Autonomic innervation of the head and neck US Medical PG Practice Questions and MCQs
Practice US Medical PG questions for Autonomic innervation of the head and neck. These multiple choice questions (MCQs) cover important concepts and help you prepare for your exams.
Autonomic innervation of the head and neck US Medical PG Question 1: A 68-year-old man comes to the physician because of double vision and unilateral right eye pain that began this morning. His vision improves when he covers either eye. He has hypertension, mild cognitive impairment, and type 2 diabetes mellitus. The patient has smoked two packs of cigarettes daily for 40 years. His current medications include lisinopril, donepezil, metformin, and insulin with meals. His temperature is 37°C (98.6°F), pulse is 85/minute, respirations are 12/minute, and blood pressure is 132/75 mm Hg. His right eye is abducted and depressed with slight intorsion. He can only minimally adduct the right eye. Visual acuity is 20/20 in both eyes. Extraocular movements of the left eye are normal. An MRI of the head shows no abnormalities. His fingerstick blood glucose concentration is 325 mg/dL. Further evaluation is most likely to show which of the following?
- A. Ptosis (Correct Answer)
- B. Dilated and fixed pupil
- C. Bitemporal hemianopsia
- D. Miosis and anhidrosis
- E. Positive swinging-flashlight test
Autonomic innervation of the head and neck Explanation: ***Ptosis***
- The patient's presentation of an **abducted and depressed right eye with minimal adduction** is highly suggestive of an **ischemic (diabetic) third nerve palsy**.
- Ischemic third nerve palsies characteristically **spare the pupillary fibers** (pupil remains normal in size and reactive) but affect the **somatomotor fibers** that innervate the extraocular muscles and the **levator palpebrae superioris**, leading to **ptosis**.
- The key clinical feature distinguishing ischemic from compressive CN III palsy is **pupil-sparing**, which is present in this case.
*Dilated and fixed pupil*
- A dilated and fixed pupil would indicate **compression of the oculomotor nerve**, often by an aneurysm (e.g., posterior communicating artery aneurysm).
- Compressive lesions affect the superficial **pupillomotor fibers** first, while ischemic third nerve palsies, as seen in patients with **diabetes**, typically affect the inner somatomotor fibers while **sparing the pupil**.
*Bitemporal hemianopsia*
- This visual field defect is characteristic of **optic chiasm compression**, commonly caused by a **pituitary adenoma**.
- This patient's symptoms are localized to a single eye and involve extraocular muscle dysfunction, not visual field loss.
*Miosis and anhidrosis*
- **Miosis** (constricted pupil) and **anhidrosis** (decreased sweating) on one side of the face, accompanied by **ptosis**, are classic signs of **Horner syndrome**.
- Horner syndrome results from a lesion in the **sympathetic pathway**, which is inconsistent with the extraocular muscle deficits observed in this patient.
*Positive swinging-flashlight test*
- A positive swinging-flashlight test (Marcus Gunn pupil) indicates an **afferent pupillary defect**, often seen in conditions affecting the **optic nerve** (e.g., optic neuritis, severe retinal disease).
- This patient's symptoms point to a **cranial nerve III palsy**, which affects efferent ocular movements and typically does not cause an afferent pupillary defect.
Autonomic innervation of the head and neck US Medical PG Question 2: A 29-year-old man presents to the emergency room with facial weakness. He first noticed that he was having trouble smiling normally while at dinner with friends the night before. He also noticed that his food had less taste than usual during the dinner. He woke up on the day of presentation with a complete inability to move the right side of his face. He recently returned from an extended camping trip in the Appalachian Mountains, but he did not find any tick bites following the camping trip. His past medical history is notable for Achilles tendonitis and carpal tunnel syndrome. He works as a computer programmer. He smokes marijuana occasionally but does not smoke cigarettes. His temperature is 98.6°F (37°C), blood pressure is 120/75 mmHg, pulse is 80/min, and respirations are 18/min. On exam, he is well-appearing in no acute distress. There is loss of facial wrinkles along the forehead, eyelids, and nasolabial folds. He is unable to completely close his right eye, raise his eyebrows, or smile with the right side of his mouth. Sensation is intact to light touch along the forehead, maxilla, and mandible bilaterally. Where is the most likely source of this patient’s lesion?
- A. Superior orbital fissure
- B. Petrotympanic fissure
- C. Inferior orbital fissure
- D. Dorsal frontal lobe
- E. Stylomastoid foramen (Correct Answer)
Autonomic innervation of the head and neck Explanation: ***Stylomastoid foramen***
- The patient presents with classic signs of **Bell's palsy**, characterized by unilateral **facial weakness affecting both the upper and lower face**, including loss of forehead wrinkles, inability to close the eye, and loss of nasolabial folds.
- The **stylomastoid foramen** is the exit point of the **facial nerve (CN VII)** from the skull, and inflammation or compression at this site is the most common cause of idiopathic facial nerve paralysis (Bell's palsy).
*Superior orbital fissure*
- Lesions in the **superior orbital fissure** would primarily affect cranial nerves **III, IV, V1, and VI**, leading to symptoms like ophthalmoplegia, ptosis, and sensory loss in the V1 distribution of the face, not a facial nerve palsy.
- While it is a bony canal, it is not the primary exit for the facial nerve.
*Petrotympanic fissure*
- The **petrotympanic fissure** transmits the **chorda tympani nerve**, which carries taste sensation from the anterior two-thirds of the tongue and parasympathetic fibers to the submandibular and sublingual glands.
- A lesion here would cause **loss of taste** and potentially dry mouth, but would not typically explain the extensive motor deficits of the entire ipsilateral face as seen in this patient, which indicates a more proximal or complete facial nerve involvement.
*Inferior orbital fissure*
- The **inferior orbital fissure** transmits the **maxillary nerve (V2)**, the zygomatic nerve, and branches of the inferior ophthalmic vein, affecting sensation to the mid-face.
- Damage here would result in **sensory deficits in the V2 distribution** and potentially orbital symptoms, not motor weakness of the facial muscles.
*Dorsal frontal lobe*
- A lesion in the **dorsal frontal lobe**, specifically involving the **motor cortex**, would cause contralateral facial weakness. However, it would typically spare the forehead and eyelid muscles due to bilateral cortical innervation of the upper facial muscles.
- The patient's presentation of **forehead and entire facial weakness** is characteristic of a **lower motor neuron lesion** of the facial nerve, not a central (upper motor neuron) lesion.
Autonomic innervation of the head and neck US Medical PG Question 3: A 72-year-old man presents to his primary care physician because he feels like his vision has been changing over the last 6 months. In particular, he feels that he cannot see as well out of his right eye as previously. His past medical history is significant for myocardial infarction as well as Lyme disease. On presentation, he is found to have a droopy right eyelid as well as persistent constriction of his right pupil. Additionally, the skin on his right half of his face is found to be cracked and dry. Which of the following is most likely associated with this patient's symptoms?
- A. Oculomotor nerve damage
- B. Drug use
- C. Syphilis
- D. Facial nerve damage
- E. Pancoast tumor (Correct Answer)
Autonomic innervation of the head and neck Explanation: ***Pancoast tumor***
- The patient's symptoms (droopy eyelid, constricted pupil, and dry skin on one side of the face) are classic for **Horner's syndrome**, which results from damage to the **sympathetic nerves** to the eye and face.
- A **Pancoast tumor** (a tumor in the apex of the lung) can compress the **sympathetic chain** in the neck/chest, leading to Horner's syndrome.
*Oculomotor nerve damage*
- Oculomotor nerve damage would typically cause a **dilated pupil** (due to unopposed sympathetic innervation) and **ptosis** (drooping eyelid), but not miosis (constricted pupil) or anhidrosis (dry skin).
- The patient's **constricted pupil** points away from oculomotor nerve involvement.
*Drug use*
- While certain drugs can affect pupil size (e.g., opiates cause miosis), drug use alone is unlikely to explain the entire triad of **Horner's syndrome** (ptosis, miosis, anhidrosis) in combination with the focal neurological findings.
- No other information in the vignette suggests drug use.
*Syphilis*
- **Neurosyphilis** can cause pupillary abnormalities, such as **Argyll Robertson pupils** (small, irregular pupils that accommodate but do not react to light).
- However, it typically does not present with the specific combination of ptosis, miosis, and anhidrosis characteristic of Horner's syndrome.
*Facial nerve damage*
- **Facial nerve damage** (e.g., Bell's palsy) affects the muscles of **facial expression** and could cause ipsilateral facial weakness or droop.
- It would not cause pupillary changes or anhidrosis, as these symptoms are related to the sympathetic nervous system and superior cervical ganglion, not the facial nerve.
Autonomic innervation of the head and neck US Medical PG Question 4: Which neurotransmitter is primarily responsible for parasympathetic effects on heart rate?
- A. Norepinephrine
- B. Dopamine
- C. Acetylcholine (Correct Answer)
- D. Epinephrine
Autonomic innervation of the head and neck Explanation: ***Acetylcholine***
- **Acetylcholine** is the primary neurotransmitter released by postganglionic parasympathetic neurons.
- It acts on **muscarinic receptors** (M2 receptors) in the heart to decrease heart rate.
*Norepinephrine*
- **Norepinephrine** is primarily associated with the **sympathetic nervous system**, increasing heart rate and contractility.
- It acts on **beta-1 adrenergic receptors** in the heart.
*Dopamine*
- **Dopamine** is a precursor to norepinephrine and epinephrine, and primarily functions as a neurotransmitter in the **central nervous system** and in regulating renal blood flow.
- While it can have cardiac effects, it is not the primary neurotransmitter for parasympathetic actions on heart rate.
*Epinephrine*
- **Epinephrine** (adrenaline) is a hormone released by the adrenal medulla and a neurotransmitter in the sympathetic nervous system, causing an **increase in heart rate** and contractility.
- It works through **beta-1 adrenergic receptors**, antagonistic to parasympathetic effects.
Autonomic innervation of the head and neck US Medical PG Question 5: A 65-year-old female with a past medical history of hypertension presents to her primary care doctor with a 3 month history of spasmodic facial pain. The pain is located in her right cheek and seems to be triggered when she smiles, chews, or brushes her teeth. The pain is sharp and excruciating, lasts for a few seconds, and occurs up to twenty times per day. She denies headaches, blurry vision, facial weakness, or changes in her memory. She feels rather debilitated and has modified much of her daily activities to avoid triggering the spasms. In the clinic, her physical exam is within normal limits. Her primary care doctor prescribes carbamazepine and asks her to follow up in a few weeks. Which cranial nerve is most likely involved in the patient's disease process?
- A. CN III
- B. CN V (Correct Answer)
- C. CN VI
- D. CN VII
- E. CN IV
Autonomic innervation of the head and neck Explanation: ***CN V***
- The patient's presentation of **recurrent, sharp, excruciating, unilateral facial pain** triggered by movements like chewing, smiling, or brushing teeth is classic for **trigeminal neuralgia**.
- **Trigeminal neuralgia** specifically affects the **trigeminal nerve (CN V)**, which has sensory branches covering the face, and is often treated with **carbamazepine**.
*CN III*
- The **oculomotor nerve (CN III)** is primarily involved in **eye movement** and **pupillary constriction**.
- Damage to CN III typically causes **diplopia, ptosis,** and **pupil dilation**, which are not present in this patient's symptoms.
*CN VI*
- The **abducens nerve (CN VI)** controls the **lateral rectus muscle**, responsible for **abducting the eye** (moving it outward).
- Dysfunction typically results in **diplopia** and an inability to move the eye laterally, not facial pain.
*CN VII*
- The **facial nerve (CN VII)** controls **facial expressions**, taste sensation from the anterior two-thirds of the tongue, and lacrimation/salivation.
- While it innervates facial muscles, its involvement typically presents as **facial weakness** or **paralysis** (e.g., Bell's palsy), not sharp, spasmodic pain.
*CN IV*
- The **trochlear nerve (CN IV)** innervates the **superior oblique muscle**, which is involved in rotating and depressing the eye.
- Lesions usually lead to **vertical diplopia**, particularly when looking down and inward, which is unrelated to the described facial pain.
Autonomic innervation of the head and neck US Medical PG Question 6: A 61-year-old man sustains an intracranial injury to a nerve that also passes through the parotid gland. Which of the following is a possible consequence of this injury?
- A. Changes in hearing (Correct Answer)
- B. Horner's syndrome
- C. Paralysis of lateral rectus muscle
- D. Loss of taste from posterior 1/3 of tongue
- E. Loss of general sensation in anterior 2/3 of tongue
Autonomic innervation of the head and neck Explanation: ***Changes in hearing***
- The **facial nerve (CN VII)** is the only cranial nerve that has both an **intracranial course** and passes **through the parotid gland**.
- The facial nerve gives off the **nerve to stapedius muscle** within the facial canal (before it exits the stylomastoid foramen).
- Damage to this nerve can lead to **hyperacusis** (increased sensitivity to sound), as the stapedius normally dampens excessive sound vibrations.
- **Note**: Facial nerve injury would also cause facial paralysis (the most prominent feature), loss of taste from anterior 2/3 of tongue via chorda tympani, and decreased lacrimation/salivation, but these are not among the answer choices.
*Horner's syndrome*
- This syndrome results from damage to the **sympathetic pathway** (hypothalamus → spinal cord → superior cervical ganglion → eye).
- Characterized by **ptosis**, **miosis**, and **anhidrosis**.
- Not related to facial nerve injury.
*Paralysis of lateral rectus muscle*
- The **lateral rectus muscle** is innervated by the **abducens nerve (CN VI)**.
- CN VI does not pass through the parotid gland.
*Loss of taste from posterior 1/3 of tongue*
- Taste from the **posterior 1/3 of the tongue** is carried by the **glossopharyngeal nerve (CN IX)**.
- CN IX does not pass through the parotid gland.
- **Note**: The facial nerve actually carries taste from the **anterior 2/3** of the tongue via the chorda tympani branch.
*Loss of general sensation in anterior 2/3 of tongue*
- **General sensation** (touch, pain, temperature) from the **anterior 2/3 of the tongue** is carried by the **lingual nerve** (branch of CN V3).
- The lingual nerve does not pass through the parotid gland.
Autonomic innervation of the head and neck US Medical PG Question 7: A 39-year-old woman is brought to the emergency department following a stab wound to the neck. Per the patient, she was walking her dog when she got robbed and was subsequently stabbed with a knife. Vitals are stable. Strength examination reveals 2/5 right-sided elbow flexion and extension, wrist extension, and finger motions. Babinski sign is upward-going on the right. There is decreased sensation to light touch and vibration on the patient's right side up to her shoulder. She also reports decreased sensation to pinprick and temperature on her left side, including her lower extremities, posterior forearm, and middle finger. The patient's right pupil is 2 mm smaller than the left with drooping of the right upper eyelid. Which of the following is the most likely cause of the patient’s presentation?
- A. Hemisection injury (Correct Answer)
- B. Syringomyelia
- C. Anterior cord syndrome
- D. Posterior cord syndrome
- E. Central cord syndrome
Autonomic innervation of the head and neck Explanation: ***Hemisection injury***
- The combination of **ipsilateral motor weakness** and **dorsal column deficits** (vibration, light touch) along with **contralateral loss of pain and temperature sensation** (spinothalamic tract) is the hallmark of a Brown-Séquard syndrome, which results from a hemisection injury to the spinal cord.
- The presence of **ipsilateral Horner's syndrome** (miosis and ptosis) indicates sympathetic nerve damage, further localizing the injury to the cervical spinal cord and supporting a hemisection.
*Syringomyelia*
- This condition is characterized by a **cavity (syrinx)** within the spinal cord, typically leading to a **cape-like distribution of pain and temperature loss** due to damage to the decussating spinothalamic fibers.
- It usually spares the dorsal columns and motor tracts in early stages, which contradicts the described ipsilateral motor and dorsal column deficits.
*Anterior cord syndrome*
- Results from damage to the **anterior spinal artery**, leading to **bilateral loss of motor function** (corticospinal tracts) and **pain/temperature sensation** (spinothalamic tracts) below the level of injury.
- **Proprioception and vibration sensation** (dorsal columns) are typically preserved in this syndrome, which is inconsistent with the patient's presentation.
*Posterior cord syndrome*
- Involves damage primarily to the **dorsal columns**, resulting in **loss of proprioception, vibration, and light touch** below the level of injury.
- **Motor function, pain, and temperature sensation** are generally preserved, which is not consistent with the motor deficits and contralateral pain/temperature loss described.
*Central cord syndrome*
- Most commonly seen after **hyperextension injuries**, leading to greater **motor weakness in the upper extremities** than the lower extremities.
- It typically causes varying degrees of **sensory loss** and can preserve sacral sensation, but the specific pattern of ipsilateral motor/dorsal column deficits and contralateral spinothalamic loss is not characteristic of central cord syndrome.
Autonomic innervation of the head and neck 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
Autonomic innervation of the head and neck 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.
Autonomic innervation of the head and neck US Medical PG Question 9: A 28-year-old man comes to the physician because of a persistent tingling sensation in the right side of his face. The sensation began after he underwent an extraction of an impacted molar 2 weeks ago. Examination shows decreased sensation of the skin over the right side of the mandible, chin, and the anterior portion of the tongue. Taste sensation is preserved. The affected nerve exits the skull through which of the following openings?
- A. Foramen rotundum
- B. Hypoglossal canal
- C. Foramen magnum
- D. Foramen ovale (Correct Answer)
- E. Stylomastoid foramen
Autonomic innervation of the head and neck Explanation: ***Foramen ovale***
- This patient presents with **paresthesia** in the distribution of branches of the **mandibular nerve (V3)** following molar extraction. The affected areas (mandible, chin, and anterior tongue sensation) indicate injury to the **inferior alveolar nerve** (lower teeth, chin, lower lip) and/or **lingual nerve** (general sensation to anterior 2/3 of tongue).
- Both the **inferior alveolar nerve** and **lingual nerve** are branches of the **mandibular nerve (V3)**, which exits the skull through the **foramen ovale**. These nerves run in close proximity during molar extraction and are commonly injured together.
- Taste sensation is preserved because the **chorda tympani** (taste fibers from CN VII) travels with the lingual nerve but does not exit through foramen ovale.
*Foramen rotundum*
- The **foramen rotundum** transmits the **maxillary nerve (V2)**, which innervates the midface, upper teeth, and palate.
- Injury to this nerve would cause sensory deficits in the upper lip and cheek, not the mandible or chin.
*Hypoglossal canal*
- The **hypoglossal canal** transmits the **hypoglossal nerve (CN XII)**, which is a motor nerve to the intrinsic and extrinsic muscles of the tongue.
- Damage to this nerve would result in **tongue weakness** or **atrophy**, not sensory changes to the face or tongue.
*Foramen magnum*
- The **foramen magnum** is the largest opening in the skull, transmitting the **spinal cord**, vertebral arteries, and accessory nerve (CN XI).
- Damage here would likely involve severe neurological deficits, not isolated sensory loss to the lower face.
*Stylomastoid foramen*
- The **stylomastoid foramen** transmits the **facial nerve (CN VII)**, which is primarily responsible for facial expression and taste sensation to the anterior two-thirds of the tongue via the chorda tympani.
- While CN VII provides taste to the tongue, it does not provide general sensory innervation to the skin of the mandible or chin, and taste is preserved in this patient.
Autonomic innervation of the head and neck US Medical PG Question 10: A 48-year-old man with retroperitoneal sarcoma requires extensive resection including portions of the sympathetic chain from T10-L2 and the celiac/superior mesenteric ganglia. Preoperative evaluation is needed to predict postoperative autonomic consequences. The multidisciplinary team must evaluate which combination of deficits is most likely based on the precise anatomical structures being resected and the potential for compensation.
- A. Pan-sympathetic failure including cardiovascular collapse due to loss of all preganglionic outflow
- B. Minimal deficits due to complete bilateral compensation from contralateral sympathetic chain
- C. Complete loss of lower extremity sweating and thermoregulation with normal GI and genitourinary function due to enteric nervous system compensation
- D. Severe orthostatic hypotension, GI dysmotility, and ejaculatory dysfunction with preserved upper body sympathetic function (Correct Answer)
- E. Isolated loss of visceral pain sensation with completely preserved motor and secretory autonomic functions
Autonomic innervation of the head and neck Explanation: ***Severe orthostatic hypotension, GI dysmotility, and ejaculatory dysfunction with preserved upper body sympathetic function***
- Resection of the **celiac and superior mesenteric ganglia** and the **sympathetic chain (T10-L2)** drastically reduces total peripheral resistance and venous return regulation, leading to **severe orthostatic hypotension**.
- Disrupting the **lumbar sympathetic chain (L1-L2)** interrupts the pathways for **emission**, while ganglionic resection causes **GI dysmotility** via loss of inhibitory sympathetic input.
*Complete loss of lower extremity sweating and thermoregulation with normal GI and genitourinary function due to enteric nervous system compensation*
- While **anhidrosis** occurs, the **enteric nervous system** cannot fully compensate for the loss of extrinsic sympathetic modulation, leading to significant GI dysfunction.
- Genitourinary function is significantly impacted as the **sympathetic input** required for the contraction of the internal urethral sphincter and seminal vesicles is removed.
*Isolated loss of visceral pain sensation with completely preserved motor and secretory autonomic functions*
- Although **visceral afferents** are interrupted, the resection of **preganglionic and postganglionic motor fibers** guarantees motor and secretory deficits.
- Sympathetic fibers are essential for the **vasoconstriction** and inhibitory signaling to the gut, which cannot remain "completely preserved" after such extensive resection.
*Pan-sympathetic failure including cardiovascular collapse due to loss of all preganglionic outflow*
- **Pan-sympathetic failure** is avoided because segments above **T10** (supplying the head, neck, and upper extremities) and the **adrenal medulla** (if T10-L2 is the primary resection) provide partial function.
- Cardiovascular collapse is unlikely because the **cardiac sympathetic nerves (T1-T4)** remain intact, maintaining heart rate and contractility.
*Minimal deficits due to complete bilateral compensation from contralateral sympathetic chain*
- Sympathetic innervation of the viscera is **bilateral**, but the **celiac and superior mesenteric ganglia** are midline structures; their resection leaves no contralateral alternative.
- Extensive **bilateral resection** of the chain segments at this level ensures profound deficits that cannot be compensated for by remaining neural pathways.
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