Medicine – Upper Motor Neuron Lesion

An upper motor neuron (UMN) lesion is damage to the descending motor pathways above the level of the anterior horn cell or motor cranial nerve nucleus. These pathways originate mainly in the cerebral cortex and descend through the brainstem and spinal cord before synapsing with lower motor neurons.

The characteristic pattern is weakness with increased tone, brisk reflexes, little early muscle wasting, and an extensor plantar response.

1. Site of the Lesion

A UMN lesion may occur anywhere along the descending motor pathway above the lower motor neuron.

Important sites include:

Motor cortex.

Corona radiata.

Internal capsule.

Brainstem.

Corticospinal tract within the spinal cord.

2. Corticospinal Tract

The corticospinal tract is the major descending pathway controlling voluntary movement.

It runs from:

Motor cortex → corona radiata → internal capsule → cerebral peduncle → pons → medullary pyramids.

Most fibres then cross in the:

Pyramidal decussation in the lower medulla.

They descend in the spinal cord as the:

Lateral corticospinal tract.

3. Effect of Lesion Relative to the Decussation

A lesion:

Above the pyramidal decussation

usually produces weakness on the:

Contralateral side of the body.

A lesion:

Below the decussation in the spinal cord

usually produces weakness on the:

Ipsilateral side below the lesion.

4. Weakness

UMN lesions cause:

Muscle weakness.

The weakness often affects groups of muscles rather than one isolated peripheral nerve distribution.

The pattern depends on the lesion site.

5. Pyramidal Pattern of Weakness

In the upper limb, UMN weakness often affects:

Extensors more than flexors.

In the lower limb, it often affects:

Flexors more than extensors.

This produces the characteristic pyramidal pattern seen after corticospinal tract damage.

6. Increased Muscle Tone

A classic UMN sign is:

Increased muscle tone.

This is usually due to:

Spasticity.

Spasticity is a velocity-dependent increase in resistance to passive movement.

7. Spasticity

With spasticity:

The faster the examiner moves the limb, the greater the resistance.

This occurs because descending inhibitory influences on spinal reflex circuits are reduced.

8. Clasp-Knife Phenomenon

In marked spasticity, passive movement may initially meet strong resistance followed by sudden release.

This is called the:

Clasp-knife phenomenon.

It is classically associated with UMN lesions.

9. Increased Reflexes

Deep tendon reflexes are usually:

Brisk

or

Exaggerated.

This is called:

Hyperreflexia.

Examples include brisk:

Knee jerk.

Ankle jerk.

Biceps reflex.

10. Why Reflexes Increase

UMN pathways normally exert inhibitory control over spinal reflex activity.

When this control is lost:

UMN damage → reduced descending inhibition → exaggerated spinal reflexes.

This produces:

Hyperreflexia.

11. Clonus

Severe hyperreflexia may produce:

Clonus.

Clonus consists of repeated rhythmic contractions triggered by sudden sustained stretch of a muscle.

It is commonly tested at the:

Ankle.

Patella.

Sustained clonus strongly supports a UMN lesion.

12. Muscle Wasting

UMN lesions usually cause:

Little muscle wasting initially.

This is because the lower motor neuron and its direct connection to the muscle remain intact.

13. Disuse Atrophy

If weakness persists for a long time, some wasting may occur due to:

Disuse.

This is usually much less severe than the neurogenic wasting seen in LMN lesions.

14. Fasciculations

Fasciculations are generally:

Absent in a pure UMN lesion.

Their presence suggests lower motor neuron involvement.

Therefore:

Brisk reflexes + fasciculations

may indicate a disease affecting both UMN and LMN systems, such as:

Motor neurone disease.

15. Plantar Response

One of the classic UMN signs is an:

Upgoing plantar response.

This is also called:

Extensor plantar response

or

Babinski sign.

16. Babinski Sign

When the lateral sole is stimulated, the abnormal response is:

Extension of the great toe

with possible

Fanning of the other toes.

This indicates corticospinal tract dysfunction in adults.

17. Normal Plantar Response

In a neurologically normal adult, plantar stimulation usually causes:

Flexion of the toes.

Therefore:

Flexor plantar = normal adult response.

Extensor plantar = UMN sign.

18. Babinski in Infants

An extensor plantar response may be normal in infants because corticospinal pathways are not yet fully myelinated.

Therefore, the Babinski sign is pathological mainly in:

Older children and adults.

19. Loss of Fine Movement

UMN lesions often impair:

Fine skilled voluntary movement.

Examples include difficulty with:

Finger tapping.

Buttoning clothes.

Writing.

Rapid alternating movements due to weakness and spasticity.

20. Pronator Drift

A subtle UMN weakness may be detected using:

Pronator drift.

The patient holds both arms outstretched with palms upward.

In pyramidal weakness, the affected arm may:

Pronate

and

Drift downward.

21. Common Causes of UMN Lesions

Important causes include:

Stroke.

Multiple sclerosis.

Spinal cord compression.

Motor neurone disease.

Cerebral palsy.

Brain tumour.

Spinal cord trauma.

Transverse myelitis.

22. Stroke

Stroke is one of the most common causes of an acute UMN syndrome.

A cerebral hemisphere lesion may cause:

Contralateral weakness.

Hyperreflexia.

Increased tone.

Extensor plantar response.

23. Internal Capsule Stroke

The corticospinal fibres are tightly packed within the:

Internal capsule.

A small lesion here can therefore produce:

Dense contralateral hemiparesis.

A lacunar infarct affecting the posterior limb may cause:

Pure motor stroke.

24. Multiple Sclerosis

Multiple sclerosis can damage corticospinal pathways within the brain or spinal cord.

This may produce:

Spastic weakness.

Brisk reflexes.

Clonus.

Extensor plantar responses.

25. Spinal Cord Compression

Compression of the spinal cord can damage corticospinal tracts.

Below the level of compression, the patient may develop:

Spastic weakness.

Hyperreflexia.

Extensor plantars.

Often there are also:

Sensory changes.

A sensory level.

Bladder dysfunction.

26. Acute Spinal Cord Lesions

Immediately after an acute severe spinal cord lesion, the patient may initially develop:

Spinal shock.

During spinal shock there may be:

Flaccid weakness.

Reduced tone.

Absent reflexes.

This may temporarily resemble an LMN lesion.

Later, the typical UMN pattern develops:

Spasticity + hyperreflexia + extensor plantars.

27. Motor Neurone Disease

Motor neurone disease can affect both:

Upper motor neurons

and

Lower motor neurons.

Therefore the same patient may show:

Spasticity.

Brisk reflexes.

Babinski sign.

together with:

Wasting.

Fasciculations.

28. Cerebral Palsy

Certain forms of cerebral palsy produce chronic UMN signs because of early injury to the developing brain.

Features may include:

Spasticity.

Hyperreflexia.

Weakness.

Abnormal gait.

29. UMN Lesion of the Face

The facial motor nucleus has an important pattern of cortical innervation.

The upper facial muscles receive:

Bilateral cortical input.

The lower facial muscles receive mainly:

Contralateral cortical input.

Therefore, a unilateral UMN facial lesion usually causes:

Contralateral lower facial weakness with relative forehead sparing.

30. UMN Facial Palsy versus LMN Facial Palsy

UMN facial palsy:

Contralateral lower face weakness.

Forehead relatively spared.

LMN facial palsy:

Ipsilateral weakness of the whole face.

Forehead affected.

Eye closure weak.

31. Upper Motor Neuron versus Lower Motor Neuron – Tone

UMN lesion:

Tone increased.

Spasticity.

LMN lesion:

Tone reduced.

Flaccidity.

32. Upper Motor Neuron versus Lower Motor Neuron – Reflexes

UMN lesion:

Reflexes brisk or exaggerated.

Clonus may occur.

LMN lesion:

Reflexes reduced or absent.

33. Upper Motor Neuron versus Lower Motor Neuron – Wasting

UMN lesion:

Little early wasting.

Late mild disuse atrophy possible.

LMN lesion:

Marked neurogenic wasting.

34. Upper Motor Neuron versus Lower Motor Neuron – Fasciculations

UMN lesion:

Absent.

LMN lesion:

May be present.

35. Upper Motor Neuron versus Lower Motor Neuron – Plantar Response

UMN lesion:

Extensor plantar response.

Babinski positive.

LMN lesion:

Usually flexor plantar response.

36. UMN Lesion – Note Form

Site:

Any lesion above the anterior horn cell or motor cranial nerve nucleus.

Weakness:

Pyramidal weakness.

Tone:

Increased.

Spastic.

Reflexes:

Brisk.

Hyperreflexic.

Clonus may occur.

Muscle bulk:

Relatively preserved early.

Only mild disuse wasting later.

Fasciculations:

Absent in a pure UMN lesion.

Plantar response:

Upgoing.

Extensor.

Babinski positive.

37. High-Yield UMN Pattern

The classic pattern is:

WEAKNESS + SPASTICITY + HYPERREFLEXIA + BABINSKI SIGN.

A useful memory sequence is:

UMN = UP.

UP tone.

UP reflexes.

UPgoing plantar.

with

little early wasting.

Key Clinical Pattern

An upper motor neuron lesion damages the descending motor pathway above the anterior horn cell or motor cranial nerve nucleus.

Think:

SPASTIC WEAKNESS.

↑ TONE.

↑ REFLEXES.

CLONUS MAY OCCUR.

LITTLE EARLY WASTING.

NO FASCICULATIONS IN A PURE UMN LESION.

UPGOING PLANTAR / BABINSKI SIGN.

The easiest contrast is:

UMN → UP tone + UP reflexes + UPgoing plantar.

whereas

LMN → LOW tone + LOW reflexes + WASTING + FASCICULATIONS.