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Motor pathways by atifa ambreen

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  • 1. CNS PHYSIOLOGY BY Atifa Ambreen (Lab technologist )
  • 2. Spinocerebellar tract • Functions of spino- cerebellar tract: – Subconscious kinesthetic sensations. – Impulses from proprioceptors  cerebellum  coordination of movements & posture maintenance. – Information to cerebellum about motor impulses, which have reached the ventral horn motor neurons along the cortico-spinal & rubro-spinal tracts.
  • 3. Miscellaneous ascending tracts: Spino-tectal tract: 1st order neurons: • Enter spinal cord through posterior nerve root  synapse with neurons in the grey matter of spinal cord. 2nd order neurons: • Arise from here  cross over to opposite side  antero-lateral white column  tract ascends  medulla  joins spinal leminiscus  terminate into superior colliculus in tectum of midbrain. Function: – Afferent pathway for spino- visual reflexes  control movement of head & eyes towards source of stimulation.
  • 4. Miscellaneous ascending tracts: Spino-reticular tract: 1st order neurons: • Enter spinal cord through posterior nerve root  synapse with neurons in lateral grey horn of spinal cord. 2nd order neurons: • Arise from here  lateral white column on same side (mainly no crossing over)  ascends as spino- reticular tract  terminates in reticular formation of medulla, pons & midbrain. Function: • Important in control of level of consciousness / alertness, awareness.
  • 5. Miscellaneous ascending tracts: Spino-olivary tract: 1st order neurons: • Enter the spinal cord through posterior nerve root  synapse with neurons in grey matter of spinal cord. 2nd order neurons: • Arise from here  no crossing over  lateral white column  ascends  medulla  synapse with neurons in inferior olivary nucleus. 3rd order neurons: • Arise here  cross to opposite side  inferior peduncle  terminate in cerebellum. Function: • Carries proprioceptive impulses.
  • 6. Descending motor pathways / tracts: 1) PYRAMIDAL / CORTICO-SPINAL. 2) EXTRA-PYRAMIDAL / EXTRA CORTICO- SPINAL. (All the descending motor pathways, other than pyramidal are called extrapyramidal).
  • 7. PYRAMIDAL TRACTS: • Consist of 1 million fibers. • Mostly myelinated fibers, but slow conducting. • Tract originates from cerebral cortex. • 30% of fibers originate from primary motor area. • Another 30% from pre-motor area & supplementary motor area. • 40% from somatic sensory area of cerebral cortex.
  • 8. • All these fibers converge through corona-radiata towards internal capsule. • In internal capsule, the tract occupies the genu (the bent portion) & anterior 2/3 of posterior limb. • When tract passes through the internal capsule, fibers for cervical parts of body are in genu & fibers for lower parts of body are in posterior limb of internal capsule. • Then tract passes into midbrain, where it occupies middle 3/5 of cerebral peduncle / crus cerebri.
  • 9. • In cerebral peduncle, fibers for cervical parts of body are medial & fibers for lower parts are lateral. • From midbrain, tract enters the pons, where tract is broken into small bundles by transverse ponto- cerebellar fibers.
  • 10. • When these bundles enter medulla, these gather / unite along the anterior border of medulla to form the pyramid (a swelling). • The tract is named pyramidal because of pyramid formation along anterior border of medulla. • In lower part of medulla, 80% of fibers cross over to opposite side, to form MOTOR DECUSSATION.
  • 11. • After motor decussation, crossed fibers enter lateral white columns of spinal cord to form lateral cortico-spinal tract. • Fibers of tract which remain uncrossed, enter anterior white column of spinal cord to form anterior cortico-spinal tract. • Fibers of anterior cortico- spinal tract terminate in ventral horn of cervical & upper thoracic segments of spinal cord. • These fibers terminate onto motor neurons ( aplha & gamma). • It is thought that these fibers are from supplementary motor area, for control of attitudinal or positional movements,e-g, in climbing posture.
  • 12. • Fibers of lateral cortico- spinal tract terminate onto the motor neurons in ventral horn of spinal cord at various levels. • From cortico-spinal tract as a whole, • 45% fibers terminate in cervical segments, • 35% in lumbar • 20% in thoracic segments of spinal cord.
  • 13. • Most of cortico-spinal fibers for their termination first synapse with inter-neurons which in turn synapse with motor neurons (alpha & gamma). • Only fibers which arise from Betz cells (Giant pyramidal cells), which form only 3% fibers, terminate directly into motor neurons.
  • 14. • Certain branches of cortico-spinal tract go to different brain parts: – To caudate & lentiform nuclei. – To red nucleus. – To olivary nuclei & reticular formation. – There are also cortico- bulbar fibers which come along cortico-spinal tract. In the brain stem these fibers cross over to opposite side to terminate with motor neurons in nuclei of cranial nerves.
  • 15. EXTRA-PYRAMIDAL TRACTS: All descending tracts other than cortico-spinal / pyramidal are included in it.
  • 16. 1) RUBRO-SPINAL TRACT: • ORIGIN: Red nucleus (midbrain). • Fibers cross over to opposite side & descend through pons & medulla  lat white column of spinal cord. • Fibers terminate on inter- neurons. • Inter-neurons synapse with alpha & gamma motor neurons.
  • 17. RUBRO-SPINAL TRACT (Cont..) • Red nucleus receives fibers from: – Cerebral cortex & – Cerebellum. • FUNCTION: – Rubro-spinal tract is an alternate pathway, through which cerebral cortex & cerebellum control activity of motor neurons in spinal cord. – This tract is excitatory for flexors & inhibitory for extensors (anti-gravity muscles). ****
  • 18. 2) TECTO-SPINAL TRACT: • ORIGIN: superior colliculus located in tectum of midbrain. • Tract fibers descend without crossing. • Fibers terminate onto motor neurons in ventral horn of upper cervical segments of spinal cord, through inter- neurons. • Function: This tract controls reflex movements of head & neck, in response to visual stimuli, e.g, something shines behind  reflex turning of head & neck back to the shining object.
  • 19. RETICULO-SPINAL TRACT: ORIGIN: Tract arises from reticular formation (groups of scattered neurons along with nerve fibers present in midbrain, Pons & medulla). • * Superiorly reticular formation is connected to cerebral cortex & • inferiorly to spinal cord. • Reticulo-spinal tract has 2 components: – A) PONTINE component – B) MEDULLARY component
  • 20. PONTINE RETICULO-SPINAL TRACT: • ORIGIN: Nuclei of reticular formation of pons. • Fibers remain uncrossed & descend to enter anterior white columns of spinal cord. • Tract terminate on motor neurons in ventral horn of spinal cord, through inter- neurons & finally motor neurons. • Function: excitatory for extensors & Inhibitory for flexors (unlike rubro-spinal).
  • 21. MEDULLARY RETICULAR FORMATION: • ORIGIN: Nuclei of reticular formation in medulla. • Fibers cross to opposite side. • Tract descends to enter lateral white column of spinal cord. • Terminate onto the motor neurons in ventral horn. • Function: It is inhibitory for extensors (like rubro- spinal).
  • 22. DESCENDING AUTONOMIC PATHWAY: • ORIGIN: Cerebral cortex, hypothalamus, amygdala & reticular formation. • This pathway accompanies reticulo-spinal tract. • These fibers enter lat. white column of spinal cord & terminate onto pre-gang. Sympathetic neurons in segments T1 – L2 & also onto pre-gang parasymp. neurons in segments S2 – S4.
  • 23. VESTIBULO-SPINAL TRACT: • ORIGIN: Vestibular nuclei in lower pons & medulla. • Mostly fibers remain uncrossed. • Then enter Ant. White column of spinal cord. • Terminate on alpha & gamma motor neurons, through interneurons.
  • 24. VESTIBULO-SPINAL TRACT: • 2 components of the tract: • Major component  Lateral V.S Tract – lat. Vest. Nuclei.  Lat. V.S Tract • Minor component  Medial V.S Tract. – med Vest. Nuclei.  Med. V.S Tract • Function: Vest-spinal tract is excitatory for extensors (unlike rubro-spinal). • cerebellar fibers  Vestibular nuclei • internal ear fibers (vestibular apparatus  Vestibular nuclei.
  • 25. OLIVO-SPINAL TRACT: • ORIGIN: Inferior olivary nucleus in medulla. • Fibers cross over to opposite side & descend into lat. White column of spinal cord. • Fibers terminate onto motor neurons in ventral horn through interneurons. • Function: This tract controls activity of motor neurons in spinal cord. • Inferior olivary nucleus receives fibers from cerebral cortex, corpus striatum, reticular formation & spinal cord.
  • 26. MOTOR SYSTEM CONSISTS OF 2 TYPES OF NEURONS: • UMN: upper motor neurons • LMN: lower motor neurons
  • 27. LMN: • These neurons include: Alpha motor neuron in ventral horn of spinal cord & also motor neurons in nuclei of cranial nerves in brain stem. – Motor neurons which innervate the skeletal muscles. – These form the final common pathways to skeletal muscles.*** – If any motor impulse has to pass to skeletal muscle, it has to pass to LMN.
  • 28. UMN: • These are present above the level of LMN. • These control motor activity through separate pathways. • These neurons may be located in cerebral cortex, basal ganglia & also in brain stem.
  • 29. FEATURES OF LMN LESION: • May involve LMN in ventral horn of spinal cord or motor nuclei of cranial nerves or their nerve fibers. • CAUSES OF LESION: – Traumatic – Infective (poliomyelitis) – Inflammatory – Degenerative – Neoplastic – Vascular (lesion)
  • 30. FEATURES of LMN: • Only a few muscles are involved in LMN lesion. • Flaccid paralysis in LMN lesion, i-e, loss of voluntary movements with hypotonia or atonia. • Loss of superficial reflexes. • Loss of deep reflexes / tendon jerks. • Muscle atrophy (*main cause is loss of trophic actions of motor nerves, supplying skeletal muscles. disuse is minor cause.
  • 31. • There are fasiculations (when bundles of muscle fibers contract) & fibrillations (individual muscle fibers contract) seen when there is slow degeneration of LMNs. • Shortening of paralyzed muscles  contractures. • Reaction of degeneration: response to faradic stimulation & galvanic stimulation. In LMN lesion, muscles respond to faradic stimulation upto 7 days & to galvanic stimulation upto 10 days. After 10 days, no response (faradic = interrupted current stimulation & galvanic = direct current stimulation). • Babinski sign is not present.
  • 32. FEATURES OF UMN LESION: • 1) FEATURES OF LESION OF PYRAMIDAL OR CORTICO-SPINAL TRACT: • 2) FEATURES OF LESION OF EXTRA-CORTICO- SPINAL OR EXTRA-PYRAMIDAL TRACT.
  • 33. FEATURES OF LESION OF PYRAMIDAL OR CORTICO-SPINAL TRACT: • FUNCTION: Control of fine skilled voluntary movements specially of distal parts of limbs. • Incase of UMN lesion of pyramidal tract: A) loss of fine skilled voluntary movements, specially of distal parts of limbs. B) + babinski sign / abnormal plantar reflex. C) loss of superficial abdom. Reflex D) loss of cremasteric reflex.
  • 34. • NORMAL PLANTAR REFLEX: – When we scratch along lateral border of sole of foot  plantar flexion of all the toes. – Segment value of normal plantar reflex is S1. • ABNORMAL PLANTAR REFLEX (Babinski’s sign): – When we scratch  dorsiflexion of big toe & fanning out of other 4 toes. – In addition, also physiologically seen in: • 1) Infants (due to incomplete myelination of cortico-spinal tract). • 2) during sleep. • 3) alcohol intoxication.
  • 35. • LOSS OF SUPERFICIAL ABDOMINAL REFLEX: – Due to loss of excitatory effect of cortico-spinal tract on inter-neurons in reflex arc. This reflex is polysynaptic because inter-neurons are also involved. – Root value = T7 – T11. • LOSS OF CREMASTERIC REFLEX: – Also due to loss of facilitation of inter-neurons by cortico-spinal tract. This reflex is also polysynaptic. – Root value is L1.
  • 36. LESIONS OF EXTRA-CORTICO-SPINAL TRACT: FEATURES: A) spastic paralysis. B) increased muscle tone. C) slight muscle atrophy. D) tendon jerks. E) ankle or knee clonus. F) clasp knife rigidity.
  • 37. LESIONS OF EXTRA-CORTICO-SPINAL TRACT: A) SPASTIC PARALYSIS: – Loss of voluntary movements with increased muscle tone. – In this lesion large no. of muscles are involved. – It may be hemiplegia. B) INCREASED MUSCLE TONE: – This is due to facilitation of stretch reflex or myotatic reflex becomes hyperactive. C) SLIGHT MUSCLE ATROPHY: – This is due to disuse  slight atrophy. D) TENDON JERKS: – They become brisk or exaggerated due to facilitation of stretch reflex. E) ANKLE OR KNEE CLONUS: – This is present when we apply a sudden maintained stretch to musles  rhythmic, repeated muscle contraction.
  • 38. F) CLASP KNIFE RIGIDITY: • In the patient, if we try to flex arm at elbow  there is initial resistance to flexion, but when we continue flexion  there is rapid flexion. • Mechanism: – Initially: stretch reflex is initiated, which is hyperactive in these patients. Triceps contracts  extension at elbow. – Later on: muscle tension increases. There is activation of inverse stretch reflex due to excitation of golgi tendon organs  muscle relaxes  rapid flexion.
  • 39. CLINICAL PICTURE OF UMN LESION: • We don’t get patients with lesion of one type of tract. The lesions involve both pyramidal & extra-pyramidal tracts. So we get mixed type of clinical features in clinical practice.
  • 40. LMN LESION: • LEVEL OF LESION: – Level is alpha motor neuron in ventral horn. • TONE: – Loss of voluntary movements with hypotonia / atonia. • No. of muscles involved: – Small no. of muscles are involved. • Type of paralysis: – Flaccid paralysis. UMN LESION (Pyramidal & Extra- pyramidal) • LEVEL OF LESION: – Level is above alpha motor neuron in cerebral cortex, basal ganglia & brain stem. • TONE: – Loss of voluntary movements with hypertonia. • No. Of muscles involved: – Large no. of muscles involved. • Type of paralysis: – Spastic paralysis (clasp knife rigidity).
  • 41. LMN LESION: • CAUSE OF ATROPHY: – Due to loss of trophic action of nerves mainly. • REFLEXES: – Loss of deep reflexes. – No ankle / knee clonus. – Negative babinski sign. • CONTRACTURE: – Present. • FASCICULATION / FIBRILLATION: – Present (slow degeneration of LMNs). • HEMIPLEGIA: – Not a common feature. • SUPERFICIAL REFLEXES: – Lost. UMN LESION: • CAUSE OF ATROPHY: – Due to disuse & only slight atrophy. • REFLEXES: – Reflexes become exaggerated due to facilitation of stretch reflex. – ankle / knee clonus. – Positive babinski sign. • CONTRACTURE: – Absent. • FASCICULATION / FIBRILLATION: – Absent . – There is loss of skilled movements of peripheral limbs. • HEMIPLEGIA: – Common • SUPERFICIAL REFLEXES: – Lost. (abdominal, cremasteric).
  • 42. Brown-Sequard Syndrome
  • 43. • Follow me on:- https://www.facebook.com/atif aambreen786

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