Motor Tasks + Lidocaine for Dyslexia
Recruiting in Palo Alto (17 mi)
Age: 18+
Sex: Any
Travel: May Be Covered
Time Reimbursement: Varies
Trial Phase: Phase 4
Recruiting
Sponsor: University of Alberta
Must not be taking: Antiarrhythmics, Anesthetics
Disqualifiers: Severe kidney disease, severe liver disease, others
No Placebo Group
Prior Safety Data
Approved in 3 Jurisdictions
Trial Summary
What is the purpose of this trial?Recent claims report that reading ability is partially dependent on speech production. While the evidence for this claim is compelling, it is not known to what extent, the speech production system contributes to successful reading performance in adult populations with dyslexia. One direct way to determine the influence of speech production feedback on reading performance is to measure reading performance in adults with dyslexia with an added motor component (i.e., sucking on a lollipop, holding a bite bar or numbing their oral mucosa with lidocaine).
To adults with and without dyslexia 18 years of age and older (60 in total; 30 in each group), three experimental tasks will be administered under four conditions (no motor task, lollipop, bite bar and lidocaine). The first task asks whether the letter string being presented is a word or a nonword. Secondly, a motor sequencing task will be administered where adults will be asked to label pictures. For all tasks, the accuracy and speed of responses will be measured by a computer while participants wear a fNIRS cap.
Will I have to stop taking my current medications?
The trial does not specify if you need to stop taking your current medications, but you cannot participate if you are taking certain heart medications (class I or III antiarrhythmic drugs) or another anesthetic containing lidocaine.
Is lidocaine generally safe for use in humans?
Lidocaine is generally safe for adults, but there are risks of toxicity, especially in children, where it can cause serious side effects like seizures. In pregnant rats, high doses showed no harmful effects on the fetus.
12345How does the drug lidocaine differ from other treatments for dyslexia?
This treatment is unique because it combines motor tasks with lidocaine, a local anesthetic known for blocking nerve signals, which is not a standard approach for dyslexia. While lidocaine is typically used for pain relief, its potential effects on learning and memory dysfunction, as well as its neuroprotective properties, are being explored in this trial, making it a novel approach for addressing dyslexia.
678910Eligibility Criteria
This trial is for adults over 18, both with and without dyslexia, who are proficient in English and weigh at least 110 lbs. It's not suitable for those with a history of reactions to anesthetics, severe kidney or liver disease, certain heart medications, damaged oral mucosa, allergies to lidocaine ingredients like parabens or artificial colors/flavors, other lidocaine treatments, or if pregnant.Inclusion Criteria
All participants will be healthy and need to be proficient in English as the assessment materials are only available in English.
I weigh at least 110 lbs (50 kg).
Exclusion Criteria
Participant being pregnant or suspecting that she might be pregnant
I am currently using another medication that contains lidocaine or a similar substance.
I have severe kidney disease.
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Trial Timeline
Screening
Participants are screened for eligibility to participate in the trial
1-2 weeks
Experimental Tasks
Participants complete three experimental tasks under four conditions (no motor task, lollipop, bite bar, and lidocaine) to measure reading performance and response times.
1 day
1 visit (in-person)
Follow-up
Participants are monitored for any immediate effects post-experiment and data is collected for analysis.
1 day
Participant Groups
The study tests how motor tasks (like sucking on a lollipop) and numbing the mouth with Lidocaine affect reading unfamiliar words in adults with dyslexia compared to those without. Participants will perform word recognition and picture labeling tasks under different conditions while their brain activity is monitored.
1Treatment groups
Experimental Treatment
Group I: ConditionExperimental Treatment1 Intervention
Typical Reader or Individual with Dyslexia
Find a Clinic Near You
Research Locations NearbySelect from list below to view details:
Department of Communication Sciences and Disorders, University of AlbertaEdmonton, Canada
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Who Is Running the Clinical Trial?
University of AlbertaLead Sponsor
References
Lidocaine overdose: another preventable case? [2019]Physicians who prescribe viscous lidocaine preparations should be aware of the adverse effects and the high risk for overdose in pediatric patients. Owing to altered pharmacokinetics (increased absorption, decreased clearance, and prolonged half-life), doses that are innocuous for adults may present a significant potential toxic hazard in children. Lidocaine should not be used to treat painful mouth lesions in children until further safety data are available. Benzocaine may be considered as a safe alternative to lidocaine. Its low incidence of side effects makes it a safer choice for infants and children. If no other choices are appropriate, then very specific instructions should be given to parents. The amount, frequency, maximum daily dose, and mode of administration should be clearly communicated (eg, cotton pledget to individual lesions, one-half dropper to each cheek every four hours, or 20 minutes before meals). They should never be prescribed on a "PRN" basis.
Toxicity--seizures in an infant caused by (or related to) oral viscous lidocaine use. [2019]A 5-month-old infant with seizures secondary to oral viscous lidocaine toxicity is described. Despite prior reports of this complication in the literature, many practitioners are unaware of the potential adverse effects of topical lidocaine usage in the pediatric patient. Complications of topical lidocaine use and recommendations regarding its use in the pediatric patient are discussed.
Trigeminal nerve injury associated with injection of local anesthetics: needle lesion or neurotoxicity? [2019]The authors used comprehensive national registry and clinical data to conduct a study of adverse drug reactions (ADRs), in particular neurosensory disturbance (NSD), associated with local anesthetics used in dentistry
[Toxicity of topical administration of lidocaine]. [2019]It is frequently described in international literature the possibility of toxicity by local anesthesics. The lidocaine is one of them. The problems with its local use are more frequent and known but topic toxicity is also possible. We want to describe a case of toxicity by topical administration of lidocaine (Xylocain) which caused neurological disease with convulsions, and cardiological disease with ventricular fibrillation, in a patient who came for a thyroplasty. Patient's evolution was satisfactory.
Toxicological assessment of lidocaine in the pregnant rat. [2017]Teratogenic and toxicological effects of lidocaine administered during pregnancy were evaluated in the Sprague Dawley rat. High doses of lidocaine administered during specific periods of gestation were shown to produce no apparent adverse toxicological or teratogenic effects. Histological, enzymological, and physical features of the fetuses, utilizing conventional toxicological parameters, were all found to be normal following maternal administration of lidocaine. Analysis of these data suggests that the administration of lidocaine during pregnancy had no detectable adverse effects on the fetus.
Neuroprotective effect of lidocaine: is there clinical potential? [2020]Local anesthetic lidocaine has been shown to be protective in animal models of focal and global ischemia as well as in in vitro hypoxic models. Lidocaine has been tested in patients for its potential protective effect on postoperative cognitive dysfunction. This mini-review summarizes the laboratory and clinical evidences and discusses its clinical applications as neuroprotective agent.
[Effects of lidocaine on learning and memory dysfunction as well neuropathologic change induced by chronic stress: experiment with mice]. [2013]To explore the effects of lidocaine on the learning and memory dysfunction as well neuropathologic change induced by chronic stress.
Transient impairment of the axolemma following regional anaesthesia by lidocaine in humans. [2021]The local anaesthetic lidocaine is known to block voltage-gated Na(+) channels (VGSCs), although at high concentration it was also reported to block other ion channel currents as well as to alter lipid membranes. The aim of this study was to investigate whether the clinical regional anaesthetic action of lidocaine could be accounted for solely by the block of VGSCs or whether other mechanisms are also relevant. We tested the recovery of motor axon conduction and multiple measures of excitability by 'threshold-tracking' after ultrasound-guided distal median nerve regional anaesthesia in 13 healthy volunteers. Lidocaine caused rapid complete motor axon conduction block localized at the wrist. Within 3 h, the force of the abductor pollicis brevis muscle and median motor nerve conduction studies returned to normal. In contrast, the excitability of the motor axons at the wrist remained markedly impaired as indicated by a 7-fold shift of the stimulus-response curves to higher currents with partial recovery by 6 h and full recovery by 24 h. The strength-duration properties were abnormal with markedly increased rheobase and reduced strength-duration time constant. The changes in threshold during electrotonus, especially during depolarization, were markedly reduced. The recovery cycle showed increased refractoriness and reduced superexcitability. The excitability changes were only partly similar to those previously observed after poisoning with the VGSC blocker tetrodotoxin. Assuming an unaltered ion-channel gating, modelling indicated that, apart from up to a 4-fold reduction in the number of functioning VGSCs, lidocaine also caused a decrease of passive membrane resistance and an increase of capacitance. Our data suggest that the lidocaine effects, even at clinical 'sub-blocking' concentrations, could reflect, at least in part, a reversible structural impairment of the axolemma.
Potential neurotoxicity of spinal anesthesia with lidocaine. [2022]Spinal (intrathecal) anesthesia has evolved into a safe, widely accepted method of anesthesia with many advantages. However, the past decade has seen a large number of case reports and incidence studies that implicate the local anesthetic (LA) lidocaine as being more neurotoxic than other commonly used LAs such as bupivacaine and tetracaine, based on patterns of clinical use current at the time of those reports. Available studies suggest a risk of persistent lumbosacral neuropathy after spinal lidocaine by single injection in about 1 in 1300 procedures and a risk as high as about 1 in 200 after continuous spinal anesthesia with lidocaine. While uncommon, this risk is probably an order of magnitude higher than the risk reported for other commonly used LAs or for general anesthesia. Spinal lidocaine is also implicated in the syndrome of transient neurologic symptoms (previously referred to as transient radicular irritation), manifest by pain or dysesthesia in the buttocks or legs after recovery from anesthesia. Although the pain typically resolves within 1 week without lasting sequelae, it can be severe in up to one third of patients with the syndrome. In addition to clinical studies, both whole animal and in vitro studies have shown that lidocaine can be neurotoxic at clinically available concentrations and that lidocaine is more neurotoxic than equipotent concentrations of other commonly used LAs. The mechanism of this neurotoxicity may involve changes in cytoplasmic calcium homeostasis and mitochondrial membrane potential.
N-ethyl lidocaine (QX-314) protects striatal neurons against ischemia: an in vitro electrophysiological study. [2014]In this study, we have investigated the neuroprotective actions of the membrane impermeable, lidocaine analog, N-ethyl lidocaine (QX-314) in the striatum. The effects of this drug were compared with those caused by the strictly-related-compound and sodium channel blocker lidocaine. To address this issue, electrophysiological recordings were performed in striatal slices, in control condition (normoxia) and during combined oxygen and glucose deprivation (in vitro ischemia). Either QX-314 or lidocaine induced, to some extent, a protection of the permanent electrophysiological alteration (field potential loss) caused by a period (12 min) of ischemia. Thus, both compounds permitted a partial recovery of the ischemic depression of the corticostriatal transmission and reduced the amplitude of the ischemic depolarization in medium spiny neurons. However, while QX-314, at the effective concentration of 100 microM, slightly reduced the amplitude of the excitatory field potential and did not affect the current-evoked spikes discharge of medium spiny striatal neurons, equimolar lidocaine depressed the field potential and eliminated repetitive spikes on a depolarizing step. On the basis of these observations, our results suggest the use of QX-314 as a neuroprotective agent in ischemic brain disorders.