Abstract
To The Editor:
Case Report
L was a 14-year-old male with bipolar disorders comorbid with SB, and without other past psychiatric history; family bruxism history; other dental problems; other neurological and systemic illness; or exposure to neuroleptic, sedative, or anxiolytic medications or drugs of abuse. For ∼5 days, he had been overactive, and his mother thought him, “mad.” He often said he could be a mayor, even a chairman, and spent all his money to buy many unnecessary things. He kept talking rapidly and frequently switched topics during the outpatient clinical examination, almost not allowing the doctor to interrupt him. He liked to be close to females and to touch them, which suggested an increased sexual drive. There had been no obvious decrease in his time spent asleep, only ∼30 minutes less than usual. There were no other psychotic symptoms. L was diagnosed as bipolar disorder type I (BD-I) by two qualified psychiatrists using the Kiddie-Schedule for Affective Disorders and Schizophrenia for School-Aged Children-Present and Lifetime Version (K-SADS-PL) (Kaufman et al. 1997). Next we used the Young Mania Rating Scale (YMRS) to measure the severity of manic symptoms and the patient's score was 38. After clinical evaluation, monotherapy with sodium valproate 500 mg/day was begun. Two weeks later, on reexamination, L's mother told us that his sleep bruxism had disappeared since he had been taking sodium valproate. We learned that he had an ∼3 year history of SB, grinding and gnashing his teeth, accompanied by a characteristic and loud sound, almost every night. There was slightly abnormal wear on his teeth but he had no discomfort, fatigue, or pain in the masticatory musculature or other abnormal clinical signs of bruxism. His mother told us that this was the first time L had used sodium valproate, and that the frequency and intensity of bruxing masticatory activities gradually disappeared ∼2 days after using the drug. Since his first episode of bruxism ∼3 years earlier, there had been no special treatment for it, such as protecting devices, muscle relaxation measures, or any drug. Approximately 2 months after initiating valproate of 500 mg/day, the frequency and intensity of elevated expansive moods dramatically decreased; however, the patient did not take medicine as usual. One week after sodium valproate was discontinued, the patient's mother observed the reappearance of grinding and the characteristic sound, but it was less severe than before. Approximately 2 weeks later, L began taking sodium valproate 500 mg/day again after the follow-up visit. We found out that his bruxism disappeared again ∼2 days after using sodium valproate.
Discussion
Sodium valproate has many mechanisms of action, including enhancement of γ-aminobutyric acid (GABA) inhibitory neurotransmission, modulation of voltage- dependent sodium channels, and decreased cerebral glucose metabolism (Reynolds et al. 2007). Various hypotheses have been proposed to explain SB, including genetics, sleep structure, psychological factors, the autonomic nervous system, central neurotransmitters, and pharmacological factors, but no single theory can fully explain the etiology of SB (de la Hoz-Aizpurua et al. 2011). Some explanations as to why it disappeared with using sodium valproate follow.
First, some literature reveals that anxiety and emotional distress are implicated in the etiology of SB (Manfredini et al. 2005). We hypothesize that L's anxiety or other emotional distress were causally related to his SB. Sodium valproate with mood stabilizing properties is used in the treatment of bipolar disorders, neuropathic pain, and anxiety disorder. To some extent, sodium valproate can relieve anxiety and stress, which means that the risk factors of bruxism maybe controlled, thereby reducing the symptoms of SB. As a result, sodium valproate may reduce bruxism indirectly.
Second, it is hypothesized that the etiology of SB is based on cerebral neurotransmitters and their control over sleep/waking cycles. Substances such as GABA may be related to the genesis of rhythmic masticatory muscle activity (Lobbezoo et al. 1997; Behr et al. 2012). Moreover, GABA as the primary central nervous system inhibiting neurotransmitter is implicated in almost all the neuronal systems that control wakefulness, sleep, and motor activity (de la Hoz-Aizpurua et al. 2011). The hypothesis has been formulated that GABA may play a role in SB. To our knowledge, sodium valproate may inhibit GABA transaminase and stimulate the synthesis of GABA (Bialer 2012). For these reasons, maybe sodium valproate produce a reduction of SB through GABA directly.
Furthermore, the condition may occur because of other unknown issues. Therefore, more studies would be useful to tell if sodium valproate could treat SB.
Footnotes
Disclosures
No competing financial interests exist.