Mirror activity : Long contractions of muscles in one hand increase involuntary reactions in the other


A team of researchers from Germany and Russia, including Vadim Nikulin from the Higher School of Economics, have demonstrated that long contraction of muscles in one hand increases the involuntary reaction of the other one.

Meanwhile, the time between muscle contractions in both hands decreases.

The results of the study have been published in Neuroscience.

Involuntary muscle activity of one limb during voluntary contraction of the other is called mirror activity.

In other words, when a human clenches the right hand into a strong fist, the left hand’s muscles react to this action with a minor involuntary activation.

It is believed that during ordinary movements that do not require significant effort the contralateral motor cortex is activated, while the other hemisphere’s motor-relevant regions are in a relatively suppressed state.

But with more force applied, the contralateral hemisphere’s motor regions may activate the other hemisphere. This happens via the corpus callosum and induces mirror activity in the contralateral hand.

Mirror movements (MM) refer to the involuntary movements on one side of the body, which mimic voluntary movements of the opposite side of the body through the activation of homologous muscles that approach the performance (i.e., mirror) of a specific task.

They may be considered a subset of motor overflow – the unintentional muscle contractions, which accompany, but are distinct from, dystonic limb movement.

Overflow includes movements induced by involuntary movement or that do not perfectly mirror voluntary action.1 

MM may be present in all limbs, but are most common in the upper limbs, especially the hands.

MM may interfere with bimanual coordination, causing difficulty in tasks that require each hand to act independently.2,3 

While patients can sometime suppress or minimize MM through the activation of antagonistic muscles, MM are often debilitating.

They may interfere with tasks such as tying shoe-laces, cutting vegetables, or buttoning shirts.

Regli et al.2 reported an 11-year-old boy who was admitted to the hospital for injuries caused by an inability to climb vertical bars in gym class — releasing one hand caused him to release the other.

Cincotta et al.4 reported another case of a 15-year-old girl with strong and sustained congenital MM affecting both hands and forearms, who complained about a painful contraction of left shoulder muscles when she wrote with her right hand.

This contraction, which subsided when MM were greatly reduced after a successful rehabilitative training, was thought to be due to a motor strategy the patient had adopted to counteract MM in the left hand during writing.

Physiological MM may appear during infancy of healthy children, persisting until around 10 years of age.5 

This may be the result of immaturity of the central nervous system.6 

Subtle physiological mirroring (sometimes only observable with electromyogram [EMG]) may be seen in normal adults, and is known to increase with fatigue, more demanding motor tasks, and/or age.7 

Nevertheless, the persistence of MM into adulthood is abnormal.

Persistent congenital MM also continue into adulthood, but may be differentiated from physiological MM by their prominence.

While persistent congenital MM may occur sporadically, they are often inherited autosomal dominantly.2,7,8 

MM may present as part of larger congenital disorders such as Klippel-Feil syndrome,9,10 X-linked Kallman’s syndrome,11 or hemiplegic cerebral palsy.3,12,13

Overt MM may also be acquired later in life as a result of either a neurodegenerative disease, such as amyotrophic lateral sclerosis,13 or an acute lesion such as in hemiplegic stroke.14

Two general mechanisms have been proposed to explain the occurrence of MM.

First, MM may stem from the same hemisphere as their voluntary counterpart by an uncrossed fast-conducting corticospinal tract that descends from the hand area of one primary motor cortex (M1) to the ipsilateral side of the spinal cord.

This abnormal ipsilateral projection could depend on either a branching of crossed corticospinal fibers or a separate ipsilateral corticospinal projection (Figure 1A or 1B).

Alternatively or complementarily, MM may result from an abnormal activation of both hemispheres during intended unimanual movement.

This could be due to dysfunction of the neural circuits that focus the generation of motor activity in the M1 contralateral to the voluntary movement (Figure 1C or D).

These mechanisms are not mutually exclusive and more than one may contribute to the generation of MM.

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Figure 1.
Possible Mechanisms for MM. A. MM caused by a common drive to bilateral homologous motoneuron pools. B. Abnormal uncrossed ipsilateral corticospinal tracts. C. Decreased transcallosal inhibition (dotted line) or increased facilitation (solid line) of the M1 contralateral to the MM hand. D. Altered interhemispheric inhibition of intracortical facilitation in the M1 contralateral to MM. Any combination of these mechanisms may be involved in the generation of MM. M1more =  more affected cortex; M1less =  less affected cortex (modified from Li et al., 2007.29)

There appears to be a difference in the pathophysiologic mechanisms of congenital MM and acquired MM.

An ipsilateral corticospinal pathway is the main neural substrate of congenital MM, as demonstrated by the presence of motor evoked potentials (MEP) in the resting hand muscles following transcranial magnetic stimulation (TMS) of the ipsilateral M1.8,9,16,17

Moreover, focal disruption of M1 activity by TMS indicates that an unintended motor output from the M1 contralateral to the mirror hand may coexist in patients with congenital MM.18

Acquired MM, by contrast, appear to stem primarily from an abnormal activation of the hemisphere contralateral to MM, however, these mechanisms will be explored further in the present article.

Herein we review the current understanding of MM as described in selected movement disorders, examining both their clinical presentation and the underlying pathophysiology that produces them.

In healthy humans, mirror activity may be invisible but is detectable with surface electromyography, which is a method used to register muscles’ electrical activity.

In humans with Parkinson’s disease, it becomes pathologic and is called ‘mirror movement’. These involuntary muscle contractions are clearly noticeable.

Previous studies of mirror activity in healthy humans have shown that as the force of one hand’s contraction increases, the amplitude of the other hand’s involuntary contraction grows.

But it has remained unclear how mirror activity changes following repetitive contractions with constant force demands.

Furthermore, another parameter of this phenomenon that has not been studied sufficiently is latency, which means the time delay between unilateral voluntary muscle activity and the contralateral involuntary muscular activity.

To analyse these indicators, a team of researchers from Germany and Russia, including Vadim Nikulin, Leading Research Fellow at the HSE Centre for Cognition & Decision Making, conducted an experiment in which participants were asked to pinch a sensor between the thumb and index finger of their right hand.

The movement was performed with constant force (80% of maximum voluntary contraction) and at certain intervals.

Data on the electrical activity of the right and left hands’ muscles were monitored with electromyography.

Analysis of the experiment’s data showed that following the growing number of voluntary repetitive contractions of the right hand, the amplitude of the left hand’s involuntary contractions grows, and the latency between contractions of the right and the left-hand decreases.

This demonstrates an inverse relationship between time and amplitude.

Previous studies of mirror activity in healthy humans have shown that as the force of one hand’s contraction increases, the amplitude of the other hand’s involuntary contraction grows.

The researchers note that growing uncontrolled motor activity may be related to participants’ fatigue caused by the considerable amount of movement and effort required during the experiment.

This may result in decreasing efficiency of inhibitory mechanisms involved in suppressing involuntarily occurring muscular activity.

Understanding the mechanisms of physiological mirror activity can help in developing a better understanding of the pathology of mirror movements clinically, for example, in Parkinson’s disease.

Higher School of Economics
Media Contacts: 
Liudmila Mezentseva – Higher School of Economics
Image Source:
The image is in the public domain.

Original Research: Open access
“Inverse relationship between amplitude and latency of physiological mirror activity during repetitive isometric contractions”. Tom Maudrich, Rouven Kenville, Vadim V. Nikulin, Dennis Maudrich, Arno Villringer, Patrick Ragert.
Neuroscience. doi:10.1016/j.neuroscience.2019.03.029


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