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vdocument.in_lower-motor-neuron-lesions.pptx
- 1. LOWER MOTOR NEURONANDLESIONS
- 2. Introduction Lower motor neuron: Comeout from the brainstem/spinal cord nuclei. Connect with skeletal motor end plate on skeletal muscle fiber They are the common final motor pathway Contribution of lower motor neuron Muscle spindle axon
- 3. Lower motor neuronsynapses with upper motor neuron, Such as Descending tracts Cortical Pyram idal cortic ospin al Extra pyram idal Cortico bulbur Cortico pontain Cortico mesencep halic Sub cortical Vesti bulos pinal balance of extensor muscles Ru bro spi nal Flex or Reticu lo spinal Pons- exten sor musc les Med ulla- flexo r mus cles Mid brain Oliv o spin al Tec tos pina l Vis ual refl ex Aud itor y refle x
- 4. LOWER MOTOR NEURONSCOMMON PATHWAY Muscle spindle is sensory organ Extra fusal fibers are contractile unit α motor neuron innervates extra fusal fibers ϒ motor neurons innervates muscle spindle Ia fibers conduct information from muscle spindle Information -> The proprioception Ia fibers synapse with α MN within spinal cord , the degree of contraction increase( α MN stimulates extra fusal fibers)
- 5. α MN ->NMJ -> Ca +2 influx -> AP-> actin-myosin function-> muscle contraction Muscle spindle / intra fusal fibers-> stretch receptors Deep tendon reflex Strech on tendon-> EFF ->I α -> spinal cord-> α MN -> NMJ-> muscle contraction When over stetch of tendon -> Golgi tendon organ-> I b fibers -> SC -> innhibitory inter neuron ->
- 6. Lesions mayoccur in these sites of lower motor neurons Lower motor neuron lesions Lesions Nuclei Cranial Nerves Spinal Nerves Axon Seddo n’s Sutherl and’s Muscle Muscle spindle Motor End Plate
- 7. Cranial motor nucleilesions belong to lower motor neuron lesions……… MID BRAIN Occulomotor nuclei Trochlear nuclei PONS Trigeminal motor nuclei Abducent motor nuclei Facial motor nuclei MEDULLA OBLONGATA Motor nuclei of Glossopharyngeal Motor nuclei of Vagus Hypoglossal nuclei
- 8. CAUSES WHICH MAYDAMAGE THE MOTOR NUCLEI IN MID BRAIN Tumor Hemorrhage Sudden movements of head Occulomotor nuclei Ipsilateral paralysis of >Lavator palpabae Superiosis >Superior Rectus >Inferior rectus >Medial rectus >Inferior oblique Trochlear motor nuclei Contralateral paralysis of >superior oblique
- 9. Damage of bothOcculomotor and Trochlear nuclei will result in impairment of occular movements
- 10. CAUSES WHICH MAYDAMAGE THE MOTOR NUCLEI OF PONS Tumor Pontine hemorrhage Facial motor nuclei Weakness of facial muscles in same side Abducent nuclei Weakness of lateral rectus one or both sides Paralysis of conjugate occular deviation Trigeminal motor nuclei Weakness of jaw muscles
- 11. CAUSES WHICH MAYDAMAGE THE MOTOR NUCLEI IN MEDULLA OBLONGATA Raised pressure in posterior cranial fossa > Glossopharyngeal motor nuclei > Motor nuclei of vagus > Hypoglossal nuclei Lateral medullary syndrome > Abducent nuclei > Nucleus ambiguus Medial medullary syndrome > Hypoglossal nuclei – Ipsilateral paralysis of tongue
- 14. Occurs whenthe axon of a neuron is crush or cut across. Injuries of the axons Axon Seddon’s Neurapraxia Axonotmesis neurotmesis Sutherland’s
- 15. Neurapraxia - Dueto blockage of nerve conduction. Axonotmesis - Disruption of nerve cell axon. - Endoneurium is intact. - With Wallerian degeneration. Neurotmesis - Most serious nerve injury. - Both the nerve and the nerve sheath are disrupted. Seddon’s Classification
- 16. Degree of injury Myelin AxonEndo- neurium Peri- neurium Epi- neurium I +/- II No Yes Yes No No III No Yes Yes Yes No IV No Yes Yes Yes Yes V Yes Yes Yes Yes Yes Sutherlands classification
- 17. Normally innervatedmuscles respond to stimulation by the application of interrupted current. Galvanic or direct current causes contraction only when the current is turned on or turned off. When the lower motor neuron is cut, After 7 days - No any muscular response to interrupted electrical stimulation 7 days after nerve section. (But it will be still responding to direct current.) After 10 days - the response to direct current also ceases. This change in muscle response to electrical stimulation is known as the Reaction Of Degeneration Reaction Of Degeneration
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- 20. Because ofinterruption of the efferent part of reflex pathways, tendon reflexes are abolished. Hyporeflexia Loss Of Reflexes
- 21. 01 Motorend plate Myasthenia gravis The immune system inappropriately produce antibodies that bind to and block some Ach receptors thereby decreasing the number of functional of skeletal muscles. More receptors are lost. Thus muscles become increasing weaker, fatigue more easily, and many eventually cease to function. Effects on muscles
- 22. 02. Musclespindle Interruption of motor , pathways anywhere between the motor area of the cerebral cortex and the muscles produce muscles paralysis. Inability to move a part of the body is called as paralysis. In some diseases damage may be confined to lower motor neurons, and the result in paralysis may be purely flaccid. Such lesions are accompanied by muscular wasting(atrophy), muscle twitching(fasciculation), and contracture of opposing muscles. eg:- poliomyelitis Effects on muscles
- 23. When lower motorneurons are destroyed or their continuity is interrupted , the muscles supplied by them loss their tone, called as flaccid. (lower motor neuron paralysis) Flaccid paralysis
- 24. Destruction ofnerve supply. (motor nerve) Abnormal excitability Sensitive to circulating Acetylcholine Irregular contraction of individual fiber (fibrillation ) Muscular Atrophy
- 25. Jerky visible contractionof group of muscle fibers. Pathological discharge of spinal motor neuron. Muscular Fasciculation
- 26. This is ashortening of the paralyzed muscles. It occurs more often in the antagonist muscles whose action is no longer opposed by the paralyzed muscles. Muscular Contracture
- 27. Lower motor neuronslesions Causes- Trauma Infection Vascular disorders Degenerative disease Neoplasm fDestroy the cell bodies in anterior gray matter or it’s axon in anterior root of spinal nerve
- 28. 28 Principal Features ofUMNL & LMNL UMNL: (1) No muscle wasting, except from disuse ( disuse atrophy) (3) Spasticity ( hypertonia ) , called “ clasp-knife spasticity ” (4) Clonus present (5) Brisk ( exaggerated ) tendon jerks (6) Extensor plantar reflex , Babinski sign ( dorsiflexion of the big toe and fanning out of the other toes ) (7) Absent abdominal reflexes (8) No fasciculations (9) No fibrillation potential in EMG { LMNL: (1) Marked muscle wasting (atrophy ) (3) Flacidity (Hypotonia ) , hence given the name “ flaccid paralysis ” (4) No clonus (5) Diminished or absent tendon reflexes (6) Absent plantar reflex (normally it is flexor ) . (7) Absent abdominal reflexes (8) Fasciculations may occur . (9) Fibrillation potentials present .
- 29. THANK YOU Presented by3rd group