Clinical Aspects of Upper and Lower Motor

Neuron Lesions

Dr Tai Keen Sang

MBBS, FRCP
IMU Clinical Campus, Seremban
 Clinical Aspects of Upper Motor Neuron (UMN) and
Lower Motor Neuron (LMN) Lesions
Outcomes:
 To be able to define and differentiate UMN and LMN lesions.
 To be able to state the presentations of UMN and LMN lesions.
 To develop an approach in evaluating a patient presenting with limb weakness
and recognize UMN and LMN lesions.
 To list common diseases presenting with UMN and LMN lesions.
 Definitions
Upper motor neurons:
The motor neurons that run from the motor cortex of the brain to the spinal
cord. They run in the corticospinal (pyramidal) tracts.

Lower motor neurons:

The neurons that run from the anterior horn cells of the spinal cord to the
peripheral nerves terminating at the motor end plates.

Lesion:
An injury or damage to an organ or tissue due to a disease process or trauma.
Upper Motor Neurons
Motor Cortex
↓
Internal Capsule
↓
Brainstem
↓
Spinal Cord

Voluntary control of muscle functions on the

contralateral side of the body
 Functions of the Corticospinal (Pyramidal) Tracts

Voluntary control of the skeletal muscles

of the contralateral side of the body.

Note: these movements are modulated

by input from the cerebellar and
extrapyramidal systems with respect to
tone, balance, posture, movement.
Basal Ganglia Cerebellum
Lower Motor Neurons
Anterior Horn Cells of Spinal
Cord
↓
Nerve Roots
↓
Nerve Plexi
↓
Peripheral Nerves
Clinical Aspects of Upper Motor Neuron Lesions
Features of Upper Motor Neuron lesions:
 Weakness*
 Hypertonia** (“clasp-knife” type, sustained clonus)
 Exaggerated deep tendon reflexes (hyperreflexia)
 Extensor plantar reflexes (positive Babinski’s sign)
 Absent abdominal reflexes
 No muscle atrophy***

*paresis (usually not total paralysis)

** early stage may be initially hypotonic
***disuse atrophy may occur
 Pattern of Weakness in Upper Motor
Neuron Lesions

The “pyramidal distribution” of weakness.

Upper limbs:
Flexors stronger than extensors.
The “anti-gravity muscles” weaker – shoulder
abduction, elbow, wrist and finger extension.

Lower limbs:
Extensors stronger than flexors.
Hip and knee flexion and ankle dorsiflexion and plantar
eversion weaker
Clinical Aspects of Lower Motor Neuron Lesions
Features of Lower Motor Neuron lesions:
 Weakness*
 Hypotonia (flaccidity)
 Hyporeflexia or areflexia
 Fasciculations
 Muscle atrophy

*may be complete paralysis

 Approach to the patient with weakness
History:
 Onset of weakness – acute or gradual.
 Muscle groups affected, unilateral or bilateral.
 Associated symptoms: speech, cranial nerves,
bulbar function, sensory system, cerebellar
system.
 Comorbidities: Hypertension, diabetes,
coronary and atherosclerotic vascular disease,
medication and social history.
Motor System Examination:
 Inspection and palpation of muscles.
 Assessment of tone.
 Assessment of movement and power.
 Assessment of reflexes.
Relevant Investigations:
 Laboratory: Full blood count, glucose, lipids
profile, renal profile, etc.
 Imaging: Computerized Tomography (CT) or
Magnetic Resonance Imaging (MRI).
 Electromyography (EMG).
 Nerve conduction studies (NCS).
Clinical Aspects of Upper Motor Neuron (UMN) and Lower
Motor Neuron (LMN) Lesions

Grading Motor Power: Grading Reflexes:

0 : No muscle contraction visible 0 Absent
1 : Contraction but no movement 1+ Diminished
2 : Movement with gravity eliminated 2+ Normal
3 : Movement against gravity but not 3+ Increased
against resistance 4+ Greatly increased (with clonus)
4: Movement against resistance but
weaker than normal
± present when using reinforcement
5: Normal power manoeuvre
 Clinical Aspects of Upper Motor Neuron (UMN) and Lower
Motor Neuron (LMN) Lesions

Investigations:

Brain & Spinal Cord:

 Computerised tomographic scan (CT)
 Magnetic resonance imaging (MRI)

Nerves:
 Nerve conduction studies (NCS)
 Electromyography (EMG) CT scan image of
brain
 Some diseases associated with Upper and Lower Motor Neuron
Lesions

Type of lesions Causes

Upper motor neuron
Lower motor neuron
Cerebrovascular Disease (stroke)
Spinal Cord Injuries
Demyelination (multiple sclerosis)
Brain trauma
Motor neurone disease
Peripheral neuropathies
Radiculopathies
Anterior horn cell disease
Motor neurone disease
 Case History 1
A 66-year-old hypertensive man Investigations:
developed sudden right-sided weakness. Computerized tomographic (CT) brain scan:
Examination findings:
BP 155/95. Pulse 90 / minute regular.
Right lower facial weakness present Cranial CT scan showing
an infarct in the left
Limbs (on right side): internal capsule

Tone: hypertonic
Power: Reduced (graded 4/5)
Deep tendon reflexes: Hyperreflexic (3+)
Extensor plantar response (Positive Babinski)
 Summary:
A 66-year-old man with sudden right-sided weakness

Diagnosis:
 Stroke with right-sided hemiparesis.

Summary of upper motor neuron signs on affected side:

 Hypertonia
 Weakness
 Hyperreflexia
 Extensor plantar response (Babinski response)
Face:
 Lower facial weakness (with sparing of the upper half of the face)
 Stroke
(Cerebrovascular Accident)

Classification of Strokes:
1. Ischaemic - interruption of the blood supply to a part of the brain.
2. Haemorrhagic – bleeding in the brain from a ruptured blood vessel.
 Ischaemic stroke

 About 80% of strokes are ischaemic.

 Due to vascular occlusion and interruption of blood supply to an area of the brain and
results in cerebral infarction.
 May be thrombotic or embolic.
 Ischaemic Stroke
Main categories:
 Large vessel disease (carotids, vertebrobasilar, intracerebral) - about 50%
 Intracranial small vessel disease (‘lacunar infarcts’) - about 25 %
 Cardioembolic (emboli originating from the heart) - about 20 %
 Others
Haemorrhagic Stroke
About 20% of strokes are haemorrhagic.
Associations:
 Advancing age
 Hypertension
 Cerebral amyloid angiopathy
 Anticoagulant & thrombolytic therapy
 Coagulopathies
 Haemorrhagic transformation of ischaemic
strokes
 Subarachnoid haemorrhage (aneurysms,
arteriovenous (AV) malformations)
 Others - intracranial neoplasms, vasculitis etc
 Case History 2
A 65-year-old man develops progressive weakness of his limbs over the last 1 year.
There is associated cramping and stiffness with difficulty in movements such as picking
up objects and buttoning clothes and he has gait difficulty with tripping and stumbling.

Examination findings:
Wasting and fasciculations in both upper and lower limb muscles.
Muscle power reduced grade 4/5.
Reflexes all brisk 3+
Extensor plantar responses (Babinski response).

Cerebellar and sensory systems: Normal

 Case History 2: A 65-year-old man with progressive limb weakness

Both upper and lower motor neuron signs are present.

Type of Lesion Upper Motor Neuron Lower Motor Neuron

Signs Hyperreflexia Wasting
Extensor plantar response Fasciculations

Investigations:
 Brain and cervical cord MRI: Normal findings.
 Nerve conduction studies (NCS): Abnormal motor NCS with reduced motor compound
muscle action potentials. Normal sensory nerve conduction studies.
 Electromyography (EMG): fibrillation and fasciculations potentials present.
Case History 2: A 65-year-old man with limb weakness and both UMN
and LMN lesions
Diagnosis:
Motor Neuron Disease
A progressive degenerative disease of the upper and lower motor neurons that may
affect the cortex, cranial nerve motor nerve nuclei and the spinal cord.

Main presentations of motor neuron disease:

 Amyotrophic lateral sclerosis: lateral corticospinal tract involved with amyotrophy
(muscle atrophy and wasting).
 Progressive bulbar palsy: lower cranial nerve nuclei affected (dysarthria, dysphagia,
nasal regurgitation, tongue atrophy and fasciculations)
 Progressive muscular atrophy: LMN affected (wasting and fasciculations of
muscles).
 Primary lateral sclerosis: Upper motor neurons affected.
 Summary:
Clinical Aspects of Upper Motor Neuron (UMN) and Lower Motor
Neuron (LMN) Lesions

In a patient presenting with weakness, obtain a focused history and perform a

systematic neurological examination.
Together with an understanding of neuroanatomy, UMN and LMN lesions can
be distinguished allowing a clinical diagnosis to be made.
Diagnoses are confirmed with relevant investigations, where indicated, and
appropriate treatment carried out.
End of Lecture

Thank you