In one breath
An upper motor neuron (UMN) lesion, anywhere from the motor cortex down to the anterior horn cells, gives a spastic paralysis with brisk tendon reflexes and a Babinski sign, while a lower motor neuron (LMN) lesion, of the anterior horn cell or its axon, gives a flaccid, wasted paralysis with lost reflexes. UMN lesions weaken muscles in groups; LMN lesions weaken the individual muscles of one nerve and add fasciculations, denervation potentials and slowed nerve conduction. Loss of the superficial reflexes is the one sign the two share.
Builds on: Corticospinal (pyramidal) tract · Stretch reflex · Muscle spindle · Leads to: Medullary integration and decerebrate rigidity · Parkinson’s and Huntington’s disease
UMN paralysis
- Definition: paralysis from damage to the descending motor fibres anywhere between their origin in the cortical motor areas and their end on the anterior horn cells.
- In clinical language, a pyramidal (CST) lesion is a UMN paralysis. The typical example is a capsular stroke (Corticospinal (pyramidal) tract).
Features
- Spasticity: tone is increased (hypertonia).
- No wasting. Only a mild disuse atrophy appears in the long run.
- Muscles are weak in groups; a single muscle is never affected alone.
- Tendon reflexes exaggerated.
- Superficial reflexes lost.
- Extensor plantar response: Babinski’s sign positive.
- No fasciculations.
- EMG: no denervation potentials.
- Nerve conduction: normal.
A pure pyramid lesion is not the "pyramidal" picture
If disease, or an experimental cut, damages only the fibres in the medullary pyramid, most of the nine features are missing. What remains is weakness of the distal limb muscles and a positive Babinski. There is no spasticity, and tone may even fall.
So the pyramid carries mostly lateral CST fibres. The full clinical picture needs damage to the corticobulbar fibres as well as the CST: the ones that reach the brainstem reticular formation and so steer the extrapyramidal pathways (see Spasticity below).
Why the UMN signs appear
Spasticity
- Tone rises because the motor neurons fire more and the motor neuron pool becomes more excitable.
- The chain:
- A UMN lesion cuts the corticoreticular fibres along with the corticospinal ones. These run from the motor cortex to the brainstem reticular formation, especially the pontine reticular nuclei.
- Those fibres normally hold back the reticulospinal pathway.
- With the brake gone, the pontine reticulospinal tract is released. It normally excites the proximal extensors (Rubrospinal, vestibulospinal, reticulospinal and tectospinal tracts).
- Motor neurons are driven harder, and tone rises: spasticity.
- The spasticity is of the clasp-knife type: resistance to stretch that suddenly gives way (Inverse stretch reflex and muscle tone). Contrast the lead-pipe rigidity of Parkinsonism (Parkinson’s and Huntington’s disease).
No wasting
- A muscle wastes only when its blood supply or its nerve supply is cut.
- In a UMN lesion the lower motor neuron, the muscle’s own nerve supply, is intact, so there is no atrophy.
- In long-standing cases a mild disuse atrophy develops.
Brisk tendon reflexes
- On balance, UMNs inhibit the lower motor neurons.
- When that inhibition is lost, motor neuron discharge rises, above all that of the γ motor neurons.
- More γ drive makes the muscle spindle more sensitive to stretch, so the deep tendon reflexes are exaggerated (Muscle spindle, Stretch reflex).
Superficial reflexes lost
- Superficial reflexes are long, polysynaptic reflexes that loop through several levels of the CNS. The stretch reflex, by contrast, is monosynaptic and completed within the cord.
- Afferent limb: up the ascending sensory systems. Efferent limb: down the descending motor pathways to the muscles.
- A UMN lesion breaks the efferent limb, so these reflexes disappear.
Worth knowing, though not in your pages: the abdominal and cremasteric reflexes are the usual examples tested.
Extensor plantar response
- The CST normally excites flexor and inhibits extensor motor neurons to the digits. So stroking the sole normally gives plantar flexion of the toes (a flexor plantar).
- When the CST’s influence on the lumbosacral motor neurons is lost, the same stroke gives dorsiflexion of the big toe and fanning of the other toes. This is the extensor plantar response, a positive Babinski sign.
Worth knowing, though not in your pages:
- To elicit it, stroke the outer border of the sole firmly with a blunt point, from the heel towards the little toe.
- An extensor plantar is normal in infants under about one year, while the CST is still myelinating.
LMN paralysis
- Cause: destruction of the anterior horn cells or of their axons, in the root, the nerve plexus or the peripheral nerve.
- Examples: nerve injury or nerve disease, poliomyelitis, motor neuron disease, lesions of the nerve roots.
A slip in your book
Your book says the axons may be damaged “in dorsal root”. Motor axons leave the cord through the ventral (anterior) root; the dorsal root carries sensory fibres. Read it as the ventral root.
Features
- Flaccid paralysis: the muscles are hypotonic.
- Marked wasting (atrophy).
- Individual muscles are affected: those supplied by the damaged nerve.
- Tendon reflexes reduced or absent.
- Superficial reflexes lost.
- Flexor plantar response: no Babinski sign.
- Fasciculations (visible twitches) are seen.
- EMG: denervation potentials (fibrillations, fasciculations, sharp waves).
- Nerve conduction reduced or absent.
Physiological basis
- Wasting: the muscle has lost its nerve, and with it the nerve growth (trophic) factors the nerve secretes. It is also no longer used.
- Distribution: only the muscles of the damaged nerve suffer, not a whole limb or one side of the body.
- Reflexes: the lesion breaks the reflex arc itself, so both the tendon reflexes and the superficial reflexes are lost.
- Flaccidity: denervation removes the γ motor neuron influence that keeps up tone.
- Sensory loss: usually accompanies the paralysis, because the same nerve carries sensory fibres into the cord.
- Nerve conduction: falls because the nerve fibres themselves are damaged.
- Plantar: with no motor neuron activity there is no Babinski sign; any response present is the normal flexor one.
- EMG: the denervated muscle shows denervation potentials (fibrillations, fasciculations).
UMN vs LMN at a glance
| Feature | UMN lesion | LMN lesion |
|---|---|---|
| Site | Cortex to cord, above the AHC | AHC, root, plexus, nerve |
| Example | Capsular stroke | Polio, nerve injury |
| Muscles hit | In groups | Individually |
| Tone | ↑ (spastic) | ↓ (flaccid) |
| Wasting | None (late disuse only) | Marked |
| Tendon reflexes | Exaggerated | Reduced or absent |
| Superficial reflexes | Lost | Lost |
| Plantar | Extensor (Babinski +) | Flexor |
| Fasciculations | Absent | Present |
| EMG | No denervation potentials | Denervation potentials |
| Nerve conduction | Normal | Reduced |
AHC = anterior horn cell.
The one shared sign
Superficial reflexes are lost in both. A UMN lesion breaks their long efferent loop; an LMN lesion breaks the final path to the muscle. Examiners like “which feature is common to UMN and LMN lesions”, and “which feature is never seen in LMN paralysis” (hypertonia).
Patterns of paralysis
- Paralysis (plegia): complete loss of voluntary movement. Paresis: weakness, an incomplete paralysis.
- Paralysis is named by the parts of the body it involves:
| Pattern | What is paralysed | Usual cause |
|---|---|---|
| Monoplegia | One whole limb | Cord or cortical lesion |
| Hemiplegia | One half of the body | Internal capsule lesion |
| Paraplegia | Both legs | Cord injury or transection |
| Quadriplegia | All four limbs | Upper cervical transection |
| Diplegia | All four, legs worse | A form of quadriplegia |
| Triplegia | Three limbs | Passing stage of quadriplegia |
| Isolated | One or more muscle groups | Disease of one nerve |
Monoplegia
- All the muscles of one limb are weak or paralysed. Paralysis of one muscle or one muscle group is not monoplegia.
- Crural (leg): trauma, myelitis, disc prolapse or tumour of the thoracolumbar cord.
- Brachial (arm): disease of the cervical cord segments.
- Either can also come from a central cortical lesion: a thrombotic or embolic infarct, or a localised tumour or abscess.
Hemiplegia and the rest
- Hemiplegia is the commonest pattern: the arm, the leg and sometimes the face of one side. It is usually a CST lesion in the internal capsule, which gives contralateral hemiplegia.
- Paraplegia usually follows spinal cord injury or disease that cuts across the cord. Rarely the cause is in the motor cortex, the cauda equina or the peripheral nerves.
- Quadriplegia (tetraplegia) usually follows transection of the upper cervical cord. Bilateral UMN disease in the cervical cord, brainstem or cerebrum can also cause it.
- Diplegia is quadriplegia with the legs worse than the arms.
- Triplegia is usually a passing stage while quadriplegia develops or partly recovers.
- Isolated paralysis of one or more muscle groups comes from disease of a single nerve or one of its branches.
Applied: reading a hemiplegia case
An elderly hypertensive or diabetic patient develops weakness of the right arm and leg, and the angle of the mouth is pulled to the left. Later the right limbs are spastic, with brisk reflexes and an extensor plantar.
- Diagnosis: right hemiplegia of UMN type. The lesion is in the left CST (the motor system).
- Commonest site: the left internal capsule, usually a bleed from Charcot’s artery.
- Other features to list: lost superficial reflexes, muscles weak in groups, no wasting, no fasciculations.
Worth knowing, though not in your pages: the mouth is pulled towards the healthy side because the lower face on the paralysed side is weak.
Exam-answer skeleton: "Differences between UMN and LMN paralysis, with the physiological basis of the UMN features" (short note)
- Define each: UMN (cortex down to, but not including, the anterior horn cell) and LMN (the anterior horn cell and its axon).
- One example of each: capsular hemiplegia; polio, nerve injury, motor neuron disease.
- The comparison table: groups vs individual muscles, tone, wasting, tendon reflexes, plantar, fasciculations, EMG, nerve conduction.
- The shared sign: superficial reflexes lost in both.
- Basis of spasticity: corticoreticular fibres cut, pontine reticulospinal tract released.
- Basis of the brisk tendon reflexes (γ drive ↑) and of the extensor plantar (lost CST action on lumbosacral neurons).
- Basis of the LMN signs: broken reflex arc, lost trophic factors, lost γ drive.
Asked in exams
- Upper and lower motor neuron lesions: Jan 2010, 2 marks · Jul 2010, 2 marks · Jul 2011, 4 marks · Jan 2021, 2 marks · Apr 2021, 3 marks · May 2022, 5 marks · Aug 2024, MCQ · Oct 2024, MCQ