1. Lecture by DR SHAIK ABDUL RAHIM

2.  Movements of our body are accomplished by contraction of the skeletal muscles  Flexion: contraction of a flexor muscle draws in a limb  Extension: contraction of extensor muscle  Skeletal muscle fibers have a striated appearance  Skeletal muscle is composed of two fiber types:  Extrafusal: innervated by alpha-motoneurons from the spinal cord: exert force  Intrafusal: sensory fibers that detect stretch of the muscle  Afferent fibers: report length of intrafusal: when stretched, the fibers stimulate the alpha-neuron that innervates the muscle fiber: maintains muscle tone  Efferent fibers: contraction adjusts sensitivity of afferent fibers. 8.2

3. 8.3  Each muscle fiber consists of a bundle of myofibrils  Each myofibril is made up of overlapping strands of actin and myosin  During a muscle twitch, the myosin filaments move relative to the actin filaments, thereby shortening the muscle fiber

4.  The neuromuscular junction is the synapse formed between an alpha motor neuron axon and a muscle fiber  Each axon can form synapses with several muscle fibers (forming a motor unit)  The precision of muscle control is related to motor unit size  Small: precise movements of the hand  Large: movements of the leg  ACh is the neuromuscular junction neurotransmitter  Release of ACh produces a large endplate potential  Voltage changes open CA ++ channels  CA ++ entry triggers myosin-actin interaction (rowing action)  Movement of myosin bridges shortens muscle fiber 8.4

5.  Smooth muscle is controlled by the autonomic nervous system  Multiunit smooth muscle is normally inactive  Located in large arteries, around hair and in the eye  Responds to neural or hormonal stimulation  Single-unit smooth muscle exhibits rhythmic contraction  Muscle fibers produce spontaneous pacemaker potentials that elicit action potentials in adjacent smooth muscle fibers  Single-unit muscle is found in gastrointestinal tract, uterus, small blood vessels  Cardiac muscle fibers resemble striated muscle in appearance, but exhibit rhythmic contractions like that of single-unit smooth muscle 8.5

6.  Striated muscle contraction is governed by sensory feedback  Intrafusal fibers are in parallel with extrafusal fibers  Intrafusal receptors fire when the extrafusal muscle fibers lengthen (load on muscle)  Intrafusal fibers activate agonist muscle fibers and inhibit antagonist muscle fibers  Extrafusal contraction eliminates intrafusal firing  Golgi tendon organ (GTO) receptors are located within tendons  Sense degree of stretch on muscle  GTO activation inhibits the agonist muscle (via release of glycine onto alpha-motoneuron  GTO receptors function to prevent over-contraction of striated muscle 8.6

7.  Spinal cord is organized into dorsal and ventral aspects  Dorsal horn receives incoming sensory information  Ventral horn issues efferent fibers (alpha- motoneurons) that innervate extrafusal fibers 8.7 Fig 3.23

8.  Monosynaptic reflexes involve a single synapse between a sensory fiber from a muscle and an alpha-motor neuron  Sensory fiber activation quickly activates the alpha motor neuron which contracts muscle fibers  Patellar reflex  Monosynaptic stretch stretch (posture)  Polysynaptic reflexes involve multiple synapses between sensory axons, interneurons, and motor neurons  Axons from the afferent muscle spindles can synapse onto  Alpha motoneuron connected to the agonist muscle  An inhibitory interneuron connected to the antagonist muscle  Signals from the muscle spindle activate the agonist and inhibit the antagonist muscle 8.8

9. 8.9

10.  Multiple motor systems control body movements  Walking, talking, postural, arm and finger movements  Primary motor cortex is located on the precentral gyrus  Motor cortex is somatotopically organized (motor homunculus)  Motor cortex receives input from  Premotor cortex  Supplemental motor area  Frontal association cortex  Primary somatosensory cortex  Planning of movements involves the premotor cortex and the supplemental motor area which influence the primary motor cortex 8.10

11. 8.11

12. 8.12

13.  Axons from primary motor cortex descend to the spinal cord via two groups  Lateral group: controls independent limb movements  Corticospinal tract: hand/finger movements  Corticobulbar tract: movements of face, neck, tongue, eye  Rubrospinal tract: fore- and hind-limb muscles  Ventromedial group control gross limb movements  Vestibulospinal tract: control of posture  Tectospinal tract: coordinate eye and head/trunk movements  Reticulospinal tract: walking, sneezing, muscle tone  Ventral corticospinal tract: muscles of upper leg/trunk 8.13

14.  Neurons of the corticospinal tract terminate on motor neurons within the gray matter of the spinal cord  Corticospinal tract starts in layer 5 of primary motor cortex  Passes through the cerebral peduncles of the midbrain  Corticospinal neurons decussate (crossover ) in the medulla  80% become the lat. corticospinal tract  20% become the ventral corticospinal tract  Terminate onto internuncial neurons or alpha-motoneurons of ventral horn  Corticospinal tracts control fine movements  Destruction: loss of muscle strength, reduced dexterity of hands and fingers  No effect of corticospinal lesions on posture or use of limbs for reaching 8.14

15.  Apraxia refers to an inability to properly execute a learned skilled movement following brain damage  Limb apraxia involves movement of the wrong portion of a limb, incorrect movement of the correct limb part, or an incorrect sequence of movements  Callosal apraxia: person cannot perform movement of left hand to a verbal request (anterior callosum interruption prevents information from reaching right hemisphere)  Sympathetic apraxia: damage to anterior left hemisphere causes apraxia of the left arm (as well as paralysis of right arm and hand)  Left parietal apraxia: difficulty in initiating movements to verbal request  Constructional apraxia is caused by right parietal lobe damage  Person has difficulty with drawing pictures or assembling objects 8.15

16. The Basal Ganglia

17.  Basal ganglia consist of the caudate nucleus, the putamen and the globus pallidus  Input to the basal ganglia is from the primary motor cortex and the substantia nigra  Output of the basal ganglia is to  Primary motor cortex, supplemental motor area, premotor cortex  Brainstem motor nuclei (ventromedial pathways)  Cortical-basal ganglia loop  Frontal, parietal, temporal cortex send axons to caudate/putamen  Caudate/putamen projects to the globus pallidus  Globus pallidus projects back to motor cortex via thalamic nuclei 8.17

18. Caudate Nucleus C shaped structure (“tail”) Lateral wall of lateral ventricle Head, body and tail

19. All regions of cerebral cortex project to the basal ganglia, but output of basal ganglia is directed towards the frontal lobe, particularly pre-motor and supplementary motor cortex

20.  Parkinson’s disease (PD) involves muscle rigidity, resting tremor, slow movements  Parkinson’s results from damage to dopamine neurons within the nigrostriatal bundle (projects to caudate and putamen)  Slow movements and postural problems result from  Loss of excitatory input to the direct circuit (caudate-Gpi-VA/VL thalamus-motor cortex)  Loss of output from the indirect circuit (which is overall an excitatory circuit for motor behavior)  Neurological treatments for PD:  Transplants of dopamine-secreting neurons (fetal subtantia nigra cells or cells from the carotid body)  Stereotaxic lesions of the globus pallidus (internal division) alleviates some symptoms of Parkinson’s disease 8.20

21.  Huntington’s disease (HD) involves uncontrollable, jerky movements of the limbs  HD is caused by degeneration of the caudate nucleus and putamen  Cell loss involves GABA-secreting axons that innervate the external division of the globus pallidus (GPe)  The GPe cells increase their activity, which inhibits the activity of the subthalamic nucleus, which reduces the activity level of the GPi, resulting in excessive movements  HD is a hereditary disorder caused by a dominant gene on chromosome 4  This gene produces a faulty version of the protein huntingtin 8.21

22.  Cerebellum consists of two hemispheres with associated deep nuclei  Flocculonodular lobe is located at the caudal aspect of the cerebellum  This lobe has inputs and outputs to the vestibular system  Involved in control of posture  Vermis is located on the midline of the cerebellum  Receives auditory and visual information from the tectum and cutaneous information from the spinal cord  Vermis projects to the fastigial nucleus which in turn projects to the vestibular nucleus and to brainstem motor nuclei 8.22

23. Classification by Phylogenetic and Ontogenic Development Archicerebellum Archicerebellum Paleocerebllum Paleocerebllum Neocerebellum Neocerebellum Classification by Afferent Connection Vestibulocerebellum Vestibulocerebellum Spinocerebellum Spinocerebellum Pontocerebellum Pontocerebellum Classification by Efferent Connection Vermis Vermis Paravermal Region Paravermal Region Cerebellar Hemisphere Cerebellar Hemisphere Cerebellum Classifications Cerebellum Classifications

24. Spinocerebellum Pontocerebellum Vestibulocerebellum

25. Cerebellum – little brain  Two hemispheres with convoluted surfaces  Responsible for maintenance of equilibrium, muscle tone and posture.  It plays a key role in accomplishing a smooth and coordinated movements by means of its comparator function.  The cerebellum plays an important role in learning of motor skills.  Damage to the cerebellum generally results in jerky, erratic and uncoordinated movements

26. Cerebellum Function Cerebellum Function  Maintenance of Equilibrium - balance, posture, eye movement - balance, posture, eye movement  Coordination of half-automatic movement of walking and posture maintenace walking and posture maintenace - posture, gait - posture, gait  Adjustment of Muscle Tone  Motor Leaning – Motor Skills  Cognitive Function

27. Balance

28. Motor Skill Pablo Casals

29. Cerebellum Clinical Syndromes Cerebellum Clinical Syndromes Ataxia: incoordination of movement - decomposition of movement - decomposition of movement - dysmetria, past-pointing - dysmetria, past-pointing - dysdiadochokinesia - dysdiadochokinesia - rebound phenomenon of Holmes - rebound phenomenon of Holmes - gait ataxia, truncal ataxia, titubation - gait ataxia, truncal ataxia, titubation Intention Tremor Hypotonia, Nystagmus Archicerebellar Lesion: medulloblastoma Paleocerebellar Lesion: gait disturbance Neocerebellar Lesion: hypotonia, ataxia, tremor

30. Posture Gait – Ataxia Tremor

31. CerebellarAtaxia Ataxic gait and position: Left cerebellar tumor Left cerebellar tumor a. Sways to the right in a. Sways to the right in standing position standing position b. Steady on the b. Steady on the right leg right leg c. Unsteady on the c. Unsteady on the left leg left leg d. ataxic gait d. ataxic gait abc d

32. Cerebellar tumors on vermis - Truncal Ataxia - Truncal Ataxia - Frequent Falling - Frequent Falling The child in this picture: - would not try to stand - would not try to stand unsupported unsupported - would not let go of the bed rail - would not let go of the bed rail if she was stood on the floor. if she was stood on the floor. CerebellarMedulloblastoma

33. BG CBLM Courtesy of Stephen C. Voron, MD

34. BG CBLM Courtesy of Stephen C. Voron, MD

35. BG CBLM pyramidal cell in the motor homunculus of the frontal lobe Courtesy of Stephen C. Voron, MD

36. BG CBLM corticospinal tract Courtesy of Stephen C. Voron, MD

37. BG CBLM decusation at the pyramids (spino- medullary junction Courtesy of Stephen C. Voron, MD

38. BG CBLM thalamus: AKA the “gate keeper” prevents unwanted movements Courtesy of Stephen C. Voron, MD T

39. BG CBLM BASAL GANGLIA consultant on automatic movements provides input into the thalamus Courtesy of Stephen C. Voron, MD T

40. Cerebellum: consultant on rapid movements provides input into the thalamus BG CBLM

41. Basal Ganglia  resting tremor  postural instability  festination  rigidity  masked facies  bradykinesia  dyskinesia  torticollis  chorea  athetosis  hemiballismus  akathisia Cerebellum  intention tremor  dysmetria  dysdiadochokinesia  hypotonia  heal to shin  finger to nose  rebound  ataxic gait  titubation  nystagmus  dysmetric saccades