Hyperreflexia of DTRs and clonus suggests a lesion in which neural pathway?

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Study for the Parkinson’s Disease Exam. Engage with detailed flashcards and multiple-choice questions, each offering hints and explanations. Prepare effectively for your exam!

Multiple Choice

Hyperreflexia of DTRs and clonus suggests a lesion in which neural pathway?

Explanation:
Upper motor neuron damage to the corticospinal tract produces hyperreflexia and clonus. The corticospinal tract normally dampens spinal reflexes; when it’s disrupted, inhibitory control is lost, making reflexes exaggerated (hyperreflexia) and allowing the stretch reflex to produce repetitive, rhythmic contractions (clonus). This pattern is a hallmark of corticospinal tract (UMN) lesions. In contrast, cerebellar lesions cause ataxia and coordination problems, basal ganglia lesions produce movement initiation issues like rigidity and bradykinesia, and peripheral nerve (LMN) lesions yield weakness with reduced or absent reflexes, atrophy, and fasciculations.

Upper motor neuron damage to the corticospinal tract produces hyperreflexia and clonus. The corticospinal tract normally dampens spinal reflexes; when it’s disrupted, inhibitory control is lost, making reflexes exaggerated (hyperreflexia) and allowing the stretch reflex to produce repetitive, rhythmic contractions (clonus). This pattern is a hallmark of corticospinal tract (UMN) lesions.

In contrast, cerebellar lesions cause ataxia and coordination problems, basal ganglia lesions produce movement initiation issues like rigidity and bradykinesia, and peripheral nerve (LMN) lesions yield weakness with reduced or absent reflexes, atrophy, and fasciculations.

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