upper and lower motor neuron lesions

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Page 1: Upper and Lower Motor Neuron Lesions

صدق الله العظيم 58االسراء اية

Page 2: Upper and Lower Motor Neuron Lesions

ByBy

Dr. Abdel Aziz M. HusseinDr. Abdel Aziz M. HusseinAssist prof of PhysiologyAssist prof of Physiology

Somatic Motor System Somatic Motor System

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• Origin:Origin:• From area (6) and area (4) → descends to

corpus striatum → Globus pallidus→ from the globus pallidus fibers pass to;

1.Reticular formation2.Vestibular nuclei3.Red nucleus 4.Tectum of midbrain. • From these nuclei the following extrapyramidal

tracts arise:

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Motor areas 4 and 6

Basal Ganglia

Corpus striatum

Globus pallidus

RF Vest. Nuclei

Ret.Spin T. Vest.Spin.T.

Red Nucl.

Rubrospin. T.

Tectum

Tectospin. T.

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Red nucleus

Cerebellum

Cerebrum

Basal ganglia

Lateral AHCs

Rubrospinal T.

++

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Functions:Functions:1.Mediates motor signals concerned with the

skilled voluntary movements performed by distal limb muscle.

2.Also facilitates & motor neurons of the distal flexors

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Pontine RF Lateral RST.

Medial AHCs

Medial RST++ ----

Medullary RF

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• Functions: Functions: • a. Medial R.S.T.• It mediates facilitatory effect on the motor

neurons of the antigravity ms to maintain postural support.

• b. Lateral R.S.T. • It inhibits the tone in the antigravity ms

under some postural conditions, which provides background to perform other motor activities.

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Lateral V.N.Medial VST.

Medial AHCsLateral VST ++ ++++

Medial VN

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• Functions: Functions: • a. Lateral V.S.T.• It is facilitatory to & motor neurons of the

antigravity ms to maintain body posture & equilibrium in response to impulses from the vestibular apparatus which evoked by charges in head position or exposure to acceleration.

• b. Medial V.S.T. • It is facilitatory to & motor neurons of the

neck and upper limb muscles that are involved in regulation of the head & upper limb position during exposure to acceleratory movements

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Superior colliculus

Medial T.S.T

Medial AHCs

Lateral TST

++++

Inferior colliculus

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• Functions: Functions: • This tract mediates reflex turning of the head

in response to sudden visual or auditory stimuli.

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MOTOR CORTEX

INTERNAL CAPSULE

BRAIN STEM

SPINAL CORD

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Def.,• It is the damage of upper motor neuron in the

higher center or the descending motor tract.Causes1.Trauma2.Tumour3.Vascular disorders as thrombosis or hemorrhage.Sites: • Most common site of UMNL is the internal

capsule.

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1. Contralateral paralysis (loss of only voluntary movements) of the distal ms of the limbs, lower facial ms and ms of the tongue.

2. Contralateral paresis (weakness i.e., the ms retains some movements) of the axial ms and upper facial ms.

• Axial ms are supplied by descending motor tracts other than CBS whereas ms of the upper face are ipsilaterally innervated by CBS tract.

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3) Spasticity (increased ms tone) of the skeletal ms due to increased supraspinal facilitation to -motor neurons.

• A lesion at the level of internal capsule interrupts the descending inhibitory cortical fibers which feeds the inhibitory reticulospinal tract leaving the facilitatory vestibulospinal and reticulospinal to act.

• This spasticity is of the clasp-knife type

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Inhibitory RF

Facilitatory RF and VST

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6) The paralyzed ms show no or minimal atrophy as the lower motor neuron is intact and the ms contracts reflexly.

7) Normal response of the paralyzed ms to electric stimulation

a) Faradic current produces clonic or tetanic contractions

b) Galvanic current produces contractions that occur only at closing (make) and opening (break)

of the circuits. CCC > ACC > AOC > COC

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1) Contralateral hemianaesthesia i.e. loss of all sensations on the opposite side of the body

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Def.,• It is damage of the lower motor neurons (the

spinal AHCS and the cranial motor nuclei or their axons) resulting in skeletal ms paralysis

Causes1.Trauma2.Neuropathy

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I) Structural changesIn Nerve (degeneration and regeneration In muscle (atrophy and increase Ach

receptorsII) Functional changes1.Flaccid paralysis 2.Fasciculation and fibrillation 3.Dennervation supersensitivity4.Reaction of degeneration

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Wallerian degeneration

Retrograde degeneration

Regeneration Atrophy of muscles

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Page 45: Upper and Lower Motor Neuron Lesions

A) Flaccid paralysis:Paralysis of denervated ms with loss of all types of

movements; "voluntary, postural and reflex".All reflexes are lost including stretch reflex

resulting in loss of ms tone and tendon jerk (flaccidity).

The extent of paralysis is usually limited to a small group of ms

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B) Fasiculations and fibrillations:• Appears few days or weeks after denervation• Disappear when the motor nerve completely

degenerates or successful re-innervation of the ms occurs.

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B) Fasiculations :• Synchronous visible contraction of the motor unit

(all ms fibers) supplied by the injured axon. • Result from spontaneous generation of action potential

(injury potentials) in distal segment of the injured axon

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Page 49: Upper and Lower Motor Neuron Lesions

B) Fibrillations:• As degeneration of the injured axon continues,

the axon terminals are now separate from the main axon and hence, from each other.

• Injury potentials are still generated along the terminals leading to asynchronous contraction of the individual ms fibers attached to terminals.

• Invisible to the observer and detected only by electromyogram (EMG).

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Fibrillations

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C) Denervation supersensitivity:• Denervated ms becomes supersensitive to

acetylcholine.• This is due to increase in the number of A.Ch.

receptors which cover the entire surface of ms cell membrane.

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D) Reaction of degeneration:• - This means abnormal response of the denervated

muscle to electric stimulation.• Reaction of degeneration (response of denervated

ms):• INCOMPLETE REACTION: • i) Faradic current produces no response. • The denervated muscle has a prolonged chronaxia. • The faradic current is faster than the excitation time

needed to produce a response.• ii) Galvanic current produces an abnormal response. • The response in general is weaker than normal and ACC

> CCC.

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D) Reaction of degeneration:COMPLETE REACTION:• When the denervation is prolonged, the ms is

atrophied and fibrosed. • Thus, no response occurs to both faradic and

galvanic currents.

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