2. The Motor Control System Learning Module Click to Begin

3. Main Menu OverviewOverview describes the module content & learning objectives Please complete this section first! ContentsContents overview of the Motor System under normal conditions and 3 interactive examples of lesion effects. Case-based practiceCase-based practice provides practice with feedback using patient cases. Exit

4. Overview Introduction Learning Objectives Overview Menu Overview Menu Main Menu Exit Main MenuExit

5. Introduction This module reviews the Motor Control System. Module organization consists of three components. Overview consists of this Introduction and the Learning Objectives. Contents consists of Navigation Instructions, a Legend, Review of the normal structure and function of the motor control system, and 3 interactive lesion lessons. Cases consists of Instructions and 2 interactive patient cases with feedback. At the bottom of each page a navigation bar contains options to move throughout the module. Material is presented at both the behavioral level and the neuroanatomical level. The behavioral level is presented first and depicts a patient’s clinical presentation. The neuroanatomical level depicts the detailed anatomy of first- order, second-order and third-order neurons. The neuroanatomical level accounts for the patient’s behavioral presentation on examination under normal and lesioned conditions. Overview Menu Overview Menu Main Menu Exit Main MenuExit

6. Learning Objectives After completing this module you should be able to: describe, in detail, the structure and function of the corticospinal tract. given a lesion, identify the signs and symptoms that would be expected. given a patient case (examination results and chief complaint), identify the location of the lesion causing the signs and symptoms. correlate neurology information between the behavioral and neuroanatomical levels. Overview Menu Overview Menu Main Menu Exit Main MenuExit

7. Contents Read these Instructions! Legend: symbols used throughout the module Overview of the Motor Control System Lesion lessons Corticospinal tract lesion Lateral corticospinal tract lesion Ventral horn lesion Main MenuExit

8. Instructions This module contains 3 interactive lesion lessons with animation. Lesson lessons begin with a question about the symptoms produced by that particular lesion. Clicking the answer button will reveal the answer to the question. Clicking the explanation button will lead to both behavioral and neuroanatomical explanations of the lesion. Each presentation is launched by clicking the animation button. The same button serves to replay the animation if desired. Any of the lessons may be accessed by simply clicking on the lesion title on the Contents page. Please refer to the Legend that defines the symbols used throughout the module. Main MenuContent MenuMain MenuContent Menu ExitExit

9. Legend Upper motor neuron Lower motor neuron Mechanism of injury Lesion Motor impairment Function intact Function lost Stimulus Main MenuContent MenuMain MenuContent Menu ExitExit

10. Voluntary Knee Extension: Behavioral Description Voluntary movement is controlled by a system of brain and spinal motor centers linked by neuronal pathways. The primary motor pathway (Corticospinal tract) is crossed such that the left hemisphere controls movement of the right half of the body and vise versa. Motor pathways consist of upper and lower motor neurons. Upper motor neurons originate in the precentral gyrus, decussate in the medulla, descend in the lateral column of the spinal cord, and terminate on lower motor neurons in the ventral horn. Lower motor neurons exit the CNS and innervate skeletal muscles via the peripheral nervous system. Click to animate Main MenuContent MenuLegendMain MenuContent MenuLegend ExitExit Neuroanatomical Explanation Stimulus UMN LMN

11. Voluntary Knee Extension: Neuroanatomical Description The cell body of the upper motor neuron is located in he precentral gyrus (somatotopically organized). The axon descends through the internal capsule, decussates in the medulla, descends through the lateral column of the spinal cord and terminates in the ventral horn. The cell body of the lower motor neuron is located in the ventral horn. The axon exits the CNS via ventral rootlets of spinal nerves and innervates skeletal muscle via a peripheral nerve. Skeletal muscles contract to produce the force to extend the knee. Main MenuContent MenuLegendMain MenuContent MenuLegend ExitExit Behavioral Explanation Stimulus UMN LMN

12. The cell body of the upper motor neuron is located in he precentral gyrus (somatotopically organized). The axon descends through the internal capsule, decussates in the medulla, descends through the lateral column of the spinal cord and terminates in the ventral horn. The cell body of the lower motor neuron is located in the ventral horn. The axon exits the CNS via spinal nerves and innervates skeletal muscle via a peripheral nerve. Skeletal muscles contract to produce the force to extend the knee. Voluntary Knee Extension: Neuroanatomical Description Main MenuContent MenuLegendMain MenuContent MenuLegend ExitExit Behavioral Explanation Stimulus UMN LMN

13. Lesion of the left corticospinal tract (at the level of the cortex) produces what impairment? Click for answer Cortical damage to the left corticospinal tract causes upper motor neuron signs on the right face and body (arm, leg, and trunk, contralateral). Stroke is the most common cause of supraspinal damage to the corticospinal tract. Click for explanation Main MenuContent MenuLegendMain MenuContent MenuLegend ExitExit

14. Corticospinal Tract Lesion: Behavioral Explanation Damage to the corticospinal tract, prior to the decussation, produces UMN signs and symptoms to the contralateral face and body. Click to animate Neuroanatomical Explanation Main MenuContent MenuLegendMain MenuContent MenuLegend ExitExit Lesion UMN LMN Lost function Impairment UMN signs: Weakness (Spastic paralysis) Hyperreflexia (+ Babinski, clonus) Hypertonia

15. Impairment is seen in the contralateral face because CN VII is crossed and the contralateral body because the UMN decussated in the medulla. Corticospinal Tract Lesion: Neuroanatomical Explanation Impairment is generalized to all body parts below the lesion level because the lateral corticospinal tract is an efferent pathway. Click to animate Behavioral Explanation Main MenuContent MenuLegendMain MenuContent MenuLegend ExitExit Lesion UMN LMN Lost function Impairment

16. Lesion of the right lateral corticospinal tract produces what impairment? Click for answer Damage to the right lateral corticospinal tract causes UMN signs and symptoms in the right (ipsilateral) side of the body, generalized below the lesion level. Impairment is ipsilateral because the pathway decussated in the medulla. Impairment is generalized below the lesion level because it is an efferent pathway. The lateral corticospinal tract exists only at the level of the spinal cord. Click for explanation Main MenuContent MenuLegendMain MenuContent MenuLegend ExitExit

17. Lateral Corticospinal Tract Lesion: Behavioral Explanation Damage to the lateral corticospinal tract, after to the decussation, produces ipsilateral UMN signs and symptoms, generalized below the lesion level. Click to animate Main MenuContent MenuLegendMain MenuContent MenuLegend ExitExit Neuroanatomical Explanation Lesion UMN LMN Lost function Impairment

18. Lateral Corticospinal Tract Lesion: Neuroanatomical Explanation Because the lesion involves UMNs that have already decussated, impairment is ipsilateral to the lesion. Impairment is generalized to all body parts below the lesion level because the lateral corticospinal tract is an efferent pathway. Click to animate Main MenuContent MenuLegendMain MenuContent MenuLegend ExitExit Behavioral Explanation Lesion UMN LMN Lost function Impairment

19. Lesion of the right ventral horn at L2-4 produces what impairment? Click for answer Lesion of the right ventral horn at L2-4 produces LMN signs (weakness and atrophy) of the right hip flexion, adduction, and knee extension muscles. Lesion of the ventral horn will damage the cell bodies of LMNs. L2-4 is the origin of femoral and obturator nerves which innervate the muscles of hip flexion, adduction, and knee extension. Because LMNs are uncrossed the impairment will be seen ipsilateral to the lesion. Click for explanation Main MenuContent MenuLegendMain MenuContent MenuLegend ExitExit

20. Ventral Horn Lesion: Behavioral Explanation Click to animate Damage to the ventral horn produces ipsilateral LMN signs and symptoms, in a myotomal distribution. LMN signs: Weakness (Flaccid paralysis) Hyporeflexia Hypotonia Atrophy Fasciculations Main MenuContent MenuLegendMain MenuContent MenuLegend ExitExit Neuroanatomical Explanation Lesion UMN LMN Lost function Impairment

21. Damage to the ventral horn (cell body of LMNs) produces ipsilateral LMN signs and symptoms, in a myotomal distribution. Signs are ipsilateral because LMNs project to skeletal muscles via spinal and peripheral nerves that remain uncrossed. The distribution is myotomal because skeletal muscles are innervated by peripheral nerves that originate from selected levels of the spinal cord. Ventral Horn Lesion: Neuroanatomical Explanation Click to animate Main MenuContent MenuLegendMain MenuContent MenuLegend ExitExit Behavioral Explanation Lesion UMN LMN Lost function Impairment

22. Case-based Practice Read these instructions! Patient Case #1 Patient Case #2 Main MenuExit

23. Case Instructions These patient cases are intended to facilitate the integration and clinical application of information about the Motor Control System by coupling the findings on examination and patient interview with their neuroanatomical correlates. Cases are presented from two perspectives. What lesion would account for a given set of examination results and patient history? For a given lesion, what signs and symptoms would be expected on examination? Click on a Case number to begin the exercise. Main MenuMain Menu Case Menu ExitCase MenuExit

24. Review Questions: Case 1 In the emergency room the patient’s wife reports her husband had a sudden onset slurring of speech, inability to stand from a chair because of the inability to accept body weight onto his right leg, and the inability to feed himself or drink with his right hand. On examination the right side of his face was hypotonic, he was drooling from the drooping right corner of his mouth, and he had lost the nasal labial fold on the right. Damage to what system(s) is causing this patient’s problems? Lesion of the left corticospinal tract above the level of the brainstem. Lesion of the left corticospinal tract, prior to the decussation (corticobulbar tract): removed cortical input to cranial nerves serving the face which are crossed (hypotonia and drooping of right face with drooling). Lesion of the left corticospinal tract, after the decussation: removal of cortical input to cervical (inability to feed himself or drink with his right hand) and lumbar regions of the cord (inability to stand from a chair because of the inability to accept body weight onto his right leg). Pathophysiology: stroke involving the perfusion territory of the left middle cerebral artery (primary motor and sensory cortical areas). Answer Show lesion Main MenuMain Menu Case Menu ExitCase MenuExit

25. Corticospinal Tract Lesion: Behavioral Explanation Damage to the corticospinal tract, prior to the decussation, produces UMN signs and symptoms to the contralateral face and contralateral body. UMN signs: Weakness (Spastic paralysis) Hyperreflexia (+ Babinski, clonus) Hypertonia Click to animate Main MenuMain Menu Case Menu ExitCase MenuExit Lesion UMN LMN Lost function Impairment Neuroanatomical Explanation

26. Impairment is seen in the contralateral face because the cranial nerves serving the face are crossed. Impairment is seen in the contralateral body because the UMN decussated in the medulla. Corticospinal Tract Lesion: Neuroanatomical Explanation Impairment is generalized to all body parts below the lesion level because the lateral corticospinal tract is an efferent pathway. Click to animate Main MenuMain Menu Case Menu ExitCase MenuExit Lesion UMN LMN Lost function Impairment

27. Review Questions: Case 2 Imaging report: The CT image reveals a mass producing impingement of the lateral region of the right lateral column of the spinal cord at L1. What signs and symptoms would be expected from this lesion? A mass impinging the right lateral column at L1 would affect the lateral corticospinal tract. The size of the mass will determine the extent of damage. The lesion will produce UMN signs in the right leg from L1 down involving all leg muscles from the hip flexors down. If the lesion is complete, there will be paralysis. If the lesion is incomplete there will be paresis. In addition to weakness (paralysis or paresis), there will be hyperreflexia and hypertonia. Answer Show lesion Main MenuMain Menu Case Menu ExitCase MenuExit

28. R L UMN Lateral corticospinal tract lesion Ipsilateral upper motor neurons signs generalized below the lesion level UMN signs Weakness (Spastic paralysis) Hyperreflexia (+ Babinski, clonus) Hypertonia Right Lateral Corticospinal Tract Lesion L2-4 Common causes include penetrating injuries, lateral compression from tumors, and MS. Click to animate Main MenuMain Menu Case Menu ExitCase MenuExit

29. The End D. Michael McKeough, PT, EdD  2008