Skip Navigation LinksHome > September 2011 - Volume 35 - Issue 3 > Intervention That Challenges the Nervous System Confronts th...
Journal of Neurologic Physical Therapy:
doi: 10.1097/NPT.0b013e31822a5087
DEPARTMENTS: Clinical Point of View

Intervention That Challenges the Nervous System Confronts the Challenge of Real-World Clinical Practice

Fisher, Beth PT, PhD

Free Access
Article Outline
Collapse Box

Author Information

Address correspondence to: Beth Fisher, E-mail: bfisher@usc.edu

Editor's Note

This article relates to Fritz et al “Feasibility of Intensive Mobility Training to ImproveGait, Balance, and Mobility in Persons With Chronic Neurological Conditions: A Case Series,” J Neurol Phys Ther. 2011;35:141–147.

Looking back a decade after the Decade of the Brain (1990–1999), it is fascinating to note how neuroplasticity has become the driving principle of neurorehabilitation. The most important insight gained during this period was that the brain at any age is a malleable, “plastic” organ that can be continually reorganized through experience. The most important translation from basic research to clinical practice was the recognition that neuroplasticity and behavioral recovery after brain injury could be facilitated through the manipulation of specific practice variables designed to promote skill acquisition.1 On the basis of this premise, greater attention was given to designing interventions in challenge the impaired nervous system through intensive, complex, repetitive task practice.

Most of our understanding of this training-induced neuroplasticity is derived from both animal and human studies of brain injury characterized by a single catastrophic event such as stroke or spinal cord injury.27 In addition, research during the Decade of the Brain culminated in the Extremity Constraint Induced Therapy Evaluation Trial (EXCITE), a federally funded rehabilitation trial. The interventions in this trial were designed to promote recovery of the brain and behavior in individuals with stroke-related impairment by challenging impaired upper extremity function with intensive task practice. The participants in this trial were within the acute poststroke period, had mild impairment of the paretic upper extremity, and had the ability to extend the paretic wrist and fingers through a specified range of movement. Individuals such as these, who are in the acute postinjury stage with mild impairment secondary to nonprogressive disorders, are thought to have the greatest potential for training-induced neuroplasticity and behavioral recovery. The question is “What about everyone else?” The case series presented by Fritz et al8 moves toward answering this question and challenges traditional modes of practice in several important ways.

First, these authors examined individuals whose chronicity and severity would previously have, at best, resulted only in a compensatory approach to physical therapy intervention. At worst, the chronicity and severity of impairment in these individuals may have eliminated them from qualifying for rehabilitation at all. Fritz et al8 challenge conventional wisdom as 3 of the 4 participants in this case study series were greater than 10 years after neurologic incident. The improvement made by these individuals with chronic conditions suggests that the potential for recovery may exist over an individual's lifetime if they are able to obtain access to intensive training and repetitive task practice.

Second, in this feasibility study, the authors adopted a strategy of intensive delivery of physical therapy services designed to challenge impaired systems in individuals with varied diagnoses. A traditional approach to physical therapy intervention (ie, teaching compensation for motor deficits) stems from the assumption that in the case of acquired or degenerative processes such as those in chronic stroke, there is no potential for neurological recovery. In addition, the frequency and duration of therapeutic intervention in traditional delivery of care is dictated by third-party reimbursement constraints, not by principles derived from the fields of neuroplasticity or motor learning, or even exercise physiology for that matter.

The limitations of the more traditional, compensation-focused intervention models have been challenged by the demonstration of experience-dependent recovery, neurorestoration, and neuroprotection associated with intensive physical training in both animal and human studies of Parkinson's disease911 as well as demonstration of neuroplastic changes in studies of chronic stroke.12,13 In their article, Fritz et al8 attempt to illustrate the external validity of these research findings. While this case series the inherent limitations of a case series, it points to the need for more controlled and rigorous examination of alternative models for delivery of care.

Research during the Decade of the Brain and beyond has brought individuals with neuropathology the hope that restoration of function, in parallel with brain recovery, is possible. Furthermore, this research has guided therapists with respect to how to evoke neuroplastic changes through manipulation of practice parameters. A frustration for both individuals with neuropathology and therapists alike is that “practice” in a research study is not the same as that in a rehabilitation setting. In a research study, squirrel monkeys may practice retrieving food pellets from a small well 9600 times over 4 weeks;14 human subjects participating in a research study will complete 31,500 repetitions of a finger sequence task over 35 days.15 The time constraints that currently exist in rehabilitation practice are not optimal for achieving the full impact of repetitive task practice on motor recovery and neuroplasticity. The length of inpatient stays have grown shorter and shorter, and limitations on outpatient rehabilitation result in more time spent teaching compensatory techniques that may not promote brain and behavioral recovery. The feasibility study conducted by Fritz et al,8 is demonstration of a safe, well-tolerated application of intensive intervention. While neuroplasticity was not specifically measured, this study represents an important first step in managing the opposing challenges of the knowledge we have of greater potential for recovery in our patients and less time to deliver therapeutic services that could help our patients access that potential.

Back to Top | Article Outline

REFERENCES

1. Kleim JA, Jones TA. Principles of experience-dependent neural plasticity: implications for rehabilitation after brain damage. J Speech Lang Hear Res. 2008;51(1):S225–S239.

2. Butefisch CM, Davis BC, Wise SP, et al. Mechanisms of use-dependent plasticity in the human motor cortex. Proc Natl Acad Sci U S A. 2000;97(7):3661–3665.

3. De Leon RD, Hodgson JA, Roy RR, Edgerton VR. Full weight-bearing hindlimb standing following stand training in the adult spinal cat. J Neurophysiol. 1998;80(1):83–91.
4. Dobkin BH, Firestine A, West M, Saremi K, Woods R. Ankle dorsiflexion as an fMRI paradigm to assay motor control for walking during rehabilitation. Neuroimage. 2004;23(1):370–381.

5. Fisher BE, Sullivan KJ. Activity-dependent factors affecting poststroke functional outcomes. Top Stroke Rehabil. 2001;8(3):31–44.

6. Nudo RJ, Plautz EJ, Frost SB. Role of adaptive plasticity in recovery of function after damage to motor cortex. Muscle Nerve. 2001;24(8):1000–1019.

7. Weiller C, Rijntjes M. Learning, plasticity, and recovery in the central nervous system. Exp Brain Res. 1999;128(1–2):134–138.

8. Fritz S, Merlo-Rains A, Rivers E, et al. Feasibility of intensive mobility training as an intervention for improving gait, balance, and mobility in persons with chronic neurological conditions: a case series. J Neurol Phys Ther. 35(3):141–147.

9. Fisher BE, Petzinger GM, Nixon K, et al. Exercise-induced behavioral recovery and neuroplasticity in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-lesioned mouse basal ganglia. J Neurosci Res. 2004;77(3):378–390.

10. Tillerson JL, Cohen AD, Caudle WM, Zigmond MJ, Schallert T, Miller GW. Forced nonuse in unilateral parkinsonian rats exacerbates injury. J Neurosci. 2002;22(15):6790–6799.

11. Vucckovic MG, Li Q, Fisher B, et al. Exercise elevates dopamine D2 receptor in a mouse model of Parkinson's disease: in vivo imaging with [(1)F]fallypride. Mov Disord. 2010;25(16):2777–2784.

12. Boyd LA, Vidoni ED, Wessel BD. Motor learning after stroke: is skill acquisition a prerequisite for contralesional neuroplastic change? Neurosci Lett. 2010;482(1):21–25.

13. Koganemaru S, Mima T, Thabit MN, et al. Recovery of upper-limb function due to enhanced use-dependent plasticity in chronic stroke patients. Brain. 2010;133(11):3373–3384.

14. Nudo RJ, Wise BM, SiFuentes F, Milliken GW. Neural substrates for the effects of rehabilitative training on motor recovery after ischemic infarct. Science. 1996;272(5269):1791–1794.

15. Karni A, Meyer G, Jezzard P, Adams MM, Turner R, Ungerleider LG. Functional MRI evidence for adult motor cortex plasticity during motor skill learning. Nature. 1995;377(6545):155–158.

© 2011 Neurology Section, APTA

Login

Article Tools

Share

Follow JNPT on Twitter