upper motor neuron lesion

**Definition/anatomy:** UMNs originate in the primary motor cortex (precentral gyrus, Brodmann area 4), premotor cortex, and supplementary motor area. They descend via the corona radiata → posterior limb of the internal capsule → cerebral peduncle (midbrain) → basilar pons → medullary pyramids. About 90% of fibers decussate at the caudal medulla (pyramidal decussation) and continue as the lateral corticospinal tract, which synapses on lower motor neurons (LMNs) in the anterior horn. Corticobulbar fibers go to cranial nerve nuclei.

**Pathophysiology:** Loss of descending input removes inhibitory control over spinal reflex arcs and disinhibits the LMN. The result is increased tone and hyperreflexia. Reticulospinal and vestibulospinal pathways are left unopposed. Because the LMN and its muscle remain intact, there is no significant denervation atrophy. Disuse atrophy may develop later.

**Clinical findings (UMN):** - Weakness or paralysis, typically in a pyramidal pattern: extensors are weaker than flexors in the arms, and flexors are weaker than extensors in the legs. - Spasticity: a velocity-dependent increase in tone with a "clasp-knife" quality. - Hyperreflexia and sustained clonus. - Positive Babinski sign (extensor plantar response). Hoffmann sign is also positive. - Loss of superficial reflexes (abdominal, cremasteric). - No fasciculations, and minimal atrophy. - Acute lesions (e.g., stroke, acute spinal cord injury) may first show flaccidity and hyporeflexia ("spinal shock" or cerebral diaschisis). Spasticity and hyperreflexia emerge over days to weeks.

**UMN vs LMN:** - UMN: spastic paralysis, ↑ reflexes, ↑ tone, Babinski present, no fasciculations, minimal atrophy. - LMN: flaccid paralysis, ↓ reflexes, ↓ tone, Babinski absent, fasciculations, marked atrophy.

**Localization pearls:** - Cortex: contralateral weakness. An MCA stroke affects the face and arm more than the leg. An ACA stroke affects the leg more than the arm. - Internal capsule (lacunar stroke): pure motor hemiparesis involving the face, arm, and leg. - Brainstem: crossed findings, with ipsilateral cranial nerve deficits and contralateral body weakness. - Spinal cord above the pyramidal decussation: ipsilateral weakness below the lesion (e.g., Brown-Séquard syndrome). - Facial nerve: a UMN (central) facial palsy spares the forehead because of bilateral cortical innervation of the upper face. An LMN (peripheral) palsy involves the whole ipsilateral face.

**Associated diseases:** - Stroke. - Multiple sclerosis. - Spinal cord compression or trauma. - Primary lateral sclerosis (pure UMN). - ALS (mixed UMN and LMN signs). - Subacute combined degeneration (B12 deficiency, which affects the dorsal columns and lateral corticospinal tracts). - Hereditary spastic paraplegia. - Cerebral palsy. - Anterior spinal artery syndrome. - Tropical spastic paraparesis (HTLV-1).

**Management concepts:** Treat the underlying cause. For spasticity, use baclofen (GABA-B agonist), tizanidine (α2 agonist), dantrolene (blocks ryanodine receptor Ca²⁺ release), benzodiazepines, and botulinum toxin for focal spasticity. Physical therapy is also used.

**High-yield buzzwords:** "Spastic paralysis," "clasp-knife," "upgoing toes," "hyperreflexia with clonus," "forehead sparing."