Midbrain nuclei US Medical PG Practice Questions and MCQs
Practice US Medical PG questions for Midbrain nuclei. These multiple choice questions (MCQs) cover important concepts and help you prepare for your exams.
Midbrain nuclei US Medical PG Question 1: During an examination of the cranial nerves, a patient shows inability to move their eye laterally past the midline. Which of the following structures in the cavernous sinus is most likely affected?
- A. Oculomotor nerve
- B. Trochlear nerve
- C. Ophthalmic nerve
- D. Abducens nerve (Correct Answer)
Midbrain nuclei Explanation: ***Abducens nerve***
- The **abducens nerve (CN VI)** innervates the **lateral rectus muscle**, responsible for **abduction** (lateral movement) of the eye.
- Inability to move the eye laterally past the midline indicates paralysis or weakness of the lateral rectus muscle, directly implicating the abducens nerve.
*Oculomotor nerve*
- The **oculomotor nerve (CN III)** controls most **extraocular muscles** (superior, inferior, medial rectus, inferior oblique) and the levator palpebrae superioris, as well as pupillary constriction.
- Damage to this nerve would primarily affect **adduction**, elevation, depression, and eyelid opening, not isolated lateral gaze.
*Trochlear nerve*
- The **trochlear nerve (CN IV)** innervates the **superior oblique muscle**, which depresses and internally rotates the eye.
- A lesion here typically presents with **vertical diplopia**, particularly when reading or descending stairs, due to impaired eye depression and intorsion.
*Ophthalmic nerve*
- The **ophthalmic nerve (V1)** is one of the three divisions of the trigeminal nerve and is purely **sensory**.
- It provides sensation to the forehead, upper eyelid, cornea, and nose, and does not control any eye movements.
Midbrain nuclei US Medical PG Question 2: A 32-year-old woman is brought to your office by her husband. The husband says that she had been acting strange lately. She has been forgetful, and she sometimes becomes angered for no reason, which is highly unusual for her. She has also been having random, uncontrollable movements, which are also new. On examination, she appears withdrawn and flat. On further questioning, she reveals that her father died at age 45 from a movement disorder. Which of the following is the pathological hallmark of the patient's condition?
- A. Lipohyalinosis
- B. Loss of neurons in the caudate nucleus and putamen (Correct Answer)
- C. Substantia nigra pars compacta
- D. Alpha-synuclein intracellular inclusions
- E. Beta-amyloid plaques
Midbrain nuclei Explanation: ***Loss of neurons in the caudate nucleus and putamen***
- The patient's symptoms (forgetfulness, anger, uncontrolled movements) and family history of an early-onset movement disorder (father died at age 45) are highly suggestive of **Huntington's disease**.
- **Huntington's disease** is characterized pathologically by **selective atrophy and loss of GABAergic neurons** in the **caudate nucleus and putamen** within the basal ganglia.
*Lipohyalinosis*
- **Lipohyalinosis** refers to the **thickening of the vessel walls** of small penetrating arteries, often seen in the brain, and is associated with **lacunar infarcts** due to hypertension and diabetes.
- While it can lead to neurological symptoms, it does not explain the specific combination of psychiatric, cognitive, and choreiform movements with an autosomal dominant family history.
*Substantia nigra pars compacta*
- Degeneration of the **substantia nigra pars compacta** and the resultant **loss of dopaminergic neurons** is the hallmark of **Parkinson's disease**.
- Parkinson's disease typically presents with tremor, rigidity, bradykinesia, and postural instability, which are different from the patient's choreiform movements.
*Alpha-synuclein intracellular inclusions*
- **Alpha-synuclein intracellular inclusions**, known as **Lewy bodies**, are the characteristic pathological finding in **Parkinson's disease** and **Lewy body dementia**.
- These are not associated with Huntington's disease, and the clinical presentation of the patient is not typical of either Parkinson's or Lewy body dementia.
*Beta-amyloid plaques*
- **Beta-amyloid plaques** are extracellular protein deposits, along with **neurofibrillary tangles** (tau protein), that are the pathological hallmarks of **Alzheimer's disease**.
- While Alzheimer's involves cognitive decline, it does not typically present with the prominent choreiform movements and specific genetic inheritance pattern seen in this patient.
Midbrain nuclei US Medical PG Question 3: A 58-year-old woman presents with vision loss in her right eye. She noticed the visual changes the morning of presentation and has never experienced this visual disturbance before. Her medical history is significant for hypertension, hypercholesterolemia, and type II diabetes mellitus. She is currently on lisinopril, lovastatin, and metformin. She has smoked a pack of cigarettes daily for the last 25 years and also is a social drinker. On physical exam, her lids and lashes appear normal and there is no conjunctival injection. Both pupils are equal, round, and reactive to light; however, when the penlight is swung from the left eye to the right eye, there is bilateral pupillary dilation. The nerve that is most likely defective in this patient relays information to which of the following?
- A. Oculomotor nucleus
- B. Edinger-Westphal nucleus
- C. Medial geniculate nucleus
- D. Lateral geniculate nucleus (Correct Answer)
- E. Ventral posteromedial nucleus
Midbrain nuclei Explanation: ***Lateral geniculate nucleus***
- The patient presents with unilateral vision loss (right eye) and a **relative afferent pupillary defect (RAPD)**, demonstrated by bilateral pupillary dilation when light swings from the unaffected left eye to the affected right eye.
- An RAPD localizes the lesion to the **afferent visual pathway anterior to the optic chiasm**, specifically the **retina or optic nerve (CN II)** of the affected eye.
- The **optic nerve** relays visual information TO the **lateral geniculate nucleus (LGN)** of the thalamus, making this the correct answer to the question "which structure does the defective nerve relay information to?"
- Note: A lesion directly AT the LGN (post-chiasmal) would cause vision loss but would NOT produce an RAPD, as the pupillary reflex integrates bilaterally at the pretectal nucleus before reaching the LGN.
*Oculomotor nucleus*
- The **oculomotor nucleus** contains motor neurons for CN III, controlling most extraocular muscles and providing parasympathetic innervation to the pupil via the Edinger-Westphal nucleus.
- A lesion here would cause **efferent deficits**: ipsilateral ptosis, eye positioned "down and out," and a dilated, fixed pupil - but NOT vision loss or RAPD.
- This is an efferent pathway issue, not an afferent visual pathway problem.
*Edinger-Westphal nucleus*
- The **Edinger-Westphal nucleus** provides preganglionic parasympathetic fibers via CN III to the ciliary ganglion, controlling pupillary constriction and accommodation.
- A lesion would cause a **dilated pupil with impaired direct and consensual light reflex** and impaired accommodation, but NOT vision loss or RAPD.
- This affects the efferent limb of the pupillary reflex, not the afferent visual pathway.
*Medial geniculate nucleus*
- The **medial geniculate nucleus (MGN)** is a thalamic relay nucleus in the **auditory pathway**, receiving input from the inferior colliculus.
- A lesion would cause hearing deficits, not visual symptoms or pupillary abnormalities.
*Ventral posteromedial nucleus*
- The **ventral posteromedial nucleus (VPM)** of the thalamus relays sensory information from the face (via trigeminal nerve) and taste sensation.
- A lesion would cause **facial sensory deficits** (numbness, altered sensation) or taste disturbances, not vision loss or RAPD.
Midbrain nuclei US Medical PG Question 4: A 73-year-old man presents to your office accompanied by his wife. He has been experiencing a tremor in his right hand for the last several months that seems to be worsening. He does not have any other complaints and says he’s “fine.” His wife thinks that he has also had more difficulty walking. His history is significant for hypertension and an ischemic stroke of the right middle cerebral artery 2 years ago. His medications include hydrochlorothiazide and daily aspirin. On physical exam you note that the patient speaks with a soft voice and has decreased facial expressions. He has a resting tremor that is worse on the right side. He has increased resistance to passive movement when you flex and extend his relaxed wrist. He has 5/5 strength bilaterally. Neuronal degeneration in which of the following locations is most likely responsible for the progression of this disease?
- A. Vermis
- B. Substantia nigra pars compacta (Correct Answer)
- C. Frontotemporal lobe
- D. Caudate and putamen
- E. Subthalamic nucleus
Midbrain nuclei Explanation: ***Substantia nigra pars compacta***
- The patient's symptoms, including **resting tremor**, **bradykinesia** (soft voice, decreased facial expressions, difficulty walking), and **rigidity** (increased resistance to passive movement), are classic signs of **Parkinson's disease**.
- Parkinson's disease is primarily caused by the degeneration of **dopaminergic neurons** in the **substantia nigra pars compacta**, leading to a lack of dopamine in the basal ganglia.
*Vermis*
- The **vermis** is a part of the cerebellum primarily involved in coordinating **truncal movements** and maintaining **posture**.
- Damage to the vermis typically causes **ataxia**, truncal instability, and gait disturbances, which are not the primary features described here.
*Frontotemporal lobe*
- The **frontotemporal lobe** is associated with cognitive functions, personality, and language.
- Degeneration in this area is characteristic of **frontotemporal dementia**, presenting with prominent behavioral changes, language difficulties, or progressive memory loss, which are not the main symptoms in this patient.
*Caudate and putamen*
- The **caudate and putamen** are components of the **striatum**, which receives dopaminergic input from the substantia nigra.
- While the lack of dopamine in the striatum contributes to Parkinsonian symptoms, the primary neuronal degeneration occurs *before* this in the substantia nigra pars compacta, which *projects* to the striatum.
*Subthalamic nucleus*
- The **subthalamic nucleus** is part of the basal ganglia circuit, and its overactivity can contribute to motor symptoms in Parkinson's disease.
- **Deep brain stimulation (DBS)** targeting the subthalamic nucleus is a treatment for Parkinson's, but the primary site of neuronal degeneration in the disease itself is not the subthalamic nucleus.
Midbrain nuclei US Medical PG Question 5: A 40-year-old man is brought to the emergency department after sustaining multiple lacerations during a bar fight. The patient’s wife says that he has been showing worsening aggression and has been involved in a lot of arguments and fights for the past 2 years. The patient has no significant past medical or psychiatric history and currently takes no medications. The patient cannot provide any relevant family history since he was adopted as an infant. His vitals are within normal limits. On physical examination, the patient looks apathetic and grimaces repeatedly. Suddenly, his arms start to swing by his side in an uncontrolled manner. Which area of the brain is most likely affected in this patient?
- A. Cerebral cortex
- B. Caudate nucleus (Correct Answer)
- C. Cerebellum
- D. Medulla oblongata
- E. Substantia nigra
Midbrain nuclei Explanation: **Caudate nucleus**
- The patient exhibits features like **worsening aggression**, **apathy**, and **uncontrolled, sudden movements** of the limbs, which are characteristic of Huntington's disease, a condition primarily affecting the **caudate nucleus**.
- **Huntington's disease** is an autosomal dominant neurodegenerative disorder linked to a trinucleotide repeat expansion (CAG) on chromosome 4, leading to atrophy of the **caudate and putamen**.
*Cerebral cortex*
- While damage to the cerebral cortex can cause personality changes and motor deficits, the specific combination of **choreiform movements** and progressive cognitive/behavioral decline seen here is more indicative of a basal ganglia disorder like Huntington's.
- Cortical lesions more commonly present with **focal neurological deficits** such as hemiparesis, aphasia, or sensory loss, which are not the primary features described.
*Cerebellum*
- Damage to the cerebellum typically results in **ataxia**, **dysmetria**, **intention tremor**, and problems with balance and coordination.
- The patient's **uncontrolled, sudden limb movements** are characteristic of chorea, not cerebellar dysfunction.
*Medulla oblongata*
- The medulla oblongata is crucial for vital autonomic functions such as **breathing, heart rate, and blood pressure regulation**.
- Lesions in this area would likely cause life-threatening symptoms, including **respiratory failure** or severe cardiovascular instability, which are not present in this patient.
*Substantia nigra*
- Damage or degeneration of the substantia nigra is primarily associated with **Parkinson's disease**, leading to symptoms like **bradykinesia**, **rigidity**, **resting tremor**, and **postural instability**.
- The patient's **hyperkinetic movements** (choreiform movements) are opposite to the hypokinetic presentation of Parkinson's disease.
Midbrain nuclei US Medical PG Question 6: A 28-year-old man presents with visual disturbances. He says that he is having double vision since he woke up this morning. His past medical history is insignificant except for occasional mild headaches. The patient is afebrile and his vitals are within normal limits. On physical examination of his eyes, there is paralysis of left lateral gaze. Also, at rest, there is esotropia of the left eye. A noncontrast CT scan of the head reveals a tumor impinging on one of his cranial nerves. Which of the following nerves is most likely affected?
- A. Trigeminal nerve
- B. Optic nerve
- C. Oculomotor nerve
- D. Trochlear nerve
- E. Abducens nerve (Correct Answer)
Midbrain nuclei Explanation: ***Abducens nerve***
- **Paralysis of left lateral gaze** and **esotropia** (inward turning of the eye) at rest are classic signs of a **left abducens nerve (CN VI) palsy**. This nerve exclusively innervates the **lateral rectus muscle**, which is responsible for abducting (moving outward) the eye.
- Impingement from a **tumor** is a common cause of cranial nerve palsies, and the presentation perfectly matches the function of the abducens nerve.
*Trigeminal nerve*
- The **trigeminal nerve (CN V)** is responsible for **facial sensation** and **mastication** (chewing).
- Dysfunction would present as facial numbness, pain, or weakness in chewing, not visual disturbances or eye movement issues.
*Optic nerve*
- The **optic nerve (CN II)** transmits **visual information** from the retina to the brain.
- Lesions typically cause **vision loss** (e.g., blindness, scotoma, visual field defects), not double vision or eye movement paralysis.
*Oculomotor nerve*
- The **oculomotor nerve (CN III)** controls most **extraocular muscles** (medial, superior, inferior rectus, inferior oblique) and the **levator palpebrae superioris** (eyelid elevation), as well as pupillary constriction.
- A palsy would typically present with a **"down and out" eye**, **ptosis** (drooping eyelid), and **mydriasis** (dilated pupil), which are not described.
*Trochlear nerve*
- The **trochlear nerve (CN IV)** innervates the **superior oblique muscle**, which depresses and intorts the eye.
- A palsy typically causes **vertical double vision**, especially when looking down and inward, and a compensatory head tilt away from the affected side. This does not match the described lateral gaze paralysis.
Midbrain nuclei US Medical PG Question 7: A 28-year-old male presents to his primary care physician with complaints of intermittent abdominal pain and alternating bouts of constipation and diarrhea. His medical chart is not significant for any past medical problems or prior surgeries. He is not prescribed any current medications. Which of the following questions would be the most useful next question in eliciting further history from this patient?
- A. "Does the diarrhea typically precede the constipation, or vice-versa?"
- B. "Is the diarrhea foul-smelling?"
- C. "Please rate your abdominal pain on a scale of 1-10, with 10 being the worst pain of your life"
- D. "Are the symptoms worse in the morning or at night?"
- E. "Can you tell me more about the symptoms you have been experiencing?" (Correct Answer)
Midbrain nuclei Explanation: ***Can you tell me more about the symptoms you have been experiencing?***
- This **open-ended question** encourages the patient to provide a **comprehensive narrative** of their symptoms, including details about onset, frequency, duration, alleviating/aggravating factors, and associated symptoms, which is crucial for diagnosis.
- In a patient presenting with vague, intermittent symptoms like alternating constipation and diarrhea, allowing them to elaborate freely can reveal important clues that might not be captured by more targeted questions.
*Does the diarrhea typically precede the constipation, or vice-versa?*
- While knowing the sequence of symptoms can be helpful in understanding the **pattern of bowel dysfunction**, it is a very specific question that might overlook other important aspects of the patient's experience.
- It prematurely narrows the focus without first obtaining a broad understanding of the patient's overall symptomatic picture.
*Is the diarrhea foul-smelling?*
- Foul-smelling diarrhea can indicate **malabsorption** or **bacterial overgrowth**, which are important to consider in some gastrointestinal conditions.
- However, this is a **specific symptom inquiry** that should follow a more general exploration of the patient's symptoms, as it may not be relevant if other crucial details are missed.
*Please rate your abdominal pain on a scale of 1-10, with 10 being the worst pain of your life*
- Quantifying pain intensity is useful for assessing the **severity of discomfort** and monitoring changes over time.
- However, for a patient with intermittent rather than acute, severe pain, understanding the **character, location, and triggers** of the pain is often more diagnostically valuable than just a numerical rating initially.
*Are the symptoms worse in the morning or at night?*
- Diurnal variation can be relevant in certain conditions, such as inflammatory bowel diseases where nocturnal symptoms might be more concerning, or functional disorders whose symptoms might be stress-related.
- This is another **specific question** that should come after gathering a more complete initial picture of the patient's symptoms to ensure no key information is overlooked.
Midbrain nuclei US Medical PG Question 8: An 87-year-old male presents to his neurologist for a follow-up visit. He is being followed for an inoperable tumor near his skull. He reports that he recently noticed that food has started to lose its taste. He also notes increasing difficulty with swallowing. He has a history of myocardial infarction, diabetes mellitus, hyperlipidemia, hypertension, and presbycusis. He takes aspirin, metoprolol, metformin, glyburide, atorvastatin, lisinopril, and hydrochlorothiazide. On examination, the patient is a frail-appearing male sitting in a wheelchair. He is oriented to person, place, and time. Gag reflex is absent on the right side. A taste evaluation is performed which demonstrates a decreased ability to detect sour and bitter substances on the right posterior tongue. The nerve responsible for this patient’s loss of taste sensation also has which of the following functions?
- A. Somatic sensory innervation to the roof of the pharynx
- B. Parasympathetic innervation to the trachea
- C. Somatic sensory innervation to the lower lip
- D. Parasympathetic innervation to the parotid gland (Correct Answer)
- E. Parasympathetic innervation to the submandibular gland
Midbrain nuclei Explanation: ***Parasympathetic innervation to the parotid gland***
- The patient's symptoms, including loss of taste on the **right posterior tongue**, difficulty swallowing, and an absent gag reflex, point to an issue with the **glossopharyngeal nerve (CN IX)**.
- The glossopharyngeal nerve provides **parasympathetic innervation to the parotid gland** via the otic ganglion, stimulating saliva production.
*Somatic sensory innervation to the roof of the pharynx*
- The glossopharyngeal nerve (CN IX) does provide somatic sensory innervation to the pharynx, but specifically the **posterior 1/3 of the tongue**, tonsils, and part of the pharynx, not primarily the roof.
- While related to the pharynx, this option is not the most precise or unique function associated with the primary nerve implicated here.
*Parasympathetic innervation to the trachea*
- **Parasympathetic innervation to the trachea** is primarily mediated by the **vagus nerve (CN X)**, which innervates the smooth muscle and glands of the trachea and bronchi.
- The glossopharyngeal nerve (CN IX) does not have a direct role in tracheal innervation.
*Somatic sensory innervation to the lower lip*
- **Somatic sensory innervation to the lower lip** is primarily provided by the **mental nerve**, a branch of the **trigeminal nerve (CN V)**.
- The glossopharyngeal nerve (CN IX) is not involved in sensory innervation of the lower lip.
*Parasympathetic innervation to the submandibular gland*
- **Parasympathetic innervation to the submandibular and sublingual glands** is provided by the **facial nerve (CN VII)** via the submandibular ganglion.
- This function is distinct from the glossopharyngeal nerve's role in innervating the parotid gland.
Midbrain nuclei US Medical PG Question 9: A 26-year-old man is brought to the emergency department by ambulance after being involved in a motor vehicle collision. He does not open his eyes on command or respond to verbal cues. A CT scan of the head shows a hyperdense fluid collection in the right medial temporal lobe with medial displacement of the uncus and parahippocampal gyrus of the temporal lobe. Which of the following cranial nerves is most likely to be injured as a result of this patient's lesion?
- A. Vagus
- B. Facial
- C. Oculomotor (Correct Answer)
- D. Abducens
- E. Trigeminal
Midbrain nuclei Explanation: ***Oculomotor***
- The description of **medial displacement of the uncus and parahippocampal gyrus** (uncus herniation) compresses the **oculomotor nerve (CN III)** as it passes between the posterior cerebral and superior cerebellar arteries.
- Compression of the oculomotor nerve leads to a **dilated pupil** (due to parasympathetic fiber involvement) and **down-and-out deviation of the eye** (due to paralysis of extraocular muscles it innervates).
*Vagus*
- The vagus nerve (CN X) is deep within the skull and brainstem, far from the temporal lobe, and is not directly affected by uncal herniation.
- Injury to the vagus nerve typically presents with dysphagia, hoarseness, or cardiac arrhythmias, symptoms not indicated here.
*Facial*
- The facial nerve (CN VII) exits the brainstem at the pontomedullary junction and is located more superiorly and laterally than the structures involved in uncal herniation.
- Damage to the facial nerve causes facial muscle weakness or paralysis, which is not the primary concern with uncal herniation.
*Abducens*
- The abducens nerve (CN VI) is a long, slender nerve that can be affected by **generalized increases in intracranial pressure**, but is less commonly directly compressed by an uncal herniation itself.
- Injury to the abducens nerve causes **lateral rectus muscle paralysis**, leading to medial deviation of the eye, whereas uncal herniation typically affects the oculomotor nerve.
*Trigeminal*
- The trigeminal nerve (CN V) exits the pons and is located superior to the tentorial notch and medial temporal lobe, making it unlikely to be directly compressed by uncal herniation.
- Injury to the trigeminal nerve causes sensory loss in the face or weakness of the muscles of mastication, which are not consistent with the described lesion.
Midbrain nuclei US Medical PG Question 10: Where does the only cranial nerve without a thalamic relay nucleus enter the skull?
- A. Superior orbital fissure
- B. Internal auditory meatus
- C. Foramen rotundum
- D. Jugular foramen
- E. Cribriform plate (Correct Answer)
Midbrain nuclei Explanation: ***Cribriform plate***
- The **olfactory nerve (CN I)** is the only cranial nerve that does not have a thalamic relay nucleus before reaching the cerebral cortex.
- It passes through the **cribriform plate** of the ethmoid bone to reach the olfactory bulbs.
*Superior orbital fissure*
- This opening transmits the **oculomotor (CN III), trochlear (CN IV), ophthalmic division of trigeminal (CN V1)**, and **abducens (CN VI)** nerves.
- These nerves all have sensory or motor components that relay through the thalamus, directly or indirectly.
*Internal auditory meatus*
- This canal transmits the **facial (CN VII)** and **vestibulocochlear (CN VIII)** nerves.
- The vestibulocochlear nerve's auditory pathway involves a thalamic relay in the **medial geniculate nucleus**.
*Foramen rotundum*
- The **maxillary division of the trigeminal nerve (CN V2)** passes through the foramen rotundum.
- Sensory information carried by CN V2 relays through the **thalamus**.
*Jugular foramen*
- This opening transmits the **glossopharyngeal (CN IX), vagus (CN X)**, and **accessory (CN XI)** nerves.
- Sensory components of these nerves, particularly taste and visceral sensation, involve thalamic nuclei.
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