|Year : 2020 | Volume
| Issue : 2 | Page : 73-78
Clinical signs in movement disorders: Phenomenology of mirror movements
Chandra S Rawat, Sanjay Pandey
Department of Neurology, Govind Ballabh Pant Postgraduate Institute of Medical Education and Research, New Delhi, India
|Date of Submission||14-Mar-2020|
|Date of Decision||26-Apr-2020|
|Date of Acceptance||18-May-2020|
|Date of Web Publication||28-Jul-2020|
Prof. Sanjay Pandey
Academic Block, Room No. 503, Department of Neurology, Govind Ballabh Pant Postgraduate Institute of Medical Education and Research, New Delhi.
Source of Support: None, Conflict of Interest: None
Mirror movements are involuntary movements that accompany the voluntary movement of the contralateral homologous body part. Etiologically, these movements could be broadly divided into two main groups: congenital and acquired mirror movements. The pathogenesis of mirror movements is different in both these groups. Minor physiological mirroring is seen in normal healthy individuals and can occur during normal childhood development, whereas apparent mirroring in adults can be present in many movement disorders. Interestingly in these neurological disorders, mirror movements are seen in a particular limb at a particular time course of the disease. This may help in making an early diagnosis and could help in the differentiation between the various movement disorders. The coordinative behavior of the central nervous system is an inherent need for an adult to work with both hands, interruption of which makes a person unable to do the coordinated task with hands. Examination of mirror movements also contributes to our understanding of movement disorders, their clinical clues, and associated pathophysiology.
Keywords: Mirror movements, M1-Primary motor cortex, Transcranial magnetic stimulation
|How to cite this article:|
Rawat CS, Pandey S. Clinical signs in movement disorders: Phenomenology of mirror movements. Ann Mov Disord 2020;3:73-8
|How to cite this URL:|
Rawat CS, Pandey S. Clinical signs in movement disorders: Phenomenology of mirror movements. Ann Mov Disord [serial online] 2020 [cited 2020 Oct 29];3:73-8. Available from: https://www.aomd.in/text.asp?2020/3/2/73/291074
| Introduction|| |
The term mirror movements were first used by Bauman in 1932, although the phenomenon had been already described in the late nineteenth century. These are involuntary movements of homologous muscles that mirror the intentional movement of the homologous body part on the opposite side. In healthy individuals, symmetrical bimanual movements are easier than nonsymmetrical bimanual movements, suggesting that mirror motions are a default tendency of the adult corticospinal motor system., Mirror movements mainly involve the distal upper limb muscles, although leg and foot mirror movements have also been reported. The intensity of mirror movements increases with the complexity of the voluntary movement. Overt mirror movements can be seen in healthy children up to 10 years of age, but their intensity decreases with age. Subtle physiological mirroring may be seen in normal adults, and is known to increase with fatigue, more demanding motor tasks, and/or age, but the persistence or the reappearance of mirror movements is considered abnormal. Mirror movements have been described in many neurodegenerative diseases such as Parkinson’s disease (PD), corticobasal syndrome (CBS), as well as other neurological disorders, such as stroke, essential tremor (ET), and focal hand dystonia (FHD). The pathophysiology of mirror movements in many neurodegenerative disorders is not known. In this article, we aimed to highlight the basic mechanism underlying pathophysiology and clinical signs of mirror movements associated with various neurodegenerative disorders.,,
Possible mechanisms for mirror movements
There have been numerous mechanisms proposed in the past to explain congenital and acquired mirror movements, which are mutually exclusive. These can be broadly divided into two main headings based on motor cortex activation as described in [Figure 1].
|Figure 1: The pathophysiology of mirror movements: (A) The black arrow shows the common corticospinal spinal tract drives the movements in both hands. (B) The yellow arrow shows mirroring is due to the ipsilateral corticospinal tract. (C) Reduced transcallosal inhibition—blue dotted line or increased facilitation (solid line) from the M1 left primary motor cortex to contralateral right motor. (D) Red altered effects of interhemispheric inhibition on intracortical inhibitory or excitatory circuits|
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- Mechanisms showing mirror movements, originating from the ipsilateral primary motor cortex (M1), which is further subdivided into the following:
- a. The corticospinal tract may abnormally connect the hand area of one primary motor cortex (M1) with both sides of the spinal cord [Figure 1A].
- b. The ipsilateral corticospinal pathways abnormally give drive to the ipsilateral motor neuron pool [Figure 1B].
- Mechanisms showing mirror movements, originating from bilateral cortical activation, which may be influenced by afferent input
- a. The reduced transcallosal inhibition or increased transcallosal facilitation may be involved [Figure 1C].
- b. Effects of transcallosal inhibition on intracortical circuits [Figure 1D].
| Classification|| |
The etiology of pathological mirror movements is diverse and is divided into two broad groups congenital and acquired.
Congenital mirror movement
Congenital mirror movements can be divided into two broad headings: physiological and pathological. Physiological mild mirror movements are frequently seen during normal childhood development, due to corpus callosum immaturity, and their frequency declines as the child grows. Generally, they disappear completely at the age of 7–10 years. Pathological congenital mirror movements are further divided into isolated or associated with complex congenital syndromes, for example, Kallmann syndrome, Klippel–Feil syndrome, hypoxic–ischemic injury
[Video 1], and congenital hemiplegia. The important characteristic features of physiological and pathological congenital mirror movements are as following [Table 1]:
- Onset in infancy or early childhood
- Progression—usually does not show change or deterioration over time
- Predominant site if involvement is upper limbs, especially in the muscles controlling the fingers and hands
- Disability is usually mild to moderate, for example, the child may feel difficult to perform tasks requiring skilled bimanual coordination
- The intensity of congenital mirror movements can be partially controlled by the will,
Congenital mirror movements are due to abnormal maturation of interhemispheric transcallosal fibers, and normal disappearance of clinically significant mirror movements after the age of 7 years is associated with the maturation of circuits mediating interhemispheric interactions between motor areas. Neuroimaging studies showed bilateral M1 (primary motor cortex) activation during unimanual tasks in patients with congenital mirror movement. Increased M1 activation on the same side as the voluntary movement may be caused due to either inhibitory processes having inefficient suppression or there may be some facilitating processes. Transcranial magnetic stimulation (TMS) studies also provide insight into the pathophysiology of mirror movements as single-pulse TMS of either M1 region produces shorter cortical silent period, whereas simultaneous bilateral TMS led to a lengthening of the cortical silent period. The shorter cortical silent period after unilateral TMS is caused by involuntary output from the nonstimulated M1, suggesting that the two M1 regions simultaneously generate outputs during voluntary unimanual tonic contraction. This shows that mirroring during intended unimanual voluntary movement may be due to activation of the mirror motor cortex through inefficient transcallosal inhibition.,,,
Acquired mirror movements
van den Berg in 1999 described the presence of mirror movements in patients with PD. Mirror movements are more commonly observed in early asymmetric Parkinson's disease patients who are less severely affected. These movements are observed typically in the less affected side of the patient, particularly hands and fingers, during voluntary movement of the more affected hand, although they have been observed in the legs and feet as well.
Prior studies suggest that mirror movements in patients with PD represent abnormal ipsilateral activation of the primary motor cortex, and they can be explained in the following manner:
- A corticocortical spread as the two hemispheres are connected via the corpus callosum and corticocortical pathways.
- Bilateral basal ganglia projections as several anatomical observations have shown that the basal ganglia are reciprocally and directly connected to the contralateral cortex. However, the precise role of the ipsilateral activation of the primary cortex in the pathophysiology of PD is unrecognized.
Cincottaet al. in 2006 explained the pathophysiology of mirror movements in patients of PD with surface electromyography and TMS, and concluded that these movements were due to motor output along with the crossed corticospinal projection from the M1 ipsilateral to the voluntary motor task. Studies also showed that suprathreshold repetitive transcranial magnetic stimulation of the contralateral M1 markedly disrupted either mirror or voluntary movements, whereas less effect was found on the mirror and voluntary movements of suprathreshold TMS on ipsilateral M1.
Regarding the characteristics of mirror movements in patients with PD, some conclusions were drawn from the previous studies, which are as follows:
Mirror movements in PD were overtly higher in the less involved limbs with an asymmetric pattern of manifestation.
Left predominant patients with PD had significantly higher mirror movements for the right side and vice versa.
Significant laterality was seen on most of the motor task examination, except in performing the pronation–supination motor task.
The mirroring and its severity in patients with PD appear to be related to the levodopa response, which means they appear to be more prominent in patients whose response to levodopa is greatest. From the off to the on medication state, patients with a larger improvement in motor impairment show greater mirroring, whereas patients with a small improvement show less mirroring.
Levodopa, especially increases mirror movements, involving hand and ankle, whereas finger tapping and pronation–supination remained the same during on and off phases.
Electrophysiological evidence strongly supports an abnormal activation of the hemisphere contralateral to mirror movements in patients with PD.,,
Mirroring in patients with PD can be assessed by asking the patient to do the finger tapping, rapid opening and closing of the fist, rapid alternating movement of hands, and foot tapping. Similarly, variations of mirroring with levodopa therapy can be evaluated at 12h after the last dose (“off” condition) and after the morning dose immediately when the patient has a maximal benefit (“on” condition). We can record the amplitude (range of excursion), distribution (the extent to which the movements matched those of the task performing limb), and proportion (fraction of time during which the movements were noted) of mirror movements in the upper as well as in the lower limbs. Mirroring can be scored for each of the motor tasks by upper and lower limbs of the left and right sides for quantification.
Apart from PD, mirror movements have been reported in various other neurological disorders, including CBS, ET, FHD, Creutzfeldt–Jakob disease, and stroke. The precise pathophysiological mechanisms of mirror movements in various neurological disorders are not yet fully understood. We have described some important movement disorders in the following paragraphs.
Mirror movements described as the imitative tendency of alien hand syndrome can be seen in CBS, which looks like symmetric movements causing competition between the hands of the patients, for example, if patient’s right hand tends to reach an object, his other hand also has a tendency to reach toward an identical nearby object. This may be due to callosal disconnection syndrome or interhemispheric motor pathway damage. Recognizing these features, that is, alien hand phenomenon and imitative mirrorlike movements with features of PD help in making a diagnosis of corticobasal ganglionic degeneration. Another clinically important point is that in CBS, mirror movements occur predominantly in the more affected side, whereas in PD, mirroring typically is observed in the less affected side.,, So, mirroring not only helps in clinching the diagnosis of the CBS but also helps in its differentiation from other neurodegenerative disorders.
Focal hand dystonia
FHD is defined as sustained muscle contraction, frequently causing twisting and repetitive movements or abnormal postures of the hand. The most common task-specific dystonia seen in clinical practice is writer’s cramp.
Sitburana and Jancovic highlighted that motor overflow and mirror dystonia are the two inherent features of patients with FHD. The phenomenology of these is different; motor overflow (ipsilateral and/or contralateral) is an unintentional muscle contraction that accompanies at the anatomically distinct site from the primary dystonic movement, and mirror dystonia represents dystonic postures or movements of the dominant hand while performing tasks with the nondominant hand. They concluded that ipsilateral overflow in patients with FHD could be due to failure of surround inhibition, whereas contralateral overflow is either due to transcallosal inhibitory failure or activation of uncrossed corticospinal fibers or both. Similarly, the importance of recognition of mirror dystonia in patients with writing dysfunction has also been previously highlighted by Jedynak et al. They reported that 29 of 65 patients with writer’s cramp had evidence of mirror dystonia, and further concluded that mirror dystonia may be useful in muscle selection for botulinum toxin injection in patients with FHD. Cohen et al., in 1992, first showed the efficacy of botulinum toxin in patients with writer’s cramp; since then, it has become the first-line therapy, producing benefits in a significant number of treated patients. As these patients tend to adapt compensatory postures to overcome their disability, and we may wrongly analyze the involved muscles, analysis of the pattern of dystonic posturing displayed in mirror dystonia may help us for the selection of muscles to be injected with botulinum toxin. Evaluation of patients for mirror dystonia can be done by simply asking them to write with their nonaffected hand while resting the affected hand on the ulnar side of the forearm [Video 1]. The patients can be asked to write the same sentences repeatedly so that they would be unaware of our focus on the detection of mirror dystonia of the resting limb.
A study conducted by Louis et al. showed an association between mirror movements and patients with ET. They studied 107 ET cases, and observed that 32.7% of them showed mirror movements compared to 23.7% in the control population. Further, their study also showed that mirror movement was more prevalent in essential tremor cases with rest tremor and they showed no correlation with age, tremor severity and duration. Results from their study explains that motor signs in essential tremor patients are not restricted to tremor but also include other features that further expand the spectrum of phenomenology seen in essential tremor cases.
Few isolated case reports show that alien hand phenomena and mirror movements could be the first sign of Creutzfeldt–Jakob disease. Movement disorders seen in Creutzfeldt–Jakob disease may reflect lesions involving cortical or basal ganglia pathology, but the pathogenesis of the mirror movements seen in patient with Creutzfeldt–Jakob disease remains unknown.
Mirror movement in stroke patients
Mirror movements, following a stroke, appear in unaffected hand when paretic hand voluntarily moves. Nelles et al. observed that greater motor deficits were associated with more occurrences of mirror movements in the unaffected hand, and patients with mirror movements in paretic hand had significantly better muscle power than patients without mirror movements. Another study by Fries et al. showed that the stroke-causing posterior internal capsule lesion could lead to degeneration of the pyramidal tract, and suprathreshold electrical stimulation of the damaged hemisphere elicited bilateral motor responses. They also found that the activity of bilaterally organized pathways could be the cause for observation of mirror movements. However, Ejaz et al. hypothesized that mirror movements might have a subcortical origin and might contradict the earlier proposed overactivation of ipsilateral or contralateral sensorimotor cortex.
| Conclusion|| |
Mirror movements are common in various movement disorders, and their knowledge gives a clue in making an early diagnosis. Pathogenesis of congenital and acquired mirror movements also shows differences, as congenital mirror movements may involve abnormal interhemispheric inhibition, functional alteration of motor planning, or abnormal persistence of the ipsilateral corticospinal tract. Although acquired mirror movements depend on bilateral cortical activation, they are more likely caused due to a deficiency of the neural mechanisms that focus the motor output in the M1 contralateral to the voluntary task. Also, predominant involvement of the hand in mirror movement varies between different movement disorders such as in corticobasal degeneration where more affected hands show mirror movements, whereas in PD, these movements appear in less affected hands, and mirroring has no relation to symptom asymmetry in patients with ET. These observations prove that mirror movements are a useful clinical tool in distinguishing a number of different movement disorders. As we know that the pathophysiology of mirror movements in various movement disorders is still not fully understood, further research is needed, which will contribute to our understanding of the normal physiology of bimanual coordination and will help in making an early clinical diagnosis of various neurological disorders.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Swinnen SP, Walter CB, Lee TD, Serrien DJ Acquiring bimanual skills: Contrasting forms of information feedback for interlimb decoupling. J Exp Psychol Learn Mem Cogn 1993;19:1328-44.
Wenderoth N, Puttemans V, Vangheluwe S, Swinnen SP Bimanual training reduces spatial interference. J Mot Behav 2003;35:296-308.
Duque J, Mazzocchio R, Dambrosia J, Murase N, Olivier E, Cohen LG Kinematically specific interhemispheric inhibition operating in the process of generation of a voluntary movement. Cereb Cortex 2005;15:588-93.
Verstynen T, Spencer R, Stinear CM, Konkle T, Diedrichsen J, Byblow WD, et al
. Ipsilateral corticospinal projections do not predict congenital mirror movements: A case report. Neuropsychologia 2007;45:844-52.
Koerte I, Eftimov L, Laubender RP, Esslinger O, Schroeder AS, Ertl-Wagner B, et al
. Mirror movements in healthy humans across the lifespan: Effects of development and ageing. Dev Med Child Neurol 2010;52:1106-12.
Mayston MJ, Harrison LM, Stephens JA A neurophysiological study of mirror movements in adults and children. Ann Neurol 1999;45:583-94.
Farmer SF, Ingram DA, Stephens JA Mirror movements studied in a patient with Klippel–Feil syndrome. J Physiol 1990;428:467-84.
Ziemann U, Ishii K, Borgheresi A, Yaseen Z, Battaglia F, Hallett M, et al
. Dissociation of the pathways mediating ipsilateral and contralateral motor-evoked potentials in human hand and arm muscles. J Physiol 1999;518:895-906.
Daskalakis ZJ, Christensen BK, Fitzgerald PB, Roshan L, Chen R The mechanisms of interhemispheric inhibition in the human motor cortex. J Physiol 2002;543:317-26.
Schott GD, Wyke MA Congenital mirror movements. J Neurol Neurosurg Psychiatry 1981;44:586-99.
Bonnet C, Roubertie A, Doummar D, Bahi-Buisson N, Cochen de Cock V, Roze E Developmental and benign movement disorders in childhood. Mov Disord 2010;25:1317-34.
Depienne C, Cincotta M, Billot S, Bouteiller D, Groppa S, Brochard V, et al
. A novel DCC mutation and genetic heterogeneity in congenital mirror movements. Neurology 2011;76: 260-4.
Carr LJ, Harrison LM, Evans AL, Stephens JA Patterns of central motor reorganization in hemiplegic cerebral palsy. Brain 1993;116:1223-47.
Cincotta M, Borgheresi A, Balestrieri F, et al
. Mechanisms underlying mirror movements in Parkinson's disease: a transcranial magnetic stimulation study. Mov Disord 2006;21:1019-25.
Cincotta M, Lori S, Gangemi PF, Barontini F, Ragazzoni A Hand motor cortex activation in a patient with congenital mirror movements: A study of the silent period following focal transcranial magnetic stimulation. Electroencephalogr Clin Neurophysiol 1996;101:240-6.
Cohen LG, Meer J, Tarkka I, Bierner S, Leiderman DB, Dubinsky RM, et al
. Congenital mirror movements. Abnormal organization of motor pathways in two patients. Brain 1991;114:381-403.
van den Berg C, Beek PJ, Wagenaar RC, van Wieringen PC Coordination disorders in patients with Parkinson’s disease: A study of paced rhythmic forearm movements. Exp Brain Res 2000;134:174-86.
Ottaviani D, Tiple D, Suppa A, Colosimo C, Fabbrini G, Cincotta M, et al
. Mirror movements in patients with Parkinson’s disease. Mov Disord 2008;23:253-8.
Thobois S, Dominey PF, Decety J, Pollak PP, Gregoire MC, Le Bars PD, et al
. Motor imagery in normal subjects and in asymmetrical Parkinson’s disease: A PET study. Neurology 2000;55:996-1002.
Espay AJ, Li JY, Johnston L, Chen R, Lang AE Mirror movements in parkinsonism: Evaluation of a new clinical sign. J Neurol Neurosurg Psychiatry 2005;76:1355-8.
Espay AJ, Morgante F, Gunraj C, Chen R, Lang AE Mirror movements in Parkinson’s disease: Effect of dopaminergic drugs. J Neurol Neurosurg Psychiatry 2006;77:1194-5.
Chatterjee P, Banerjee R, Choudhury S, Mondal B, Kulsum MU, Chatterjee K, et al
. Mirror movements in Parkinson’s disease: An under-appreciated clinical sign. J Neurol Sci 2016;366:171-6.
Gottlieb D, Robb K, Day B Mirror movements in the alien hand syndrome. Case report. Am J Phys Med Rehabil 1992;71:297-300.
Fisher CM Alien hand phenomena: A review with the addition of six personal cases. Can J Neurol Sci 2000;27:192-203.
Pal PK, Gunraj CA, Li JY, Lang AE, Chen R Reduced intracortical and interhemispheric inhibitions in corticobasal syndrome. J Clin Neurophysiol 2008;25:304-12.
Sitburana O, Jankovic J Focal hand dystonia, mirror dystonia and motor overflow. J Neurol Sci 2008;266:31-3.
Jedynak PC, Tranchant C, de Beyl DZ Prospective clinical study of writer’s cramp. Mov Disord 2001;16:494-9.
Cohen LG, Hallett M, Geller BD, Hochberg F Treatment of focal dystonias of the hand with botulinum toxin injections. J Neurol Neurosurg Psychiatry 1989;52:355-63.
Karp BI Botulinum toxin treatment of occupational and focal hand dystonia. Mov Disord 2004;19:S116-9.
Louis ED, Rios E, Henchcliffe C Mirror movements in patients with essential tremor. Mov Disord 2009;24:2211-7.
Park IS, Song IU, Lee SB, Lee KS, Kim HT, Kim JS Mirror movements and involuntary homolateral limb synkinesis in a patient with probable Creutzfeldt–Jakob disease. Clin Neurol Neurosurg 2009;111:380-3.
Nelles G, Cramer SC, Schaechter JD, Kaplan JD, Finklestein SP Quantitative assessment of mirror movements after stroke. Stroke 1998;29:1182-7.
Fries W, Danek A, Witt TN Motor responses after transcranial electrical stimulation of cerebral hemispheres with a degenerated pyramidal tract. Ann Neurol 1991;29:646-50.
Ejaz N, Xu J, Branscheidt M, Hertler B, Schambra H, Widmer M, et al
. Evidence for a subcortical origin of mirror movements after stroke: A longitudinal study. Brain 2018;141:837-47.