Impaired motor learning and diffuse axonal damage in motor and visual systems of the rat following traumatic brain injury

被引:53
作者
Ding, YC
Yao, B
Lai, Q
McAllister, JP
机构
[1] Wayne State Univ, Sch Med, Dept Neurol Surg, Detroit, MI 48201 USA
[2] Wayne State Univ, Sch Med, Dept Anat & Cell Biol, Detroit, MI 48201 USA
[3] Wayne State Univ, Sch Educ, Div Hlth Phys Educ & Recreat, Detroit, MI USA
关键词
motor learning; traumatic brain injury; axon degeneration; motor system; visual pathway;
D O I
10.1179/016164101101198334
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Cognitive-motor functioning or motor skill learning is impaired in humans following traumatic brain injury. A more complete understanding of the mechanisms involved in disorders of motor skill learning is essential for any effective rehabilitation. The specific goals of this study were to examine motor learning disorders, and their relationship to pathological changes in adult rats with mild to moderate closed head injury. Motor learning deficits were determined by comparing the ability to complete a series of complex motor learning tasks with simple motor activity. The extent of neuronal damage was determined using silver impregnation. At all post-injury time points (day 7 to day 14) statistically significant deficits were observed in parallel bar traversing, foot placing, ladder climbing, and rope climbing. Performance improved with time, but never reached control levels. In contrast, no deficits were found in simple motor activity skills tested with beam balance and runway traverse. Histologically, axonal degeneration was widely distributed in several brain areas that relate to motor learning, including the while matter of sensorimotor cortex, corpus callosum, striatum, thalamus and cerebellum. Additionally, severely damaged axons were observed in the primary visual pathway, including the optic chiasm, optic tract, lateral geniculate nuclei, and superior colliculus. These findings suggest that motor learning deficits could be detected in mild or moderate brain injury, and this deficit could be attributed to a diffuse axonal injury distributed both in the motor and the visual systems.
引用
收藏
页码:193 / 202
页数:10
相关论文
共 69 条
[1]  
Adams J H, 1983, Acta Neurochir Suppl (Wien), V32, P15
[2]   DIFFUSE AXONAL INJURY IN HEAD-INJURY - DEFINITION, DIAGNOSIS AND GRADING [J].
ADAMS, JH ;
DOYLE, D ;
FORD, I ;
GENNARELLI, TA ;
GRAHAM, DI ;
MCLELLAN, DR .
HISTOPATHOLOGY, 1989, 15 (01) :49-59
[3]   ASSOCIATION BETWEEN PATIENT REPORT OF SYMPTOMS AFTER MILD HEAD-INJURY AND NEUROBEHAVIORAL PERFORMANCE [J].
ARCIA, E ;
GUALTIERI, CT .
BRAIN INJURY, 1993, 7 (06) :481-489
[4]   NEUROBEHAVIORAL PERFORMANCE OF ADULTS WITH CLOSED-HEAD INJURY, ADULTS WITH ATTENTION-DEFICIT, AND CONTROLS [J].
ARCIA, E ;
GUALTIERI, CT .
BRAIN INJURY, 1994, 8 (05) :395-404
[5]  
Asanuma H, 1997, NEUROREPORT, V8, pR1
[6]   FUNCTIONAL SUBDIVISIONS OF THE RAT SOMATIC SENSORIMOTOR CORTEX [J].
BARTH, TM ;
JONES, TA ;
SCHALLERT, T .
BEHAVIOURAL BRAIN RESEARCH, 1990, 39 (01) :73-95
[7]   The impact-acceleration model of head injury: Injury severity predicts motor and cognitive performance after trauma [J].
Beaumont, A ;
Marmarou, A ;
Czigner, A ;
Yamamoto, M ;
Demetriadou, K ;
Shirotani, T ;
Marmarou, C ;
Dunbar, J .
NEUROLOGICAL RESEARCH, 1999, 21 (08) :742-754
[8]   HU-211, A NOVEL NONCOMPETITIVE N-METHYL-D-ASPARTATE ANTAGONIST, IMPROVES NEUROLOGICAL DEFICIT AND REDUCES INFARCT VOLUME AFTER REVERSIBLE FOCAL CEREBRAL-ISCHEMIA IN THE RAT [J].
BELAYEV, L ;
BUSTO, R ;
ZHAO, WZ ;
GINSBERG, MD .
STROKE, 1995, 26 (12) :2313-2319
[9]   LEARNING CAUSES SYNAPTOGENESIS, WHEREAS MOTOR-ACTIVITY CAUSES ANGIOGENESIS, IN CEREBELLAR CORTEX OF ADULT-RATS [J].
BLACK, JE ;
ISAACS, KR ;
ANDERSON, BJ ;
ALCANTARA, AA ;
GREENOUGH, WT .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1990, 87 (14) :5568-5572
[10]   Current status of neuroprotection trials for traumatic brain injury: Lessons from animal models and clinical studies [J].
Bullock, MR ;
Lyeth, BG ;
Muizelaar, IP .
NEUROSURGERY, 1999, 45 (02) :207-217