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Behavioral & Nervous Physiology — Step 1 practice questions
46 questions in this area, with an explanation for every answer choice.
Three samples below, free and without an account.
How this shows up on Step 1
Physiology questions in this section combine two things the exam tests separately elsewhere. Physiology questions can be reasoned rather than recalled, which makes them the best return on study time. Neuroanatomy questions are localisation problems: a deficit is described and you name the lesion site.
Sample questions
Sample question 1
A 22-year-old woman has irresistible daytime sleep attacks, vivid hallucinations while falling asleep, episodes of paralysis on awakening, and sudden bilateral leg weakness when she laughs. Which of the following underlies her condition?
Explanations
A. Excessive GABA activity in the reticular formation
Excess GABA is not the mechanism.
B. Loss of hypothalamic orexin (hypocretin)-producing neurons, likely autoimmune, with HLA-DQB1*06:02 association · correct
Narcolepsy type 1 results from destruction of orexin/hypocretin neurons in the lateral hypothalamus, producing low CSF orexin, strong HLA-DQB1*06:02 association, and intrusion of REM phenomena into wakefulness: cataplexy (sudden loss of tone with emotion), hypnagogic/hypnopompic hallucinations, and sleep paralysis. Diagnosis uses polysomnography with a multiple sleep latency test showing short REM latency. Treat sleepiness with modafinil and cataplexy with sodium oxybate or venlafaxine.
C. Deficiency of dopamine in the substantia nigra
Nigral dopamine loss is Parkinson disease.
D. Iron deficiency affecting dopaminergic pathways
Iron deficiency is linked to restless legs syndrome.
E. Obstruction of the upper airway during sleep
Airway obstruction is obstructive sleep apnea, which causes sleepiness but not cataplexy.
Sample question 2
Which of the following best describes the physiologic basis of the deep tendon (myotatic/stretch) reflex, such as the knee-jerk reflex?
Explanations
A. A reflex with no clinical utility
Deep tendon reflexes have significant clinical utility in neurologic examination, localizing lesions along the reflex arc.
B. A monosynaptic reflex arc involving muscle spindle afferents directly synapsing on alpha motor neurons innervating the same muscle · correct
The deep tendon reflex is a classic monosynaptic reflex arc: muscle spindle stretch receptors (Ia afferents) directly synapse on alpha motor neurons innervating the same muscle, causing rapid reflexive contraction in response to stretch, without requiring higher brain processing.
C. A polysynaptic reflex requiring cortical processing for every response
This reflex is specifically MONOsynaptic (a single synapse), not polysynaptic, and does not require cortical processing for its basic response.
D. A reflex that requires conscious voluntary effort to occur
This is an involuntary reflex, not requiring conscious voluntary effort.
E. A reflex mediated entirely by the cerebellum with no spinal cord involvement
This reflex is mediated at the SPINAL CORD level, not primarily the cerebellum.
Sample question 3
A patient receiving a nondepolarizing neuromuscular blocking agent during surgery is given neostigmine at the end of the case along with glycopyrrolate. Which of the following best explains this combination?
Explanations
A. Neostigmine directly antagonizes the blocking agent at its binding site
Neostigmine works indirectly by increasing the competing neurotransmitter.
B. Glycopyrrolate crosses the blood-brain barrier to prevent central effects
Its inability to cross the barrier is precisely why it is chosen.
C. Glycopyrrolate potentiates the neuromuscular blockade
Glycopyrrolate has no effect on the neuromuscular junction.
D. Neostigmine reverses depolarizing blockade from succinylcholine
Cholinesterase inhibitors PROLONG succinylcholine blockade.
E. Neostigmine raises synaptic acetylcholine to outcompete the competitive blocker at nicotinic receptors, while glycopyrrolate blocks the resulting MUSCARINIC effects such as bradycardia and secretions · correct
Nondepolarizing agents such as rocuronium and vecuronium COMPETITIVELY block nicotinic receptors, so raising acetylcholine with an acetylcholinesterase inhibitor restores transmission. Because the increased acetylcholine also stimulates MUSCARINIC receptors — causing bradycardia, bronchoconstriction, salivation, and gastrointestinal hypermotility — an antimuscarinic (glycopyrrolate or atropine) is co-administered. Glycopyrrolate is preferred because it does NOT cross the blood-brain barrier, avoiding central anticholinergic delirium. Sugammadex encapsulates rocuronium directly, avoiding this entirely.
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