park, M.D., Ph.D.1, Sun Im, M.D.1, Soon Hei Yoo, M.D.2, Jin Jun, M.D.2, Jin Ook Kwon, M.D.1, Sung Hee Jung, M.D.2, Hee Chan Jung, M.D.2 Department of Rehabilitation Medicine, 1Bucheon St. Mary's Hospital, The Catholic University of Korea, Bucheon 420-717, 2Seoul St. Mary's Hospital, The Catholic University of Korea, Seoul 137-040, Korea Rare side effects of bromocriptine, such as, trigermial neuralgia, have been reported in patients with pituitary adenoma but no such case has been reported in post-stroke patients. This case reports on a stroke patient who developed trigeminal neuralgia after bromocriptine therapy. A 48-year-old man, diagnosed with left middle cerebral artery territory infarction and transcortical motor aphasia, was prescribed with 2.5 mg of bromocriptine. After two days, he complained of pain in the right trigeminal nerve distribution. Brain MRI, facial EMG, blink reflex, revealed no abnormalities. His pain showed no relief to various pharmacological agents. However, pain disappeared with discontinuation of bromocriptine and recurred again with readministration. In addition, pain intensity correlated with increase of bromocriptine dosage. Based on these findings, we concluded that patient’s trigerminal neuralgia was related to bromocriptine administration. An antidote, which consisted of a dopamine antagonist was prescribed together with bromocriptine and the patient subsequently showed relief of pain and improvement of aphasia. Key Words Trigeminal neuralgia, Bromocriptine, Stroke INTRODUCTION somnolence, and there is only one report of non-func- tional pituarity tumor patient who developed a trigemi- Trigeminal neuralgia is a disease that appears in the nal neuralgia with an administration of bromocriptine.1 distribution along one or more divisions of the fifth However, there is no report about a stroke patient cranial nerve with repetitively extreme paroxysmal attack. who developed a trigeminal neuralgia with bromocri- The most commonly identified abnormalities are known ptine. Nevertheless we have experienced the case after to be the compression of the trigeminal nerve by the administration of bromocriptine for the post stroke vessel. Rarely, cerebello-pontine angle tumor, pontine aphasia, and therefore, would like to report about the infarction, arteriovenous malformation and multiple scle- case. rosis can lead to trigeminal neuralgia. Bromocriptine is an ergot-derived dopamine receptor agonist which is a treatment for Parkinson’s disease, CASE REPORT hyperprolactinemia and post stroke aphasia. Common adverse effects are nausea, headache, dizziness and A 48-year-old man was admitted at 2 months post- Received July 1, 2010; Accepted September 10, 2010 Corresponding author: Joo Hyun Park Department of Rehabilitation Medicine, College of Medicine, The Catholic University of Korea, Banpo 4-dong, Seocho-gu, Seoul 137-701, Korea Tel: +82-2-2258-2822, Fax: +82-2-2258-2825, E-mail: [email protected] Copyright © 2010. Korean Academy of Rehabilitation Medicine Joo Hyun Park, et al. icus of left middle cerebral artery infarction, for com- prehensive rehabilitation of aphasia and right motor weakness. Patient had no specific underlying disease like diabetes, hypertension and migraine. Brain mag- netic resonance imaging showed acute infarction on left basal ganglia, insular lobe, frontoparietal perculum and part of parietal lobe. When admitted, he was able to perform two-step command, and mini-mental state examination was 24 points. Korean paradise western aphasia examination showed transcortical motor aphasia, with aphasia quo- tient of 51/100 and language quotient of 52/100. We started speech therapy twice a week and bromocriptine therapy after admission. At that time, the patient ad- ministered aspirin, artemisiae asiatica 95% ethanol ex- tract, donepezil and tizanidine. We added no other drug except bromocriptine while admission. Before bromo- Fig. 1. (A) Figure shows the pain distribution that patient criptine therapy, he was able to express one word, experienced with administration of bromocriptine. The pa- while after, his status improved to connecting 2-3 tient’s pain distribution corresponds to the ophthalmic and words to make a simple sentence. On the second day mandibular territory of trigeminal nerve. (B) The pain in- after initiating 2.5 mg bromocriptine, the patient com- tensity is seven by the visual analog scale. plained of a series of repetitive excruciating neuralgic pain in the right trigeminal nerve distribution. His pain from 7,000/μl to 3,000/μl. Due to the fact that the scored 3 by a visual analogue scale. Physical examina- pain attacks developed after bromocriptine admin- tion (including eye movements, visual acuity and fields, istration, pain intensity was proportional to dosage, and corneal reflex, facial sensory test and visual inspection all studies for the purpose of differential diagnosis of on face and oral cavity) showed no abnormalities. facial pain showed no abnormalities, we assumed that Prodromal symptom of migraine and abnormality of vi- this rare case of trigeminal neuralgia was induced by tal sign were not shown. We increased the amount of bromocriptine administration. To confirm our hypoth- bromocriptine to 5 mg on the 4th day. This aggravated esis, we evaluated the causal relationship between the the pain to 7. We administered tyrenol and meloxicam pain attack and bromocriptine therapy by a single- for relieving the pain, but it did not work. In order to blinded pharmacologic test. After informed consent was properly evaluate the nature, intensity and distribution obtained, we observed the change of pain intensity of pain, we examined through pictures and texts. Pain with administration of placebo. On the 11th day of neu- was dull but consistent, and got worse for a short time ralgic attack, we reduced amount of bromocriptine from periods by paroxysmal attack. Pain appeared in the dis- 7.5 mg to 2.5 mg. This alleviated the pain from 7 to 3. tribution along the ophthalmic and madibular branch of On the 14th day, as soon as we stopped bromocriptine, trigeminal nerve (Fig. 1). We assumed that the cause of neuralgic pain totally disappeared. However, language pain was trigeminal neuralgia based on the nature and fluency became worse after bromocriptine therapy distribution of pain. Therefore we administered carba- stopped. To reconfirm the relationship between the pain mazepine 300 mg for pain relief. In order to identify attack and bromocriptine, we re-initiated bromocriptine the cause of pain, we performed a series of studies therapy. On the first day of re-initiation, the patient that included brain magnetic resonance imaging, soma- complained of a neuralgic pain in the same distribution, tosensory evoked potential study, blink reflex and facial which resembled the pain nature of previous attack. nerve conduction studies with EMG, but none of these Pain intensity was also proportional to dosage. Despite tests revealed any abnormalities. We administered 300 the examination to prove the relationship between dop- mg of carbamazepine as a treatment of trigeminal neu- amine system and bromocriptine-induced trigeminal neu- ralgia, which failed to alleviate the pain. Then, we stop- ralgia, the examined blood prolactin level was within ped carbamazepine therapy because WBC level dropped the normal range. The bromocriptine therapy was need- 778 Trigeminal Neuralgia after Bromocriptine Therapy in a Stroke Patient ed to improve the fluency and therefore domperidone, bromocriptine turned out to increase the risk of valvu- antagonist of bromocriptine, was dosed in combination lar heart disease if highly dosed for a long period of for pain relief. The pain intensity scored 6 by VAS time.5 score with only bromocriptine 5 mg dose, but with the In the past, Ferrari et al.1 proposed the relationship combination of domperidone 50 mg, pain intensity re- between bromocriptine and trigeminal neuralgia for the duced to 2. Trigeminal neuralgia was resolved and first time through the report of non-functional pituarity speaking fluency also improved after one month with tumor patient that developed a trigeminal neuralgia combination treatment of bromocriptine 5mg and dom- with bromocriptine. Past case suggested that bromoc- peridone 50 mg. riptine induced transient increase in total pituitary vol- ume by accumulation of prolactin storage granule, pro- ducing intermittent pressure on the ophthalmic branch of DISCUSSION the fifth nerve, resulting in trigeminal neuralgia attack. But in this case, we concluded that some functional ab- Bromocriptine has been used as the treatment for normalities, not structural abnormalities like com- Parkinson’s disease, hyperprolactinemia and post stroke pression of trigeminal nerve by pituitary gland, may led aphasia since the introduction of the early 1970’s, and to trigeminal neuralgia for some reasons. First, pro- is widely used due to the rare fatal adverse effect. lactin plasma level was not associated with bromo- There has been a report about trigeminal neuralgia with criptine dose. Second, blink reflex study and MRI showed an administration of bromocriptine in pituarity tumor no structural abnormalities. We administered domperi- patient, but no such case has been reported in post- done, dopamine antagonist, on the base of previous stroke patients. case1 of relieving the neuralgic
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