Upper Motor Neuron lesions (UMNL) / Pyrimidal Lower motor neuron lesions

insufficiency (LMNL)
Location From pyrimidal cells of precentral gyrus of frontal Anterior horn cells distally to
cortex (primary motor cortex) to anterior horn muscles (anterior horn, nerve
cells of the spinal segment (brain, internal roots, plexuses, peripheral
capsule, brainstem, spinal cord before anterior nerve, neruomuscular junction,
horn) muscle)
Why Lose ability of spinal pathway to send signals In nerve crush injury, directly
from upper cortical center down to anterior horn, lose innervation direct to the
dysregulated innervation of the muscles, muscles muscle
go uncontrolled “crazy”
Pronator May be present May be some drift/movement
drift of arm(s) if weak or de-
afferented, but not pronator
Weakness Paralysis of movements on the affected side, Flaccid muscle paresis or
weakness in groups of muscles rather than paralysis - Weakness
individually in “pyrimidal” pattern typically corresponds to muscles
extensors (upper limbs) or flexors (lower limbs supplied by the involved
neurons, limited to segmental
or focal pattern, Root
innervated pattern
Tone Hypertonia, velocity-dependant spasticity on arm Hypotonia or atonia, little
flexors and leg extensors, “clasp-knife response” resistance to passive stretch,
where initial higher resistance to movement is (floppy and soft)
followed by a lesser resistance
Reflexes Hyperreflexia (Exaggerated or brisk), increased Hyporeflexia or areflexia
deep tendon reflexes and sustained clonus, (reduced or absent), decreased
however superficial abdominal reflexes and deep tendon reflexes
cremasteric reflex are absent
Atropy No muscle atrophy seen initially, but later some Denervation atrophy / muscle
Disuse atrophy or muscle wasting wasting much earlier
Plantar Extensor plantar response (Babinski +) Normal, flexor plantar
reflexes response (Babinski -)
Fine Loss of performance of fine-skilled volunttary
movements movements especially at distal end of the limbs
Other Decreased endurance, Decreased control of Muscle fibrillations
findings active movement, particularly slowness (contraction of individualised
fibers) indicated by abnormal
EMG potentials

Muscle fasciculations
(contraction of a group of
fibers) due to irritation of the
motor neurons – seen with
naked eye

Muscle contracture (shortening

of paralyzed muscles)

Reaction of degeneration:
When the LMN is cut, a muscle
 will no longer respond to
interrupted electrical
stimulation 7 days after nerve
section, although it will still
respond to direct current. After
10 days, response to direct
current also ceases.

Forehead involvements
Examples Pseudobulbar palsy Bells palsy
Acquired brain injury e.g. Stroke Bulbar palsy
Multiple sclerosis Poliomyelitis
Cerebral palsy Amyotrophic Lateral Sclerosis
Spinal cord injury Gullian-Barre syndrome
Myasthenia Gravis

In UMNL, everything goes up. In LMNL, everything goes down.

Upper motor neurons lesions can be further localised by the other symptoms that go along with the
weakness. For example:

A cord lesion may also cause sphincter symptoms, a sensory level, bilateral motor signs.

A brain stem lesion may also cause dysarthria, dysphagia, Horner's syndrome, cerebellar signs,
spinothalamic sensory loss.

A lesion of the motor cortex may be associated with frontal signs, dysphasia, hemianopia,
disturbance of higher sensory function eg agnosias.

Lower motor neuron lesions can generally be inferred from accompanying symptoms and signs, for
example:

Back pain and sciatica suggests a root problem

Weakness of the biceps with absence of the biceps reflex, with upper motor neurone signs in the
legs suggests cord disease (eg a disc) at C5/6 (LMN at that level, UMN below).

Weakness of thumb abduction, wasting of the thenar eminence and numbness in the thumb and
lateral 21/2 fingers suggests median nerve pathology.