A 54-year-old man comes to the physician for the evaluation of difficulty swallowing of both solids and liquids for 1 month. During the past 5 months, he has also had increased weakness of his hands and legs. He sails regularly and is unable to hold the ropes as tightly as before. Ten years ago, he was involved in a motor vehicle collision. Examination shows atrophy of the tongue. Muscle strength is decreased in the right upper and lower extremities. There is muscle stiffness in the left lower extremity. Deep tendon reflexes are 1+ in the right upper and lower extremities, 3+ in the left upper extremity, and 4+ in the left lower extremity. Plantar reflex shows an extensor response on the left foot. Sensation to light touch, pinprick, and vibration is intact. Which of the following is the most likely diagnosis?

Subacute combined degeneration of spinal cord

Cervical spondylosis with myelopathy

A 76-year-old woman with hypertension and coronary artery disease is brought to the emergency department after the sudden onset of right-sided weakness. Her pulse is 83/min and blood pressure is 156/90 mm Hg. Neurological examination shows right-sided facial drooping and complete paralysis of the right upper and lower extremities. Tongue position is normal and she is able to swallow liquids without difficulty. Knee and ankle deep tendon reflexes are exaggerated on the right. Sensation to vibration, position, and light touch is normal bilaterally. She is oriented to person, place, and time, and is able to speak normally. Occlusion of which of the following vessels is the most likely cause of this patient's current symptoms?

Contralateral lenticulostriate artery

Ipsilateral anterior cerebral artery

Contralateral middle cerebral artery

Ipsilateral posterior inferior cerebellar artery

A 17-year-old boy is brought to the emergency department after being stabbed with a knife during an altercation. Physical examination shows a 4-cm stab wound on the right lateral border of the T1 spinous process. An MRI of the spinal cord shows damage to the area of the right lateral corticospinal tract at the level of T1. Further evaluation will most likely show which of the following findings?

Absence of right-sided motor function below T1

Absence of left-sided proprioception below T1

Presence of left-sided Babinski sign

Absence of left-sided fine touch sensation below T1

Absence of right-sided temperature sensation below T1

A 23-year-old man presents to the emergency room following a stab wound to the back. He was in a bar when he got into an argument with another man who proceeded to stab him slightly right of the midline of his back. He is otherwise healthy and does not take any medications. He has one previous admission to the hospital for a stab wound to the leg from another bar fight 2 years ago. His temperature is 99°F (37.2°C), blood pressure is 115/80 mmHg, pulse is 100/min, and pulse oximetry is 99% on room air. Cardiopulmonary and abdominal exams are unremarkable; however, he has an abnormal neurologic exam. If this wound entered his spinal cord but did not cross the midline, which of the following would most likely be seen in this patient?

Ipsilateral flaccid paralysis at the level of the lesion

Contralateral spasticity below the level of the lesion

Ipsilateral loss of pain and temperature sensation below the lesion

Contralateral loss of tactile, vibration, and proprioception below the lesion

Contralateral loss of sensation at the level of the lesion

UMN vs LMN lesions for USMLE Step 1: High-Yield Anatomy Lessons

Corticospinal Tracts - The Command Pathway

Origin: Primary motor cortex (precentral gyrus).
Function: Main voluntary motor pathway for contralateral, skilled, fine motor control, especially of distal limbs.
Somatotopic Organization: Follows the motor homunculus.

Corticospinal Tract Pathway: UMN and LMN

⭐ High-Yield: The posterior limb of the internal capsule is a common site for lacunar strokes, causing pure motor hemiparesis of the contralateral body.

Lesion Signs - UMN vs. LMN Locator

UMN Lesion: Injury to CNS pathways above the anterior horn cell (e.g., brain, spinal cord).
LMN Lesion: Injury to anterior horn cells or their peripheral axons (e.g., nerve root, peripheral nerve).

UMN vs LMN Lesion Signs

Sign	UMN Lesion (Central)	LMN Lesion (Peripheral)
Tone	Hypertonia (Spastic paralysis)	Hypotonia (Flaccid paralysis)
Reflexes	Hyperreflexia, Clonus	Hyporeflexia, Areflexia
Babinski	Present (Toes extend)	Absent (Toes curl down)
Atrophy	Late & mild (disuse atrophy)	Severe & rapid (denervation)
Fasciculations	Absent	Present
Weakness	Affects muscle groups (Pyramidal)	Affects individual muscles (Myotomal)

⭐ Exam Pearl: Acute UMN lesions can initially present as "spinal shock" with flaccid paralysis and ↓ reflexes, mimicking an LMN lesion, before spasticity and hyperreflexia develop over days to weeks.

Clinical Correlations - Syndromes Spotlight

Amyotrophic Lateral Sclerosis (ALS)
- Combined UMN & LMN signs. Affects corticospinal tracts & anterior horn cells.
- UMN: Spasticity, hyperreflexia, Babinski sign.
- LMN: Fasciculations, atrophy, weakness.
- 📌 Mnemonic: Arm Leg Speech deficits.
Brown-Séquard Syndrome (Hemisection of Cord)
- Ipsilateral UMN signs (spastic paralysis) below the lesion.
- Ipsilateral LMN signs (flaccid paralysis) at the level of the lesion.
- Ipsilateral loss of proprioception/vibration below lesion.
- Contralateral loss of pain/temperature starting 2-3 segments below lesion.

Brown-Séquard syndrome sensory and motor deficits

Pure LMN Syndromes
- Poliomyelitis / Werdnig-Hoffman disease: Destruction of anterior horn cells; presents with flaccid paralysis, atrophy, fasciculations.

⭐ The presence of both UMN and LMN signs in the same limb is a classic finding for Amyotrophic Lateral Sclerosis (ALS).

High‑Yield Points - ⚡ Biggest Takeaways

UMN lesions cause spastic paralysis, ↑ reflexes (hyperreflexia), and ↑ tone (hypertonia).

LMN lesions result in flaccid paralysis, ↓ reflexes (hyporeflexia), and ↓ tone (hypotonia).

The Babinski sign is present in UMN lesions but absent in LMN lesions.

Severe muscle atrophy and fasciculations are classic signs of LMN damage.

UMN pathways originate in the cortex; LMN pathways start at the anterior horn cell.

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