Other Optic Neuropathies — MCQs
A case of injury to right brow due to a fall from scooter presents with sudden loss of vision in the right eye. The pupil shows absent direct reflex but a normal consensual pupillary reflex is present. The fundus is normal. The treatment of choice is:
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 a patient with chronic alcoholism, which nutrient deficiency is most likely to cause neurological symptoms?
An affected male does not have affected children but an affected female always has affected children. Type of inheritance?
Most common CNS tumor associated with NF1
A 40F presents with double vision, headaches, and a progressively enlarging thyroid mass. She has proptosis and limited eye movement. TSH is suppressed. Likely cause of her symptoms?
Which visual disturbance is commonly associated with Vitamin B12 deficiency?
Anion-gap metabolic acidosis with decreased vision occurs with the following poisoning.
Identify the visual field defect shown in the image.
Early fundoscopic sign in papilloedema is
Other Optic Neuropathies Indian Medical PG Practice Questions and MCQs
Question 1: A case of injury to right brow due to a fall from scooter presents with sudden loss of vision in the right eye. The pupil shows absent direct reflex but a normal consensual pupillary reflex is present. The fundus is normal. The treatment of choice is:
- A. Pulse methyl Prednisolone 250 mg four times daily for three days
- B. Emergency optic canal decompression
- C. Oral Prednisolone 1.5 mg/kg body weight
- D. Intensive intravenous corticosteroids as prescribed for spinal injuries to be instituted within six hours (Correct Answer)
Explanation: ***Intensive intravenous corticosteroids as prescribed for spinal injuries to be instituted within six hours*** - The sudden **loss of vision** with a **traumatic brow injury** and **afferent pupillary defect** (absent direct reflex, normal consensual) suggests **traumatic optic neuropathy (TON)**. - While the efficacy of corticosteroids is debated, high-dose intravenous corticosteroids, often following the **National Acute Spinal Cord Injury Study (NASCIS)** protocols (similar to spinal injury treatment), are a common initial treatment for TON, especially when administered within 6-8 hours of injury to reduce inflammation and edema around the optic nerve. *Pulse methyl Prednisolone 250 mg four times daily for three days* - This dosage regimen is a form of **pulse steroid therapy**, but the specific dose and frequency may not align with the standard high-dose IV corticosteroid protocols used for TON (e.g., typically 1g methylprednisolone daily). - While corticosteroids are used, the precise protocol and optimal dosing for TON are critical and vary from this option. *Emergency optic canal decompression* - **Optic canal decompression surgery** is considered in cases of TON where there is direct compression of the optic nerve or a lack of response to corticosteroid therapy. - It is not the initial treatment of choice for all TON cases and carries significant surgical risks; corticosteroid therapy is usually attempted first. *Oral Prednisolone 1.5 mg/kg body weight* - **Oral corticosteroids** are generally not sufficient for the acute, severe inflammation seen in traumatic optic neuropathy. - **Intravenous administration** is preferred for its rapid and higher systemic bioavailability to achieve therapeutic levels at the optic nerve.
Question 2: 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 3: In a patient with chronic alcoholism, which nutrient deficiency is most likely to cause neurological symptoms?
- A. Vitamin B6
- B. Thiamine (Correct Answer)
- C. Folate
- D. Vitamin B12
Explanation: ***Thiamine*** - **Thiamine (Vitamin B1)** deficiency is extremely common in chronic alcoholism due to poor nutrition and impaired absorption, leading to neurological disorders like **Wernicke-Korsakoff syndrome** [1]. - **Wernicke-Korsakoff syndrome** manifests with symptoms such as **ataxia**, **ophthalmoplegia**, **confusion**, and **memory impairment** [2]. *Vitamin B6* - While **Vitamin B6 (pyridoxine)** deficiency can occur in alcoholism, it is more commonly associated with peripheral neuropathy rather than the extensive neurological picture seen with thiamine deficiency. - Severe B6 deficiency can cause **seizures** and **encephalopathy**, but these are less common as primary neurological manifestations in typical chronic alcoholics compared to Wernicke-Korsakoff syndrome. *Folate* - **Folate deficiency** is very common in chronic alcoholism and primarily leads to **macrocytic anemia**. - While it can indirectly contribute to neurological issues due to anemia, it does not directly cause the classic acute neurological syndromes seen with thiamine deficiency. *Vitamin B12* - **Vitamin B12 deficiency** can cause neurological symptoms, including **peripheral neuropathy**, **ataxia**, and **cognitive impairment**, but it is less directly associated with alcoholism compared to thiamine deficiency. - B12 deficiency is more commonly seen in strict vegetarians, pernicious anemia, or malabsorption conditions involving the ileum.
Question 4: An affected male does not have affected children but an affected female always has affected children. Type of inheritance?
- A. Autosomal recessive
- B. Mitochondrial (Correct Answer)
- C. X linked recessive
- D. X linked dominant
Explanation: ***Correct Option: Mitochondrial*** - This pattern describes **mitochondrial inheritance**, where all children of an **affected mother** inherit the condition because mitochondria are exclusively inherited from the ovum (maternal inheritance). - An **affected father** cannot pass on the condition to his children, as sperm contribute only nuclear DNA and essentially no mitochondria. - This is the **only inheritance pattern** where an affected male has no affected children while an affected female has all children affected. *Incorrect Option: Autosomal recessive* - This pattern would typically show affected individuals having unaffected parents (who are carriers) and both males and females being affected in equal proportions. - It does not explain the complete absence of transmission from an affected father or universal transmission from an affected mother. - An affected individual could have unaffected children if their partner is not a carrier. *Incorrect Option: X linked recessive* - In **X-linked recessive inheritance**, affected males cannot pass the trait to their sons, but all their daughters would be carriers (not affected). - An affected mother would pass the trait to all her sons (affected) and make all her daughters carriers (not affected), which does not match the described pattern of all children being affected. *Incorrect Option: X linked dominant* - In **X-linked dominant inheritance**, an affected father passes the trait to all his daughters but none of his sons (contradicts "no affected children"). - An affected mother has a 50% chance of passing the trait to **each child**, which is inconsistent with all children of an affected female being affected.
Question 5: Most common CNS tumor associated with NF1
- A. Optic glioma (Correct Answer)
- B. Astrocytoma
- C. Bilateral acoustic neuroma
- D. Optic nerve schwannoma
Explanation: ***Optic glioma*** - **Optic gliomas** (specifically **pilocytic astrocytomas**) are the most common CNS tumor found in association with **Neurofibromatosis type 1 (NF1)** [1]. - These tumors typically affect the **optic nerve** and can cause vision impairment. *Optic nerve schwannoma* - **Schwannomas** are tumors arising from Schwann cells, and while they can affect cranial nerves, an **optic nerve schwannoma** is very rare and not characteristic of NF1. - The most common schwannoma associated with neurofibromatosis is a **vestibular schwannoma** (acoustic neuroma) in NF2, not NF1 [2]. *Astrocytoma* - While optic gliomas are a type of astrocytoma, simply stating "astrocytoma" is too broad; the specific location (optic nerve) and type (pilocytic) are key in NF1 [1]. - Other types of astrocytomas (e.g., glioblastoma) are not typically associated with NF1 as the *most common* CNS tumor. *Bilateral acoustic neuroma* - **Bilateral acoustic neuromas** (vestibular schwannomas) are the hallmark CNS tumor of **Neurofibromatosis type 2 (NF2)**, not NF1 [2]. - This symptom strongly points to NF2, a distinct genetic disorder from NF1 [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1319-1320. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Manifestations Of Central And Peripheral Nervous System Disease, pp. 727-728.
Question 6: A 40F presents with double vision, headaches, and a progressively enlarging thyroid mass. She has proptosis and limited eye movement. TSH is suppressed. Likely cause of her symptoms?
- A. Pituitary adenoma
- B. Orbital cellulitis
- C. Graves' orbitopathy (Correct Answer)
- D. Thyroid carcinoma
Explanation: Graves' orbitopathy - The combination of **proptosis**, **limited eye movement (ophthalmoplegia)** causing double vision, and a suppressed TSH (indicating hyperthyroidism) is highly characteristic of **Graves' disease** with orbital involvement [1]. - An **enlarging thyroid mass** further supports Graves' disease, as it often presents with goiter and hyperthyroidism, leading to the autoimmune sequelae in the orbit [1]. *Pituitary adenoma* - While it can cause **headaches** and **double vision** due to oculomotor nerve compression, a pituitary adenoma would not typically cause a progressively **enlarging thyroid mass** or **proptosis** with suppressed TSH. - Hypersecreting pituitary adenomas (e.g., ACTH, GH) affect other endocrine axes, and non-secreting ones primarily cause mass effect. *Orbital cellulitis* - This is an **acute infection** of the orbital tissues, usually presenting with **pain, fever, rapidly progressing proptosis**, and erythema, which is not suggested by the chronic and progressive nature of this patient's symptoms. - It would not be associated with a suppressed TSH or an enlarged thyroid gland. *Thyroid carcinoma* - A thyroid carcinoma can present as an **enlarging thyroid mass** and may cause local symptoms like dysphagia or hoarseness if advanced, but it does not directly cause **proptosis**, **double vision**, or suppressed TSH. - Although some rare thyroid cancers can metastasize to the orbit, primary presentation with bilateral proptosis and ophthalmoplegia is not typical.
Question 7: Which visual disturbance is commonly associated with Vitamin B12 deficiency?
- A. Centrocaecal scotoma (Correct Answer)
- B. Binasal hemianopia
- C. Constriction of peripheral vision
- D. Bitemporal hemianopia
Explanation: No relevant citations could be added to the original explanation because the provided references did not specifically address the association between Vitamin B12 deficiency and centrocaecal scotoma. ***Centrocaecal scotoma*** - **Vitamin B12 deficiency** can lead to optic neuropathy, which often manifests as a **centrocaecal scotoma**, affecting central and paracentral vision. - This visual impairment is due to **demyelination of the optic nerve fibers** caused by the deficiency. *Binasal hemianopia* - This type of visual field defect is rare and typically caused by lesions that compress the uncrossed retinal nerve fibers, such as **bilateral internal carotid artery aneurysms** or **bilateral optic nerve disease**. - It does not directly correlate with **Vitamin B12 deficiency**. *Constriction of peripheral vision* - **Peripheral vision loss** is associated with conditions like **glaucoma** or advanced **retinitis pigmentosa**. - It is not a characteristic visual disturbance of **Vitamin B12 deficiency**. *Bitemporal hemianopia* - This visual field defect is commonly caused by compression of the **optic chiasm**, most often due to a **pituitary adenoma**. - It results in loss of vision in the outer half of both visual fields and is not linked to **Vitamin B12 deficiency**.
Question 8: Anion-gap metabolic acidosis with decreased vision occurs with the following poisoning.
- A. Cadmium
- B. Mercury
- C. Ethanol
- D. Methanol (Correct Answer)
Explanation: ***Methanol*** - **Methanol poisoning** leads to the formation of **formic acid**, which causes **anion-gap metabolic acidosis** and direct toxicity to the optic nerve, resulting in **decreased vision** and potential **blindness**. - The delayed onset of symptoms (12-24 hours) is due to the time required for methanol to be metabolized into its toxic byproducts. *Cadmium* - **Cadmium poisoning** primarily affects the **kidneys** (proximal tubular dysfunction), **lungs**, and **bones**, leading to conditions like osteomalacia and emphysema. - It does not typically cause **anion-gap metabolic acidosis** or acute visual disturbances. *Mercury* - **Mercury poisoning**, whether elemental, inorganic, or organic, primarily affects the **nervous system** (tremors, ataxia, cognitive impairment) and kidneys. - While it can cause neurological deficits, **decreased vision** and **anion-gap metabolic acidosis** are not characteristic features. *Ethanol* - **Ethanol** (drinking alcohol) poisoning can cause **respiratory depression**, **hypoglycemia**, and **metabolic acidosis** (often ketosis or lactic acidosis at very high levels), but it typically results in a **normal anion gap** unless there are co-ingestions or severe complications. - It does not directly cause **decreased vision** via toxic metabolites like methanol does.
Question 9: Identify the visual field defect shown in the image.
- A. Binasal hemianopia
- B. Bitemporal hemianopia (Correct Answer)
- C. Homonymous hemianopia
- D. Altitudinal defect
Explanation: ***Bitemporal hemianopia*** - The image shows loss of vision in the **temporal (outer) halves of both visual fields**, which is characteristic of bitemporal hemianopia. - This defect typically results from a lesion at the **optic chiasm**, compressing the crossing nasal retinal fibers, often due to a **pituitary tumor**. *Binasal hemianopia* - This condition involves visual loss in the **nasal (inner) halves of both visual fields**, which is the opposite of what is depicted. - It is a rare defect that can be caused by lesions affecting the **uncrossed temporal retinal fibers** on both sides, such as from bilateral carotid artery aneurysms. *Homonymous hemianopia* - A homonymous hemianopia involves the **same half of the visual field in both eyes** (e.g., right visual field loss in both eyes), resulting from a lesion posterior to the optic chiasm. - The image clearly shows different halves affected in each eye (temporal fields), not the same half. *Altitudinal defect* - An altitudinal defect involves the **loss of vision in the upper or lower half of the visual field** in one or both eyes, respecting the horizontal midline. - The visual field loss shown in the image is vertical, affecting the temporal halves, not the upper or lower halves.
Question 10: Early fundoscopic sign in papilloedema is
- A. Blurring of the disc margin (Correct Answer)
- B. Hyperemia of the disc
- C. Splinter hemorrhages
- D. Blurring of the peripapillary nerve fiber layer
Explanation: ***Blurring of the disc margin*** - The earliest fundoscopic sign of **papilledema** is the blurring of the superior and inferior optic disc margins, followed by nasal and then temporal margins. - This blurring is due to the **axoplasmic stasis** and edema in the optic nerve head caused by increased intracranial pressure. *Hyperemia of the disc* - While disc **hyperemia** (redness) can occur in papilledema, it typically manifests after the initial blurring of the disc margins. - It results from **venous engorgement** and capillary dilation within the swollen optic disc. *Splinter hemorrhages* - **Splinter hemorrhages** on or near the optic disc are a sign of more advanced or rapidly progressive papilledema, indicating capillary rupture. - These are not usually the *earliest* sign but suggest severe **venous congestion**. *Blurring of the peripapillary nerve fiber layer* - While the **peripapillary nerve fiber layer** does become edematous and blurred in papilledema, the **disc margin blurring** is the *initial* and most characteristic sign identifying the onset of the condition. - This occurs as part of the overall swelling but is often preceded by changes directly at the disc boundary.
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