Good luck figuring out what a premotor therapy is and you need robotics besides. I believe most of my premotor cortex was destroyed so nothing here will help me even if I could figure it out.
Targeted engagement of a dorsal premotor circuit in the treatment of post-stroke paresis
2013, NeuroRehabilitation
Lucy Dodakian a,
Lucy Dodakian a,
Kelli G. Sharp a,
Jill See a,
Neil S. Abidi a,
Khoa Mai a,
Brett W. Fling a,
Vu H. Le a
and Steven C. Cramer a,b,∗
a Department of Anatomy & Neurobiology, University of California, Irvine, CA, USA
b Department of Neurology, University of California, Irvine, CA, USA
a Department of Anatomy & Neurobiology, University of California, Irvine, CA, USA
b Department of Neurology, University of California, Irvine, CA, USA
* Address for correspondence: Steven C. Cramer, MD, University of California, Irvine Medical Center, 200S. Manchester Ave. Suite206, Orange, CA 92868, USA. Tel.: +1 714 456 6876; Fax: +1 714456 8805; E-mail: scramer@uci.edu
BACKGROUND:
Good motor outcome after stroke has been found to correlate with increased activity in a dorsal premotor(PMd) brain circuit, suggesting that therapeutic strategies targeting this circuit might have a favorable, causal influence on motor status.
OBJECTIVE:
This study addressed the hypothesis that a Premotor Therapy that exercises normal PMd functions would providegreater behavioral gains than would standard Motor Therapy; and that Premotor Therapy benefits would be greatest in patients with greater preservation of PMd circuit elements.
METHODS:
Patients with chronic hemiparetic stroke (n=15) were randomized to 2-weeks of Premotor Therapy
or Motor Therapy, implemented through a robotic device.
RESULTS:
Overall, gains were modest but significant (change in FM score, 2.1±2.8 points, p<0.02) and did not differ by treatment assignment. However, a difference between Therapies was apparent when injury to the PMd circuit was considered, as the interaction between treatment assignment and degree of corticospinal tract injury was significantly related to the change inFM score (p=0.018): the more the corticospinal tract was spared, the greater the gains provided by Premotor Therapy. Similar results were obtained when looking at the interaction between treatment assignment and PMd function (p=0.03).
CONCLUSIONS:
Targeted engagement of a brain circuit is a feasible strategy for stroke rehabilitation. This approach has maximum impact when there is less stroke injury to key elements of the targeted circuit.Keywords: Stroke, premotor cortex, robot, motor recovery, corticospinal tract
1. Introduction
Motor deficits are among the most common forms of impairment after stroke, present in>80% of patients acutely (Rathore, Hinn, Cooper, Tyroler, & Rosamond,2002). Most patients show spontaneous improvement in motor status during the weeks following stroke. Several forms of brain plasticity that contribute to this recovery have been identified (S. C. Cramer, 2008;Nudo, 2011). In particular, anatomical and functional evidence support a role for dorsal premotor cortex in support of return of motor function (Alagona et al.,2001; S. Cramer et al., 1997; Denny-Brown, 1950;Fries, Danek, Scheidtmann, & Hamburger, 1993; Gau-thier, Taub, Mark, Barghi, & Uswatte, 2012; Laplane,Talairach, Meininger, Bancaud, & Bouchareine, 1977;Seitz et al., 1998; Weiller, Chollet, Friston, Wise, &Frackowiak, 1992). Activity within ipsilesional dorsal premotor cortex (PMd) has been associated withachieving spontaneous recovery (Fridman et al., 2004;Platz et al., 2000; Rehme, Eickhoff, Wang, Fink, &Grefkes, 2011; Sharma, Baron, & Rowe, 2009; Wardet al., 2006) as well as treatment-induced recovery(Careyetal.,2002;Johansen-Berg,Dawes,etal.,2002;
1053-8135/13/$27.50 © 2013 – IOS Press and the authors. All rights reserved
L. Dodakian et al. / Targeted dorsal premotor engagement
Page,Szaflarski,Eliassen,Pan,&Cramer,2009;Strup-pler et al., 2007) after stroke. Evidence suggests that contralesional PMd might contribute to recovery, too,particularly in patients with more severe stroke (Bute-fisch et al., 2005; Kantak, Stinear, Buch, & Cohen,2012; Lotze et al., 2011; Rehme, Fink, von Cramon,&Grefkes,2011).Changes in PMd activity are thought to support behavioral gains through connections with ipsilesional primary motor cortex (M1), contralesional brain areas, spinal cord targets, and possibly reticulospinal brain stem neurons (Fregni & Pascual-Leone,2006; Fridman, et al., 2004; James et al., 2009; Kantak, et al., 2012). Together, these findings suggest that therapies that increase PMd activity could improve motor status after stroke. This idea was examined in the current study by testing two main hypotheses. The first is that practicing a motor behavior known to engage PMd circuitry will improve motor status after stroke to a greater extent than will practicing a repetitive motor behavior unrelated to PMd. These cond is that the extent to which such a PMd-based therapy provides superior gains in motor status will vary with the availability of PMd anatomically, and perhaps functionally–a therapy can not provide benefit if its biological target is excessively injured by stroke(Nouri & Cramer, 2011). These two hypotheses were examined in the cur-rent study, with a focus on the distal upper extremity. A Premotor Therapy
was designed, the features of which emphasized normal functions of a PMd circuit.Key anatomical components of the PMd circuit include PMd, which processes novel external cues in order to guide the timing and the choice of voluntary movements(Askim,Indredavik,&Haberg,2010;Chouinard&Paus,2006;Geyer,Matelli,Luppino,&Zilles,2000;Koch et al., 2006; Kurata & Hoffman, 1994; O’Shea,Johansen-Berg,Trief,Gobel,&Rushworth,2007;Pass-ingham, 1993; Rushworth, Johansen-Berg, Gobel, &Devlin, 2003; Schluter, Rushworth, Passingham, &Mills, 1998), as well as M1 and the corticospinaltract, important for expressing the output of corticalcomponents of the circuit. A study of healthy control subjects (described below) confirmed that performing the timed movement tasks that constitute Premotor Therapy
was associated with increased activity within a dorsal premotor circuit. A robotic device (Takahashi,Der-Yeghiaian, Le, Motiwala, & Cramer, 2008), found to improve post-stroke arm motor function in a prior study, served as an ideal vehicle for implementing the timed cues central to
Premotor Therapy, and furthermore allowed inclusion of therapy in a gaming context, an approach useful to modulating the function of selected brain circuits (Bavelier, Levi, Li, Dan, &Hensch, 2010; Colzato, van den Wildenberg, Zmigrod,& Hommel, 2012). In the current study, this Premotor Therapy
was contrasted with Motor Therapy
, in which subjects performed the same distal arm movements as with
Premotor Therapy but without cues or novelty. Patients with chronic stroke underwent a baseline example plus MRI for assessing anatomical and functional features of a PMd circuit, were randomized to two weeks of Motor Therapy vs. Premotor Therapy via the robotic device, and then had their motor outcome assessed 1 month after completion of therapy. These data were used to address the above two hypotheses.
Abstract
.BACKGROUND:
Good motor outcome after stroke has been found to correlate with increased activity in a dorsal premotor(PMd) brain circuit, suggesting that therapeutic strategies targeting this circuit might have a favorable, causal influence on motor status.
OBJECTIVE:
This study addressed the hypothesis that a Premotor Therapy that exercises normal PMd functions would providegreater behavioral gains than would standard Motor Therapy; and that Premotor Therapy benefits would be greatest in patients with greater preservation of PMd circuit elements.
METHODS:
Patients with chronic hemiparetic stroke (n=15) were randomized to 2-weeks of Premotor Therapy
or Motor Therapy, implemented through a robotic device.
RESULTS:
Overall, gains were modest but significant (change in FM score, 2.1±2.8 points, p<0.02) and did not differ by treatment assignment. However, a difference between Therapies was apparent when injury to the PMd circuit was considered, as the interaction between treatment assignment and degree of corticospinal tract injury was significantly related to the change inFM score (p=0.018): the more the corticospinal tract was spared, the greater the gains provided by Premotor Therapy. Similar results were obtained when looking at the interaction between treatment assignment and PMd function (p=0.03).
CONCLUSIONS:
Targeted engagement of a brain circuit is a feasible strategy for stroke rehabilitation. This approach has maximum impact when there is less stroke injury to key elements of the targeted circuit.Keywords: Stroke, premotor cortex, robot, motor recovery, corticospinal tract
1. Introduction
Motor deficits are among the most common forms of impairment after stroke, present in>80% of patients acutely (Rathore, Hinn, Cooper, Tyroler, & Rosamond,2002). Most patients show spontaneous improvement in motor status during the weeks following stroke. Several forms of brain plasticity that contribute to this recovery have been identified (S. C. Cramer, 2008;Nudo, 2011). In particular, anatomical and functional evidence support a role for dorsal premotor cortex in support of return of motor function (Alagona et al.,2001; S. Cramer et al., 1997; Denny-Brown, 1950;Fries, Danek, Scheidtmann, & Hamburger, 1993; Gau-thier, Taub, Mark, Barghi, & Uswatte, 2012; Laplane,Talairach, Meininger, Bancaud, & Bouchareine, 1977;Seitz et al., 1998; Weiller, Chollet, Friston, Wise, &Frackowiak, 1992). Activity within ipsilesional dorsal premotor cortex (PMd) has been associated withachieving spontaneous recovery (Fridman et al., 2004;Platz et al., 2000; Rehme, Eickhoff, Wang, Fink, &Grefkes, 2011; Sharma, Baron, & Rowe, 2009; Wardet al., 2006) as well as treatment-induced recovery(Careyetal.,2002;Johansen-Berg,Dawes,etal.,2002;
1053-8135/13/$27.50 © 2013 – IOS Press and the authors. All rights reserved
L. Dodakian et al. / Targeted dorsal premotor engagement
Page,Szaflarski,Eliassen,Pan,&Cramer,2009;Strup-pler et al., 2007) after stroke. Evidence suggests that contralesional PMd might contribute to recovery, too,particularly in patients with more severe stroke (Bute-fisch et al., 2005; Kantak, Stinear, Buch, & Cohen,2012; Lotze et al., 2011; Rehme, Fink, von Cramon,&Grefkes,2011).Changes in PMd activity are thought to support behavioral gains through connections with ipsilesional primary motor cortex (M1), contralesional brain areas, spinal cord targets, and possibly reticulospinal brain stem neurons (Fregni & Pascual-Leone,2006; Fridman, et al., 2004; James et al., 2009; Kantak, et al., 2012). Together, these findings suggest that therapies that increase PMd activity could improve motor status after stroke. This idea was examined in the current study by testing two main hypotheses. The first is that practicing a motor behavior known to engage PMd circuitry will improve motor status after stroke to a greater extent than will practicing a repetitive motor behavior unrelated to PMd. These cond is that the extent to which such a PMd-based therapy provides superior gains in motor status will vary with the availability of PMd anatomically, and perhaps functionally–a therapy can not provide benefit if its biological target is excessively injured by stroke(Nouri & Cramer, 2011). These two hypotheses were examined in the cur-rent study, with a focus on the distal upper extremity. A Premotor Therapy
was designed, the features of which emphasized normal functions of a PMd circuit.Key anatomical components of the PMd circuit include PMd, which processes novel external cues in order to guide the timing and the choice of voluntary movements(Askim,Indredavik,&Haberg,2010;Chouinard&Paus,2006;Geyer,Matelli,Luppino,&Zilles,2000;Koch et al., 2006; Kurata & Hoffman, 1994; O’Shea,Johansen-Berg,Trief,Gobel,&Rushworth,2007;Pass-ingham, 1993; Rushworth, Johansen-Berg, Gobel, &Devlin, 2003; Schluter, Rushworth, Passingham, &Mills, 1998), as well as M1 and the corticospinaltract, important for expressing the output of corticalcomponents of the circuit. A study of healthy control subjects (described below) confirmed that performing the timed movement tasks that constitute Premotor Therapy
was associated with increased activity within a dorsal premotor circuit. A robotic device (Takahashi,Der-Yeghiaian, Le, Motiwala, & Cramer, 2008), found to improve post-stroke arm motor function in a prior study, served as an ideal vehicle for implementing the timed cues central to
Premotor Therapy, and furthermore allowed inclusion of therapy in a gaming context, an approach useful to modulating the function of selected brain circuits (Bavelier, Levi, Li, Dan, &Hensch, 2010; Colzato, van den Wildenberg, Zmigrod,& Hommel, 2012). In the current study, this Premotor Therapy
was contrasted with Motor Therapy
, in which subjects performed the same distal arm movements as with
Premotor Therapy but without cues or novelty. Patients with chronic stroke underwent a baseline example plus MRI for assessing anatomical and functional features of a PMd circuit, were randomized to two weeks of Motor Therapy vs. Premotor Therapy via the robotic device, and then had their motor outcome assessed 1 month after completion of therapy. These data were used to address the above two hypotheses.
No comments:
Post a Comment