2. PhD MD MBBS Faculty of Medicine Al Maarefa Colleges of Science & Technology Faculty of Medicine Al Maarefa Colleges of Science & Technology Lecture – 6: Motor System - 2 Nervous System Physiology By Dr. SHAHAB SHAIKH PhD MD MBBS Faculty of Medicine Al Maarefa Colleges of Science & Technology Faculty of Medicine Al Maarefa Colleges of Science & Technology

3. EXTRA PYRAMIDAL SYSTEM The basal ganglia, brain stem, and cerebellum all receive strong motor signals from the Pyramidal system every time a signal is transmitted down the spinal cord to cause a motor activity. The term extrapyramidal motor system is used to denote all those portions of the brain and brain stem that contribute to motor control but are not part of the direct corticospinal pyramidal system. These include pathways through the basal ganglia, the reticular formation of the brain stem, the vestibular nuclei, and the red nuclei. 2

4. COMPONENTS OF EXTRAPYRAMIDAL SYSTEM BRAINSTEM giving rise to following tracts: oRubrospinal tract oVestibulospinal tract oReticulospinal tract oTectospinal tract 3

5. RUBROSPINAL TRACT only func Origin – Red nucleus in mid brain Input - Red nucleus gets input from both cerebellum and cerebral cortical motor areas Output - Via Rubrospinal tract is directed to contralateral spinal motor neurons ( crosses to opposite side at the level of nucleus and axons are located in lateral spinal white matter anterior to Corticospinal tract. Functions - Involved in movements of distal limbs (hand & feet) also regulates tone and posture. It is excitatory to flexors and inhibitory to extensor muscles. Correction of movement mainly inhibitory **** Damage= hypertonia, over excitation 4

6. VESTIBULOSPINAL TRACT, don’t cross Location - Vestibular nuclei located in Pons & Medulla Input - receive input from Vestibular apparatus in the inner ear and Cerebellum Output – Mainly From Lateral vestibular nuclei to spinal cord in Vestibulospinal tract. It remains ipsilateral. Function - Excitatory to ipsilateral extensor. Inhibitory to flexor muscles Regulates muscle tone for maintaining balance in response to head movement 5

7. RETICULOSPINAL TRACT Location - Reticular formation in the central grey matter of brain stem Input - Afferent input to reticular formation comes from spinal cord, vestibular nuclei, cerebellum, Sensory motor cortex, globus pallidus & Lat. Hypothalamus Output - Descending tract arise from nuclei in pons and medulla 1]Pons – Pontine Reticulospinal tract runs ipsilaterally; Function - Excitatory to Axial extensor muscles 2]Medulla – Medullary reticulospinal tract runs ipsilaterally (some cross also) Function - Inhibitory to axial extensor Muscle 6

8. TECTOSPINAL TRACT Origin – originates in superior colliculus in midbrain Input – from visual stimuli Output - Conveys nerve impulses from superior colliculus (midbrain) to contralateral skeletal muscles that move the head and eyes in response to visual stimuli Function – Involved in control of neck muscle in response to visual stimuli Axial ms postural and balance 7

9. EXTRA PYRAMIDAL TRACT 8 These tracts terminate on interneurons usually. Occasionally they terminate directly on anterior horn motor neurons

10. FUNCTIONS OF EXTRA PYRAMIDAL SYSTEM REGULATION OF BODY POSTURE, INVOLVING INVOLUNTARY MOVEMENTS OF LARGE MUSCLE GROUPS OF TRUNK AND LIMBS REGULATION OF VOLUNTARY MOVEMENT REGULATION OF TONE 9

11. APPLIED Of the Extra pyramidal tracts, some are excitatory and other have inhibitory influence on muscle tone but overall there is strong inhibitory effect over Gamma Motor Neuron in anterior horn cell. Therefore in UMN lesions, this inhibitory effect is lost resulting in Hypertonia. 10

12. Difference between Pyramidal and Extrapyramidal tracts PYRAMIDAL TRACTS 1.-Lateral corticospinal -Ant. or ventral corticospinal - Corticobulbar 2.Cell bodies that contribute to pyramidal tracts are located in precentral gyrus ( Primary, Premotor and supplimentary motor cortex) and somatosensory area. 3.Pyramidal tract descend directly without synaptic interruption from cerebral motor cortex to spinal cord ( on interneuron and ant. Horn cells) 11 EXTRA PYRAMIDAL TRACTS 1.-Rubrospinal -Vestibulospinal -Reticulospinal -Tectospinal 2.They originate in Midbrain and brainstem nuclei and have influence of cerbral cortex, basal ganglia and cerebellum which can stimulate or inhibit these nuclei 3.No direct control of motor cortex or basal ganglia on spinal cord but via nuclei in midbrain and brainstem Didn’t focus but said know them

13. Difference between Pyramidal and Extrapyramidal Tract PYRAMIDAL TRACTS 4.80 % of Corticospinal tracts (lateral) cross in medulla 20 % of corticospinal tract (ventral) cross in spinal cord Because of crossing cerebral cortex controls opposite side of the body 5.Function: - Lat. Corticospinal tract – fine movement of fingers eg. Writing, needle work - Ventral corticospinal tract – Axial or Postural Movement 12 EXTRA PYRAMIDAL TRACTS Major extra pyramidal tracts, some cross and others are uncrossed Function: Control of body posture involving involuntary movements of axial and Proximal limb muscle

14. 13 Motor System It is two neuron system 1- Upper motor neuron – From motor cortex to anterior horn cell of spinal cord 2- Lower motor neuron – Starts from anterior horn cell and ends on muscle e.g. all peripheral nerves

15. MOTOR NEURON LESIONS 14

16. UMN lesion causes: loss inhibitory oIncreased tone (Spasticity) oIncreased reflexes oClonus: Repetitive contraction and relaxation of muscle in oscillating fashion every second or so oBabinski sign: oNote: below one year of age Babinski reflex is normally present 15

17. LMN lesion causes: total paralysis oDecreased tone (Hypotonia / Flaccidity). oDecreased power of the muscles. oDecreased reflexes. oWasting of muscles. Ms not use so ms waste 16

18. DIFFERENCE BETWEEN UPPER & LOWER MOTOR NEURON LESION UMN LESION Paralysis affect movement rather than muscles Muscle wasting is only from disuse, therefore slight. Occasionally marked in chronic severe lesions. Spasticity of clasp-knife’ type. Muscles hypertonic. LMN LESION Individual muscle or group of muscles are affected. Wasting pronounced. Flaccidity. Muscles hypotonic. 17

19. UMN LESION UMN LESION Tendon reflexes increased. Clonus often present. Superficial reflexes diminished or modified. Abdominal reflex absent. Babinski’s sign +ve, --Increased jaw jerk. LMN LESION Tendon reflexes diminished or absent. Superficial reflexes often unaltered. 18

20. COMMON TERMINOLOGIES IN CLINICAL NEUROLOGY HEMIPLEGIA – –Paralysis (loss of power) of half side of the body HEMIPARESIS – –Partial loss of power of half side of the body PARAPLEGIA – lwr half of body –Paralysis in both legs PARAPARESIS – 4 limbs, above brachial plesxus –Partial loss of power in both legs QUADRIPEGIA – –Paralysis in all four limbs MONOPLEGIA – –Paralysis in one limb 19

21. PhD MD MBBS Faculty of Medicine Al Maarefa Colleges of Science & Technology Faculty of Medicine Al Maarefa Colleges of Science & Technology Sensory & Motor System Lesions Nervous System Physiology By Dr. SHAHAB SHAIKH PhD MD MBBS Faculty of Medicine Al Maarefa Colleges of Science & Technology Faculty of Medicine Al Maarefa Colleges of Science & Technology

22. What is the impairment caused by Lesion of the right dorsal column at L1? Click for answer Damage to the right dorsal column at L1 causes the absence of light touch, vibration, and position sensation in the right leg. Only fasciculus gracilis exists below T6. Click for explanation RL 21

23. Right Dorsal Column Lesion Dorsal column lesion Ipsilateral loss of light touch, vibration, and position sense generalized below the lesion level Below T6 only the fasciculus gracilis is present. RL DRG L1 Common causes include MS, penetrating injuries, and compression from tumors. Click to animate 22

24. Click for answer Damage to the right lateral spinothalamic tract at L1 causes the absence of pain and temperature sensation in the left leg. Click for explanation what impairment Lesion of the right lateral Spinothalamic tract at L1 produces? R L 23

25. R L DRG Lateral spinothalamic tract lesion Contralateral loss of pain and temperature sense Right Lateral Spinothalamic Tract Lesion L1 Common causes include MS, penetrating injuries, and compression from tumors. Click to animate 24

26. what impairment Lesion of the right lateral Corticospinal tract at L1 produces? Click for answer Damage to the right lateral corticospinal tract at L1 causes upper motor neurons signs (weakness or paralysis, hyperreflexia, and hypertonia) in the right leg. Click for explanation RL 25

27. 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 L1 Common causes include penetrating injuries, lateral compression from tumors, and MS. Click to animate 26

28. Click for answer Damage to the right dorsal columns at L1 causes the absence of light touch, vibration, and position sense in the right leg. Damage to the lateral corticospinal tract causes upper motor neuron signs in the right leg (Monoplegia), and damage to the lateral spinothalamic tract causes the absence of pain and temperature sensation in the left leg. Click for explanation Complete transection of the right half the spinal cord (Hemicord or Brown-Sequard syndrome) at L1 produces what impairments? RL 27

29. RL Hemicord Lesion (Brown-Sequard Syndrome) Dorsal column lesion Ipsilateral loss of light touch, vibration, and position sense Lateral corticospinal tract lesion Ipsilateral upper motor neurons signs Lateral spinothalamic tract lesion Contralateral loss of pain and temperature sense Hemicord lesion Build the lesion L1 Common causes include penetrating injuries, lateral compression from tumors, and MS. Click to animate 28

30. Hemicord Lesion (Brown-Sequard Syndrome) Dorsal column lesion Ipsilateral loss of light touch, vibration, and position sense Lateral corticospinal tract lesion Ipsilateral upper motor neurons signs Lateral spinothalamic tract lesion Contralateral loss of pain and temperature sense UMN Hemicord lesion RL DRG L1 Click to animate 29