Original

Paresis of an upper extremity. Action observation and motor imagery in recovery of patients with chronic stroke

G. Valadez-Roque, J. Cantillo-Negrete, R.I. Carino-Escobar, A. Torres-Chávez [REV NEUROL 2024;78:307-315] PMID: 38813788 DOI: https://doi.org/10.33588/rn.7811.2024017 OPEN ACCESS
Volumen 78 | Number 11 | Nº of views of the article 2.729 | Nº of PDF downloads 34 | Article publication date 01/06/2024
Icono-PDF-OFF Download PDF Castellano Icono-PDF-OFF Download PDF English Citation Search in PubMed
Share in: Facebook Twitter
Go to another issue
ABSTRACT Artículo en español English version
INTRODUCTION Action observation (AO) and motor imagery (MI) are considered functionally equivalent forms of motor representation related to movement execution (ME). Because of their characteristics, AO and MI have been proposed as techniques to facilitate the recovery of post-stroke hemiparesis in the upper extremities.

PATIENTS AND METHODS An experimental, longitudinal, prospective, single-blinded design was undertaken. Eleven patients participated, and were randomly assigned to each study group. Both groups received 10 to 12 sessions of physical therapy. Five patients were assigned to the control treatment group, and six patients to the experimental treatment group (AO + MI). All were assessed before and after treatment for function, strength (newtons) and mobility (percentage) in the affected limb, as well as alpha desynchronisation (8-13 Hz) in the supplementary motor area, the premotor cortex and primary motor cortex while performing AO + MI tasks and action observation plus motor execution (AO + ME).

RESULTS The experimental group presented improvement in function and strength. A negative correlation was found between desynchronisation in the supplementary motor area and function, as well as a post-treatment increase in desynchronisation in the premotor cortex of the injured hemisphere in the experimental group only.

CONCLUSIONS An AO + MI-based intervention positively impacts recovery of the paretic upper extremity by stimulating the supplementary motor area, a cortex involved in movement preparation and learning. AO + MI therapy can be used as adjunctive treatment in patients with upper extremity paresis following chronic stroke.
VIDEOS
KeywordsAction observationAlpha desynchronisationMotor executionMotor imageryParesis of the upper extremityStroke CategoriesPatología vascular
FULL TEXT Artículo en español English version

Introduction


Action observation (AO) [1,2] and motor imagery (MI) [3] are considered functionally equivalent forms of motor representation related to movement execution (ME) [4,5]. According to neuroimaging evidence, both the supplementary motor area and the premotor cortex are activated in similar ways during AO and MI tasks [6]. Both regions interact with the primary motor cortex in the planning and initiation of sequenced movements [7,8]. Because of their functional characteristics, AO and MI have been proposed as techniques to facilitate recovery from post-stroke hemiparesis in the upper extremities [9-13].

Several studies of the effects of interventions based on AO for stroke patients report improvements in clinical motor function scales compared to a baseline or controls [14-18]. Treatments focusing on MI have also been administered in order to evaluate their clinical effects [19,20] (for a review, see Fernández-Gómez and Sánchez-Cabeza [21]) involving reducing the degree of involvement of the paretic limb, increasing its use and maintaining the positive effects [22-25]. However, some studies have reported contrary results for AO- and MI-based interventions with stroke patients; in their respective studies, Ietswaart et al [26] and Braun et al [27] conclude that treatments do not lead to motor recovery in these cases.

Although AO- and MI-based interventions for patients with paresis of an upper extremity as a sequela of stroke have been shown to lead to clinical improvement [28,29], Vogt et al [9] note that ‘Typically only one form of treatment, either MI or AO, has been used as an intervention’, and argue that this approach ignores the potential benefits of multimodal motor training with both AO and MI (AO + MI). Research with healthy subjects by Conson et al [30] supports this proposition by demonstrating that AO has facilitation effects for MI, while Sun et al [31] claim that an AO- + MI-focused intervention improves activation in the sensorimotor cortex, and facilitates recovery of the paretic upper extremity in stroke patients.

The present study aimed to investigate the effects of an AO- + MI-based intervention complementing physical rehabilitation in patients with chronic stroke, based on the hypothesis that AO + MI stimulation enhances the recovery of strength, mobility and function of the paretic upper extremity. The following steps were taken to overcome some of the limitations presented by the state of the art: the intervention was based on AO and MI together (AO + MI) [32]; clinical strength and mobility were measured using a computerised robotic device; the patients had a time to progression of at least 12 months, so that the expected recovery in the first six months would have reached a plateau [33-35]; and electroencephalographic recordings were performed to determine whether stimulation via AO + MI led to long-term (6 weeks) changes in brain electrical activity in the motor areas [32,36].
 

Patients and methods


Study design


An experimental, longitudinal, prospective design was undertaken. Each patient was assigned to a group by randomisation by a draw. The study was single-blinded, with third-party blinded evaluation; neither the evaluators nor the patients knew which group they belonged to.

Patients


The patients were recruited from the acquired brain injury service of the Luis Guillermo Ibarra Ibarra National Rehabilitation Institute (INR-LGII) in Mexico City, and had to meet the following inclusion criteria: a) first stroke with time to progression of more than 12 months; b) right-handed; c) over 18 years of age; and d) Mini-Mental test score of 20 or over. Patients were excluded: a) if they had a stroke secondary to traumatic brain injury; b) if they were in concurrent treatment for paresis of the upper extremity; c) if they had quadriparesis; d) if they were visually impaired; and e) if they had an uncontrolled chronic condition. The sociodemographic characteristics of the sample are shown in Table I.

 

Table I. Sociodemographic characteristics of the total sample and for each group.
 

Age in years

Time to progression (weeks)

Sex

Paresis

Type of stroke

Injured hemisphere


Total sample (N = 11)
 

50.4 (±10.6)

141 (±92.2)

M = 6. F = 5

R = 6

L = 5

Isq = 8

Hem = 3

R = 5

L = 6


Experimental group (n = 6)
 

53.1 (±11.1)

136.8 (±107)

M = 4. F = 2

R = 3

L = 3

Isq = 3

Hem = 3

R = 3

L = 3


Control group (n = 5)
 

47.2 (±10)

146.2 (±82.8)

M = 2. F = 3

R = 3

L = 2

Isq = 5

Hem = 0


R = 2

L = 3

Hem: haemorrhagic; Isch: ischemic; L: left; R: right; M: male; F: female.
 

 

The study was approved by the Research and Ethics Committee of the INR-LGII. The patients gave their written informed consent in accordance with the standards of the Declaration of Helsinki.

Study variables


Primary

The variable of interest function is derived from the domain known as motor function according to the Fugl-Meyer assessment scale, which clinically determines post-stroke recovery by directly observing performance. The Fugl-Meyer assessment scale also measures other domains, including sensation, balance, joint motion and joint pain, rating them on an ordinal scale with three possible answers (0 = none; 1 = partial; and 2 = full) [37,38]. In accordance with the objectives of this study, the evaluation focused only on the items related to movement of the upper extremity (the shoulder, elbow and wrist), considering changes in reflex activity and volitional movement in relation to motor synergies.

The AMADEO® robot-assisted rehabilitation system was used for measurement, control and intervention. The patient’s arm and hand is fastened to a device composed of levers, to which the fingers are attached by means of magnets (Fig. 1a). The robot applies various flexion and extension resistances to each finger, and measures the ranges of mobility, forces received and power of mobility. The variables of interest were the combined force (newtons) of flexion and extension of the fingers, and the range of motion (percentage) of the hand. The AMADEO® physical therapy programme was also applied [39].

 

Figure 1. a) Evaluation using the AMADEO® system; b) Electroencephalographic recording; c) Intervention focused on AO + MI.






 

Secondary

Electroencephalographic recording was performed in a lit, semi-soundproofed room, with the patients seated comfortably and their arms resting on the armrests of a padded armchair (Fig. 1b), using a g.USBamp model g.TEC 16-channel biosignal amplifier with a sampling frequency of 256 Hz and active electrodes. The data for the quantitative electroencephalographic analysis were obtained during three tasks: resting with eyes open (baseline), AO + MI and action observation plus movement execution (AO + ME). The movements shown on video (lifting a bottle and lifting a spoon) were presented on a 50-centimetre monitor placed on a table one metre in front of the patients.

The trials had the following structure (Fig. 2a): a) a fixed white cross appeared in the centre of the monitor for three seconds; b) a beep and an arrow pointed randomly to the left or right for 1-1.5 seconds to indicate which hand should be used for the task; c) a short video randomly showed a first-person perspective of a hand lifting a bottle or spoon for 3.5-4 seconds; and d) a blue screen for 3-5 seconds indicated the end of the test. Fluctuations in the display times of the arrow, video and blue screen stimuli were randomly distributed among trials, and all patients were subjected to them in equal proportion. All the patients performed all the tasks. For control purposes, half of the trials were performed with the paretic upper extremity and the other half with the non-paretic upper extremity.

 

Figure 2. a) Structure of the electroencephalographic trials; b) position of the electroencephalogram electrodes.






 

While the video was displayed, the patients had to imagine (AO + MI) or perform (AO + ME) the movement they saw, as instructed at the beginning of each series of trials. The order of the AO + IM and AO + EM series was randomised in order to prevent carryover effects. Eight series of 20 tests were performed for each patient, with rest periods of 3-5 minutes after every two series. Four series (80 trials) were for AO + MI, and another four for AO + ME. Each series lasted for approximately 4-5 minutes, and the recording had a total duration of 35-45 minutes.

The AO + EM task was included in the electroencephalographic recording due to evidence for the functional equivalence and involvement of similar neural substrates during motor representation (AO and MI) and motor execution (ME), which would enable training in the former to facilitate the latter [4-6,9,31].

The electroencephalographic analysis focused on one-second windows during the first three seconds of the video for each condition, separating the paretic upper extremity and non-paretic upper extremity trials. Six surface electrodes arranged according to the international 10-20 system and located over the supplementary motor area (Fz and Cz), the premotor cortex (F3 and F4) and the primary motor cortex (C3 and C4) were recorded (Fig. 2b). The quantitative electroencephalographic variable of interest for this study was event-related desynchronisation of the alpha rhythm (8-13 Hz) [40-42].

Intervention


The patients who met the inclusion criteria were evaluated using the Fugl-Meyer assessment scale, AMADEO® and a quantitative electroencephalogram prior to their randomisation to the groups. During the intervention, both the patients and the professionals responsible for the physical therapy and evaluations were unaware of the group which the patients belonged to. At the conclusion of the treatment, the patients were re-evaluated using the Fugl-Meyer assessment scale, AMADEO® and a quantitative electroencephalogram.

The experimental group received 10-12 treatment sessions, consisting of 10-12 minutes of physical therapy plus 25-30 minutes of AO + MI, focused exclusively on the paretic upper extremity. Two sessions were administered per week, on Mondays and Thursdays, for six weeks. The physical therapy consisted of continuous flexion and extension movements of the fingers at a frequency of 0.5 Hz. Exercises involving stretching of the hand (flexion and extension of the fingers and wrist) and arm (flexion and extension of the elbow and shoulder) were performed before each session as a warm-up to prevent injuries, as specified by a physiotherapist specialising in neurorehabilitation. The AO + MI intervention consisted of watching videos showing repetitive hand movements in daily life actions (lifting a bottle and lifting a spoon), from a first-person perspective, presented on a computer screen at a distance of 50 centimetres from the patient (Fig. 1c). While watching the movements, the patients were instructed to imagine themselves performing them with the paretic upper limb, but keeping it immobile, evoking how it would feel to touch the bottle or spoon (the temperature and texture), the force and tension they would have to exert on the arm and hand, the position of the arm and fingers needed to perform the task, and the feeling of completing the movement (drinking from the bottle or eating from the spoon). Each task was displayed with the same frequency (50% lifting the bottle and 50% lifting the spoon).

The control group received from 10 to 12 sessions of physical therapy, with parameters identical to those of the experimental treatment. In order to ensure consistency between conditions, after the physical therapy, 25-30 minutes were allocated to an informal interview between the experimenter and patient, during which the same videos used for the experimental intervention were presented at a distance of 50 cm in the patient’s field of vision, with no cues provided, so that both groups were exposed to the same stimuli, with the difference that the experimental group was trained in AO + MI.

During the intervention, neither group performed the AO + EM task required for electroencephalographic recordings, in order to prevent any possible interference between the treatments.

Statistics


Version 22.0 of the SPSS® statistical package (IBM Corp., New York, United States) was used to analyse the variables studied. The equivalence of the groups was initially established for the variables age, time to progression and cognitive status (Mini-Mental test) using the Mann-Whitney U test. The same analysis was subsequently performed with the variables of interest function, strength, mobility and desynchronisation.

The measurements of function, strength, mobility and desynchronisation before (PRE) and after (POS) treatment were compared using the Wilcoxon test to determine the effect of the intervention in the overall sample and for each group. The POS measurements of the same variables were then compared between the groups using the Mann-Whitney U test to determine whether the experimental group presented a greater degree of improvement. Effect sizes were calculated for all the comparisons using Cohen’s d or Hedges’ g as appropriate.

Finally, the main variables that presented significant changes were correlated with desynchronisation using Spearman’s rho test to ascertain whether the clinical improvement was related to brain electrical activity in any specific region (the supplementary motor area, premotor cortex or primary motor cortex). The level of significance established for all the analyses was alpha < 0.05.
 

Results


Fourteen patients were recruited. Three of them were excluded, as two did not meet the inclusion criteria and one refused to participate.

The groups were considered equivalent, as none of the variables measured before treatment showed any significant differences (p < 0.05) (Table II).

 

Table II. Comparison of pre-treatment variables.
 

Control (MR)

Experimental (MR)

U

Z

p


Age (years)
 

5

6.83

10

–0.913

0.361


Time to progression (weeks)
 

6.6

5.5

12

–0.548

0.584


Cognitive status
 

6.8

5.33

11

–0.746

0.456


Functionality PRE
 

6.5

5.58

12.5

–0.457

0.647


Strength PRE
 

6.4

5.67

13

–0.369

0.712


Mobility PRE
 

4.8

7

9

–1.095

0.273


Desynchronisation
         

Fz AO + ME NP PRE
 

5.8

6.17

14

–0.183

0.855


Fz AO + ME PA PRE
 

5.4

6.5

12

–0.548

0.584


F INJ AO + ME PA PRE
 

7

5.17

10

–0.913

0.855


AO + ME: action observation plus motor execution; F: frontal; Fz: medial frontal; INJ: injured; MR: mean range; NP: not paretic; PA: paretic; PRE: pre-treatment.
 

 

Function, strength and mobility


PRE vs. POS comparison of the total sample showed significant differences in function (PRE, median 17 and range 34, vs. POS, median 18 and range 34; Z = -2.546, p = 0.011 and d = 0.234), but not in strength or mobility. When comparing the changes by group, there were significant increases in function in the experimental group (PRE, median 12 and range 34, vs. POS, median 20.5 and range 34; Z = –2.032, p = 0.042 and d = 0.312) and strength (PRE, median 43.5 and range 64, vs. POS, median 58.5 and range 66; Z = –2.201, p = 0.028 and d = 0.599), while there were no significant changes in any of the variables in the control group (Fig. 3).

 

Figure 3. Comparison of pre-treatment (PRE) versus post-treatment (POS) clinical variables in the total sample, the control group and the experimental group.






 

POS comparison between groups revealed significantly greater strength in the experimental group (experimental, median 58.5 and range 66, versus control, median 29 and range 68; U = 4, p = 0.045 and g = 0.824), and no significant differences in function or mobility (Fig. 4).

 

Figure 4. Comparison of post-treatment clinical variables (POS) between the control group and the experimental group. 






 

Desynchronisation


Significant changes were found during AO + ME, but not during AO + MI. PRE vs. POS comparison of the total sample at Fz during AO + ME of the paretic upper extremity (AO + ME PA) showed a significant increase in POS desynchronisation (PRE, median 0.059 and range 0.346, vs. POS, median –0.183 and range 0.344; Z = –2.49, p = 0.013 and d = 1.399). When the groups were compared, this difference remained significant in the experimental group (PRE, median 0.042 and range 0.237, vs. POS, median –0.188 and range 0.181; Z = –2.201, p = 0.028 and d = 2.819), but not in the control group. A significant increase at the same electrode (Fz) during AO + ME of the non-paretic upper extremity (AO + ME NP) was also found for the experimental group (PRE, median –0.047 and range 0.375, vs. POS, median –0.18 and range 0.3; Z = –1.992, p = 0.046 and d = 1.628) (Fig. 5).

 

Figure 5. Pre-treatment (PRE) versus post-treatment (POS) desynchronisation at the medial frontal electrode (Fz) during action observation plus motor execution (AO + ME) of the non-paretic upper extremity (NP) and paretic upper extremity (PA) in the total sample, the control group and the experimental group






 

The only significant difference in POS desynchronisation between the groups was in the frontal electrode of the injured hemisphere (F INJ) during AO + ME PA, in which the experimental group presented greater POS desynchronisation (experimental, median –0.057 and range 0.296, vs. control, median –0.269 and range 0.335; U = 3, p = 0.03 and g = 1.421) (Fig. 6).

 

Figure 6. Comparison between the control and experimental groups of post-treatment desynchronisation (POS) in healthy frontal cortex (F HEA) and injured frontal cortex (F INJ) during action observation plus motor execution (AO + ME) of the non-paretic upper extremity (NP) and paretic upper extremity (PA).






 

Correlation between recovery in the paretic upper extremity and desynchronisation


Correlations were performed for the total sample, between function, strength and POS desynchronisation at Fz during AO + ME PA and AO + ME NP, with no significant results. We then performed the same analysis for each group, and found a significant strong positive correlation between function and strength (rho(4) = 0.829 and p = 0.042), as well as a significant strong negative correlation between function and POS desynchronisation at Fz during AO + ME PA (rho(4) = –0.829 and p = 0.042) for the experimental group, but not for the control group.
 

Discussion


Our findings show that an AO- + MI-based intervention facilitates recovery of the paretic upper extremity in chronic stroke patients in terms of function and strength, which is consistent with the suggestions of Vogt et al [9] and Eaves et al [13], concerning the benefits of multimodal motor training in these cases; this is partially consistent with the results reported by Sun et al [31], who reported an increase in function related to greater activation of the primary motor cortex, whereas in our study the relationship was between function and greater activation of the supplementary motor area; a possible explanation for this difference could be the time to progression, since our chronic patients are less likely to present changes in areas directly related to movement.

Likewise, the increased desynchronisation in the supplementary motor area during movement of both upper limbs (AO + ME PA and AO + ME NP) after treatment in the experimental group suggests a bilateral facilitating effect that is consistent with the findings of Welniarz et al [43], who refer to a modulatory function of the supplementary motor area during movement preparation, while the increased desynchronisation in the injured premotor cortex (F INJ) during movement of the paretic upper limb (AO + ME PA) in the experimental group indicates neuroplastic processes related to recovery in movement planning [44] and even reorganisation for control of the basic movement parameters usually assigned to the primary motor cortex, consistent with that described by Fridman et al [45].

With regard to increased strength, the study by Scott et al [46] is the only precedent reporting an improvement related to AO + MI. Taken together, the findings could indicate a facilitating effect on intramuscular tension; however, these authors focused on the hamstring muscles, so the results should be considered with caution, as these are very different muscle groups and movements. The correlation between function and strength is also expected, as the former includes aspects of motion for which the latter is necessary [38].

An interesting but nevertheless logical result was that during the AO + ME task and not during the AO + MI task, the most post-treatment changes were observed in the experimental group, which seems to be consistent with Jeannerod’s proposal [4,5] concerning AO and MI as functionally equivalent phenomena, and hidden constituents of movement execution.
 

Conclusions


In this study, we examined the effects of an AO- + MI-based intervention for chronic stroke patients on the assumption that it enhances recovery of strength, mobility, and function of the paretic upper extremity. According to the results, the treatment favoured improvement in strength and function, but not directly in mobility.

It is likely that the AO + MI-based intervention had an overall impact on the recovery of the paretic upper extremity by stimulating the supplementary motor area, a region involved in the preparation, initiation, control and learning of movement [6,47-49]. This would indicate that it has an indirect positive effect on the generation of movement, which only the primary motor cortex is capable of [50], and the latter showed no changes in desynchronisation. No changes in the mobility variable were detected either.

In the authors’ opinion, this is complemented by the fact that the changes in desynchronisation occurred during motor execution tasks (AO + ME), and that the function variable is in turn made up of both reflex movements and voluntary movements related to motor synergies, i.e. the effects of the intervention could affect some motion parameters without necessarily favouring the recovery of the primary motor cortex.

In summary, our findings indicate that AO + MI-focused therapy as a complement to physical rehabilitation can be used as a treatment for patients with post-stroke paresis in the upper extremity, and that its effects are positive even in chronic cases.

It is important to note that although the effect sizes were moderate to high for the clinical variables and very high for cortical activation, the results should be considered with caution, as the study had important limitations, such as the size and heterogeneity of the sample, in addition to the low level of spatial resolution in the electroencephalogram. In future research, we recommend increasing the sample size and homogenising its characteristics in order to increase the robustness of the statistical analysis, and including functional imaging studies during the tasks to establish the cortical areas involved more precisely. Finally, we suggest administering different versions of the AO + MI based treatment to determine the effects of duration, frequency and time of exposure on recovery.

 

References
 


 1. Fabbri-Destro M, Rizzolatti G. Mirror neurons and mirror systems in monkeys and humans. Physiology 2008; 23: 171-9.

 2. Buccino G. Action observation treatment: a novel tool in neurorehabilitation. Philos Trans R Soc Lond B Biol Sci 2014; 369: 20130185.

 3. Lotze M, Cohen LG. Volition and imagery in neurorehabilitation. Cogn Behav Neurol 2006; 19: 135-40.

 4. Jeannerod M. Neural simulation of action: a unifying mechanism for motor cognition. Neuroimage 2001; 14: 103-9.

 5. Jeannerod M. Motor cognition: what actions tell the self. Oxford: Oxford University Press; 2006.

 6. Hardwick RM, Caspers S, Eickhoff SB, Swinnen SP. Neural correlates of action: comparing meta-analyses of imagery, observation, and execution. Neurosci Biobehav Rev 2018; 94: 31-44.

 7. Hoshi E, Tanji J. Distinctions between dorsal and ventral premotor areas: anatomical connectivity and functional properties. Curr Opin Neurobiol 2007; 17: 234-42.

 8. Ohbayashi M. The roles of the cortical motor areas in sequential movements. Front Behav Neurosci 2021; 15: 640659.

 9. Vogt S, Di Rienzo F, Collet C, Collins A, Guillot A. Multiple roles of motor imagery during action observation. Front Hum Neurosci 2013; 7: 807.

 10. Lotze M, Halsband U. Motor imagery. J Physiol 2006; 99: 386-95.

 11. Mulder T. Motor imagery and action observation: cognitive tools for rehabilitation. J Neural Transm 2007; 114: 1265-78.

 12. Holmes P. Evidence from cognitive neuroscience supports action observation as part of an integrated approach to stroke rehabilitation. Man Ther 2011; 16: 40-1.

 13. Eaves DL, Riach M, Holmes PS, Wright DJ. Motor imagery during action observation: a brief review of evidence, theory and future research opportunities. Front Neurosci 2016; 10: 514.

 14. Ertelt D, Small S, Solodkin A, Dettmers C, McNamara A, Binkofski F, et al. Action observation has a positive impact on rehabilitation of motor deficits after stroke. Neuroimage 2007; 36: 164-73.

 15. Franceschini M, Agosti M, Cantagallo A, Sale P, Mancuso M, Buccino G. Mirror neurons: action observation treatment as a tool in stroke rehabilitation. Eur J Phys Rehabil Med 2010; 46: 517-23.

 16. Franceschini M, Ceravolo MG, Agosti M, Cavallini P, Bonassi S, Dall’Armi V, et al. Clinical relevance of action observation in upper-limb stroke rehabilitation: a possible role in recovery of functional dexterity. A randomized clinical trial. Neurorehabil Neural Repair 2012; 26: 456-62.

 17. Sugg K, Müller S, Winstein C, Hathorn D, Dempsey A. Does action observation training with immediate physical practice improve hemiparetic upper-limb function in chronic stroke? Neurorehabil Neural Repair 2015; 29: 807-17.

 18. Celnik P, Webster B, Glasser DM, Cohen LG. Effects of action observation on physical training after stroke. Stroke 2008; 39: 1814-20.

 19. Feenstra W, Tepper M, Boonstra AM, Otten B, de Vries S. Recovery of motor imagery ability in the first year after stroke. Int J Rehabil Res 2016; 39: 171-5.

 20. Johnson SH, Sprehn G, Saykin AJ. Intact motor imagery in chronic upper limb hemiplegics: evidence for activity-independent action representations. J Cogn Neurosci 2002; 14: 841-52.

 21. Fernández-Gómez E, Sánchez-Cabeza Á. Imaginería motora: revisión sistemática de su efectividad en la rehabilitación de la extremidad superior tras un ictus. Rev Neurol 2018; 66: 137-46.

 22. Page SJ, Levine P, Sisto S, Johnston MV. A randomized efficacy and feasibility study of imagery in acute stroke. Clin Rehabil 2001; 15: 233-40.

 23. Page SJ, Levine P, Leonard A. Mental practice in chronic stroke: results of a randomized, placebo-controlled trial. Stroke 2007; 38: 1293-7.

 24. Page SJ, Levine P, Leonard AC. Effects of mental practice on affected limb use and function in chronic stroke. Arch Phys Med Rehabil 2005; 86: 399-402.

 25. Page SJ, Murray C, Hermann V, Levine P. Retention of motor changes in chronic stroke survivors who were administered mental practice. Arch Phys Med Rehabil 2011; 92: 1741-5.

 26. Ietswaart M, Johnston M, Dijkerman HC, Joice S, Scott CL, MacWalter RS, et al. Mental practice with motor imagery in stroke recovery: randomized controlled trial of efficacy. Brain 2011; 134: 1373-86.

 27. Braun SM, Beurskens AJ, Kleynen M, Oudelaar B, Schols JM, Wade DT. A multicenter randomized controlled trial to compare subacute ‘treatment as usual’ with and without mental practice among persons with stroke in Dutch nursing homes. J Am Med Dir Assoc 2012; 13: 85. e1-7.

 28. Gatti R, Tettamanti A, Gough PM, Riboldi E, Marinoni L, Buccino G. Action observation versus motor imagery in learning a complex motor task: a short review of literature and a kinematics study. Neurosci Lett 2013; 540: 37-42.

 29. Malouin F, Jackson PL, Richards CL. Towards the integration of mental practice in rehabilitation programs. A critical review. Front Hum Neurosci 2013; 7: 576.

 30. Conson M, Sarà M, Pistoia F, Trojano L. Action observation improves motor imagery: specific interactions between simulative processes. Exp Brain Res 2009; 199: 71-81.

 31. Sun Y, Wei W, Luo Z, Gan H, Hu X. Improving motor imagery practice with synchronous action observation in stroke patients. Top Stroke Rehabil 2016; 23: 245-53.

 32. Eaves DL, Behmer LP Jr, Vogt S. EEG and behavioural correlates of different forms of motor imagery during action observation in rhythmical actions. Brain Cogn 2016; 106: 90-103.

 33. Lee KB, Lim SH, Kim KH, Kim KJ, Kim YR, Chang WN, et al. Six-month functional recovery of stroke patients: a multi-time-point study. Int J Rehabil Res 2015; 38: 173.

 34. Nakayama H, Jørgensen HS, Raaschou HO, Olsen TS. Recovery of upper extremity function in stroke patients: the Copenhagen Stroke Study. Arch Phys Med Rehabil 1994; 75: 394-8.

 35. Andrews K, Brocklehurst J, Richards B, Laycock P. The rate of recovery from stroke-and its measurement. Int Rehabil Med 1981; 3: 155-61.

 36. Berends HI, Wolkorte R, Ijzerman MJ, van Putten MJ. Differential cortical activation during observation and observation-and-imagination. Exp Brain Res 2013; 229: 337-45.

 37. Fugl-Meyer AR, Jaasko L, Leyman I, Olsson S, Steglind S. The post-stroke hemiplegic patient. 1. a method for evaluation of physical performance. Scand J Rehabil Med 1975; 7: 13-31.

 38. Gladstone DJ, Danells CJ, Black SE. The fugl-meyer assessment of motor recovery after stroke: a critical review of its measurement properties. Neurorehabil Neural Repair 2002; 16: 232-40.

 39. Sale P, Lombardi V, Franceschini M. Hand robotics rehabilitation: feasibility and preliminary results of a robotic treatment in patients with hemiparesis. Stroke Res Treat 2012; 2012.

 40. Ramoser H, Muller-Gerking J, Pfurtscheller G. Optimal spatial filtering of single trial EEG during imagined hand movement. IEEE Trans Rehabil Eng 2000; 8: 441-6.

 41. Sinkkonen J, Tiitinen H, Naatanen R. Gabor filters: an informative way for analysing event-related brain activity. J Neurosci Methods 1995; 56: 99-104.

 42. Pfurtscheller G, Lopes da Silva FH. Event-related EEG/MEG synchronization and desynchronization: basic principles. Clin Neurophysiol 1999; 110: 1842-57.

 43. Welniarz Q, Gallea C, Lamy JC, Méneret A, Popa T, Valabregue R, et al. The supplementary motor area modulates interhemispheric interactions during movement preparation. Hum Brain Mapp 2019; 40: 2125-42.

 44. Mizuguchi N, Kanosue K. Changes in brain activity during action observation and motor imagery: their relationship with motor learning. Prog Brain Res 2017; 234: 189-204.

 45. Fridman EA, Hanakawa T, Chung M, Hummel F, Leiguarda RC, Cohen LG. Reorganization of the human ipsilesional premotor cortex after stroke. Brain 2004; 127: 747-58.

 46. Scott M, Taylor S, Chesterton P, Vogt S, Eaves DL. Motor imagery during action observation increases eccentric hamstring force: an acute non-physical intervention. Disabil Rehabil 2018; 40: 1443-51.

 47. Picard N, Strick PL. Motor areas of the medial wall: a review of their location and functional activation. Cereb Cortex 1996; 6: 342-53.

 48. Rizzolatti G, Cattaneo L, Fabbri-Destro M, Rozzi S. Cortical mechanisms underlying the organization of goal-directed actions and mirror neuron-based action understanding. Physiol Rev 2014; 94: 655-706.

 49. Nachev P, Kennard C, Husain M. Functional role of the supplementary and pre-supplementary motor areas. Nat Rev Neurosci 2008; 9: 856-69.

 50. Bhattacharjee S, Kashyap R, Abualait T, Annabel Chen S-H, Yoo W-K, Bashir S. The role of primary motor cortex: more than movement execution. J Motor Behav 2021; 53: 258-74.

 

Paresia de una extremidad superior. Recuperación mediante observación de la acción más imaginería motora en pacientes con ictus crónico


Introducción. La observación de la acción (OA) y la imaginería motora (IM) se consideran formas de representación motora funcionalmente equivalentes, relacionadas con la ejecución del movimiento (EM). Debido a sus características, la OA y la IM se han propuesto como técnicas para facilitar la recuperación de las hemiparesias de la extremidad superior posterior a ictus.

Pacientes y métodos. Se realizó un diseño experimental, longitudinal y prospectivo simple ciego. Participaron 11 pacientes, quienes fueron asignados aleatoriamente a cada grupo de estudio. Ambos grupos recibieron de 10 a 12 sesiones de terapia física. Cinco pacientes fueron asignados al grupo de tratamiento control y seis pacientes al grupo de tratamiento experimental (OA + IM). A todos se les evaluó antes y después del tratamiento para determinar la función, la fuerza (newtons) y la movilidad (porcentaje) de la extremidad afectada, así como la desincronización de alfa (8-13 Hz) en el área motora suplementaria, la corteza premotora y la corteza motora primaria durante tareas de OA + IM y observación de la acción más ejecución motora (OA + EM).

Resultados. El grupo experimental presentó mejoría en la función y la fuerza. Se encontró correlación negativa entre la desincronización en el área motora suplementaria y la función, así como incremento postratamiento de la desincronización en la corteza premotora del hemisferio lesionado únicamente para el grupo experimental.

Conclusiones. Una intervención basada en OA + IM impacta positivamente en la recuperación de la extremidad superior parética mediante la estimulación del área motora suplementaria, corteza involucrada en la preparación y aprendizaje del movimiento. La terapia OA + IM puede usarse como tratamiento complementario en pacientes con paresia de una extremidad superior posterior a un ictus crónico.

Palabras clave. Desincronización de alfa. Ejecución motora. Ictus. Imaginería motora. Observación de la acción. Paresia de extremidad superior.
 

 

© 2024 Revista de Neurología

Si ya es un usuario registrado en Neurologia, introduzca sus datos de inicio de sesión.


Rellene los campos para registrarse en Neurologia.com y acceder a todos nuestros artículos de forma gratuita
Datos básicos
He leído y acepto la política de privacidad y el aviso legal
Seleccione la casilla si desea recibir el número quincenal de Revista de Neurología por correo electrónico. De forma quincenal se le mandará un correo con los títulos de los artículos publicados en Revista de Neurología.
Seleccione la casilla si desea recibir el boletín semanal de Revista de Neurología por correo electrónico. El boletín semanal es una selección de las noticias publicadas diariamente en Revista de Neurología.
Seleccione la casilla si desea recibir información general de neurologia.com (Entrevistas, nuevos cursos de formación, eventos, etc.)
Datos complementarios

Se os solicita los datos de redes para dar repercusión por estos medios a las publicaciones en las que usted participe.



Estimado usuario de Revista de Neurología,

Debido a la reciente fusión por absorción de VIGUERA EDITORES, S.L.U., la entidad gestora de las publicaciones de Viguera Editores, entre ellas, Revista de Neurología, por EVIDENZE HEALTH ESPAÑA, S.L.U., una de las sociedades también pertenecientes al Grupo Evidenze, y con la finalidad de que Usted pueda seguir disfrutando de los contenidos y distintos boletines a los que está suscrito en la página web de neurologia.com, es imprescindible que revise la nueva política de privacidad y nos confirme la autorización de la cesión de sus datos.

Lamentamos informarle que en caso de no disponer de su consentimiento, a partir del día 28 de octubre no podrá acceder a la web de neurologia.com

Para dar su consentimiento a seguir recibiendo la revista y los boletines de neurologia.com vía correo electrónico y confirmar la aceptación de la nueva política de privacidad, así como la cesión de sus datos a Evidenze Health España S.L.U., el resto de las entidades del Grupo Evidenze y sus partners y colaboradores comerciales, incluyendo la posibilidad de llevar a cabo transferencias internacionales a colaboradores extranjeros, pulse en el siguiente enlace:

ACEPTAR

Cancelar

Atentamente

El equipo de Revista de Neurología