SN11 SHORT NOTE 5M

Write a short note on the differentiation of upper and lower motor neurone lesions.

General Medicine · Final Professional

Anatomy

The upper motor neurone (UMN) originates in the precentral gyrus (motor cortex) and descends through the corona radiata, internal capsule, cerebral peduncle, pons and medulla as the corticospinal (pyramidal) tract. It decussates at the pyramids of the medulla and descends in the lateral corticospinal tract to synapse on the anterior horn cell.

The lower motor neurone (LMN) comprises the anterior horn cell, nerve root, plexus, peripheral nerve, neuromuscular junction and muscle — the "final common pathway" to the muscle.

Localisation follows from this: a lesion above the decussation causes contralateral signs; below it, ipsilateral signs.

The Core Differences

Feature	Upper motor neurone	Lower motor neurone
Weakness pattern	"Pyramidal" distribution — upper limb extensors and lower limb flexors weaker; hemiparesis, paraparesis or quadriparesis	Distribution of the affected root, nerve or muscle group
Tone	INCREASED — spasticity with "clasp-knife" quality, velocity-dependent	DECREASED — flaccidity, hypotonia
Reflexes	EXAGGERATED (brisk), with clonus and spread	REDUCED or ABSENT
Plantar response	EXTENSOR — Babinski sign positive	Flexor (normal) or absent
Wasting	Absent (mild disuse atrophy late)	PRESENT and early — marked
Fasciculations	Absent	PRESENT (especially anterior horn cell disease)
Superficial reflexes (abdominal, cremasteric)	Lost	Preserved
Sensation	Depends on the level; may show a sensory level	Distribution of the nerve or root
Electromyography	Normal muscle	Denervation — fibrillations, positive sharp waves, giant motor units

The Babinski Sign

Firm stroking of the lateral border of the sole from heel towards the toes, curving medially across the ball, normally produces plantar flexion of the great toe. An extensor response — dorsiflexion of the great toe with fanning of the others — is the Babinski sign, and indicates corticospinal (pyramidal) tract dysfunction.

Important caveats: it is normal in infants under about one year, before myelination of the corticospinal tract is complete; it may be transiently present after a seizure, in deep coma, in hypoglycaemia and under anaesthesia; and equivalent responses can be elicited by other manoeuvres (Chaddock, Oppenheim, Gordon, Gonda).

Spasticity Versus Rigidity — a Common Examination Pair

Feature	Spasticity (pyramidal)	Rigidity (extrapyramidal)
Distribution	Selective — flexors of arm, extensors of leg	Uniform — affects all muscle groups equally
Velocity-dependence	Yes — worse with rapid movement	No — constant throughout the range
Character	"Clasp-knife" — sudden give-way	"Lead-pipe", or "cogwheel" when combined with tremor
Reflexes	Exaggerated with clonus	Normal
Plantar	Extensor	Flexor
Associated	Weakness, Babinski	Bradykinesia, tremor, postural instability

Clinical Localisation of Umn Lesions

Site	Features
Cortex	Contralateral monoparesis or focal weakness; seizures, aphasia, neglect (cortical signs)
Internal capsule	Dense contralateral hemiplegia involving face, arm and leg equally; classic stroke
Brainstem	CROSSED signs — ipsilateral cranial nerve palsy with contralateral hemiparesis
Spinal cord	Para- or quadriparesis with a SENSORY LEVEL and sphincter involvement; signs below the level
Cervical cord	Quadriparesis; LMN signs at the level and UMN signs below it

Causes

UMN lesions: stroke, tumour, multiple sclerosis, traumatic brain and spinal cord injury, cord compression, transverse myelitis, cerebral palsy, motor neurone disease (which has both UMN and LMN signs), hereditary spastic paraplegia, subacute combined degeneration of the cord (UMN signs with absent ankle jerks from coexisting neuropathy).

LMN lesions: anterior horn cell (poliomyelitis, spinal muscular atrophy, motor neurone disease), root (disc prolapse, radiculopathy), plexus (brachial plexus injury), peripheral nerve (Guillain–Barré syndrome, diabetic and other neuropathies, leprosy — the commonest treatable neuropathy in India, trauma, entrapment), neuromuscular junction (myasthenia gravis, botulism) and muscle (myopathy, muscular dystrophy).

CLINICAL PEARL

Mixed UMN and LMN signs in the same patient is a highly localising finding. The classic combinations are motor neurone disease (wasting and fasciculations with brisk reflexes and extensor plantars, and no sensory signs), subacute combined degeneration of the cord (absent ankle jerks with extensor plantars, from B12 deficiency), Friedreich's ataxia, and a cervical myelopathy with radiculopathy (LMN signs in the arms, UMN signs in the legs). Spotting this combination narrows the differential immediately.

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