ArticlePhysiological reports2013
Spinal plasticity in stroke patients after botulinum neurotoxin A injection in ankle plantar flexors.
Article in Physiological reports, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.
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Who cites it
20 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.
- From Neurophysiological Mechanisms to Rehabilitation After Botulinum Toxin Type A in Post-Stroke Spasticity.Toxins · 2026Pooled it
- Advances in Clostridial Neurotoxins: Passage of the Intestinal Barrier and Targeting of Specific Neuronal Cells.Toxins · 2026Review
- Spastic co-contraction: A misdirected central command.Clinical neurophysiology practice · 2026Article
- Review
- Effect of Early Treatment of Spasticity After Stroke on Motor Recovery: Protocol for the Baclotox Multicenter, Double-Blind, Double-Dummy Randomized Controlled Trial.JMIR research protocols · 2025Article
- Article
- Memory-Guided Saccades and Non-Motor Symptoms Improve after Botulinum Toxin Therapy in Cervical Dystonia.Journal of clinical medicine · 2024Article
- Article
- LONG-TERM REPEATED BOTULINUM TOXIN A TREATMENT OVER 12 YEARS GRADUALLY CHANGES GAIT CHARACTERISTICS: SINGLE-CASE STUDY.Journal of rehabilitation medicine. Clinical communications · 2024Article
- Pathogenicity and virulence ofVirulence · 2023Review
- The effect of oral baclofen and botulinum toxin treatments in hemiplegic spasticity on the nociceptive flexor reflex: A randomized clinical trial.Turkish journal of physical medicine and rehabilitation · 2022Article
- Lasting Peripheral and Central Effects of Botulinum Toxin Type A on Experimental Muscle Hypertonia in Rats.International journal of molecular sciences · 2022Article
- Botulinum Neurotoxins in Central Nervous System: An Overview from Animal Models to Human Therapy.Toxins · 2021Review
- Dramatic neurological and biological effects by botulinum neurotoxin type A on SH-SY5Y neuroblastoma cells, beyond the blockade of neurotransmitter release.BMC pharmacology & toxicology · 2020Article
- Evidence for central antispastic effect of botulinum toxin type A.British journal of pharmacology · 2020Article
- Transynaptic Action of Botulinum Neurotoxin Type A at Central Cholinergic Boutons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Contribution of muscle activity at different gait phases for improving walking performance in chronic stroke patients with hemiparesis.Journal of physical therapy science · 2018Article
- Review
- Botulinum toxin injection causes hyper-reflexia and increased muscle stiffness of the triceps surae muscle in the rat.Journal of neurophysiology · 2016Article
- Interneuronal Transfer and Distal Action of Tetanus Toxin and Botulinum Neurotoxins A and D in Central Neurons.Cell reports · 2016Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The effect of botulinum neurotoxin A (BoNT-A) in stroke patients' upper limbs has been attributed to its peripheral action only. However, BoNT-A depressed recurrent inhibition of lumbar motoneurons, likely due to its retrograde transportation along motor axons affecting synapses to Renshaw cells. Because Renshaw cells control group Ia interneurons mediating reciprocal inhibition between antagonists, we tested whether this inhibition, particularly affected after stroke, could recover after BoNT-A. The effect of posterior tibial nerve (PTN) stimulation on tibialis anterior (TA) electromyogram (EMG) was investigated in 13 stroke patients during treadmill walking before and 1 month after BoNT-A injection in ankle plantar flexors. Before BoNT-A, PTN stimuli enhanced TA EMG all during the swing phase. After BoNT-A, the PTN-induced reciprocal facilitation in TA motoneurons was depressed at the beginning of swing and reversed into inhibition in midswing, but at the end of swing, the reciprocal facilitation was enhanced. This suggests that BoNT-A induced spinal plasticity leading to the recovery of reciprocal inhibition likely due to the withdrawal of inhibitory control from Renshaw cells directly blocked by the toxin. At the end of swing, the enhanced reciprocal facilitation might be due to BoNT-induced modification of peripheral afferent inputs. Therefore, both central and peripheral actions of BoNT-A can modify muscle synergies during walking: (1) limiting ankle muscle co-contraction in the transition phase from stance to swing, to assist dorsiflexion, and (2) favoring it from swing to stance, which blocks the ankle joint and thus assists the balance during the single support phase on the paretic limb.
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