Peripheral magnetic theta burst stimulation to muscles can effectively reduce spasticity: a randomized controlled trial

NOT GOOD ENOUGH! What will it take to cure spasticity? That is what survivors want. Not your fucking tyranny of low expectations - 'reduction'.

Peripheral magnetic theta burst stimulation to muscles can effectively reduce spasticity: a randomized controlled trial

• Nevine El Nahas,
• Fatma Fathalla Kenawy,
• Eman Hamid Abd Eldayem,
• Tamer M. Roushdy,
• Shahinaz M. Helmy,
• Ahmed Zaki Akl,
• Aya Ahmed Ashour,
• Tamer H. Emara,
• Marwa Mohamed Moawad,
• Randa M. Amin &
• Ahmed M. Elbokl 

Journal of NeuroEngineering and Rehabilitation volume 19, Article number: 5 (2022) Cite this article

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Abstract

Background

Spasticity is a common complication of many neurological diseases and despite contributing much disability; the available therapeutic options are limited. Peripheral magnetic stimulation is one promising option. In this study, we investigated whether peripheral intermittent theta burst stimulation (piTBS) will reduce spasticity when applied directly on spastic muscles.

Methods

In this sham-controlled study, eight successive sessions of piTBS were applied directly to spastic muscles with supra threshold intensity. Assessment was done by modified Ashworth scale (mAS) and estimated Botulinum toxin dose (eBTD) at baseline and after the 8th session in both active and sham groups.

Results

A total of 120 spastic muscles of 36 patients were included in the analysis. Significant reduction of mAS and eBTD was found in the active compared to sham group (p < 0.001). The difference in mAS was also significant when tested in upper limb and lower limb subgroups. The degree of reduction in mAS was positively correlated with the baseline scores in the active group.

Conclusion

piTBS could be a promising method to reduce spasticity and eBTD. It consumes less time than standard high frequency protocols without compromising treatment efficacy.

Trial registration: Clinical trial registry number: PACTR202009622405087. Retrospectively Registered 14th September, 2020.

Introduction

Spasticity is a disabling motor disorder which commonly complicates many neurological diseases. It represents one of the components of upper motor neuron syndrome and is characterized clinically by velocity dependent increase in muscle tone and stretch reflex [1]. Its mechanism is related to loss of supraspinal activation of intraspinal inhibitory circuits on both Ia muscle spindle afferents (presynaptic inhibition) and alpha motor neurons (post synaptic inhibition) [2]. Another possible mechanism that is apparently not under supraspinal control and not mediated by the intraspinal inhibitory circuits is the reduction in post activation depression [2]. Post activation depression reflects an intrinsic neuronal ability to decrease neurotransmitter release following repetitive stimulation of Ia afferents [3]. It was found that limb immobilization and its related changes of mechanical muscle properties is an additional cause of spasticity through reduction of post activation depression of Ia muscle spindle afferents, a mechanism that might play a pivotal role in development of spasticity [4, 5]. Moreover, the delayed appearance of spasticity after acute neurological insult suggests underlying abnormal plasticity, occurring in the spinal cord and also in the brain and that spasticity is beyond being just a release phenomenon [2].The prevalence of spasticity is variable in different neurological diseases. For example, leg spasticity is reported in about 41–66% in patients with multiple sclerosis, 28–38% in patients with stroke, and 13% in patients with traumatic brain injury [6]. Thus, spasticity is a common problem that has its negative implications on motor functions, can cause pain and end up in deformities.

Among the conventional treatments available for spasticity, only Botulinum toxin injections have been proven effective in spasticity reduction [7]. However, the limitations of cost, the need for repeated injections and the limited effectiveness in higher grades of spasticity are major concerns in clinical settings that call for other alternatives.

Non-invasive peripheral stimulation is a promising option that could contribute to motor recovery specially the relatively novel repetitive peripheral magnetic stimulation (rPMS), that adopts the same techniques of cranial stimulation, yet applies the coil to the muscle or nerve [8]. rPMS was reported to reduce spasticity in wrist and finger flexors with active but not with sham stimulation [9].

Also, improvement of kinematics of finger movements was observed following rPMS and that was associated with activation of the parieto-premotor network as shown by PET study. This denotes that rPMS has a central modulatory effect on the brain [10].

rPMS is assumed to act by generating massive proprioceptive inflow either directly by stimulating Ia sensory afferents or indirectly by the repetitive muscle/joint contractions induced by magnetic pulses [8]. This proprioceptive inflow would influence and modulate the activity of the neuronal networks involved in motor control. Being painless, with deeper penetration and preferentially recruiting the proprioceptive afferents, rPMS might be more advantageous over the more popular trans-cutaneous electrical stimulation for motor recovery. It can be a treatment option in conditions like spasticity through its ability to produce repetitive muscle contractions [11]. Nevertheless, studies of rPMS effectiveness in spasticity are still scant and diverse. [12,13,14].

One form of magnetic stimulation is theta burst stimulation which is a patterned form using less pulses and shorter duration of stimulation than typical repetitive transcranial magnetic stimulation paradigms. Intermittent theta burst stimulation (iTBS) is one form of this patterned stimulation that has a stimulatory effect similar to high frequency rTMS [15] and previous studies have shown that it is as effective as standard high frequency rTMS protocol for depression[16]. However, iTBS can be delivered over a period of 3 min as compared to 37.5 min for the standard 10 Hz protocol of high frequency magnetic stimulation. Applying the 10 Hz protocol for several muscles per patient per session seems too lengthy to be practical. Thus, using iTBS to target several spastic muscles for each patient, we can increase the number of treated patients, without compromising the clinical benefit.

Therefore, in this pilot study, we investigated the efficacy of peripheral intermittent theta burst stimulation (piTBS) applied directly on the spastic muscle belly as shown by change in modified Ashworth scale (mAS) and on reduction of estimated dose of Botulinum toxin (eBTD). This modality might be more appropriate when the amount of toxin required exceeds the therapeutic dose, or in cases where transcranial magnetic stimulation is contraindicated. Also, it can be more convenient in developing countries where the cost of repeated Botulinum injection is an issue and is more time saving than the previously studied rPMS.

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