Answer 1:
B) Serum acetylcholine receptor antibody (AChR-Ab) titer; Sensitivity >95%

Explanation:
The gold standard for diagnosing acquired MG is the measurement of circulating antibodies against the nicotinic acetylcholine receptor. This test has a sensitivity >95% and high specificity in generalized cases. EMG may support the diagnosis via a decremental response but is less sensitive. The Tensilon test is less reliable in dogs and mostly of historical interest.

​

Answer 2:
C) Progressive exercise-induced appendicular weakness and regurgitation from megaesophagus

Explanation:
Generalized MG typically presents with symmetrical skeletal muscle weakness that worsens with activity and improves with rest. Megaesophagus is common due to impaired neuromuscular control of the esophagus. Regurgitation may lead to aspiration pneumonia, which worsens the prognosis. The disease does not typically involve systemic inflammation or hematologic abnormalities.

​​

​

Answer 3:
C) Pyridostigmine with cautious immunosuppression, oxygen support, and antibiotics

Explanation:
Pyridostigmine is a reversible cholinesterase inhibitor that improves neuromuscular transmission. In cases complicated by aspiration pneumonia, antimicrobial therapy and oxygen are essential. Immunosuppression (e.g., prednisolone) may be introduced cautiously once infection is controlled. NSAIDs are contraindicated in MG due to risk of GI and renal side effects, especially in debilitated patients.

​

​

Answer 4:
C. Third-order neuron (postganglionic)

Explanation:

• The sympathetic pathway to the eye involves three neurons:

  • First-order (central): Hypothalamus → cervical spinal cord (T1–T3).

  • Second-order (preganglionic): Spinal cord → thoracic cavity → vagosympathetic trunk → cranial cervical ganglion.

  • Third-order (postganglionic): Cranial cervical ganglion → through middle ear → orbit and ocular muscles.

• Pharmacologic localization testing with 1% phenylephrine:

  • Rapid dilation (<20 min): Postganglionic lesion due to denervation hypersensitivity.

  • Delayed or absent dilation (>45 min): Central or preganglionic lesion.

• In this case, rapid dilation supports a third-order lesion, commonly associated with otitis media/interna or orbital disease.

​

​

Answer 5:
B. Ptosis of the upper eyelid

Explanation:

• Horner’s syndrome is caused by sympathetic denervation of ocular and periocular structures, leading to:

  • Miosis (loss of sympathetic dilator control)

  • Ptosis (Müller’s muscle paralysis in upper eyelid)

  • Enophthalmos (loss of orbital smooth muscle tone)

  • Third eyelid protrusion (secondary to globe recession)

• Differentiation from other disorders:

  • Mydriasis with absent PLR suggests CN III dysfunction.

  • Absent dazzle reflex may indicate retinal or optic nerve pathology, not Horner’s.

  • Corneal ulceration may cause conjunctival hyperemia and third eyelid elevation but lacks miosis and ptosis.

​

​

Answer 6:
B. Most traumatic or idiopathic cases resolve within weeks to months

Explanation:

• Causes of Horner’s syndrome:

  • First-order lesions: Intracranial disease, spinal cord trauma, neoplasia.

  • Second-order lesions: Brachial plexus injury, thoracic masses, cervical trauma.

  • Third-order lesions: Otitis media/interna, orbital masses, idiopathic causes.

• Idiopathic cases are most common in dogs (up to 50%) and often resolve spontaneously within 6–8 weeks.

• Prognosis is favorable unless caused by underlying neoplasia, severe CNS disease, or progressive infections.

• Treatment focuses on managing the primary cause; phenylephrine can improve cosmetic appearance but doesn’t influence recovery time.