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Motor system pathways for students
- 1. Motor System • Starts at the motor cortex • Motor cortex is located at the frontal lobe – precentral cortex
- 6. Brodmann areas Primary motor cortex Area 4
- 7. Motor cortex • different areas of the body are represented in different cortical areas in the motor cortex • Motor homunculus – somatotopic representation – not proportionate to structures but proportionate to function – distorted map – upside down map
- 8. Motor cortical areas • primary motor cortex (MI) – precentral gyrus • Movements are executed • secondary motor cortex (MII) – premotor cortex – supplementary motor area (SMA) • Movements are planned together with cerebellum, basal ganglia and other cortical areas
- 9. Primary motor cortex • Corticospinal tract (pyramidal tract) originates from the primary motor cortex • Corticobulbar tract also originates from the motor cortex and supplies brainstem and the cranial nerves • Cell bodies of the corticospinal tracts are called Betz cells (large pyramidal shaped cells) • Corticospinal tract descends down the internal capsule
- 10. Course of the corticospinal tract • Descends through – internal capsule – at the medulla • cross over to the other side • uncrossed tracts – descends down as the corticospinal tract – ends in each anterior horn cell – synapse at the anterior horn cell (directly or through interneurons)
- 12. Primary and secondary cortical areas • Primary areas are primarily connected with the peripheral organs/structures – Primary motor cortex (area 4) • Secondary areas are inter-connected to each other by cortico-cortical pathways and perform complex processing – Premotor cortex (area 6) – Supplementary motor area (superomedial part of area 6)
- 14. Functional role of primary and secondary motor areas • SMA (Supplementary motor area) assembles global instructions for movements • It issues these instructions to the Premotor cortex (PMC) • Premotor cortex works out the details of smaller components • And then activates specific Primary motor cortex (MI) • Primary motor cortex through Corticospinal tracts (CST) activate specific motor units SMA PMC MI CST Motor units
- 15. Complex nature of Cortical Control of Movement 8.15
- 16. idea •premotor area •supplementary motor area (SMA) •Prefrontal cortex (PFC) Primary motor cortex movement basal ganglia cerebellum cerebellum plan execute memory, emotions
- 17. Motor system • Consists of – Upper motor neuron – Lower motor neuron
- 18. Lower motor neuron • consists of mainly • alpha motor neuron – and also gamma motor neuron alpha motor neuron gamma motor neuron
- 19. alpha motor neuron gamma motor neuron corticospinal tract Arrangement at the anterior horn cell
- 20. alpha motor neuron • this is also called the final common pathway • Contraction of the muscle occurs through this whether – voluntary contraction through corticospinal tract or – involuntary contraction through gamma motor neuron - stretch reflex - Ia afferent
- 21. motor unit • muscle contraction occurs in terms of motor units rather than by single muscle fibres • a motor unit is defined as – anterior horn cell – motor neuron – muscle fibres supplied by the neuron • Muscle power/strength is obtained by the principle of “Recruitment of motor units”
- 22. motor unit • Innervation ratio – motor neuron:number of muscle fibres • in eye muscles – 1:23 offers a fine degree of control • in calf muscles – 1:1000 more strength
- 23. Upper motor neuron • Consists of – Corticospinal tract (pyramidal tract) – Extrapyramidal tracts • Start from the brainstem • Ipsilateral/contralateral • Cortical pathways can excite/inhibit these tracts • Modify the movement that is initiated by the CST • Influence (+/-) gamma motor neuron, stretch reflex, muscle tone • Important for postural control • Cerebellar and basal ganglia influence on the lower motor neuron will be through extrapyramidal tracts
- 24. Extrapyramidal tracts • starts at the brain stem • descends down either ipsilaterally or contralaterally • ends at the anterior horn cell • modifies the motor functions
- 25. Extrapyramidal tracts • there are 4 tracts – reticulospinal tracts – vestibulospinal tracts – rubrospinal tracts – tectospinal tracts
- 26. reticulospinal tract • relay station for descending motor impulses except pyramidal tracts • receives & modifies motor commands to the proximal & axial muscles • maintain normal postural tone • excitatory to alpha & gamma motorneurons • end on interneurons too • this effect is inhibited by cerebral influence • mainly ipsilateral
- 28. • pontine reticular formation – medial reticulospinal tracts • controls proximal muscles (axial), excitatory to flexor • medullary reticular formation – lateral reticulospinal tracts (also medial) • excitatory or inhibitory to axial muscles
- 29. Reticular formation • A set of network of interconnected neurons located in the central core of the brainstem • It is made up of ascending and descending fibers • It plays a big role in filtering incoming stimuli to discriminate irrelevant background stimuli • There are a large number of neurons with great degree of convergence and divergence
- 30. Functions • Maintain consciousness, sleep and arousal • Motor functions (postural and muscle tone control) – Reticulospinal pathways are part of the extrapyramidal tracts • Pain modulation (inhibition) – Several nuclei (PAG, NRM) are part of the descending pain modulatory (inhibitory) pathway
- 31. vestibular nuclei & tracts • responsible for maintaining tone in antigravity muscles & for coordinating the postural adjustments in limbs & eyes • connections with vestibular receptors (otolith organs) & cerebellum • mainly ipsilateral • supplies extensors
- 33. • vestibulospinal tracts – lateral vestibulospinal tract – medial vestibulospinal tract – excitatory to antigravity alpha motor neurons & supplies interneurons too – lateral tract • excitation of extensor muscles & relaxation of flexor muscles – medial tract • inhibition of neck & axial muscles
- 34. red nucleus • present in the midbrain • rubrospinal tract originates from the red nucleus • ends on interneurons • control the distal muscles of limbs • excite limb flexors & inhibit extensors • higher centre influence (cerebral cortex) • mainly contralateral • supplies flexors • Functionally this tract is not important in human motor system
- 36. tectospinal tract • tectospinal tract originates from the tectum of the midbrain • ends on interneurons • mainly contralateral • supplies cervical segments only • Functionally this tract is not important in human motor system
- 38. inferior olivary nucleus • present in the medulla • function: – motor coordination • via projections to the cerebellum • sole source of climbing fibres to the cerebellum – motor learning – Functionally this nucleus is not important in human motor system
- 39. Upper motor neuron Lower motor neuron extrapyramidal tracts pyramidal tracts alpha motor neurone gamma motor neurone
- 40. Clinical Importance of the motor system examination • Tests of motor function: – Muscle power • Ability to contract a group of muscles in order to make an active movement – Muscle tone • Resistance against passive movement
- 41. Basis of tests • Muscle power – Test the integrity of motor cortex, corticospinal tract and lower motor neuron • Muscle tone – Test the integrity of stretch reflex, gamma motor neuron and the descending control of the stretch reflex
- 42. Muscle tone • Resistance against passive movement – Gamma motor neuron activate the spindles – Stretching the muscle will activate the stretch reflex – Muscle will contract involuntarily – Gamma activity is under higher centre inhibition
- 43. • There is a complex effect of corticospinal and extrapyramidal tracts on the alpha and gamma motor neurons (in addition to the effect by muscle spindle) • There are both excitatory and inhibitory effects • Sum effect – excitatory on alpha motor neuron – Inhibitory on gamma motor neuron Corticospinal tract Extrapyramidal tracts Alpha motor neuron Gamma motor neuron•Voluntary movement •Muscle tone Muscle spindle
- 44. Clinical situations • Muscle power – Normal – Reduced (muscle weakness) • Paralysis, paresis, plegia • MRC grades 0 - no movement 1 - flicker is perceptible in the muscle 2 - movement only if gravity eliminated 3 - can move limb against gravity 4 - can move against gravity & some resistance exerted by examiner 5 - normal power • Muscle tone – Normal – Reduced • Hypotonia (Flaccidity) – Increased • Hypertonia (Spasticity)
- 45. Main abnormalities • Muscle Weakness / paralysis – Reduced muscle power • Flaccidity – Reduced muscle tone • Spasticity – Increased muscle tone
- 46. • Lower motor neuron lesion causes – flaccid paralysis (flaccid weakness) • Upper motor neuron lesion causes – spastic paralysis (spastic weakness)
- 47. Lower motor neuron lesion • muscle weakness • flaccid paralysis • muscle wasting (disuse atrophy) • reduced muscle tone (hypotonia) • reflexes: reduced or absent (hyporeflexia or areflexia) • spontaneous muscle contractions (fasciculations) • plantar reflex: flexor • superficial abdominal reflexes: present • eg. Brachial plexus damage
- 48. Upper motor neuron lesion • muscle weakness • spastic paralysis • increased muscle tone (hypertonia) • reflexes: exaggerated (hyperreflexia) • Babinski sign: positive • superficial abdominal reflexes: absent • muscle wasting is very rare • clonus can be seen: – rhythmical series of contractions in response to sudden stretch • clasp knife effect can be seen – passive stretch causing initial increased resistance which is released later • eg. Stroke
- 49. Babinski sign • when outer border of the sole of the foot is scratched • upward movement of big toe • fanning out of other toes • feature of upper motor neuron lesion • extensor plantar reflex • seen in infants during 1st year of life (because of immature corticospinal tract)
- 51. • Observation • When the spinal cord is suddenly transected, essentially all cord functions, including spinal cord reflexes, immediately become depressed • This is called “spinal shock” • Period of spinal shock is about 2 weeks in humans • It may vary depending on the level spinal cord injury • Higher the animal in evolution greater is the spinal shock period Spinal cord transection and spinal shock
- 52. During spinal shock period • complete loss of all reflexes • no tone • paralysis • complete anaesthesia • no peristalsis • bladder and rectal reflexes absent • no sweating • arterial blood pressure decreases
- 53. Possible mechanism of spinal shock • Normal activity of the spinal cord reflexes depends to a great extent on continual tonic excitation from higher centers (pyramidal and extrapyramidal tracts) • Spinal shock may be due to the sudden cessation of tonic bombardment of spinal cord interneuron pool by descending influences • During recovery from spinal shock, the excitability of spinal cord reflexes increase due to the lack of descending inhibition and possible denervation hypersensitivity • After the spinal shock period typical upper motor neuron features appear
- 54. after the spinal shock • reflexes will reappear, mostly exaggerated • bladder become reflex • mass reflex will appear – afferent stimuli irradiate to several reflex centres – noxious stimulus causes: withdrawal response, evacuation of bladder, rectum, sweating, pallor
- 55. Site of lesions Cortex Internal capsule Brain stem Spinal cord Anterior horn cell Motor nerve Neuromuscular junction Muscle
- 56. Neurological diseases Disease Involvement • Stroke UMN • Peripheral neuropathy LMN – Mononeuropathy – Polyneuropathy • Plexopathy LMN • Radiculopathy LMN • Myelopathy LMN, UMN • Motor neuron disease LMN, UMN • Monoplegia (monoparesis) • Hemiplegia (hemiparesis) • Paraplegia (paraparesis) • Quadriplegia (quadriparesis)
- 57. Site of lesions monoplegia only 1 limb is affected either UL or LL, lower motor neuron lesion hemiplegia one half of the body including UL and LL lesion in the Internal capsule paraplegia both lower limbs thoracic cord lesion quadriplegia (tetraplegia) all 4 limbs are affected cervical cord or brain stem lesion
- 59. Stroke • Cerebrovascular accident (CVA) • A serious neurological disease • Large number of deaths per year • Cerebrovascular ischaemia causing infarction or haemorrhage • Sudden onset hemiplegia • Hypertension, diabetes, obesity are risk factors
- 60. Peripheral neuropathies • Mononeuropathies – Carpal tunnel syndrome (CTS) – Ulnar neuropathy - claw hand – Saturday night palsy (radial nerve lesion) – wrist drop – Common peroneal nerve lesion – foot drop – Posterior tibial nerve lesion – tarsal tunnel syndrome – Sciatic nerve lesion – Facial nerve lesion – Bell’s palsy • Polyneuropathies – Diabetic, vitamin deficiency, toxic
- 61. Median nerve compression (Carpal tunnel syndrome)
- 62. Ulnar nerve lesion (Ulnar tunnel syndrome) Clawing of the hand
- 63. Radial nerve lesion (Saturday night palsy) Wrist drop Wrist guard
- 64. Common peroneal nerve lesion Foot drop Ankle guard
- 65. Posterior tibial nerve lesion (Tarsal tunnel syndrome)
- 67. Facial nerve lesion (Facial palsy or Bell’s palsy)
- 70. Sciatica
- 72. MND or Motor neuron disease • Anterior horn cell disease • MND: motor neuron disease • ALS: Amyotrophic lateral sclerosis • Weakness of lower limbs, upper limbs • Speech defect: dysarthria • Difficulty in swallowing: dysphagia
- 73. MND or Motor neuron disease