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 fiber
They are the common final motor pathway
Contribution of lower motor neuron
Muscle spindle

axon

Lower motor neuron synapses with upper motor

neuron,
Such as
Descending
tracts
Cortical
Pyram
idal

Extra
pyram
idal

Cortico
bulbur

Vesti
bulos
pinal

Cortico
mesencep
halic

Cortico
pontain

cortic
ospin
al

Sub
cortical

balance of
extensor
muscles

Ru
bro
spi
nal

Flex
or

Retic
ulo
spinal

Ponsexten
sor
musc
les
Mid
brain

Med
ullaflexo
r
mus
cles

Oliv
o
spin
al

Tec
tos
pina
l

Vis
ual
refl
ex

Aud
itor
y
reflee
x
x

LOWER MOTOR NEURONS COMMON

PATHWAY

Muscle spindle is sensory organ

Extra fusal fibers are contractile unit
motor neuron innervates extra fusal fibers
motor neurons innervates muscle spindle
Ia fibers conduct information from muscle
spindle
Information -> The proprioception
Ia fibers synapse with MN within spinal cord ,
the degree of contraction increase( MN
stimulates extra fusal fibers)

 MN -> NMJ -> Ca

contraction

+2

influx -> AP-> actin-myosin function-> muscle

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 ->

Lower motor neuron lesions

Lesions may occur in these sites of lower
motor neurons
Lesions
Nuclei
Crani
al
Nerve
s

Spinal
Nerve
s

Axon
Sedd
ons

Suthe
rland
s

Muscle
Muscl
e
spindl
e

Motor
End
Plate

Cranial motor nuclei lesions belong to

lower motor neuron lesions

MID
BRAIN
Occulomotor
nuclei

Trochlear nuclei

PONS

MEDULLA
OBLONGA
TA

Trigeminal
motor nuclei

Motor nuclei of
Glossopharyng
eal

Abducent
motor nuclei

Motor nuclei of
Vagus

Facial motor
nuclei

Hypoglossal
nuclei

CAUSES WHICH MAY DAMAGE THE MOTOR

NUCLEI IN
MID BRAIN
Tumor
Hemorrhage
Sudden movements of head

Occulomot
or nuclei

Trochlear
motor
nuclei

Ipsilateral paralysis of

Contralateral
paralysis of

>Lavator palpabae
Superiosis
>Superior Rectus
>Inferior rectus
>Medial rectus
>Inferior oblique

>superior oblique

Damage of both Occulomotor and Trochlear nuclei

will result in impairment of occular movements

CAUSES WHICH MAY DAMAGE 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

Trigemina
l motor
nuclei
Weakness
of jaw
muscles

CAUSES WHICH MAY DAMAGE 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

Injuries of the axons

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

Axon

Neurapraxi
a

Seddons

Sutherland
s

Axonotme
sis

neurotmes
is

Seddons Classification

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.

Sutherlands classification

Degree
of
injury

Myelin

Axon

Endoneuriu
m

Perineuriu
m

Epineuriu
m

+/-

II

No

Yes

Yes

No

No

III

No

Yes

Yes

Yes

No

IV

No

Yes

Yes

Yes

Yes

Yes

Yes

Yes

Yes

Yes

Reaction Of Degeneration
Normally 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 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
Degeneration

Neural
Degeneration

Wallerian
degeneration

Transneural
degeneration

Axonal/Retrogra
de
degeneration

Loss Of Reflexes
Because of interruption of the efferent part
of reflex pathways, tendon reflexes are
abolished.

Hyporeflexia

Effects on muscles
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 muscles
02. 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

Flaccid paralysis

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)

Muscular Atrophy
Destruction of nerve supply.
(motor nerve)
Abnormal excitability
Sensitive to circulating Acetylcholine
Irregular contraction of individual fiber
(fibrillation )

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

Muscular Contracture
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.

Lower motor neurons lesions

Causes-

Trauma
Infection
Vascular
disorders
Degenerative
disease
Neoplasm

fDestroy the cell bodies in

anterior gray matter or its
axon in anterior root of
spinal nerve

Principal Features of UMNL & 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
{

28

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 .

THANK YOU

Presented by 3rd group