1272 CLINICAL NOTES Bruxism After Brain Injury: Successful Treatment With Botulinurn Toxin-A Cindy B. Ivanhoe, MD, Jenny M. Lai, MD, Gerard E. Francisco, MD ABSTRACT. Ivanhoe CB, Lai JM, Francisco GE. Bruxism after brain injury: successful treatment with botulinum toxin- A. Arch Phys Med Rehabil 1997;78:1272-3. Bruxism, the rhythmic grinding of teeth-usually during sleep-is not an infrequent complication of traumatic brain injury. Its prevalence in the general population is 21%, but its incidence after brain injury is unknown. Untreated, bruxism causes masseter hypertrophy, headache, temporomandibular joint destruction, and total dental wear. We report a case of complete resolution of postanoxic bruxism after treatment with botulinum toxin-A (BTX-A). The patient was a 28year-old man with no history of bruxism who sustained an anoxic brain injury secondary to cardiac arrest of unknown etiology. On admission to our rehabilitation unit 2 months after the injury, the patient presented with severe bruxism and heavy dental wear. The patient was injected with a total of 200 units of BTX- A to each masseter and temporalis. There was total resolution of bmxism 2 days after injection, with no complications. On follow-up 3 months after injection, the patient remained free of bruxism. We propose that botulinum toxin be considered as a treatment for bmxism secondary to anoxic brain injury. Further studies regarding muscle selection and medication dosage are warranted to elucidate the toxin’s efficacy in this condition. 0 1997 by the American Congress of Rehabilitation Medicine and the American Academy of Physical Medicine and Rehabili- tation T HE TERM BRUXISM is derived from the Greek work brychein, which means “to grind or gnash the teeth.“’ Untreated, this rhythmic grinding can cause masseter hypertro- phy, headache, temporomandibular joint destruction, and total dental wear. In the general population the incidence of bruxism was once reported to be as high as 21 %.2 Bruxism is often noted in patients with altered states of consciousness, but its incidence after brain injury is still unknown. Resolution of bruxism is often associated with improvement in consciousness, and the appearance of bruxism has been closely linked to the return of sleep-wake cycles and improvement of level of consciousness in patients who were initially comatose.3 To prevent dental wear, mouth guards, spasmolytic medications, and relaxation therapy have been used with variable success. In this report, we describe our experience with successful treatment of bmxism in From the Department of Physical Medicine and Rehabilitation, Baylor College of Medicine (Dr. Ivanhoe); the Department of Physical Medicine and Rehabilita- tion, The University of Texas Health Science Center (Drs. Lai. Francisco): and the Brain Injury Program, The Institute. for Rehabilitation and Research (Drs. Ivanhoe, Francisco), Houston, TX. Submitted for publication December 20, 1996. Accepted in revised form May 6, 1997. No commercial party having a direct financial interest in the results of the research supporting this article has or will confer a benefit upon the authors or upon any organization with which the authors are associated. Reprint requests to Cindy B. Ivanhoe, MD, Brain Injury Program, TIRR, 1333 Moursund, Houston, TX 77030-3405. 0 1997 by the American Congress of Rehabilitation Medicine and the American Academy of Physical Medicine and Rehabilitation 0003.9993/97/781 l-4291$3.00/0 Arch Phys Med Rehabil Vol78, November 1997 a patient with anoxic brain injury using botulinum toxin-A (BTX-A). CASE REPORT A 28-year-old man had an acute onset of dyspnea and subse- quently fell unconscious while playing basketball. He had no history of bruxism or other illnesses. The patient was immedi- ately given two-person cardiopulmonary resuscitation for ap- proximately 15 minutes before the emergency medical team arrived. Initially, the patient was in ventricular fibrillation, which was converted to normal sinus rhythm following several defibrillations. On arrival in the emergency room, the patient had fixed pupils with a Glasgow Coma Scale score of 3. Computed tomography of the head revealed attenuated artifact of the right middle fossa with no evidence of facial or skull fractures, cerebral ischemia, or hemorrhage. Echocardiogram showed mild concentric left ventricular hypertrophy. The patient was diagnosed with anoxic encephalopathy secondary to cardiac arrest of unknown etiol- ogy. The only medical complication during the acute hospital- ization was pneumonia. Apart from tracheostomy and gastros- tomy tube placement, no other surgical procedure was performed. On admission to the rehabilitation unit 2 months later, the patient had spontaneous eye opening and occasional tracking. He had only unintelligible and nonmeaningful vocalizations. Severe, continuous grinding of the teeth and dental wear were observed. Three months after anoxic brain injury, the patient was in- jected with BTX-A to the masseter and temporalis muscles, respectively. Since the patient was not cooperative, the injec- tions were performed in the operating room under general anes- thesia with the guidance of an oromaxillofacial specialist. A needle was inserted until it came in contact with the mandibular and temporal bones. It was then withdrawn approximately 4mm to reach the bulk of the masseter and temporalis muscles. The patient tolerated the procedure well. There was no evidence of muscle atrophy, bleeding, or infection 2 days after injection. Bruxism started to resolve within 2 days. Three months after treatment, the patient demonstrated unchanged neurologic status but remained free of bruxism. DISCUSSION The pathophysiology of bruxism after anoxic brain injury has not been well described. The complications of chronic bruxism include dental wear, temporomandibular joint destruction, and pain. Traditionally, bruxism has been treated with mouth guards to prevent dental wear. In patients with severe tonic bite re- flexes, mouth guards can be difficult to insert or remove. Painful bruxism usually continues, with eventual wear of the temporo- mandibular joint.4 Because the primary muscles involved in bruxism are the temporalis and masseter, it was postulated that weakening these muscles with BTX-A would resolve the condi- tion. Botulinurn toxin-A was first introduced clinically by Scott5 in 1980 in the treatment of strabismus. Since that time, its