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LOWER MOTOR NEURON AND LESIONS

Lower Motor Neuron Lesions

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Lower motor neuron lesions

LOWER MOTOR NEURON AND LESIONS

Introduction

Lower motor neuron:Come out from the brainstem/spinal cord nuclei.Connect with skeletal motor end plate on skeletal muscle fiberThey are the common final motor pathway

Contribution of lower motor neuron

Muscle spindle

axonLower motor neuron synapses with upper motor neuron,Such as

LOWER MOTOR NEURONS COMMON PATHWAY

Muscle spindle is sensory organExtra fusal fibers are contractile unit motor neuron innervates extra fusal fibers motor neurons innervates muscle spindleIa fibers conduct information from muscle spindleInformation -> The proprioceptionIa fibers synapse with MN within spinal cord , the degree of contraction increase( MN stimulates extra fusal fibers)

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4 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 -> spinal cord-> MN -> NMJ-> muscle contraction

When over stetch of tendon ->

Golgi tendon organ-> I b fibers -> SC -> innhibitory inter neuron ->

Lesions may occur in these sites of lower motor neurons

Lower motor neuron lesionsCranial motor nuclei lesions belong to lower motor neuron lesions CAUSES WHICH MAY DAMAGE THE MOTOR NUCLEI IN MID BRAINTumor HemorrhageSudden movements of head Damage of both Occulomotor and Trochlear nuclei will result in impairment of occular movements

CAUSES WHICH MAY DAMAGE THE MOTOR NUCLEI OF PONSTumorPontine hemorrhageCAUSES WHICH MAY DAMAGE THE MOTOR NUCLEI IN MEDULLA OBLONGATARaised pressure in posterior cranial fossa > Glossopharyngeal motor nuclei > Motor nuclei of vagus > Hypoglossal nucleiLateral medullary syndrome > Abducent nuclei > Nucleus ambiguusMedial medullary syndrome > Hypoglossal nuclei Ipsilateral paralysis of tongue

Occurs when the axon of a neuron is crush or cut across.

Injuries of the axons

Neurapraxia- Due to 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.

Seddons ClassificationDegree of injuryMyelinAxonEndo-neuriumPeri-neuriumEpi-neuriumI+/-IINoYesYesNoNoIIINoYesYesYesNoIVNoYesYesYesYesVYesYesYesYesYesSutherlands classificationNormally innervated muscles 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 stillresponding 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 DegenerationReaction Of Degeneration

Reaction Of DegenerationBecause of interruption of the efferent part of reflex pathways, tendon reflexes are abolished.

Hyporeflexia

Loss Of Reflexes

01 Motor end 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 muscles02. Muscle spindle 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 When lower motor neurons are destroyed or their continuity is interrupted , the muscles supplied by them loss their tone, called as flaccid. (lower motor neuron paralysis) Flaccid paralysis Destruction of nerve supply. (motor nerve)Abnormal excitability Sensitive to circulating AcetylcholineIrregular contraction of individual fiber (fibrillation )Muscular Atrophy

Jerky visible contraction of group of muscle fibers.Pathological discharge of spinal motor neuron.Muscular Fasciculation

This is a shortening of the paralyzed muscles.It occurs more often in the antagonist muscles whose action is no longer opposed by the paralyzed muscles.Muscular ContractureLower motor neurons lesionsCauses- Trauma Infection Vascular disorders Degenerative disease Neoplasm

fDestroy the cell bodies in anterior gray matter or its axon in anterior root of spinal nerve28Principal Features of UMNL & LMNLUMNL: (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 .

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Presented by 3rd group