Traumatic Optic Neuropathy — MCQs
In head injury, unilateral dilatation of the pupil is seen due to?
Following injury to the right temple region, a patient complains of pain in the right eye and loss of vision. On examination, the eye movements are normal, and the pupil normally reacts to light. The affected eye shows increased intraocular pressure of 32 mmHg (normal: 10-21 mmHg), mild corneal edema, and a small hyphema visible in the anterior chamber. The diagnosis is
Which test is used to detect a relative afferent pupillary defect (RAPD)?
A 20 year old man complains of difficulty in reading the newspaper with his right eye, three weeks after sustaining a gun shot injury to his left eye. The most likely diagnosis is:
In which condition is the swinging light test positive?
Which of the following medications is contraindicated in head trauma patients?
Treatment of choice in traumatic facial nerve injury with delayed onset or incomplete paralysis is -
A 27-year-old female patient presents with sudden diminishing vision associated with a relative afferent pupillary defect in the right eye. On examination, the left eye is normal. Which of the following combinations of investigations would be most appropriate?
All of the following are complications of traumatic hyphema except which of the following?
Which drug does NOT cause optic neuropathy?
Traumatic Optic Neuropathy Indian Medical PG Practice Questions and MCQs
Question 1: In head injury, unilateral dilatation of the pupil is seen due to?
- A. Ophthalmic N. compression
- B. Trigeminal N. compression
- C. Oculomotor nerve compression (Correct Answer)
- D. None of the options
Explanation: Oculomotor nerve compression - Unilateral pupillary dilation, often referred to as a **blown pupil**, is a classic sign of **oculomotor nerve (CN III) compression** due to increased intracranial pressure, typically from a **herniating uncus** [1]. - The parasympathetic fibers responsible for pupillary constriction run on the superficial aspect of the oculomotor nerve and are thus vulnerable to extrinsic compression [1], [2]. *Ophthalmic N. compression* - The **ophthalmic nerve (CN V1)** is a sensory nerve responsible for sensation to the forehead, scalp, upper eyelid, and cornea, not pupillary control. - Compression of this nerve would cause **sensory deficits** in its distribution and potentially abolish the **corneal reflex**, but not pupillary dilation. *Trigeminal N. compression* - The **trigeminal nerve (CN V)** is primarily responsible for sensation to the face and motor control of the muscles of mastication. - Compression would lead to **facial numbness or pain** and **weakness in chewing**, with no direct impact on pupillary size. *None of the options* - This option is incorrect because oculomotor nerve compression is a well-established cause of unilateral pupillary dilation in head injuries [1].
Question 2: Following injury to the right temple region, a patient complains of pain in the right eye and loss of vision. On examination, the eye movements are normal, and the pupil normally reacts to light. The affected eye shows increased intraocular pressure of 32 mmHg (normal: 10-21 mmHg), mild corneal edema, and a small hyphema visible in the anterior chamber. The diagnosis is
- A. Traumatic glaucoma (Correct Answer)
- B. Optic nerve atrophy
- C. Sub-arachnoid haemorrhage
- D. Functional loss of vision
Explanation: ***Traumatic glaucoma*** - Increased **intraocular pressure (32 mmHg)** after a **temple injury** with **corneal edema** and **hyphema** are classic signs of traumatic glaucoma. - The hyphema (blood in the anterior chamber) obstructs the **trabecular meshwork**, impeding aqueous humor outflow and leading to elevated IOP. *Optic nerve atrophy* - While optic nerve atrophy can cause **vision loss**, it is a chronic condition and typically not an acute presentation following trauma unless there is direct optic nerve damage. - It would not explain the acute findings of **hyphema**, **corneal edema**, or acutely elevated **intraocular pressure**. *Sub-arachnoid haemorrhage* - A **sub-arachnoid hemorrhage** might present with headache and loss of consciousness, or **papilledema** in severe cases, but typically would not cause such specific eye findings as **hyphema** or **corneal edema** from elevated IOP. - While a blow to the head could cause this, the direct eye findings point to a local ocular issue. *Functional loss of vision* - **Functional vision loss** (or psychogenic vision loss) is a diagnosis of exclusion where no organic cause can be found. - The presence of clear organic signs such as **hyphema**, **corneal edema**, and significantly elevated **intraocular pressure** rules out a functional cause.
Question 3: Which test is used to detect a relative afferent pupillary defect (RAPD)?
- A. Tonometry
- B. Slit-lamp examination
- C. Swinging flashlight test (Correct Answer)
- D. Perimetry
Explanation: ***Swinging flashlight test*** - The **swinging flashlight test** is the classic and most reliable method to detect a **relative afferent pupillary defect (RAPD)**. - It involves alternately shining a light into each eye, observing for unequal pupillary constriction and dilation, which indicates a defect in the afferent visual pathway of the affected eye. *Tonometry* - **Tonometry** is used to measure **intraocular pressure**, which is important for detecting and monitoring conditions like glaucoma. - It does not assess pupillary function or the integrity of the afferent visual pathway. *Slit-lamp examination* - A **slit-lamp examination** provides a magnified view of the anterior and posterior segments of the eye, helping to identify various ocular diseases like cataracts or uveitis. - While it can reveal structural abnormalities, it is not designed to detect an RAPD. *Perimetry* - **Perimetry**, also known as visual field testing, assesses the extent of a person's **field of vision** and can detect visual field defects. - It is used to evaluate the function of the retina and optic nerve but does not directly measure pupillary responses or an RAPD.
Question 4: A 20 year old man complains of difficulty in reading the newspaper with his right eye, three weeks after sustaining a gun shot injury to his left eye. The most likely diagnosis is:
- A. Optic nerve avulsion
- B. Sympathetic ophthalmia (Correct Answer)
- C. Delayed vitreous hemorrhage
- D. Macular edema
Explanation: ***Sympathetic ophthalmia*** - This is a rare, bilateral **granulomatous uveitis** occurring after penetrating trauma or surgery to one eye, with symptoms typically appearing weeks to months later in the **contralateral eye**. - The delayed onset of visual difficulty in the uninjured right eye, following **gunshot injury** to the left eye three weeks prior, strongly points to an autoimmune reaction affecting both eyes. *Optic nerve avulsion* - This injury involves the complete or partial tearing of the **optic nerve** from the back of the globe, usually due to direct trauma to the eye. - Symptoms would be immediate and severe vision loss in the **injured eye**, not delayed vision loss in the contralateral eye. *Delayed vitreous hemorrhage* - A delayed **vitreous hemorrhage** would cause sudden vision loss in the **injured eye** due to blood obscuring the visual axis. - It would not explain the vision loss in the **contralateral, uninjured eye**. *Macular edema* - **Macular edema** can cause blurred or distorted vision, but it is typically a localized phenomenon, often resulting from inflammation, diabetes, or vascular occlusion. - It would affect the **injured eye** as a direct consequence of trauma, not the contralateral eye in a delayed fashion and with the specific clinicopathological features of sympathetic ophthalmia.
Question 5: In which condition is the swinging light test positive?
- A. Conjunctivitis
- B. Glaucoma
- C. Keratoconus
- D. Optic neuritis (Correct Answer)
Explanation: ***Optic neuritis*** - The swinging light test (also known as the **Marcus Gunn pupil** or relative afferent pupillary defect, RAPD) is positive when there is a significant **asymmetry in the afferent visual pathway** between the two eyes. - In optic neuritis, the **optic nerve** is inflamed and demyelinated, impairing the transmission of light signals to the brain, which leads to a paradoxical pupillary dilation when the light is swung from the unaffected to the affected eye. *Conjunctivitis* - This is an **inflammation of the conjunctiva**, the membrane lining the eyelid and sclera, which primarily affects the ocular surface. - It does not involve the optic nerve or afferent pupillary pathways, so the swinging light test would be **negative**. *Glaucoma* - Glaucoma is a condition characterized by **progressive optic nerve damage**, often associated with elevated intraocular pressure, leading to peripheral vision loss. - While it causes optic neuropathy, a positive swinging light test is typically seen only in **severe, asymmetric cases** and is not its primary diagnostic feature. *Keratoconus* - This is a non-inflammatory eye condition in which the normally round dome-shaped cornea **thins and bulges outward into a cone-like shape**. - It affects the **cornea's shape and vision quality**, but not the optic nerve or the afferent pupillary reflex pathway, thus the swinging light test would be negative.
Question 6: Which of the following medications is contraindicated in head trauma patients?
- A. Furosemide
- B. Thiopentone
- C. Mannitol
- D. Corticosteroids (Correct Answer)
Explanation: ***Corticosteroids*** - While previously used, **corticosteroids** are now contraindicated in traumatic brain injury (TBI) due to evidence suggesting they may increase mortality. - **CRASH trial** showed that corticosteroids increased the risk of death in patients with head injury, possibly by exacerbating secondary brain injury. *Furosemide* - **Furosemide** can be used in certain situations to reduce intracranial pressure by inducing diuresis and reducing cerebral edema, especially when combined with mannitol. - It works by inhibiting the Na-K-2Cl cotransporter in the thick ascending limb of the loop of Henle, leading to increased water excretion. *Thiopentone* - **Thiopentone** (a barbiturate) can be used in severe head trauma to reduce cerebral metabolic rate, thereby decreasing cerebral blood flow and intracranial pressure. - It induces a **pharmacological coma** and provides neuroprotection by scavenging free radicals and stabilizing cell membranes. *Mannitol* - **Mannitol** is an osmotic diuretic commonly used to reduce intracranial pressure in head trauma by creating an osmotic gradient that draws water out of the brain parenchyma. - It is administered intravenously and works rapidly to decrease brain volume and improve cerebral perfusion pressure.
Question 7: Treatment of choice in traumatic facial nerve injury with delayed onset or incomplete paralysis is -
- A. Facial decompression
- B. Masterly inactivity (Correct Answer)
- C. Facial sling
- D. Systemic corticosteroid
Explanation: ***Masterly inactivity*** - In traumatic facial nerve injuries with **delayed onset or incomplete paralysis**, the prognosis for **spontaneous recovery** is excellent (up to 90%). - This approach involves careful observation with serial clinical examinations, allowing time for nerve recovery without the risks of surgical intervention. - **Surgical exploration** is reserved for immediate complete paralysis or when electrodiagnostic tests (electromyography, electroneuronography) show >90% degeneration. *Facial decompression* - This surgical procedure is considered only in cases of **immediate complete paralysis** with temporal bone fractures and confirmed severe nerve degeneration on testing. - It is **not indicated** for delayed-onset or incomplete injuries, as these have excellent spontaneous recovery rates. - Carries risks of further nerve damage, CSF leak, and hearing loss. *Facial sling* - A facial sling is a **late reconstructive procedure** used for permanent facial paralysis when nerve recovery has failed after 1-2 years. - It is a palliative measure to improve facial symmetry and eye protection, not a treatment for acute nerve injury. *Systemic corticosteroid* - While corticosteroids have a role in **Bell's palsy** (idiopathic facial paralysis), their benefit in **traumatic facial nerve injury is unproven**. - The primary pathology in trauma is mechanical disruption, not inflammatory edema that would respond to steroids. - Some clinicians use steroids empirically, but evidence does not support this as standard treatment.
Question 8: A 27-year-old female patient presents with sudden diminishing vision associated with a relative afferent pupillary defect in the right eye. On examination, the left eye is normal. Which of the following combinations of investigations would be most appropriate?
- A. MRI brain and orbits + Visual evoked potentials
- B. Visual evoked potentials + Blood tests
- C. MRI brain and orbits + Blood tests
- D. MRI brain and orbits + Visual evoked potentials + Blood tests (Correct Answer)
Explanation: ***MRI brain and orbits + Visual evoked potentials + Blood tests*** - The combination of **sudden diminishing vision** and a **relative afferent pupillary defect (RAPD)** in one eye strongly suggests **optic neuritis**. - **MRI brain and orbits** is crucial to identify demyelinating lesions characteristic of **multiple sclerosis** and to rule out other causes of optic neuropathy, while **visual evoked potentials (VEPs)** confirm optic nerve dysfunction and can detect subclinical demyelination. **Blood tests** are essential to exclude other inflammatory or autoimmune conditions that can mimic optic neuritis. *MRI brain and orbits + Visual evoked potentials* - While these two investigations are critical for diagnosing **optic neuritis** and assessing for **multiple sclerosis**, they might miss systemic causes of optic neuropathy that can be identified via targeted **blood tests**. - Excluding systemic inflammatory or autoimmune conditions is crucial for complete patient management and preventing recurrence or progression. *Visual evoked potentials + Blood tests* - This combination is insufficient as it omits the **MRI brain and orbits**, which is vital for visualizing the optic nerve and brain for demyelinating lesions and ruling out compressive or infiltrative etiologies. - An **MRI** provides structural information that VEPs and blood tests alone cannot, making it indispensable in this clinical scenario. *MRI brain and orbits + Blood tests* - This combination lacks **Visual evoked potentials (VEPs)**, which provide objective evidence of **optic nerve demyelination** and can detect subclinical involvement, aiding in diagnosis and prognosis. - VEPs are particularly valuable in diagnosing **optic neuritis** and monitoring its recovery or progression.
Question 9: All of the following are complications of traumatic hyphema except which of the following?
- A. Pupillary Block
- B. Posterior synechiae
- C. Rebleeding
- D. Corneal Ulcer (Correct Answer)
Explanation: ***Corneal Ulcer*** - A **corneal ulcer** is typically caused by infection, trauma, or exposure keratitis and is not a direct complication of blood in the anterior chamber from a **traumatic hyphema**. - While prolonged elevation of **intraocular pressure** from hyphema could theoretically impair corneal health, a direct ulcer is not a typical or primary complication. *Rebleeding* - **Rebleeding** is a common and serious complication of hyphema, usually occurring 2-7 days after the initial injury. - It often results in a more significant bleed and carries a higher risk of complications such as **elevated intraocular pressure** and **blood staining of the cornea**. *Pupillary Block* - **Pupillary block** can occur if the amount of blood from the hyphema prevents the flow of aqueous humor from the posterior to the anterior chamber. - This blockage leads to a buildup of **aqueous humor** in the posterior chamber, causing the iris to bow forward and potentially precipitating **acute angle-closure glaucoma**. *Posterior synechiae* - **Posterior synechiae** can develop due to inflammation (uveitis) associated with the hyphema, where the iris adheres to the anterior lens capsule. - This complication can lead to **irregular pupil shape**, **pupillary block glaucoma**, or other visual disturbances.
Question 10: Which drug does NOT cause optic neuropathy?
- A. Chloramphenicol
- B. Penicillin (Correct Answer)
- C. Ethambutol
- D. INH
Explanation: ***Penicillin*** - Penicillin is a widely used antibiotic that is **not associated with optic neuropathy** - Its primary side effects are **allergic reactions and hypersensitivity** - Visual disturbances or optic nerve damage are **not characteristic** of penicillin therapy *Chloramphenicol* - Known to cause **dose-dependent and duration-dependent optic neuropathy**, especially with prolonged use - Can lead to visual impairment, including reduced visual acuity and color vision defects - May be **irreversible** in some cases *Ethambutol* - **Most notorious** antitubercular drug for causing optic neuritis - Causes **dose-dependent bilateral visual loss** and **red-green color blindness** - Requires regular visual monitoring during therapy - Potentially **irreversible** optic nerve damage *INH (Isoniazid)* - Can cause optic neuropathy, though **less frequently** than ethambutol - Usually associated with **high doses** or prolonged therapy - Risk increases in slow acetylators and those with nutritional deficiencies
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