Centrally mediated late motor recovery after botulinum toxin injection: Case reports and a  review of current evidence

Mas, Manuel F.; Li, Sheng; Francisco, Gerard E.

doi:10.2340/16501977-2257

Cited by 6 publications

(4 citation statements)

References 79 publications

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“…Briefly, peripheral deafferentation at the injection site produces alterations in presynaptic input from the neuromuscular connection to the γ-motoneuronal endings and intrafusal muscle fibers, modifying the excitability of spinal pathways and causing alterations of motor maps at the cortical level. The block of the afferent inflow of the spindle directed to the spinal motor neurons therefore interferes with the spinal circuits, producing possible alterations in the brain stem and cortical circuits, causing an alteration of cortical excitability and a plasticity/reorganization of various cortical areas, including thalamus and sensorimotor cortex [28]. As basal ganglia receive projection from thalamus and sensorimotor cortex, activity of basal ganglia is also altered by BoNTs-induced changes in motor afferent feedback.…”

Section: Indirect Central Effects Following Peripheral Injection Of Bontsmentioning

confidence: 99%

Botulinum Neurotoxins in Central Nervous System: An Overview from Animal Models to Human Therapy

Luvisetto

2021

Toxins

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Botulinum neurotoxins (BoNTs) are potent inhibitors of synaptic vesicle fusion and transmitter release. The natural target of BoNTs is the peripheral neuromuscular junction (NMJ) where, by blocking the release of acetylcholine (ACh), they functionally denervate muscles and alter muscle tone. This leads them to be an excellent drug for the therapy of muscle hyperactivity disorders, such as dystonia, spasticity, and many other movement disorders. BoNTs are also effective in inhibiting both the release of ACh at sites other than NMJ and the release of neurotransmitters other than ACh. Furthermore, much evidence shows that BoNTs can act not only on the peripheral nervous system (PNS), but also on the central nervous system (CNS). Under this view, central changes may result either from sensory input from the PNS, from retrograde transport of BoNTs, or from direct injection of BoNTs into the CNS. The aim of this review is to give an update on available data, both from animal models or human studies, which suggest or confirm central alterations induced by peripheral or central BoNTs treatment. The data will be discussed with particular attention to the possible therapeutic applications to pathological conditions and degenerative diseases of the CNS.

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Section: Indirect Central Effects Following Peripheral Injection Of Bontsmentioning

confidence: 99%

Botulinum Neurotoxins in Central Nervous System: An Overview from Animal Models to Human Therapy

Luvisetto

2021

Toxins

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“…This BoNT-related muscle weakness is not well studied, but may contribute to the observation that BoNT therapy does not lead to functional improvement [ 34 ]. However, there are unusual cases when the outcome of BoNT injections surpasses this expectation and results in increase in functional abilities in chronic stroke survivors [ 13 , 39 , 40 ].…”

Section: Introductionmentioning

confidence: 99%

The Effects of Botulinum Toxin Injections on Spasticity and Motor Performance in Chronic Stroke with Spastic Hemiplegia

Chen

Zhang

Liu

et al. 2020

Toxins

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Spastic muscles are weak muscles. It is known that muscle weakness is linked to poor motor performance. Botulinum neurotoxin (BoNT) injections are considered as the first-line treatment for focal spasticity. The purpose of this study was to quantitatively investigate the effects of BoNT injections on force control of spastic biceps brachii muscles in stroke survivors. Ten stroke survivors with spastic hemiplegia (51.7 ± 11.5 yrs; 5 men) who received 100 units of incobotulinumtoxinA or onabotulinumtoxinA to the biceps brachii muscles participated in this study. Spasticity assessment (Modified Ashworth Scale (MAS) and reflex torque) and muscle strength of elbow flexors, as well as motor performance assessment (force variability of submaximal elbow flexion) were performed within one week before (pre-injection) and 3~4 weeks (3-wk) after BoNT injections. As expected, BoNT injections reduced the MAS score and reflex torque, and elbow flexor strength on the spastic paretic side. However, motor performance remained within similar level before and after injections. There was no change in muscle strength or motor performance on the contralateral arm after BoNT injections. The results of this study provide evidence that BoNT injections can reduce spasticity and muscle strength, while motor performance of the weakened spastic muscle remains unchanged.

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“…In dystonic and spastic movement disorders commonly treated with BoNT-A, abnormalities of motor control and somatosensory processing have been reported, as well as cortical modulations associated with clinical improvement after BoNT-A treatment, [ 31 , 33 , 43 , 44 ] but electrophysiological evidence (SEPs) remains controversial.…”

Section: Discussionmentioning

confidence: 99%

Cortical somatosensory processing after botulinum toxin therapy in post-stroke spasticity

et al. 2021

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In dystonic and spastic movement disorders, abnormalities of motor control and somatosensory processing as well as cortical modulations associated with clinical improvement after botulinum toxin A (BoNT-A) treatment have been reported, but electrophysiological evidence remains controversial. In the present observational study, we aimed to uncover central correlates of post-stroke spasticity (PSS) and BoNT-A-related changes in the sensorimotor cortex by investigating the cortical components of somatosensory evoked potentials (SEPs). Thirty-one chronic stroke patients with PSS of the upper limb were treated with BoNT-A application into the affected muscles and physiotherapy. Clinical and electrophysiological evaluations were performed just before BoNT-A application (W0), then 4 weeks (W4) and 11 weeks (W11) later. PSS was evaluated with the modified Ashworth scale (MAS). Median nerve SEPs were examined in both upper limbs with subsequent statistical analysis of the peak-to-peak amplitudes of precentral P22/N30 and postcentral N20/P23 components. At baseline (W0), postcentral SEPs were significantly lower over the affected cortex. At follow up, cortical SEPs did not show any significant changes attributable to BoNT-A and/or physiotherapy, despite clear clinical improvement. Our results imply that conventional SEPs are of limited value in evaluating cortical changes after BoNT-A treatment and further studies are needed to elucidate its central actions.

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Centrally mediated late motor recovery after botulinum toxin injection: Case reports and a review of current evidence

Abstract: Additional research is required to further elucidate these hypotheses, as well as providing specific dosing specifications, patient selection criteria and the interplay with other therapeutic modalities necessary to promote late motor recovery.

Cited by 6 publications

References 79 publications

Botulinum Neurotoxins in Central Nervous System: An Overview from Animal Models to Human Therapy

Botulinum Neurotoxins in Central Nervous System: An Overview from Animal Models to Human Therapy

The Effects of Botulinum Toxin Injections on Spasticity and Motor Performance in Chronic Stroke with Spastic Hemiplegia

Cortical somatosensory processing after botulinum toxin therapy in post-stroke spasticity

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