Bruxism occurring after stroke is an underrecognized complication that can impair oral function, contribute to orofacial pain, damage dentition, and negatively affect rehabilitation outcomes. The literature documents use of botulinum toxin type A (BoNT‑A) for bruxism in non‑stroke populations, but reports of its application in post‑stroke patients are limited. This case illustrates a structured assessment and treatment approach for bruxism that developed after a left basal ganglia intracerebral hemorrhage.
A 40‑year‑old man developed bruxism while recovering from a massive left hemispheric intracerebral hemorrhage. He had previously undergone decompressive craniectomy and hematoma evacuation. Approximately three months after admission, caregivers noted new nocturnal grinding. On clinical examination the patient had bilateral masseter muscle hypertrophy with marked tenderness on palpation, temporomandibular joint pain, visible dental wear, and drooling from the right mouth corner. The patient had no prior history of bruxism.
The treating team used the Standardized Tool for the Assessment of Bruxism (STAB) to provide a structured, multidimensional evaluation. Axis A (subject, clinical, and instrument domains) yielded the following:
The use of STAB offered a reproducible framework to document symptom presence and to integrate subjective, objective, and instrumented findings prior to intervention.
Initial management included occlusal splint therapy combined with hot compresses. The patient’s symptoms proved refractory to these conservative measures. Given persistent pain, muscle hypertrophy, and functional disturbance, the team elected to proceed with intramuscular injection of botulinum toxin type A into the bilateral masseter muscles with electromyography guidance.
Surface electromyography served two roles: confirming pathological masseter activity and guiding injection placement. The reported injection protocol was intramuscular administration into the bilateral masseters, with a dose of 50 units of BoNT‑A per side. Each side received injections divided across three sites. The procedure was performed under sEMG guidance as described in the report.
At 48 hours after the EMG‑guided BoNT‑A injections, the patient demonstrated a marked reduction in masseter muscle tension and tenderness. The clinical improvement reported at 48 hours was sustained at a 6‑month follow‑up evaluation. The case therefore describes a temporal association between BoNT‑A administration and symptom relief in post‑stroke bruxism.
This report is a single‑case description and therefore has limited generalizability. The authors note that these are descriptive findings and that controlled studies are needed to determine the efficacy and safety of BoNT‑A for bruxism in post‑stroke populations. Details such as adverse events, longer‑term dosing strategies, and comparative effectiveness versus other interventions were not reported in this single case. Clinicians should weigh the limited evidence base when considering BoNT‑A for post‑stroke bruxism and consider structured assessment tools such as STAB and objective measures like sEMG when documenting baseline status and guiding treatment.
This case highlights: (1) the potential for new‑onset bruxism after basal ganglia hemorrhage; (2) the value of a multidimensional assessment using STAB with clinical and instrumented confirmation; and (3) a temporal association between EMG‑guided intramuscular botulinum toxin type A injections to the masseters (50 U per side, divided into three sites) and rapid, sustained symptom improvement up to 6 months. Controlled research is required to establish treatment recommendations for the post‑stroke population.