Trial of Oral Metoclopramide on Diurnal Bruxism of Brain Injury
A 51-year-old man was admitted for subarachnoid hemorrhage caused by a rupture of the left anterior communicating artery aneurysm. After acute treatment for a month, he was transferred to the department of rehabilitation for intensive therapy. Physical and neurological examinations were done. The score of the Korean version of the Mini-Mental Status Examination (K-MMSE) was 16. There were no abnormal findings on cranial nerve function tests, and no definite extraocular movement limitations or facial palsies were noted. Manual muscle power test showed that the Medical Research Council (MRC) grade of both the upper and lower extremities was grade II and I, respectively. The patient had been suffering from teeth grinding and jaw clenching, which had begun 3 weeks after the onset of a cerebral hemorrhage. Dystonia of the tongue, face or any other part of the body was absent. This symptom was aggravated during the daytime, especially during meals, and subsided during sleep. Teeth grinding worsened as time went on. An injection of botulinum toxin was given 5 weeks after the onset of bruxism; 40 units to each side of the bilateral masseter, 15 units to each side of the bilateral lateral pterygoid, and 15 units to each side of the bilateral medial pterygoid muscles. The symptom was followed up after 2 weeks, and the injected botulinum toxin showed no effect. His bruxism was also refractory to bromocriptine therapy. Thus, a 10 mg intramuscular metoclopramide HCl injection was administered for treatment of the bruxism. The bruxism subsided dramatically 5 hours after the injection and did not recur for the subsequent 12 hours. Oral metoclopramide medication in dosages of 15 mg per day was initiated the next day, which successfully abolished his bruxism after 2 days. Bruxism did not recur during the metoclopramide therapy. Magnetic resonance imaging of the brain showed a subacute intracranial hemorrhage at the left basal frontal lobe (). Positron emission tomography (PET) also showed a metabolic defect at the left basal frontal lobe, along with diffuse hypometabolism at the bilateral frontal, temporal, and parietal cortexes. A blink reflex study and electroencephalography (EEG) were normal. Transcranial and carotid Doppler were also normal. Anticholinergic agents, which are known to decrease the effectiveness of metoclopramide, were not administered for any reason. Any drug that induced bruxism or decreased the effect of levodopa was not administered either.