Brainstem nuclei

Brainstem nuclei US Medical PG Question 1: A 45-year-old female is admitted to the hospital after worsening headaches for the past month. She has noticed that the headaches are usually generalized, and frequently occur during sleep. She does not have a history of migraines or other types of headaches. Her past medical history is significant for breast cancer, which was diagnosed a year ago and treated with mastectomy. She recovered fully and returned to work shortly thereafter. CT scan of the brain now shows a solitary cortical 5cm mass surrounded by edema in the left hemisphere of the brain at the grey-white matter junction. She is admitted to the hospital for further management. What is the most appropriate next step in management for this patient?

• A. Seizure prophylaxis and palliative pain therapy
• B. Chemotherapy
• C. Irradiation to the brain mass
• D. Surgical resection of the mass (Correct Answer)

Brainstem nuclei Explanation: ***Surgical resection of the mass*** - The presence of a **solitary cortical mass** with significant edema [1], [2] in a patient with a history of **breast cancer** [3] strongly suggests a resectable brain metastasis that is causing symptomatic cerebral edema. - **Surgical resection** offers the best chance for immediate symptom relief, pathological diagnosis, and improved prognosis in cases conducive to complete removal [1]. *Seizure prophylaxis and palliative pain therapy* - While seizure prophylaxis might be considered due to the mass effect, it is a **supportive measure** and does not address the underlying cause of the symptoms (the mass) that can be surgically removed. - **Palliative pain therapy** would also be a supportive measure only and would not achieve a definitive diagnosis or treatment of the mass. *Chemotherapy* - **Chemotherapy** for brain metastases often has limited efficacy due to the **blood-brain barrier** and is generally reserved for systemic disease or multiple, unresectable brain lesions. - Prior to initiating chemotherapy, a definitive **histopathologic diagnosis** is usually required, and surgical resection would provide tissue for this purpose. *Irradiation to the brain mass* - While **brain irradiation** (like stereotactic radiosurgery or whole-brain radiation therapy) is an option for brain metastases, especially for multiple or unresectable lesions, **surgical resection** is generally preferred for a solitary, accessible metastasis with significant mass effect. - Irradiation alone might not provide the same immediate symptomatic relief from brain edema as surgical decompression [2].

Brainstem nuclei US Medical PG Question 2: A 60-year-old woman presents with progressive difficulty swallowing solid foods for the past 2 months. She also says her voice has gradually changed, and she has had recent episodes of vertigo associated with nausea and vomiting and oscillating eye movements while reading. She denies any problems with the movement of her face or extremities. Past medical history is significant for hypertension, managed with enalapril, and dyslipidemia, which she is managing with dietary modifications. The patient reports a 40-pack-year smoking history. Vital signs are within normal limits. On physical examination, there is decreased pain and temperature sensation on the right side of her body, and she cannot touch her nose with her eyes closed. Which of the following is the most likely site of vascular occlusion in this patient?

• A. Anterior cerebral artery
• B. Anterior inferior cerebellar artery
• C. Posterior inferior cerebellar artery (Correct Answer)
• D. Middle cerebral artery
• E. Anterior spinal artery

Brainstem nuclei Explanation: ***Correct: Posterior inferior cerebellar artery*** - This presentation is classic for **Wallenberg syndrome (lateral medullary syndrome)**, which is most commonly caused by occlusion of the **posterior inferior cerebellar artery (PICA)**. - Key symptoms like **dysphagia**, **hoarseness (nucleus ambiguus involvement)**, **vertigo, nausea, vomiting, nystagmus (vestibular nuclei)**, **ipsilateral ataxia (inferior cerebellar peduncle/cerebellum)**, and **contralateral pain and temperature loss (spinothalamic tract)** are all present. *Incorrect: Anterior cerebral artery* - Occlusion of the anterior cerebral artery typically causes **contralateral leg weakness and sensory loss**, with **gait dysfunction** and **behavioral changes**. - It does not explain the **brainstem symptoms** like dysphagia, vertigo, or ataxia. *Incorrect: Anterior inferior cerebellar artery* - An **anterior inferior cerebellar artery (AICA) stroke** would present with symptoms of lateral pontine syndrome, including **ipsilateral facial weakness and sensory loss**, **tinnitus and hearing loss**, and **ataxia**. - While some vestibular symptoms can occur, the prominent **dysphagia and hoarseness** point more strongly to medullary involvement. *Incorrect: Middle cerebral artery* - A **middle cerebral artery (MCA) stroke** typically results in **contralateral hemiparesis**, **hemianesthesia**, and possibly **aphasia** (if dominant hemisphere affected) or **hemineglect** (if non-dominant hemisphere affected). - This does not account for the brainstem signs observed in the patient. *Incorrect: Anterior spinal artery* - Occlusion of the **anterior spinal artery** primarily affects the spinal cord, causing **bilateral motor weakness, bilateral loss of pain and temperature sensation below the lesion**, and **bladder dysfunction**. - It does not cause the cerebellar, vestibular, or bulbar symptoms seen in this patient.

Brainstem nuclei US Medical PG Question 3: A 25-year-old man presents to the emergency department with the sudden onset of neck pain and a severe spinning sensation for the last 6 hours. The symptoms initially began while he was lifting weights in the gym. He feels the room is spinning continuously, and he is unable to open his eyes or maintain his balance. The dizziness and pain are associated with nausea and vomiting. Past medical history is unremarkable. His blood pressure is 124/88 mm Hg, the heart rate is 84/min, the temperature is 37.0°C (98.6°F), the respiratory rate is 12/min, and the BMI is 21.6 kg/m2. On physical examination, he is awake and oriented to person, place, and time. Higher mental functions are intact. There are several horizontal beats of involuntary oscillatory eye movements on the left lateral gaze. He has difficulty performing repetitive pronation and supination movements on the left side. Electrocardiogram reveals normal sinus rhythm. Which of the following additional clinical features would you expect to be present?

• A. Sensory aphasia
• B. Past-pointing (Correct Answer)
• C. Expressive aphasia
• D. Hemiplegia
• E. Bitemporal hemianopsia

Brainstem nuclei Explanation: ***Past-pointing*** - The patient's symptoms (sudden onset of neck pain, severe spinning sensation, inability to maintain balance, horizontal nystagmus, and dysdiadochokinesia on the left) strongly suggest a posterior circulation stroke, likely involving the **cerebellum** or brainstem. - **Past-pointing**, a form of dysmetria, is a classic sign of cerebellar dysfunction, characterized by the inability to accurately touch a target due to issues with movement coordination and range. *Sensory aphasia* - **Sensory aphasia** (Wernicke's aphasia) is characterized by impaired comprehension and is typically associated with damage to the **left superior temporal gyrus** (Wernicke's area) in the dominant hemisphere. - The patient's higher mental functions are intact, making sensory aphasia an unlikely finding. *Expressive aphasia* - **Expressive aphasia** (Broca's aphasia) involves difficulty in speech production while comprehension remains relatively intact; it is usually linked to damage in the **left inferior frontal gyrus** (Broca's area). - Given the intact higher mental functions and the presentation of **posterior circulation symptoms**, expressive aphasia is not expected. *Hemiplegia* - **Hemiplegia** (paralysis of one side of the body) points to damage in the **contralateral motor cortex** or descending motor pathways, often from an anterior circulation stroke. - While vertebrobasilar stroke can sometimes cause motor deficits, the prominent symptoms here point to cerebellar and brainstem involvement rather than widespread motor cortex damage. *Bitemporal hemianopsia* - **Bitemporal hemianopsia** is a visual field defect characterized by loss of vision in the outer half of both visual fields, typically caused by compression of the **optic chiasm**, often by a pituitary tumor. - This condition is not associated with the acute onset of vertigo, neck pain, and cerebellar signs seen in this patient's presentation.

Brainstem nuclei US Medical PG Question 4: 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?

• A. Ipsilateral anterior cerebral artery
• B. Contralateral middle cerebral artery
• C. Anterior spinal artery
• D. Contralateral lenticulostriate artery (Correct Answer)
• E. Ipsilateral posterior inferior cerebellar artery

Brainstem nuclei Explanation: ***Contralateral lenticulostriate artery*** - The patient presents with **pure motor hemiparesis** affecting the face, arm, and leg equally on the right side, with **no sensory deficits, aphasia, or cognitive impairment**. - This clinical pattern is classic for a **lacunar stroke** affecting the **internal capsule**, which is supplied by the **lenticulostriate arteries** (branches of the middle cerebral artery). - The internal capsule contains tightly packed corticospinal and corticobulbar fibers; a small infarct here causes complete contralateral motor deficits without cortical signs. - The **absence of cortical findings** (normal speech, cognition, and sensation) distinguishes this from cortical MCA stroke. *Contralateral middle cerebral artery* - A **cortical MCA stroke** would typically present with **cortical signs** such as aphasia (if left hemisphere), neglect (if right hemisphere), sensory loss, and visual field defects. - MCA strokes usually show **arm and face > leg** weakness (the leg area is supplied by ACA). - This patient's **pure motor syndrome** without cortical signs points to a subcortical lesion, not cortical MCA occlusion. *Ipsilateral anterior cerebral artery* - First, the lateralization is incorrect - symptoms are right-sided, indicating left hemisphere pathology, so it would be **contralateral** ACA. - ACA occlusion causes weakness predominantly in the **contralateral leg > arm**, with relative sparing of the face. - This patient has equal involvement of face, arm, and leg, which is inconsistent with ACA territory. *Anterior spinal artery* - The **anterior spinal artery** supplies the anterior two-thirds of the spinal cord, including the corticospinal tracts and anterior horn cells. - Occlusion causes **bilateral** motor weakness below the lesion level and bilateral loss of pain/temperature sensation. - It does not cause **unilateral facial weakness** or the distribution of deficits seen in this patient. *Ipsilateral posterior inferior cerebellar artery* - Again, lateralization is incorrect - symptoms would be from **contralateral** PICA for motor findings, but PICA supplies the lateral medulla and inferior cerebellum. - PICA occlusion causes **lateral medullary syndrome (Wallenberg syndrome)**: ataxia, vertigo, dysphagia, dysarthria, Horner syndrome, and contralateral pain/temperature loss. - The patient's **pure motor hemiparesis** without cerebellar or brainstem signs is incompatible with PICA occlusion.

Brainstem nuclei US Medical PG Question 5: An 18-year-old man presents to his primary care physician with a complaint of excessive daytime sleepiness. He denies any substance abuse or major changes in his sleep schedule. He reports frequently dozing off during his regular daily activities. On further review of systems, he endorses falling asleep frequently with the uncomfortable sensation that there is someone in the room, even though he is alone. He also describes that from time to time, he has transient episodes of slurred speech when experiencing heartfelt laughter. Vital signs are stable, and his physical exam is unremarkable. This patient is likely deficient in a neurotransmitter produced in which part of the brain?

• A. Hippocampus
• B. Midbrain
• C. Pons nucleus
• D. Hypothalamus (Correct Answer)
• E. Thalamus

Brainstem nuclei Explanation: ***Hypothalamus*** - The patient's symptoms of excessive daytime sleepiness, cataplexy (falling asleep with strong emotions like laughter), and hypnagogic hallucinations (sensing someone in the room upon falling asleep) are classic for **narcolepsy**. - Narcolepsy type 1 is characterized by a significant loss of **orexin (hypocretin)** neurons, a neuropeptide primarily produced in the **lateral hypothalamus** (specifically the lateral and perifornical areas), which plays a crucial role in maintaining wakefulness. *Hippocampus* - The **hippocampus** is primarily involved in **memory formation** and spatial navigation. - Deficiencies in neurotransmitters produced or acting in the hippocampus are typically associated with memory disorders, not narcolepsy. *Midbrain* - The **midbrain** contains nuclei involved in dopamine, serotonin, and norepinephrine pathways, which are critical for mood, reward, and sleep-wake regulation. - While these neurotransmitters influence the sleep-wake cycle, the primary deficiency in narcolepsy type 1 is specifically orexin, which originates from the hypothalamus, not the midbrain. *Pons nucleus* - The **pons** is essential for regulating sleep stages, particularly **REM sleep**, and contains nuclei involved in breathing and motor control. - While it contributes to sleep architecture, the core pathology of narcolepsy type 1, the loss of orexin-producing neurons, is located higher in the brain, in the hypothalamus. *Thalamus* - The **thalamus** acts as a crucial relay station for sensory and motor signals to the cerebral cortex and is involved in regulating consciousness and alertness. - While it is involved in arousal regulation, it is not the primary site of orexin production, nor is a neurotransmitter deficiency directly from the thalamus the primary cause of narcolepsy.

Brainstem nuclei US Medical PG Question 6: 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

Brainstem 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.

Brainstem nuclei US Medical PG Question 7: 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

Brainstem 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.

Brainstem nuclei US Medical PG Question 8: A 57-year-old man was brought into the emergency department unconscious 2 days ago. His friends who were with him at that time say he collapsed on the street. Upon arrival to the ED, he had a generalized tonic seizure. At that time, he was intubated and is being treated with diazepam and phenytoin. A noncontrast head CT revealed hemorrhages within the pons and cerebellum with a mass effect and tonsillar herniation. Today, his blood pressure is 110/65 mm Hg, heart rate is 65/min, respiratory rate is 12/min (intubated, ventilator settings: tidal volume (TV) 600 ml, positive end-expiratory pressure (PEEP) 5 cm H2O, and FiO2 40%), and temperature is 37.0°C (98.6°F). On physical examination, the patient is in a comatose state. Pupils are 4 mm bilaterally and unresponsive to light. Cornea reflexes are absent. Gag reflex and cough reflex are also absent. Which of the following is the next best step in the management of this patient?

• A. Second opinion from a neurologist
• B. Withdraw ventilation support and mark time of death
• C. Electroencephalogram
• D. Repeat examination in several hours
• E. Apnea test (Correct Answer)

Brainstem nuclei Explanation: ***Apnea test*** - The patient exhibits classic signs of **brain death**, including a **coma**, fixed and dilated pupils, and absent brainstem reflexes (corneal, gag, cough). The next step is to perform an apnea test to confirm the absence of spontaneous respiratory drive. - An apnea test confirms brain death by demonstrating the **absence of respiratory effort** despite a rising pCO2, provided that spinal cord reflexes are not mistaken for respiratory efforts. *Second opinion from a neurologist* - While consulting a neurologist is often helpful in complex neurological cases, the current clinical picture presents such clear signs of brain death that **further confirmatory testing** for brain death (like the apnea test) is more immediately indicated before seeking additional opinions on diagnosis. - A second opinion would typically be sought to confirm the diagnosis or guide management, but establishing brain death requires a specific protocol which is incomplete without the apnea test. *Withdraw ventilation support and mark time of death* - It is **premature to withdraw ventilation** before brain death is unequivocally confirmed by all necessary clinical and confirmatory tests, including the apnea test. - Withdrawing support without full confirmation could lead to ethical and legal issues, as the patient might still have residual brainstem function, however minimal. *Electroencephalogram* - An **EEG** can show absent electrical activity, supporting brain death, but it is **not a mandatory part of the core brain death criteria** in many protocols, especially when clinical signs are clear and an apnea test can be performed. - The primary diagnostic criteria for brain death usually prioritize clinical examination and the apnea test for proving irreversible cessation of all brain functions. *Repeat examination in several hours* - Repeating the examination in several hours is typically done if there are **confounding factors** (e.g., severe hypothermia, drug intoxication) that might mimic brain death, or if the initial assessment is incomplete. - In this case, there are no mentioned confounding factors, and the immediate priority is to complete the brain death protocol with an apnea test, given the current clear clinical picture.

Brainstem nuclei US Medical PG Question 9: 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

Brainstem 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.

Brainstem 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)

Brainstem 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.

Brainstem nuclei Flashcard 1 of 10

Question: ID Nucleus: _____

Answer: Hypoglossal nucleus - Situated near the midline just beneath the fourth ventricle

Brainstem nuclei Flashcard 2 of 10

Question: ID Nucleus: _____

Answer: Spinal trigeminal nucleus

Brainstem nuclei Flashcard 3 of 10

Question: ID Brainstem Level: _____

Answer: Open medulla - Presence of 4th ventricle - Inferior olivary nucleus - Presence of CN IX, X and XII

Extra Information:  https://onlinemeded.org/spa/neuroscience/brainstem/acquire?ref=anki Netters: Other: 

Brainstem nuclei Flashcard 4 of 10

Question: Which cranial nerves (4) are located in the medulla? _____

Answer: IX, X, XI*, and XII

Brainstem nuclei Flashcard 5 of 10

Question: ID Brainstem Level: _____

Answer: Closed medulla - Absence of 4th ventricle - Decussation of medullary pyramids

Brainstem nuclei Flashcard 6 of 10

Question: paramedian pontine reticular formation (PPRF)

Answer: eyes look away from side of lesion

Brainstem nuclei Flashcard 7 of 10

Question: Where is the locus ceruleus located?

Answer: pons

Brainstem nuclei Flashcard 8 of 10

Question: Where is the raphe nucleus located?

Answer: pons

Brainstem nuclei Flashcard 9 of 10

Question: medial geniculate nucleus (MGN)

Answer: superior olive, inferior colliculus of tectum

Extra Information: hearing medial = music auditory cortex (temporal lobe)

Brainstem nuclei Flashcard 10 of 10

Question: ID Nucleus: _____

Answer: Nucleus of CN III - Located in rostral midbrain - Anterolateral to cerebral aqueduct - Anterior to nucleus of Edinger-Westphal

Extra Information:  https://onlinemeded.org/spa/pediatrics/ophthalmology/acquire?ref=anki Netters: Other: