Bit · Neuro

UMN vs LMN signs

Two patterns of motor neuron damage with opposite physical findings. The pivot is tone and reflexes.

Mechanism

The motor pathway is two neurons in series:

Some diseases give both — ALS is the classic mixed UMN+LMN disease.

Differentiator Table

SignUMN lesionLMN lesion
Tone↑ Spasticity (clasp-knife)↓ Flaccidity
Reflexes (DTRs)↑ Hyperreflexia, clonus↓ Hyporeflexia or absent
Babinski signPRESENT (upgoing toes)Absent (downgoing toes)
Muscle bulkMild disuse atrophy lateSignificant atrophy early
FasciculationsAbsentPRESENT
Weakness patternPyramidal (extensors weaker in arms; flexors weaker in legs)Segmental — follows nerve / nerve root
Classic exampleStroke (corticospinal tract), spinal cord injury above conus, MSPolio, Guillain-Barré, peripheral nerve injury, cauda equina, spinal muscular atrophy
Mixed (BOTH UMN and LMN)Amyotrophic lateral sclerosis (ALS) — pathognomonic combination

The Pivot

Four findings tell you which one:

  1. Tone — spastic → UMN. Flaccid → LMN.
  2. Reflexes — brisk/clonus → UMN. Absent → LMN.
  3. Babinski sign present → UMN (in an adult).
  4. Fasciculations and atrophy → LMN.

If you see both patterns in different muscle groups in the same patient — think ALS. Hyperreflexic biceps in an arm that also has atrophy and fasciculations is the classic finding.

NBME-Style Stem

A 58-year-old man presents with 8 months of progressive weakness. Examination shows atrophy and fasciculations of the tongue and intrinsic hand muscles, brisk reflexes throughout, bilateral Babinski signs, and a spastic gait. Sensation is intact. Which of the following is the most likely diagnosis?
Concept Anchor
UMN damage disinhibits the spinal reflex (everything goes up — tone, reflexes, plantar response); LMN damage cuts the muscle off from all input (everything goes down — tone, bulk, reflexes — plus fasciculations as denervated fibres twitch). ALS is the disease that does both at once.

← Bit Library  ·  Log a missed question →