Question:

A 45-year-old man comes to the clinic due to a 2-month history of progressive left arm clumsiness and weakness. The patient initially attributed his symptoms to a left rotator cuff injury he sustained several years ago; however, he has recently developed problems with his gait. The patient's symptoms have interfered with daily activities such as bathing and dressing. He has had no recent injury, headaches, or bowel/bladder symptoms. On physical examination, there is reduced muscle strength in the left upper extremity. Further evaluation with brain MRI reveals a lesion involving the corticospinal tract. Which of the following additional signs is most likely to be seen in this patient?

Hyperactive deep tendon reflexes

Muscle atrophy

Muscle fasciculation

Muscle hypotonia

Resting tremor

Sensory loss in the affected area

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Upper & lower motor neuron signs
UMN signs	Spastic paralysis Clasp-knife rigidity Hyperreflexia Babinski sign
LMN signs	Flaccid paralysis Hypotonia Hyporeflexia Muscle atrophy & fasciculations
LMN = lower motor neuron; UMN = upper motor neuron.

Voluntary muscle activity is mediated by the corticospinal (pyramidal) tracts. First-order neurons of these tracts are located in the premotor and motor cortex of the frontal lobe (Brodmann areas 6 and 4, respectively). Their efferent fibers descend through the internal capsule, midbrain, and pons, and continue to form the pyramids on the anterior aspect of the medulla. In the medulla, 90% of the fibers decussate (cross) to form the lateral corticospinal tract. Fibers that do not decussate descend as the anterior corticospinal tract. The axons of both tracts synapse on the motor neurons of the anterior horn (second-order neurons). Damage to the corticospinal tract is divided into upper and lower motor neuron lesions:

Upper motor neuron (UMN) refers to anything above the anterior horn. Lesions to UMNs (eg, due to stroke, brain tumor) cause a combination of spastic paralysis, clasp-knife rigidity, hyperreflexia (including clonus), and upgoing plantar reflexes (Babinski sign). This likely occurs due to loss of descending inhibition over second-order neurons in the anterior horn.
Damage to the motor neurons of the anterior horn is considered a lower motor neuron (LMN) lesion. This type of injury leads to flaccid paralysis, hypotonia, hyporeflexia, muscle atrophy, and fasciculations. Poliomyelitis and infantile spinal muscular atrophy are examples of LMN lesions (Choices B, C, and D).

Combined UMN and LMN lesions are characteristic of amyotrophic lateral sclerosis (Lou Gehrig disease).

(Choice E) Resting tremor is characteristic of Parkinson disease, which occurs due to loss of dopaminergic neurons in the substantia nigra.

(Choice F) Sensory information is transmitted by the spinothalamic tract (pain and temperature) and dorsal column pathway (vibration and proprioception). Lesions to the corticospinal tract do not cause sensory deficits.

Educational objective:
Upper motor neuron damage leads to spastic paralysis, hyperreflexia, and an upgoing plantar reflex (Babinski sign) due to loss of descending inhibition over lower motor neurons in the anterior horn. Conversely, lower motor neuron lesions cause flaccid paralysis, hypotonia, hyporeflexia, muscle atrophy, and fasciculations.