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The Control of Movement Following Traumatic Brain Injury

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Abstract

Traumatic brain injury (TBI) results in a variety of impairments in cognition, mood, sensation, and movement, depending upon the location and severity of injury. Although not as extensively studied as cognitive impairments, motor impairments are common, especially in moderately to severely injured patients. The recovery of these deficits is not usually complete; however, extensive effort is put into the rehabilitation of motor skills to enhance independence and quality of life. Understanding the motor recovery process and how it can be influenced by rehabilitation has been extensively studied in animal models of stroke and focal lesions, albeit to a lesser extent following animal models of TBI. Injury‐induced neural plasticity is intricately involved in motor recovery and influenced by behavioral compensation and rehabilitation following stroke and focal lesions. New studies in animal models of TBI indicate that neural plasticity and the processes of motor recovery and rehabilitation following brain injury may not mirror those processes shown to occur following stroke. Further examination of motor recovery, rehabilitation, and plasticity in animal models of TBI as well as in individuals with TBI will be necessary to fully understand the control of movement following brain injury. © 2013 American Physiological Society. Compr Physiol 3:121‐139, 2013.

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Figure 1. Figure 1.

Basic overview of the organization of the motor system [with permission from reference (123)].

Figure 2. Figure 2.

Animal models of TBI. Fluid percussion injury (left) and controlled cortical impact (right).

Figure 3. Figure 3.

(Top) Amputation of digit 3 in the owl monkey resulted in a loss of the motor representation for the digit and an expansion of the representations for adjacent digits 2 and 4. (Bottom) Training of digit 3 on a sensorimotor task results in expansion of its representation in motor cortex. [Figure taken, with permission, from reference (123)].

Figure 4. Figure 4.

(Top) Demonstration of the location of electrolytic lesions, ischemic infarcts, and TBIs of the forelimb sensorimotor cortex (FL‐SMC) and the resulting forelimb impairments. (Bottom) Electrolytic lesions to FL‐SMC result in time‐dependent changes in astrocytes, dendritic arborization, and synapses. [Reproduced, with permission, from reference (68)].

Figure 5. Figure 5.

Exaggeration of Injury in electrolytic lesions [top, taken, with permission, from reference (83)] and following fluid percussion injury (bottom). Following electrolytic lesions, forelimb immobilization for the first week postlesion results in an exaggeration of the injury size (E) compared to injured animals without immobilization (A) and an inhibition of behavioral recovery (greater unsuccessful forelimb placing). Following fluid percussion injury, an area of cell loss occurs in the forelimb sensorimotor cortex in animals forced to use the impained forelimb. This cell loss corresponds to an area of enhanced glucose metabolism (right) seen in animals forced to use the impaired forelimb.

Figure 6. Figure 6.

Examples of techniques used for rehabilitation and motor skills training in the rodent. (A‐E = techniques used in motor skills training; F = alley used in yoked animals to control for activity, G = single pellet reaching training, H = forelimb immobilization). [Adapted, with permission, from reference (69)].

Figure 7. Figure 7.

Comparison of plasticity measures in stroke versus traumatic brain injury (TBI) (top). Whereas plasticity is increased in the contralateral cortex following stroke, it is decreased or not changed significantly following TBI. Dendritic arborization following a controlled cortical impact is decreased bilaterally at all time points postinjury (bottom A‐D). [Adapted, with permission, from reference (71)].



Figure 1.

Basic overview of the organization of the motor system [with permission from reference (123)].



Figure 2.

Animal models of TBI. Fluid percussion injury (left) and controlled cortical impact (right).



Figure 3.

(Top) Amputation of digit 3 in the owl monkey resulted in a loss of the motor representation for the digit and an expansion of the representations for adjacent digits 2 and 4. (Bottom) Training of digit 3 on a sensorimotor task results in expansion of its representation in motor cortex. [Figure taken, with permission, from reference (123)].



Figure 4.

(Top) Demonstration of the location of electrolytic lesions, ischemic infarcts, and TBIs of the forelimb sensorimotor cortex (FL‐SMC) and the resulting forelimb impairments. (Bottom) Electrolytic lesions to FL‐SMC result in time‐dependent changes in astrocytes, dendritic arborization, and synapses. [Reproduced, with permission, from reference (68)].



Figure 5.

Exaggeration of Injury in electrolytic lesions [top, taken, with permission, from reference (83)] and following fluid percussion injury (bottom). Following electrolytic lesions, forelimb immobilization for the first week postlesion results in an exaggeration of the injury size (E) compared to injured animals without immobilization (A) and an inhibition of behavioral recovery (greater unsuccessful forelimb placing). Following fluid percussion injury, an area of cell loss occurs in the forelimb sensorimotor cortex in animals forced to use the impained forelimb. This cell loss corresponds to an area of enhanced glucose metabolism (right) seen in animals forced to use the impaired forelimb.



Figure 6.

Examples of techniques used for rehabilitation and motor skills training in the rodent. (A‐E = techniques used in motor skills training; F = alley used in yoked animals to control for activity, G = single pellet reaching training, H = forelimb immobilization). [Adapted, with permission, from reference (69)].



Figure 7.

Comparison of plasticity measures in stroke versus traumatic brain injury (TBI) (top). Whereas plasticity is increased in the contralateral cortex following stroke, it is decreased or not changed significantly following TBI. Dendritic arborization following a controlled cortical impact is decreased bilaterally at all time points postinjury (bottom A‐D). [Adapted, with permission, from reference (71)].

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Dorothy A. Kozlowski, J. Leigh Leasure, Timothy Schallert. The Control of Movement Following Traumatic Brain Injury. Compr Physiol 2013, 3: 121-139. doi: 10.1002/cphy.c110005