Upper Motor Neuron Lesion
(UMNL , Pyramidal Lesion)
& Lower Motor Neuron Lesion (LMNL)
Lecture
by
DR SHAIK ABDUL RAHIM
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Upper Motor Neuron Lesion (UMNL)
 In upper motor neuron (pyramidal) lesion , the spinal
cord is disconnected from the modulating influences
of the supraspinal controlling centers.
 Therefore , in UMNL , after a period of “spinal shock”
the stretch reflex recovers , but resumes function in
a primitive and uninhibited manner: there are
exaggerated tendon reflexes and “ spastic ” increase
in muscle tone , greater in the extensors of the lower
limbs (LLs ) and the flexors of the upper limbs ( ULs) .
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Lower Motor Neuron Lesion ( LMNL)
The lower motor neuron ( LMN) constitutes
part of the reflex arc - the integrity of the
reflex arc is essential for (1) maintenace of
muscle tone (2) adequate nutrition of the
muscle itself.
LMN lesion leads to atonia or hypotonia , lost
or depressed tendon reflexes , and muscle
atrophy (wasting ).
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Examples of Conditions in Which there is UMNL
or LMNL
Upper Motor Neuron
Lesion (UMNL)
Can result from
(1) Haemorrhage ,
thrombosis or embolism
in the internal capsule
(e.g. Hemiplegia)
(2) Spinal cord transection
or hemisection
(e.g. Brown- Sequard
syndrome)
Lower Motor Neuron
Lesion (LMNL)
Can result from
(1) Spinal root lesions or
peripheral nerve lesion
(e.g. nerve injury by
trauma or compressive
lesion
(2) Anterior horn cell lesions
(e.g. , poliomyelitis, motor
neuron disease )
Principal Features of UMNL & LMNL
UMNL:
(1) No muscle wasting, except
from disuse ( disuse atrophy)
(2) Spasticity ( hypertonia ),
called “ clasp-knife spasticity ”
(3) Clonus present
(4) Brisk ( exaggerated ) tendon
jerks
(5) Extensor plantar reflex ,
Babinski sign ( dorsiflexion of
the big toe and fanning out of
the other toes )
(6) Absent abdominal reflexes
(7) No fasciculations
(8) No fibrillation potential in
EMG
LMNL:
(1) Marked muscle wasting
(atrophy )
(2) Flacidity (Hypotonia ) , hence
given the name “ flaccid
paralysis ”
(3) No clonus
(4) Diminished or absent tendon
reflexes
(5) Absent plantar reflex
(normally it is flexor )
(6) Absent abdominal reflexes
(7) Fasciculations may occur
(8) Fibrillation potentials present
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Hemiplegia
Causes : cerebral heamorrhage , thrombosis or embolism results in
paralysis of the oppsite half of the body. The commonest cause of
cerebral haemorrhage is hypertension, usually associated with rupture
of
the lenticulo-striate branch of the middle cerebral artery in the
internal capsule.
Features :
(1)UMNL involving the half of the body contralateral to the site of the
lesion .
(2) Hypertonia causes the limbs to acquire a specific posture 
A/ upper limb is (a) adducted to the side of the trunk , (b) flexed at the
elbow ,(c) the forearm is semipronated,(d) with flexion of the wrist and
fingers.
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Hemiplegia
B/ lower limb is (a) adducted and (b) extended at the
knee and ankle.
In extensive lesions the patient may have , in addition :
(3) Loss of sensation on the opposite side of the body
(Hemianesthesia), due to damage of the
thalamocortical fibers.
(4) Homonymous hemianopia ( loss of vision in two
corresponding halves of the visual fields in both eyes),
may occur if the optic radiation is lesioned
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Brown-Sequard syndrome
(Hemi section of the spinal cord)
 Occurs as a result of unilateral lesion or
hemisection of the spinal cord
(e.g. due to stab injury, bullet , car-accident, or
tumor). The manifestations of the BrownSequard syndrome depend on the level of the
lesion.
A/ At the level of the lesion, all manifestations
occur on the same side:
1. Paralysis of the lower motor neuron type,
involving only the muscle supplied by the
damaged segments.
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Brown-Sequard syndrome
(Hemi section of the spinal cord)
2. Vasodilatation of the blood vessels that receive
vasoconstrictor fibres from the damaged segments.
3. Loss of all sensations in the areas supplied by the
afferent fibres that enter the spinal cord in the
damaged segments +/- band of hyperesthesia
B/ Ipsilaterally ( on the same side of lesion ) below the
level of the lesion :
1.spastic lower limb (with upper motor neuron type of
lesion ).
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Brown-Sequard syndrome
(Hemi section of the spinal cord)
2. Fine touch, position and vibration sense are
lost as a result of damage of the dorsal column
tracts .
3. Vasodilatation due to interruption of the
descending pathways from the medullary
vasomotor centres.
C/ On the opposite side to the lesion :
Pain and temperature sensations are lost.
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COMPARISON OF MOTOR SYSTEMS
http://library.med.utah.edu/neurologicexam/html/home_exam.html
Lowe r Motor Neuron
Spina l Cord
Uppe r Motor Neuron
Corticospina l Tract
Cerebellum
Basal Ganglia
Efferent part of
monosynaptic reflex
Volunta ry movement
Muscle tone by
inhibiting antagonists
Maintains muscle
fibers (trophic factors)
Muscle tone
Rapid coordinated alternating
skilled movements that are
learned
Eye-head movements
Facilitates intentional
movements and inhib it
extraneous movements
Autopilot for motor activities
Normal
Weakness or paralysis
Fine control, espec. finger
flexors
Inhibitory to Lower motor
neurons
Weakness or paralysis
Posture and Gait
Balance, equili brium,
orientation in space
timi ng, duration, and amplitude
Voluntary movements in an
automatic manor.
Hyperreflexia
Hyperactive deep tendon
reflexes
Babins ki- extensor plantar
reflex
Spasticity
Trunca l ataxia, gait ataxia
Shuffling or festinating gait,
small steps, hard to turn
Nystagmus, Dizziness,
Masked facies, few blinks
Decomposition of movement
Diffi culty turning or starting,
hypo kinetic = bradykinesia
Paucity of associated
movements
Abno rmal
Areflexia
Fasciculation
Muscle Atrophy
Flaccid paralysis
Dysmetria- ataxia of arms
Dysynergia
Dysdiadocho kinesia- inabili ty
to do rapid alternating
movements
Hypotonia- pendular reflexes
Intention tremor
Scanning speech
Chorea, athetosis,
hyperkinetic
Rigidity ( lead-pipe )
(cogwheel),
Resting tremor
Soft speech