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Transient Acquired Speech Dysfluency Temporally Associated with Dexmedetomidine- Assisted Sedation During Spinal Anesthesia: A Case Report

This case report describes a 63-year-old woman who experienced a transient, fully reversible episode of speech dysfluency shortly after dexmedetomidine-assisted sedation during spinal anesthesia, suggesting a potential, albeit unproven, drug-related modulation of speech networks after acute cerebrovascular causes were ruled out.

Original authors: Wudong Zhuang, Ruizhao Lyu, Rui Liu, Yang Bai, Xiaoyuan Li, Yukun Xu, Haoyang Geng

Published 2026-09-11

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CC BY 4.0

Original authors: Wudong Zhuang, Ruizhao Lyu, Rui Liu, Yang Bai, Xiaoyuan Li, Yukun Xu, Haoyang Geng

Original paper licensed under CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/). ✨ This is an AI-generated explanation of the paper below. It is not written or endorsed by the authors. For technical accuracy, refer to the original paper. Read full disclaimer

The human ability to speak fluently relies on a vast, invisible network of connections within the brain. This network does not just store words; it coordinates the precise timing and initiation of sounds, ensuring that thoughts flow smoothly into sentences. While we often take this flow for granted, it can be disrupted by injury, disease, or even the subtle chemical shifts caused by medication. When this disruption happens suddenly in a person who has never stuttered before, it is known as acquired speech dysfluency. For doctors, the sudden onset of such symptoms is a medical alarm bell, usually pointing first toward a stroke or a temporary blockage of blood flow to the brain. However, the brain is a complex organ, and sometimes the cause is not a broken vessel, but a temporary glitch in how its circuits are firing, perhaps triggered by the very drugs used to keep a patient calm during surgery.

In a recent report from a hospital in Hebei, China, a team of anesthesiologists and neurologists described a rare instance where a woman developed a sudden, temporary stuttering-like condition shortly after receiving a common sedative. The patient was a 63-year-old woman undergoing a routine knee surgery. She had a history of high blood pressure and diabetes, and a preoperative scan had already revealed that she had small, old scars in the deep parts of her brain known as the basal ganglia, areas critical for movement and speech timing. Despite these old scars, she had never had any speech problems before. During her operation, she received spinal anesthesia to numb her lower body and was given dexmedetomidine, a drug widely used to keep patients calm and cooperative without stopping their breathing. The surgery went smoothly, and she woke up without issue.

The unusual event began about 30 minutes after the sedative was turned off. While sitting in her hospital room, fully awake and aware of her surroundings, the woman suddenly found she could not start speaking. She could understand everything people said to her, she knew the names of objects, and her voice was clear, but when she tried to talk, she would get stuck. She would repeat the first sound of a word or hold a sound out longer than intended, a pattern characteristic of stuttering. This was not a case of confusion or muscle weakness; her mind was sharp, and her body was strong, but the flow of her speech had been interrupted. Because this happened so suddenly, the medical team immediately suspected a stroke. They performed urgent scans of her brain, including detailed images that can detect even the smallest fresh blockages. The results were clear: there was no stroke, no bleeding, and no new damage to her blood vessels. The only abnormalities found were the old, silent scars in her basal ganglia that had been there before the surgery.

Over the next hour and a half, the woman's speech slowly returned to normal without any specific treatment. About 97 minutes after the symptoms began, she was speaking as fluently as she had before. She was discharged three days later with no lasting effects, and a follow-up call a week after confirmed she had fully recovered. The researchers carefully considered other possibilities. They ruled out low oxygen, low blood sugar, or the lingering effects of the spinal anesthesia, none of which typically cause isolated speech issues. They also noted that she had not received other common sedatives or painkillers that might interact with the drug she was given. While the team could not prove with absolute certainty that the dexmedetomidine caused the episode, the timing was too close to be a coincidence. They suggest that the drug may have temporarily altered the activity in the brain's speech networks, and because the patient already had small, old injuries in the deep brain circuits that control speech, her brain was more vulnerable to this temporary glitch.

This case serves as a reminder that the brain's response to medication can be unpredictable, especially in patients with pre-existing, silent brain changes. While the drug dexmedetomidine is generally considered safe and is prized for allowing patients to remain alert during procedures, this report highlights that it might occasionally trigger a temporary disruption in speech for a small subset of people. The medical team emphasized that whenever a patient develops new speech problems after anesthesia, doctors must first treat it as a potential stroke until proven otherwise. In this specific instance, the quick thinking of the medical staff allowed them to rule out a life-threatening emergency and observe as the patient's natural recovery took place, offering a glimpse into how delicate the balance of our neural circuits can be.

Technical Summary: Transient Acquired Speech Dysfluency Associated with Dexmedetomidine-Assisted Sedation

Problem Statement
Dexmedetomidine (DEX), a selective $\alpha_2$ -adrenoceptor agonist, is widely utilized for perioperative sedation due to its ability to provide cooperative sedation while preserving spontaneous respiration. While its safety profile regarding respiratory depression and hemodynamics is well-established, neurological adverse events specifically involving speech production remain rarely reported. New-onset speech abnormalities in the perioperative period typically necessitate immediate evaluation for acute cerebrovascular disease (e.g., stroke or transient ischemic attack). However, distinguishing between acute ischemic events and transient, reversible functional disturbances caused by pharmacological modulation or interactions with pre-existing structural abnormalities presents a diagnostic challenge. This case report addresses the occurrence of transient acquired speech dysfluency temporally associated with DEX-assisted sedation in a patient with chronic basal ganglia abnormalities.

Methodology
This study is a single-case report adhering to the CARE guidelines. The subject was a 63-year-old female (ASA physical status II) undergoing elective arthroscopic left knee surgery under spinal anesthesia.

Anesthetic Protocol: Spinal anesthesia was induced with 3 mL of 0.25% bupivacaine. DEX was administered for sedation via a loading dose (0.5 µg/kg over 10 minutes) followed by a maintenance infusion (0.3 µg/kg/h). The infusion ceased 10 minutes prior to surgery completion. No opioids, benzodiazepines, propofol, or inhalational anesthetics were used.
Clinical Monitoring: Hemodynamic and respiratory parameters were continuously monitored. Sedation depth was assessed using the Richmond Agitation–Sedation Scale (RASS).
Diagnostic Workup: Upon the onset of speech symptoms, an urgent neurological evaluation was conducted, including the National Institutes of Health Stroke Scale (NIHSS). Diagnostic imaging included Brain MRI, Diffusion-Weighted Imaging (DWI), and Intracranial Magnetic Resonance Angiography (MRA) performed while the patient was symptomatic.
Causality Assessment: The Naranjo Adverse Drug Reaction Probability Scale was applied to evaluate the likelihood of a drug-induced event.
Follow-up: The patient was monitored for spontaneous resolution of symptoms, discharged on postoperative day 3, and followed up via telephone at 7 days.

Key Results

Clinical Presentation: Approximately 30 minutes after the discontinuation of DEX, the patient developed sudden difficulty initiating speech. The dysfluency was characterized by the repetition of initial sounds/syllables and sound prolongation. Crucially, the patient remained fully conscious, oriented, and retained intact comprehension, naming ability, semantic expression, and articulation. The NIHSS score was 1, attributed solely to the speech abnormality.
Diagnostic Findings:
- Imaging: Preoperative CT revealed chronic bilateral lacunar infarctions in the basal ganglia. Post-event MRI and DWI showed no evidence of acute cerebral infarction or diffusion restriction. MRA ruled out intracranial arterial occlusion, dissection, or severe stenosis.
- Physiology: Hemodynamic and respiratory parameters remained stable throughout the event. Metabolic and electrolyte imbalances were excluded.
Outcome: The speech disturbance resolved spontaneously approximately 97 minutes after onset without pharmacological intervention. The patient was discharged without neurological sequelae, and the 7-day follow-up confirmed complete recovery with no recurrence.
Causality Analysis: The Naranjo scale yielded a score of 3, indicating a "possible" adverse drug reaction. This assessment relied on the clear temporal relationship between DEX administration and symptom onset but was limited by the lack of rechallenge and the absence of prior identical reports.

Key Contributions

Documentation of a Rare Phenomenon: This report describes a case of transient acquired speech dysfluency occurring in close temporal association with DEX-assisted sedation, a neurological adverse event not commonly associated with this agent.
Differential Diagnosis Framework: The case highlights the necessity of distinguishing between acute cerebrovascular events and transient functional speech disturbances in the perioperative setting, particularly when neuroimaging is negative for acute ischemia.
Susceptibility Factors: The report suggests that patients with pre-existing structural abnormalities in the basal ganglia (specifically chronic lacunar infarctions) may possess reduced functional reserve, rendering them more susceptible to transient disruptions in speech-related neural networks induced by pharmacological modulation.
Mechanistic Hypothesis: While causality is not proven, the authors propose that DEX-induced modulation of the cortico-striato-thalamo-cortical network—specifically involving noradrenergic activity in the locus coeruleus and its connections to speech motor planning regions—may represent a plausible mechanism for the observed dysfluency in susceptible individuals.

Significance and Claims
The authors conclude that while a direct causal relationship between dexmedetomidine and speech dysfluency cannot be definitively established from a single case, the temporal association and exclusion of other perioperative triggers suggest a possible link. The paper posits that dexmedetomidine-related modulation of speech-associated neural networks may contribute to such events in patients with pre-existing basal ganglia abnormalities.

The significance of this report lies in its clinical warning: clinicians must remain vigilant when new-onset speech abnormalities occur after anesthesia or sedation. Acute cerebrovascular events must be rigorously excluded via imaging and clinical evaluation before attributing symptoms to medication effects or functional mechanisms. The authors emphasize that transient acquired speech dysfluency can occur even in the absence of acute structural abnormalities on conventional neuroimaging. They maintain a modest stance, noting that further clinical observations are required to determine if this represents a reproducible neurological adverse effect of dexmedetomidine.

Technical Summary: Transient Acquired Speech Dysfluency Associated with Dexmedetomidine-Assisted Sedation

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